EOS Med Chem, Medicinal Chemical is Big: EOS Med Chem Building block stock list 2345

EOS Med Chem is TOP 100 of China CRO & CMO company, mainly in custom synthesis.
2019 CHINA CPHI E2A62
2019 WORLD CPHI 101C45
FDA New, GMP Do
Clinical Phase II, III Intermediates
GMP Custom synthesis, Full Document

R&D Center: 8000 sq, More than 100 hoods
Pilot Plant: 20000sq, 40 reactors from 5-200L
Manufacturing Site: 800000sq, 40 reactors from 100-5000L
Web:

www.eosmedchem.com
Email: info@eosmedchem.com ; eosmedchem@gmail.com

Name: 2,6-Dimethoxybenzoic acid, CAS: 1466-76-8, stock 25.8g, assay 98.6%, MWt: 182.17, Formula: C9H10O4, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: 2,6-Dimethoxybenzoic acid is a member of organic compounds known as o-methoxybenzoic acids and derivatives.

Name: (S)-Leucic acid, CAS: 13748-90-8, stock 7.6g, assay 98.5%, MWt: 132.16, Formula: C6H12O3, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: (S)-Leucic acid is an amino acid metabolite.

Name: AKT inhibitor VIII AKTi-1/2, CAS: 612847-09-3, stock 11.7g, assay 98.9%, MWt: 551.64, Formula: C34H29N7O, Solubility: DMSO : 20 mg/mL (36.26 mM; Need ultrasonic); H2O : < 0.1 mg/mL (insoluble), Clinical_Informat: No Development Reported, Pathway: Apoptosis;PI3K/Akt/mTOR, Target: Apoptosis;Akt, Biological_Activity: AKT inhibitor VIII (AKTi-1/2) is a cell-permeable quinoxaline compound that has been shown to potently, selectively, allosterically, and reversibly inhibit Akt1, Akt2, and Akt3 activity with IC50s of 58 nM, 210 nM, and 2119 nM, respectively.
IC50 & Target: IC50: 58 nM (Akt1), 210 nM (Akt2), 2119 nM (Akt3)
In Vitro: When LnCaP cells are pretreated with AKT inhibitor VIII and then incubated with TRAIL, a dramatic increase in caspase-3 activity (6-10-fold relative to control or TRAIL alone) is observed. This sensitization of tumor cell lines with AKT inhibitor VIII is not limited to LnCaP cells as similar apoptosis induction is observed in HT29, MCF7, and A2780 cells, among others, with chemosensitizers such as camptothecin, herceptin, and doxorubicin[1]. The furanodiene-induced decrease of p-Akt and Akt expressions is enhanced by the Akt inhibitor VIII pretreatment. Furthermore, the furanodiene-induced PARP cleavage is enhanced by Akt inhibitor VIII pretreatment. The Akt inhibitor VIII shows no effect on cleaved PARP expression but decreases the p-Akt and Akt expressions[2]. AKT inhibitor VIII decreases cell viability and increases phosphatidylserine (PS) translocation to the outer leaflet of the plasma membrane, DNA fragmentation, Caspase-9 cleavage, Caspase-3 activation and PARP proteolysis in hESC lines WA01 (H1) and WA09 (H9) and in a hiPSCs cell line generated in our laboratory (FN2.1)[3].
In Vivo: Mice are dosed with AKT inhibitor VIII (50 mpk, 3 doses, ip, every 90 min) achieving plasma concentrations of 1.5-2.0 μM, and then the animals are tail vein injected with IGF to stimulate Akt phosphorylation. By IP Western, both basal and IGF stimulated Akt1 and Akt2 phosphorylation are inhibited in mouse lung, with no effect on Akt3 phosphorylation[1].

Name: MK-2206 (dihydrochloride) MK-2206 (2HCl), CAS: 1032350-13-2, stock 3.4g, assay 99%, MWt: 480.39, Formula: C25H23Cl2N5O, Solubility: DMSO : 20 mg/mL (41.63 mM; Need ultrasonic); H2O : 3.81 mg/mL (7.93 mM; Need ultrasonic and warming), Clinical_Informat: Phase 2, Pathway: PI3K/Akt/mTOR;Autophagy, Target: Akt;Autophagy, Biological_Activity: MK-2206 dihydrochloride (MK-2206 (2HCl)) is an orally active allosteric AKT inhibitor with IC50s of 5 nM, 12 nM, and 65 nM for AKT1, AKT2, and AKT3, respectively[1].
IC50 & Target: IC50: 5 nM (AKT1), 12 nM (AKT2), 65 nM (AKT3)[1]
In Vitro: MK-2206 dihydrochloride (MK-2206 (2HCl)) (0-10 μM; 72 and 96 hours) inhibits the nasopharyngeal carcinoma (NPC) cell lines CNE-1, CNE-2, HONE-1, and SUNE-1 proliferation in dose- and time-dependent manner[1]. 
MK-2206 dihydrochloride (0-10 μM; 24 and 48 hours) results in a dose-dependent increase in the percentage of cells in G0/G1 phase and a concomitant reduction of cell numbers in S phase in CNE-2 and HONE-1 cells[1]. 
MK-2206 dihydrochloride (0-10 μM; 24 hours) attenuates phosphorylation levels of PRAS40 and S6 in a dose-dependent manner. MK-2206 does not effect phosphorylation of GSKα/β and AKT[1]. 
MK-2206 dihydrochloride (0-10 μM; 24 hours) increases the appearance of LC3-II in CNE-2 cells dose-dependently. Microtubule-associated protein 1 LC3 is an essential autophagy protein[1].
In Vivo: Both MK-2206 dihydrochloride (MK-2206 (2HCl)) doses (oral gavage; 480 mg/kg once a week and 240 mg/kg three times a week; for 2 weeks) can inhibit the growth of human CNE-2 xenografts in nude mice. In the two MK-2206 dihydrochloride groups, the tumor weights are much lighter than the control group. Temporal body weight reduction is observed after receiving the MK-2206 dihydrochloride treatment[1]. 
No other obvious toxicity is observed in mice[1]. 
MK-2206 dihydrochloride (orally; 120 mg/kg; alternate days; for 3 weeks) significantly inhibits tumor growth[2].

Name: CCR2-RA-[R], CAS: 512177-83-2, stock 32.5g, assay 98.7%, MWt: 351.80, Formula: C18H19ClFNO3, Solubility: DMSO : ≥ 125 mg/mL (355.32 mM); H2O : < 0.1 mg/mL (insoluble), Clinical_Informat: No Development Reported, Pathway: Immunology/Inflammation;GPCR/G Protein, Target: CCR;CCR, Biological_Activity: CCR2-RA-[R] is an allosteric antagonist of the C-C chemokine receptor type 2 (CCR2) with an IC50 of 103 nM.
IC50 & Target: IC50: 103 nM (CCR2)[1]
In Vitro: The chemokine receptor CCR2 is a G protein-coupled receptor that is involved in many diseases characterized by chronic inflammation, and therefore a large variety of CCR2 small molecule antagonists has been developed. CCR2-RA-[R] displaces [125I]CCL2 from CCR2 with an pIC50 value of 6.1. The pKD of CCR2-RA-[R] for CCR2 and CCR5 is 8.8±0.1 and 7.0±0.1, respectively[2]. CCR2-RA-[R] inhibits CCR2 non-competitively by blocking activation-associated conformational changes and formation of the G protein-binding interface. The binding pocket of CCR2-RA-[R] is highly enclosed and possesses a balanced combination of hydrophobic and polar features, all of which favors pocket “druggability”[3].

Name: Sorbinil, CAS: 68367-52-2, stock 39.5g, assay 98.7%, MWt: 236.20, Formula: C11H9FN2O3, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Aldose Reductase, Biological_Activity: Sorbinil, is an Aldose reductase inhibitor (ARI).
Sorbinil plays therapeutic role in treating diabetes and diabetic complications, decreases AR activity and inhibits polyol pathway, it to be found comparatively safer than other ARIs for human use[1].

Name: Diammonium Glycyrrhizinate, CAS: 79165-06-3, stock 34.1g, assay 98.3%, MWt: 856.99, Formula: C42H68N2O16, Solubility: 10 mM in DMSO, Clinical_Informat: Launched, Pathway: Others, Target: Others, Biological_Activity: Diammonium Glycyrrhizinate, isolated from the licorice root, is a widely used anti-inflammatory agent[1].

Name: GS-6201 CVT-6883, CAS: 752222-83-6, stock 28.4g, assay 98.4%, MWt: 446.43, Formula: C21H21F3N6O2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein, Target: Adenosine Receptor, Biological_Activity: GS-6201 (CVT-6883) is a selective adenosine A2B receptor antagonist. GS-6201 displays high affinity and selectivity for the human adenosine A2B receptors (Ki=22 nM)[1]. GS-6201 reduces caspase-1 activity in the heart, and attenuates cardiac remodeling after acute myocardial infarction (AMI) in the mouse[2]. GS-62013 attenuates the airway reactivity induced by NECA, AMP, or allergen in sensitized mice[3].
IC50 & Target: Ki: 22 nM (human A2B receptors), 1070 nM (human A3 receptors), 1940 nM (human A1 receptors), 3280 nM (human A2A receptors)[1]
In Vivo: GS-6201 (CVT-6883) (4 mg/kg; i.p.; every 12 h for 14 days) significantly reduces IL-6, TNF-α, E-selectin, ICAM-1, and VCAM plasma levels[2]. 
GS-6201 (4 mg/kg; i.p.; every 12 h for 14 days) leads to a significant attenuation of left and right ventricular enlargement and dysfunction at 7 days, which was maintained at 14 days and also at 28 days[2]. 
GS-6201 (2 mg/kg; p.o.) treatment shows the Cmax, dAUC and t1/2 are 1110 ng/mL, 6500 ng h/mL, and 4.25 hours, respectively[1].

Name: Filibuvir, CAS: 877130-28-4, stock 27.4g, assay 98.1%, MWt: 503.64, Formula: C29H37N5O3, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Anti-infection, Target: HCV, Biological_Activity: Filibuvir is a potent, selective non-nucleoside inhibitor (NNI) of the HCV nonstructural 5B protein (NS5B) RNA-dependent RNA polymerase, and it binds noncovalently in the “Thumb 2” pocket of NS5B. In vitro, filibuvir is equipotent against genotype 1a and 1b replicons, with an EC50 of 59 nM[1].

Name: Tecalcet (Hydrochloride) R-568 (hydrochloride), CAS: 177172-49-5, stock 26g, assay 98.5%, MWt: 340.29, Formula: C18H23Cl2NO, Solubility: DMSO : 50 mg/mL (146.93 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein, Target: CaSR, Biological_Activity: Tecalcet Hydrochloride (R 568 Hydrochloride), an orally active calcimimetic compound, allosterically and positively modulates the calcium-sensing receptor (CaSR). Tecalcet Hydrochloride (R 568 Hydrochloride) increases the sensitivity to activation by extracellular Ca2+[1][2][3].

Name: KT5720, CAS: 108068-98-0, stock 14.9g, assay 98.3%, MWt: 537.61, Formula: C32H31N3O5, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Stem Cell/Wnt;Protein Tyrosine Kinase/RTK, Target: PKA;PKA, Biological_Activity: KT5720 is a cell-permeable, potent, specific, reversible, ATP-competitive inhibitor of protein kinase A (PKA), with a Ki of 60 nM[1][2].
IC50 & Target: Ki: 60 nM (PKA)[1][2].

Name: Sonolisib PX-866, CAS: 502632-66-8, stock 29.3g, assay 98.9%, MWt: 525.59, Formula: C29H35NO8, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: PI3K/Akt/mTOR, Target: PI3K, Biological_Activity: Sonolisib (PX-866), an improved Wortmannin analogue, is an oral, irreversible, and pan-isoform inhibitor of PI3K (IC50=0.1 nM (p110α), 1.0 nM (p120γ), 2.9 nM (p110δ)). Antitumor activity[1][2].
IC50 & Target: IC50: 0.1 nM (p110α), 1.0 nM (p120γ), 2.3 nM (p110δ)[2]
In Vitro: Sonolisib (PX-866) inhibits the production of the secondary messenger phosphatidylinositol-3,4,5-trisphosphate (PIP3) and activation of the PI3K/Akt signaling pathway, which may result in inhibition of tumor cell growth and survival in susceptible tumor cell populations[3].

Name: Gaboxadol (hydrochloride) Lu 02-030 (hydrochloride); THIP (hydrochloride), CAS: 85118-33-8, stock 20.8g, assay 98.6%, MWt: 176.60, Formula: C6H9ClN2O2, Solubility: DMSO : 75 mg/mL (424.69 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Neuronal Signaling;Membrane Transporter/Ion Channel, Target: GABA Receptor;GABA Receptor, Biological_Activity: Gaboxadol hydrochloride (Lu 02-030 hydrochloride) is a selective agonist at GABAA receptors that contain α4-δ subunits, and has anxiolytic and sedative effects[1].
IC50 & Target: GABAA[1]

Name: MK-0608, CAS: 443642-29-3, stock 0.5g, assay 98%, MWt: 280.28, Formula: C12H16N4O4, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Anti-infection, Target: HCV, Biological_Activity: MK-0608 is a potent and orally bioavailable inhibitor of HCV replication in vitro with an EC50 of 0.3 μM (EC90=1.3 μM) in the subgenomic-replicon assay[1].
IC50 & Target: EC50: 0.3 μM (HCV replication)[1]
In Vivo: Oral dosing of MK-0608 results in a potent antiviral effect. In preclinical pharmacokinetic experiments with rats, dogs, and rhesus monkeys, MK-0608 demonstrates good to excellent oral bioavailability (50 to 100%) and long plasma half-lives in dogs and rhesus macaques (9 and 14 h, respectively)[1].

Name: Odiparcil SB-424323, CAS: 137215-12-4, stock 36.3g, assay 98.8%, MWt: 324.35, Formula: C15H16O6S, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Thrombin, Biological_Activity: Odiparcil (SB-424323) is an orally active beta-d-thioxyloside analog with antithrombotic activity associated with a reduced risk of adverse bleeding events. Odiparcil (SB-424323) is indirect thrombin inhibitor that exerts its anticoagulant effect through activation of antithrombin II (heparin cofactor II) [1][2].
IC50 & Target: Thrombin[2]

Name: TTA-Q6, CAS: 910484-28-5, stock 39.2g, assay 98.7%, MWt: 405.80, Formula: C20H15ClF3N3O, Solubility: DMSO : 125 mg/mL (308.03 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Membrane Transporter/Ion Channel;Neuronal Signaling, Target: Calcium Channel;Calcium Channel, Biological_Activity: TTA-Q6 is a selective T-type Ca2+ channel antagonist, used in the neurological disease.
IC50 & Target: T-type Ca2+ channel[1]
In Vitro: TTA-Q6 is a selective T-type Ca2+ channel antagonist, with 14 nM and 590 nM in FLIPR depolarized assaay and FLIPR hyperpolarized assay[1].

Name: Eprotirome KB2115, CAS: 355129-15-6, stock 9.8g, assay 98.3%, MWt: 487.14, Formula: C18H17Br2NO5, Solubility: DMSO : 125 mg/mL (256.60 mM; Need ultrasonic), Clinical_Informat: Phase 3, Pathway: Others, Target: Thyroid Hormone Receptor, Biological_Activity: Eprotirome is a liver-selective thyroid hormone receptor agonist.
IC50 & Target: Thyroid hormone receptor[1]
In Vivo: Eprotirome is a liver-selective thyroid hormone receptor agonist. Histological analysis of livers from mice treated with Eprotirome reveals that Eprotirome elicits a near complete elimination of lipid filled vacuoles that are characteristic of the livers from untreated control mice. Eprotirome treated mice also exhibit increased fasting glucose, but Eprotirome does not increase fasting insulin levels. Glucose levels of mice treated with Eprotirome continues to increase over time, leading to pronounced hyperglycemia by the end of the study. Temperature of mice treated with Eprotirome is decreased relative to untreated control mice[1].

Name: SC75741, CAS: 913822-46-5, stock 38.6g, assay 98.2%, MWt: 565.67, Formula: C29H23N7O2S2, Solubility: DMSO : ≥ 125 mg/mL (220.98 mM), Clinical_Informat: No Development Reported, Pathway: Anti-infection;NF-κB, Target: Influenza Virus;NF-κB, Biological_Activity: SC75741 is a broad and efficient NF-κB inhibitor with an IC50 of 200 nM for p65[1]. SC75741 blocks influenza viruses (IV) replication in non-toxic concentrations. SC75741 impairs DNA binding of the NF-κB subunit p65, resulting in reduced expression of cytokines, chemokines, and pro-apoptotic factors. SC75741 subsequently inhibits caspase activation and blocks caspase-mediated nuclear export of viral ribonucleoproteins[2].
IC50 & Target: 200 nM (NF-κB)[1], caspase[2]
In Vitro: SC75741 (5 μM; 24-96 hours) inhibits long-term A549 cells proliferation[2]. 
SC75741 (1-10 μM; 5.5-65 hours) reduces A549 cells viability in a concentration-dependent manner indicating a cytostatic effect for A549 cells within a time frame of about 50 and 65 hours[2]. 
SC75741 (5 μM; 24 hours) strongly inhibits cleavage of the effector caspase 3 induced upon H7N7-infection[2].
In Vivo: SC75741 (intraperitoneal injection; 15 mg/kg; for 2 days) leads to a reduced propagation of the H5N1 virus mRNA by 90% in the lungs of infected mice[2]. 
The plasma-levels of SC74751 (intravenously of 5 mg/kg and intraperitoneally of 15 mg/kg; for 3.5 and 6 hours) after i.v. administration decreases mono-exponentially and half-life is roughly 40 min. After i.p. administration, elimination of SC75741 seems to be limited by a slow uptake from the peritoneum and a half-life of 55 min is observed[1].

Name: Eniluracil 5-Ethynyluracil;GW776C85, CAS: 59989-18-3, stock 30.9g, assay 98.4%, MWt: 136.11, Formula: C6H4N2O2, Solubility: DMSO : 62.5 mg/mL (459.19 mM; Need ultrasonic), Clinical_Informat: Phase 3, Pathway: Others, Target: Others, Biological_Activity: Eniluracil (5-Ethynyluracil), a uracil analogue and a mechanism-based irreversible inhibitor of dihydropyrimidine dehydrogenase (DPD), increases the oral bioavailability of 5-fluorouracil (5-FU) to 100%, facilitating uniform absorption and predictable toxicity[1].
IC50 & Target: Dihydropyrimidine dehydrogenase[1]

Name: Arterolane OZ 277;RBx 11160, CAS: 664338-39-0, stock 7.7g, assay 98.4%, MWt: 392.53, Formula: C22H36N2O4, Solubility: DMSO : 100 mg/mL (254.76 mM; Need ultrasonic), Clinical_Informat: Launched, Pathway: Anti-infection, Target: Parasite, Biological_Activity: Arterolane is an antimalarial agent, with IC50 of both 1.1 nM against P. falciparum Ro73 and W2, respectively.
IC50 & Target: IC50: 1.1 nM (P. falciparum Ro73), 1.1 nM (P. falciparum W2)[1]
In Vitro: Arterolane (Trioxolane 7; OZ277; RBx-11160) is an antimalarial agent, with IC50s of both 1.1 nM (0.43 ng/mL) against P. falciparum Ro73 and W2, respectively. Arterolane also shows inhibitory activity against several other P. falciparums, with IC50s of 1.0, 1.6, 0.90, 0.91, 1.4, 1.5, 0.83, and 0.84 ng/mL for P. falciparum K1, Fc27, FVO, NF54, HB3, FCB1, ITG2-F6, and MAD20, respectively[1].

Name: Temanogrel APD791, CAS: 887936-68-7, stock 28.7g, assay 98.4%, MWt: 436.50, Formula: C24H28N4O4, Solubility: DMSO : 125 mg/mL (286.37 mM; Need ultrasonic), Clinical_Informat: Phase 1, Pathway: Neuronal Signaling;GPCR/G Protein, Target: 5-HT Receptor;5-HT Receptor, Biological_Activity: Temanogrel is a highly selective 5-HT2A receptor antagonist with a Ki of 4.9 nM.
IC50 & Target: Ki: 4.9 nM (5-HT2A receptor)
In Vitro: Temanogrel is a highly selective 5-HT2A receptor antagonist with a Ki of 4.9 nM. Temanogrel inhibits inositol phosphate accumulation with an IC50 of 5.2 nM. Temanogrel exhibits potent inhibition of serotonin mediated amplification of ADP-stimulated human and dog platelet aggregation (IC50=8.7 and 23.1 nM, respectively)[1]. Pretreatment of aortic rings with Temanogrel prevents the vasoconstriction caused by 20 μM 5-HT in a concentration-dependent manner. Preincubation with Temanogrel also significantly inhibits the 5-HT-stimulated DNA synthesis with an IC50 of 13±7 nM[3].
In Vivo: There are no differences in heart rate or mean arterial pressure between saline-treated and Temanogrel-treated groups at any time during the experiment (that is, for mean arterial pressure, P=0.508 between groups, and P=0.540 for group-time interaction). In dogs assigned to receive Temanogrel, plasma Temanogrel levels show a rapid and sustained increase, averaging 25.5±4.1, 28.7±4.6 and 31.2±4.5 ng/mL, respectively, at 10 min, 1.25 h and 2.25 h after the start of treatment[3].

Name: BMS-688521, CAS: 893397-44-9, stock 17.2g, assay 98.4%, MWt: 536.37, Formula: C26H19Cl2N5O4, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Cytoskeleton, Target: Integrin, Biological_Activity: BMS-688521 is a highly potent, orally active inhibitor of the LFA-1/ICAM interaction, with an IC50 of 2.5 nM in the adhesion assay and an IC50 of 60 nM in the MLR assay. BMS-688521 is efficacious in a mouse allergic eosinophilic lung inflammation model[1].
In Vitro: BMS-688521 in a mouse specific adhesion assay employed mouse splenocytes and a mouse ICAM-1 expression cell line, b.END3. BMS-688521 has an IC50 of 78 nM, representing an approximately 30-fold decrease in activity relative to the human T-cell/HUVEC assay data (ICIC50=2.5 nM)[1].
In Vivo: BMS-688521 (1-10 mg/kg; p.o.; BID for a three-day) is efficacious in a mouse allergic eosinophilic lung inflammation model[1]. 
BMS-688521 (5 mg/kg; p.o.) treatment shows the Cmax, Tmax, AUC, F values are 0.32 μM, 1.0 μM, 1.5 μM h, and 50%, respectively[1]. 
BMS-688521 (1 mg/kg; i.v.) treatment shows the T1/2, MRT, CL and Vss values are 1.6 hours, 1.7 hours, 50 mL/mim/kg, and 5.1 L/kg, respectively in BALB/c mice[1].

Name: PF-00446687, CAS: 862281-92-3, stock 11.2g, assay 98.5%, MWt: 470.59, Formula: C28H36F2N2O2, Solubility: DMSO : 62.5 mg/mL (132.81 mM; Need ultrasonic), Clinical_Informat: Phase 2, Pathway: GPCR/G Protein;Neuronal Signaling, Target: Melanocortin Receptor;Melanocortin Receptor, Biological_Activity: PF-00446687 is a potent, selective melanocortin-4 receptor (MC4R) agonist with EC50 of 12 ± 1 nM[1]. Pf-446687 is brain penetrant[2].
IC50 & Target: EC50: 12 ± 1 nM (MC4R)[1]
In Vitro: PF-00446687 binds MC4 receptor with a Ki of 27±4 nM. PF-00446687 has a relatively weak activity at the MC1, MC3, and MC5 receptors with EC50s of 1.02±0.30 μM, 1.16±0.35 μM, and 1.98±0.20 μM, respectively. The broad off-target profiles of PF-00446687 are assessed in the CEREP Bioprint wide ligand screening panel, with the most potent binding activities being at the σ receptor (Ki=330 nM), the sodium ion channel (Ki=690 nM), and the muscarinic M2 receptor (Ki=730 nM)[1].
In Vivo: Pf-446687 is highly selective for MC4R and is both brain penetrant and stable in vivo. Peripheral administration of the brain penetrant MC3/4R receptor peptide agonist, Melanotan II (MTII), and the highly selective, small molecule MC4R agonist, Pf-446687, enhances partner preference formation in the prairie vole, but not in the non-monogamous meadow vole[2].

Name: SB-657510, CAS: 474960-44-6, stock 27.6g, assay 98%, MWt: 505.81, Formula: C19H22BrClN2O5S, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: SB-657510 is a selective urotensin II (UII) receptor (UT) antagonist. The Ki values are 61, 17, 30, 65 and 56 nM for human, monkey, cat, rat and mouse receptors, respectively. SB-657510 exerts anti-inflammatory effects by inhibiting UII-induced upregulation of inflammatory mediators such as adhesion molecules, cytokines, and tissue factor in human vascular endothelial cells[1][2].
In Vitro: SB-657510 dramatically blocks the UII-induced increase in adhesion between U937 and EA.hy926 cell. SB-657510 (1 μM; 0.5-8 hours) blocks the expression of tissue factor induced by UII in endothelial cells[1]. 
SB-706375 (1-10000 nM) inhibits [Ca2+]i mobilization elicited by 10 nM hU-II with an IC50 of 180 nM[2].
In Vivo: SB-657510 inhibits the progression of high-fat diet induced atherosclerosis and diabetes-associated atherosclerosis[1]. 
Levels of phosphorylated ERK are significantly attenuated in the aorta of SB-657510-treated (30 mg/kg/day) diabetic mice (Male Apoe KO mice)[3].

Name: Pridopidine ACR16;ASP2314;FR310826, CAS: 346688-38-8, stock 1.8g, assay 98.6%, MWt: 281.41, Formula: C15H23NO2S, Solubility: DMSO : 50 mg/mL (177.68 mM; Need ultrasonic), Clinical_Informat: Phase 3, Pathway: GPCR/G Protein;Neuronal Signaling, Target: Dopamine Receptor;Dopamine Receptor, Biological_Activity: Pridopidine, a dopamine (DA) stabilizer, acts as a low affinity dopamine D2 receptor (D2R) antagonist. Pridopidine exerts high affinity towards sigma 1 receptor (S1R) with Ki between 70 and 80 nM, which is ~100× higher than its affinity toward D2R.
IC50 & Target: Ki: 70-80 nM (sigma 1 receptor)[1] 
Dopamine[1] 
Dopamine D2 receptor[1]
In Vitro: Pridopidine, a dopamine (DA) stabilizer, Pridopidine may be a neuromodulatory agent with neuroprotective properties in Huntington disease (HD). To clarify the neuroprotective efficacy of Pridopidine and to explore the potential underling molecular mechanism, the ability of Pridopidine is evaluated to protect cells from apoptosis and to eventually activate pro-survival targets. Administration of Pridopidine (150 μM), the most effective dose, significantly reduces apoptosis in immortalized striatal knock-in cells expressing endogenous levels of mutant Htt (STHdh111/111) and markedly enhances phosphorylation state of prosurvival kinase ERK[2].
In Vivo: Pridopidine is known to act as a low affinity D2R antagonist. Pridopidine’s activity may be attributed to binding the sigma 1 receptor (S1R), an endoplasmic reticulum (ER). To strengthen the hypothesis that the BDNF pathway is upregulated due to activation of the S1R, SD rats are treated with lower doses of Pridopidine (range 0.3-60 mg/kg), and analysed the expression of seven selected genes in the BDNF pathway by qPCR. Pridopidine doses of 3 and 15 mg/kg in rats occupy 57±2% and 85±2% of S1R, respectively, and both do not show occupancy of the D2R, as determined by in vivo PET imaging. The significant occupancy proportion of the D2R (44-66%) is observed only at a dose of 60 mg/kg. This PET study supports the conclusion that the upregulation of genes in rats treated with 15 mg/kg Pridopidine are a result of specific activation of the S1R. At 30 mg/kg, partial/low occupancy of the D2R is at levels of 22-33% (assuming linearity), and S1R is saturated. Indeed, qPCR analysis reveals that the upregulation of EGR1 (already up at 3 mg/kg), EGR2, HOMER1A, KLF5, and ARC expression are upregulated at the low 15 mg/kg dose and expression of CDNK1A and CEBPB are significantly upregulated from a low dose of 30 mg/kg (CEBPB is significantly increased at 3 mg/kg but not at 15 mg/kg)[1]. To further confirm the beneficial effect of Pridopidine on HD motor phenotype and to elucidate whether Pridopidine may act also as neuroprotective agent, preclinical studies in R6/2 mice have been undertaken. Daily administration of Pridopidine at a dose of 5 mg/kg, the most effective dose with no adverse effects, starting at the pre-symptomatic stage at 5 weeks for 6 weeks, significantly preserves motor function and prevents the progressive and dramatic motor worsening commonly observed in R6/2 mice. The beneficial effects of Pridopidine are maintained for about 4 weeks, after which mice show a slight worsening in performing both the horizontal ladder task and the open field. In addition, according to a Kaplan-Meier survival curve analysis, Pridopidine efficiently extends lifespan in the same mice[2].

Name: Ximelagatran H 376/95, CAS: 192939-46-1, stock 40g, assay 99%, MWt: 473.57, Formula: C24H35N5O5, Solubility: Methanol : 62.5 mg/mL (131.98 mM; Need ultrasonic); DMSO : 250 mg/mL (527.91 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Thrombin, Biological_Activity: Ximelagatran (H 376/95) is an orally active thrombin inhibitor that selectively and competitively inhibits both free and clot-bound thrombin. Ximelagatran is an anticoagulant agent with a rapid onset of anticoagulant effect, predictable, dose-dependent pharmcokinetics and pharmacodynamics[1][2].
In Vitro: Ximelagatran is an orally administered direct thrombin inhibitor under development as an anticoagulant agent for prophylaxis against and treatment of thromboembolism. Ximelagatran is rapidly absorbed and quickly converted into its active form Melagatran, a reversible, active-site inhibitor of both free and clot-bound thrombin that has stable and reproducible pharmacokinetic properties. Initial studies have shown Ximelagatran to have good efficacy and safety in the prevention of venous thromboembolism after total knee or total hip replacement[3].

Name: Ritanserin R 55667, CAS: 87051-43-2, stock 9.8g, assay 98.8%, MWt: 477.57, Formula: C27H25F2N3OS, Solubility: DMSO : 25 mg/mL (52.35 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Neuronal Signaling;GPCR/G Protein, Target: 5-HT Receptor;5-HT Receptor, Biological_Activity: Ritanserin (R 55667) is a highly potent, relatively selective, orally active, long acting antagonist of 5-HT2 receptor, with an IC50 of 0.9 nM, less active on Histamine H1, Dopamine D2, Adrenergic α1, Adrenergic α2 receptors[1].
IC50 & Target: IC50: 0.9 nM (5-HT2 receptor), 35 nM (H1 receptor), 70 nM (D2 receptor), 97 nM (α1 receptor), 150 nM (α2 receptor)[1]
In Vitro: Ritanserin (R 55667) is a highly potent, relatively selective, long acting antagonist of 5-HT2 receptor, with an IC50 of 0.9 nM, less active on Histamine-H1 (IC50, 35 nM), Dopamine-D2 (IC50, 70 nM), Adrenergic-α1 (IC50, 97 nM), Adrenergic-α2 receptor (IC50, 150 nM)[1].

Name: Cruzain-IN-1, CAS: 1199523-24-4, stock 15.3g, assay 98.2%, MWt: 300.27, Formula: C14H10F2N6, Solubility: H2O : < 0.1 mg/mL (insoluble); DMSO : 80 mg/mL (266.43 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Cruzain-IN-1 is a covalent and reversible Cruzain inhibitor, with an IC50 of 10 nM.
IC50 & Target: IC50:10 nM (Cruzain)[1].

Name: S 18986, CAS: 175340-20-2, stock 2.3g, assay 98.2%, MWt: 224.28, Formula: C10H12N2O2S, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Membrane Transporter/Ion Channel;Neuronal Signaling, Target: iGluR;iGluR, Biological_Activity: S 18986 is a selective, orally active, brain penetrant positive allosteric modulator of AMPA-type receptors. S 18986 shows cognitive enhancing properties in rodents. S 18986 activates the release of noradrenaline and acetylcholine in rat hippocampus and enhances rat memory in object-recognition tests[1][2].
In Vivo: S 18986 is robust memory-enhancing effects in middle-aged animals compared with aged ones. S 18986 shows antiamnesic properties in middle-aged rodents in spatial memory models [1]. 
S 18986 (5-50 mg/kg; i.p.) significantly increases both the induction and the maintenance of 4 and 20 bursts tetanus-evoked potentiation[1].

Name: Pifithrin-μ PFTμ;2-Phenylethynesulfonamide, CAS: 64984-31-2, stock 15g, assay 98.8%, MWt: 181.21, Formula: C8H7NO2S, Solubility: DMSO : ≥ 108 mg/mL (595.99 mM), Clinical_Informat: No Development Reported, Pathway: Autophagy;Metabolic Enzyme/Protease;Cell Cycle/DNA Damage;Apoptosis, Target: Autophagy;HSP;HSP;MDM-2/p53, Biological_Activity: Pifithrin-μ is an inhibitor of p53 and HSP70, with antitumor and neuroprotective activity.
IC50 & Target: p53[1], HSP70[2]
In Vitro: Pifithrin-μ (10 μM) is a p53 inhibitor, which inhibits p53 binding to mitochondria by reducing its affinity to antiapoptotic proteins Bcl-xL and Bcl-2 but has no effect on p53-dependent transactivation, activity of caspases 2, 8, 9 and 10 in a cell-free system, or NF-κB-dependent transcription[1]. Pifithrin-μ (PES) time- and dose-dependently reduces viability in A549 cells, with IC50s of 44.9 and 25.7 µM at 24 h and 48 h. Pifithrin-μ (20 μM) suppresses the cell migration, induces cell cycle arrest and cell apoptosis in A549 and H460 cells. Pifithrin-μ (10 or 20 µM) inhibits activities of AKT, ERK, and Hsp70 in A549 and H460 cells. Pifithrin-μ (20 µM) sensitizes A549 and H460 cell lines to TRAIL-induced cell proliferation inhibition and apoptosis[2].
In Vivo: Pifithrin-μ (40 mg/kg, i.p.) shows no protective effect against doses of radiation that cause gastrointestinal syndrome in mice[1]. Pifithrin-μ (PES, 10 mg/kg) shows antitumor effect in mice bearing A549 cells[2]. Pifithrin-μ exhibits neuroprotective effect with the P53-inhibitor pifithrin-μ after cardiac arrest in a rodent model[3].

Name: Toloxatone MD 69276, CAS: 29218-27-7, stock 21.6g, assay 98.6%, MWt: 207.23, Formula: C11H13NO3, Solubility: DMSO : 125 mg/mL (603.19 mM; Need ultrasonic), Clinical_Informat: Launched, Pathway: Neuronal Signaling, Target: Monoamine Oxidase, Biological_Activity: Toloxatone (MD 69276) is a reversible monoamine oxidase A (MAOA) inhibitor[1]. Antidepressant[1].
IC50 & Target: MAOA[1]

Name: Ditolylguanidine 1,3-Di-o-tolylguanidine;DTG, CAS: 97-39-2, stock 37g, assay 98.2%, MWt: 239.32, Formula: C15H17N3, Solubility: DMSO : 150 mg/mL (626.78 mM; Need ultrasonic); H2O : < 0.1 mg/mL (insoluble), Clinical_Informat: Phase 4, Pathway: Neuronal Signaling;GPCR/G Protein, Target: Sigma Receptor;Sigma Receptor, Biological_Activity: Ditolylguanidine (1,3-Di-o-tolylguanidine) is an agonist of sigma receptor (σ1/σ2 receptor)[1].
IC50 & Target: Sigma receptor[1]

Name: Fadrozole hydrochloride CGS 16949A, CAS: 102676-31-3, stock 32.6g, assay 98.3%, MWt: 259.73, Formula: C14H14ClN3, Solubility: H2O : 100 mg/mL (385.02 mM; Need ultrasonic); DMSO : 100 mg/mL (385.02 mM; Need ultrasonic and warming), Clinical_Informat: No Development Reported, Pathway: Others, Target: Aromatase, Biological_Activity: Fadrozole hydrochloride is a potent, selective and nonsteroidal inhibitor of aromatase with an IC50 of 6.4 nM.
IC50 & Target: IC50: 6.4 nM (aromatase)[1]
In Vitro: Fadrozole hydrochloride is a potent, selective and nonsteroidal inhibitor of aromatase with an IC50 of 6.4 nM. In hamster ovarian slices, Fadrozole hydrochloride inhibits the production of estrogen with an IC50 of 0.03 μM. The production of progesterone is inhibited with an IC50 of 120 μM. Synthesis of other cytochrome P-450 dependent steroids can be suppressed to various degrees with higher doses of Fadrozole hydrochloride[1].
In Vivo: Fadrozole hydrochloride is able to inhibit the aromatase-mediated androstenedione-induced uterine hypertrophy in immature female rats with an ED50 of 0.03 mg/kg when given orally. In the same model, aminoglutethimide elicits the same effect with an ED50 of 30 mg/kg when given orally[1]. Fadrozole hydrochloride prevents the development of both benign and malignant spontaneus mammary neoplasns in female Sprague-Dawley rats. It also slows the spontaneous development of ptuitary pars distalis adenomas in female rats, and reduces the incidence of spontaneous hepatocellular tumours in male and female rats[2]. Administration of Fadrozole hydrochloride in male and female mice suppresses the production of 17b-estradiol, accompanied with a 70% reduction in parasite burden. This protective effect is associated in male mice with a recovery of the specific cellular immune response. Interleukin-6 (IL-6) serum levels, and its production by splenocytes, is augmented by 80%, together with a 10-fold increase in its expression in testes of infected male mice. Fadrozole hydrochloride treatment returns these levels to baseline values[3].

Name: Pericyazine Propericiazine;RP 8909, CAS: 2622-26-6, stock 29.9g, assay 98.9%, MWt: 365.49, Formula: C21H23N3OS, Solubility: DMSO : 250 mg/mL (684.01 mM; Need ultrasonic), Clinical_Informat: Launched, Pathway: GPCR/G Protein;Neuronal Signaling, Target: Dopamine Receptor;Dopamine Receptor, Biological_Activity: Pericyazine (Propericiazine) is a first-generation antipsychotic drug that is used as an adjunct to the short-term management of severe anxiety states and psychosis[1]. Pericyazine (Propericiazine) is a selective D2-dopamine receptor antagonist[2][3].
IC50 & Target: D2-dopamine receptor[2]

Name: Cyamemazine, CAS: 3546-03-0, stock 23.6g, assay 98.8%, MWt: 323.46, Formula: C19H21N3S, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Neuronal Signaling;GPCR/G Protein, Target: 5-HT Receptor;5-HT Receptor, Biological_Activity: Cyamemazine is a neuroleptic agent that contains the phenothiazine chromophore. Cyamemazine is often used as an anxiolytic. Cyamemazine is a potent 5-HT3 (Ki of 12 nM), 5-HT2A (Ki = 1.5 nM) and 5-HT2C (Ki of 75 nM) receptors antagonist with antipsychotic activity[1][2].
In Vitro: Cyamemazine exhibits a high affinity for dopamine receptors, which is consistent with its antipsychotic activity. The antagonist activity of Cyamemazine at muscarinic receptors is consistent with its affinity for M1 (Ki = 13 nM), M2 (Ki = 42 nM), M3 (Ki = 321 nM), M4 (Ki = 12 nM), and M5 (Ki = 35 nM) receptors[1].
In Vivo: Cyamemazine behaves as an antagonist at the 5-HT3, 5-HT2C, and 5-HT2A receptors in 5-HT3-dependent contraction of isolated guinea pig ileum and bradycardic responses in rats, in 5-HT2C-dependent phospholipase C stimulation in the rat brain membrane, and in 5-HT2A-dependent contraction of isolated rat aorta rings and isolated guinea pig trachea. Cyamemazine antagonizes 5-HT3 and 5-HT2C receptors and that this effect is partially involved in its therapeutic activity in anxiety disorders. Acute administration of low doses of Cyamemazine can reduces extracellular dopamine and metabolite concentrations in rat striatum[1].

Name: Gallopamil Methoxyverapamil, CAS: 16662-47-8, stock 36.3g, assay 98.1%, MWt: 484.63, Formula: C28H40N2O5, Solubility: DMSO : 100 mg/mL (206.34 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Membrane Transporter/Ion Channel;Neuronal Signaling, Target: Calcium Channel;Calcium Channel, Biological_Activity: Gallopamil (Methoxyverapamil), a methoxy derivative of Verapamil, is a phenylalkylamine calcium antagonist[1]. Gallopamil inhibits acid secretion in a concentration-dependent manner with an IC50 of 10.9 μM[2]. Gallopamil is a potent antiarrhythmic and vasodilator agent[3].
In Vivo: Gallopamil (Methoxyverapamil; i.v.; 0.2 mg/kg; for 5 min) markedly reduces ventricular tachycardia (VT) and totally prevents fibrillation (VF). Gallopamil significantly reduces systolic and diastolic blood pressure measured 5 min after injection without markedly influencing heart rate[3].

Name: Marizomib Salinosporamide A;NPI-0052, CAS: 437742-34-2, stock 32.8g, assay 98.7%, MWt: 313.78, Formula: C15H20ClNO4, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Proteasome, Biological_Activity: Marizomib (Salinosporamide A) is second-generation, irreversible, brain-penetrant, pan-proteasome inhibitor. Marizomib inhibits the CT-L (β5), CT-T-laspase-like (C-L, β1) and trypsin-like (T-L, β2) activities of the 20S proteasome (IC50=3.5, 28, and 430 nM, respectively)[1][2][3].
IC50 & Target: IC50: 3.5 nM (CT-L), 28 nM (CT-T-laspase-like), 430 nM (trypsin-like)[1]
In Vitro: Marizomib (Salinosporamide A) (0.1-10000 nM; 72 hours) effectively reduces survival of D-54 and U-251 cells in a dose-dependent manner. The IC50s are ∼52 nM for U-251 and ∼20 nM for D-54[1]. 
Marizomib (24 hours; 60 nM) induces apoptosis and caspase-3 activation in glioma cells[1].
In Vivo: Marizomib (Salinosporamide A) (0.15 mg/kg; i.v; twice a week for three weeks) significantly decreases tumor growth, and is not associated with any toxicity[3].

Name: Elinogrel PRT060128, CAS: 936500-94-6, stock 19.3g, assay 98.9%, MWt: 523.95, Formula: C20H15ClFN5O5S2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein, Target: P2Y Receptor, Biological_Activity: Elinogrel (PRT060128) is a potent, direct acting, competitive, and reversible platelet P2Y12 antagonist (IC50=20 nM). It is orally and intravenously available and has potent antiplatelet effects[1].
IC50 & Target: IC50: 20 nM (P2Y12)[2]

Name: GSK-690693, CAS: 937174-76-0, stock 31.9g, assay 98.1%, MWt: 425.48, Formula: C21H27N7O3, Solubility: DMSO : 25 mg/mL (58.76 mM; Need ultrasonic), Clinical_Informat: Phase 1, Pathway: PI3K/Akt/mTOR;Autophagy;Epigenetics;PI3K/Akt/mTOR, Target: Akt;Autophagy;AMPK;AMPK, Biological_Activity: GSK-690693 is an ATP-competitive pan-Akt inhibitor with IC50s of 2, 13, 9 nM for Akt1, Akt2 and Akt3, respectively. GSK-690693, an AMP-activated protein kinase (AMPK) inhibitor, affects Unc-51-like autophagy activating kinase 1 (ULK1) activity and robustly inhibits STING-dependent IRF3 activation[1][2][3].
IC50 & Target: IC50: 2 nM (Akt1), 13 nM (Akt2), 9 nM (Akt3)
In Vitro: GSK690693 is very selective for the Akt isoforms versus the majority of kinases in other families. However, GSK690693 is less selective for members of the AGC kinase family including PKA, PrkX, and PKC isozymes with IC50 of 24 nM, 5 nM, and 2-21 nM, respectively. GSK690693 also potently inhibits AMPK and DAPK3 from the CAMK family with IC50 of 50 nM and 81 nM, respectively, and PAK4, 5, and 6 from the STE family with IC50 of 10 nM, 52 nM, and 6 nM, respectively. GSK690693 inhibits the phosphorylation of GSK3β in tumor cells with IC50 ranging from 43 nM to 150 nM. GSK690693 treatment leads to a dose-dependent increase in the nuclear accumulation of the transcription factor FOXO3A. GSK690693 potently inhibits the proliferation of T47D, ZR-75-1, BT474, HCC1954, MDA-MB-453, and LNCaP cells with IC50 of 72 nM, 79 nM, 86 nM, 119 nM, 975 nM, and 147 nM, respectively. GSK690693 treatment induces apoptosis at concentrations > 100 nM in both LNCaP and BT474 cells[1]. Consistent with the role of AKT in cell survival, GSK690693 induces apoptosis in sensitive ALL cell lines[2].
In Vivo: A single administration of GSK690693 inhibits GSK3β phosphorylation in human breast carcinoma (BT474) xenografts in a dose- and time-dependent manner. Similarly, GSK690693 induces a reduction in phosphorylation of the Akt substrates, PRAS40, and FKHR/FKHRL1. GSK690693 also results in an acute increase in blood glucose, returning to baseline 8 to 10 hours after drug administration. Administration of GSK690693 induces reductions in phosphorylated Akt substrates in vivo, and potently inhibits the growth of human SKOV-3 ovarian, LNCaP prostate, and BT474 and HCC-1954 breast carcinoma xenografts, with maximal inhibition of 58% to 75% at the dose of 30 mg/kg/day[1]. GSK690693 exhibits efficacy irrespective of the mechanism of Akt activation involved. GSK690693 is most effective in delaying tumor progression in Lck-MyrAkt2 mice expressing a membrane-bound, constitutively active form of Akt[3].

Name: SNT-207707, CAS: 1064662-40-3, stock 11g, assay 98%, MWt: 550.18, Formula: C32H44ClN5O, Solubility: DMSO : ≥ 250 mg/mL (454.40 mM); Methanol : 250 mg/mL (454.40 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein;Neuronal Signaling, Target: Melanocortin Receptor;Melanocortin Receptor, Biological_Activity: SNT-207707 is a selective, potent and orally active melanocortin MC-4 receptor antagonist with an IC50 of 8 nM (binding) and 5 nM (function) on the MC-4 receptor.
IC50 & Target: IC50: 8 nM (binding MC-4), 5 nM (function MC-4)[1]
In Vitro: SNT-207707 binds to the MC-4 receptor with an affinity of 8 nM and shows a more than 200-fold selectivity vs. MC-3 and MC-5. SNT207858 is a 22 nM MC-4 antagonist with a 170-fold selectivity vs. MC-3 and a 40-fold selectivity versus MC-5[1].
In Vivo: Single subcutaneous injection of 20 mg/kg of SNT-207707 distinctly increases food intake of the mice. Once daily oral administration of both compounds SNT207858 and SNT-207707 starting the day after tumor implantation significantly reduces the tumor induced weight loss[1].

Name: SNT-207858, CAS: 1104080-42-3, stock 27.8g, assay 98.5%, MWt: 689.54, Formula: C32H45Cl4N5O3, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein;Neuronal Signaling, Target: Melanocortin Receptor;Melanocortin Receptor, Biological_Activity: SNT207858 is a selective, blood brain barrier penetrating, potent and orally active melanocortin-4 (MC-4) receptor antagonist. SNT207858 has an IC50 of 22 nM (binding) and 11 nM (function) on the MC-4 receptor[1].
IC50 & Target: IC50: 22 nM (binding, MC-4 receptor), 11 nM (function, MC-4 receptor)[1]
In Vitro: SNT207858 binds to the MC-4 receptor with an affinity of 22 nM and shows a 170-fold selectivity vs. MC-3 and a 40-fold selectivity vs. MC-5[1].
In Vivo: SNT207858 (30 mg/kg; oral administration; once daily; 15 days) significantly reduces the tumor induced weight loss in mice[1].

Name: CVT-12012, CAS: 1018675-35-8, stock 34.6g, assay 98.4%, MWt: 434.41, Formula: C21H21F3N4O3, Solubility: DMSO : 125 mg/mL (287.75 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Stearoyl-CoA Desaturase (SCD), Biological_Activity: CVT-12012 is a potent and orally bioavailable stearoyl-coA desaturase (SCD) inhibitor, with IC50s of 38 nM, 6.1 nM for rat microsomal and human HEPG2, respectively.
IC50 & Target: IC50: 38 nM (rat microsomal), 6.1 nM (human HEPG2)[1][2].
In Vitro: CVT-12012 (Compound 5b) displays the highest potency in both the microsomal and the HEPG2 SCD assays (IC50 38 nM and 6.1 nM, respectively) compared to the other methyl-substituted compounds[1].
In Vivo: In a rat PK study, CVT-12012 demonstrates good oral bioavailability (78%). It appears that the oral absorption of CVT-12012 is not affected by a significant Pgp efflux, which is expected based on Caco-2 assay result. The plasma clearance of CVT-12012 is high (88 mL/min/kg) with elimination half-life of approximately 1 h[1].

Name: PF-03654746 (Tosylate), CAS: 1039399-17-1, stock 38.4g, assay 98.9%, MWt: 494.59, Formula: C25H32F2N2O4S, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Immunology/Inflammation;GPCR/G Protein;Neuronal Signaling, Target: Histamine Receptor;Histamine Receptor;Histamine Receptor, Biological_Activity: PF-03654746 Tosylate is a potent and selective histamine H3 receptor antagonist with high brain penetration. PF-03654746 Tosylate reduces allergen-induced nasal symptoms[1]. PF-03654746 Tosylate has potential for treatment of human cognitive disorders, improves cognitive efficacy and disease-modifying effects in Alzheimer's disease (AD)[2].
IC50 & Target: H3 receptor[1]

Name: GW-803430 GW-3430, CAS: 515141-51-2, stock 26.1g, assay 98.5%, MWt: 481.99, Formula: C25H24ClN3O3S, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein;Neuronal Signaling, Target: MCHR1 (GPR24);MCHR1 (GPR24), Biological_Activity: GW-803430 (GW-3430) is a potent and selective melanin-concentrating hormone receptor 1 (MCH R1) antagonist with a pIC50 of 9.3. GW-803430 is orally active in an animal model of obesity[1].
IC50 & Target: pIC50: 9.3 (MCH R1)[1]
In Vitro: GW-803430 demonstrates a potent antagonist activity towards MCH induced MCHR1 receptor with an IC50 value of ~13 nM[2].
In Vivo: GW-803430 (0.3, 3, and 15 mg/kg ; oral administration; once daily) causes a sustained dose-dependent weight loss relative to vehicle controls[1]. 
GW-803430 is a suitable compound for its good pharmacokinetic properties (bioavailability=31%, t1/2=11 h) and brain penetration (6:1 brain:plasma concentration) in mice[1].

Name: Verubulin (hydrochloride) MPC-6827 (hydrochloride), CAS: 917369-31-4, stock 23.1g, assay 98.3%, MWt: 315.80, Formula: C17H18ClN3O, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Cell Cycle/DNA Damage;Cytoskeleton, Target: Microtubule/Tubulin;Microtubule/Tubulin, Biological_Activity: Verubulin hydrochloride (MPC-6827 hydrochloride) is a blood brain barrier permeable microtubule-disrupting agent, with potent and broad-spectrum in vitro and in vivo cytotoxic activities. Verubulin hydrochloride (MPC-6827 hydrochloride) exhibits potent anticancer activity in human MX-1 breast and other mouse xenograft cancer models. Verubulin hydrochloride (MPC 6827 hydrochloride) is a promising candidate for the treatment of multiple cancer types[1][2].
IC50 & Target: microtubule[1]

Name: Purpurogallin, CAS: 569-77-7, stock 10.4g, assay 98.9%, MWt: 220.18, Formula: C11H8O5, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Xanthine Oxidase, Biological_Activity: Purpurogallin is a naturally phenol extracted from the plants of Quercus spp, has potent xanthine oxidase (XO) inhibitory activity with an IC50 of 0.2 µM. Purpurogallin has antioxidant and anti-inflammatory effects[1][2][3].
IC50 & Target: IC50: 0.2 µM (xanthine oxidase)[3]
In Vitro: Purpurogallin (50 or 100 µM; 7 or 25 hours; BV2 murine microglial cells) treatment attenuates the production of pro-inflammatory cytokines, including interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α) by suppressing their mRNA and protein expression in LPS-stimulated BV2 microglial cells[1]. 
Purpurogallin (100 µM; 75-120 minutes; BV2 murine microglial cells) exhibits anti-inflammatory properties by suppressing the phosphatidylinositol 3-kinase/Akt and mitogen-activated protein kinase signaling pathways in LPS-stimulated BV2 microglial cells[1].
In Vivo: Purpurogallin (100-400 μg/kg; intraperitoneal injection; for 48 or 72 hours; male Sprague-Dawley rats) exerts its neuroinflammation effect through the dual effect of inhibiting IL-6 and TNF-α mRNA expression and reducing HMGB1 protein and mRNA expression[2].

Name: Vofopitant GR 205171, CAS: 168266-90-8, stock 31.7g, assay 98%, MWt: 432.44, Formula: C21H23F3N6O, Solubility: 10 mM in DMSO, Clinical_Informat: Phase 2, Pathway: Neuronal Signaling;GPCR/G Protein, Target: Neurokinin Receptor;Neurokinin Receptor, Biological_Activity: Vofopitant is potent tachykinin NK1 receptor antagonist, with pKis of 10.6, 9.5, and 9.8 for human, rat and ferret NK1 receptor, respectively.
IC50 & Target: pKi: 10.6 (Human NK1 receptor), 9.5 (Rat NK1 receptor), 9.8 (Ferret NK1 receptor)[1]
In Vitro: Vofopitant is potent tachykinin NK1 receptor antagonist, with pKis of 10.6, 9.5, and 9.8 for human, rat and ferret NK1 receptor, respectively. Vofopitant less potently inhibits rat 5-HT1A, bovine 5-HT1D, rat 5-HT2A, rat Histamine H1, guinea-pig Histamine H2 and rat Ca2+ channel, with pKis of 6.3, 6.6, 6.5, 6.5, 6.6, and 5.6, respectively. Vofopitant shows negligible affinity at NK2 and NK3, with pIC50 of <5.0[1]. GR205171 (300 µM) potentiates the effects of paroxetine on cortical [5-HT]ext, and inhibits paroxetine-induced increase in [5-HT]ext in the dorsal raphe nucleus[3].
In Vivo: Vofopitant (GR205171, 30 mg/kg, s.c.) increases the number of choices of the 25-s delayed reward in a T-maze[2]. Vofopitant (GR205171, 30 mg/kg, i.p.) increases the extracellular 5-HT levels in the frontal cortex of paroxetine-treated wild-type mice, rather than in wild-type mice and paroxetine-treated NK1 receptor knockout mice[3].

Name: CCMI, CAS: 917837-54-8, stock 22.5g, assay 98.8%, MWt: 388.25, Formula: C19H15Cl2N3O2, Solubility: DMSO : 100 mg/mL (257.57 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Neuronal Signaling;Membrane Transporter/Ion Channel, Target: nAChR;nAChR, Biological_Activity: CCMI is a potent and selective α7 nAChR-positive allosteric modulator, does not bind to or activate α7 nAChRs via the orthosteric site, and causes significant positive modulation of agonist-induced currents at α7 nAChRs. CCMI has potential in CNS diseases with cognitive dysfunction[1].
IC50 & Target: α7 nAChR[1]
In Vitro: CCMI (Compound 6) is a potent and selective α7 nAChR-positive allosteric modulator, does not bind to or activate α7 nAChRs via the orthosteric site, and causes significant positive modulation of agonist-induced currents at α7 nAChRs[1].

Name: NS 1738 NSC 213859, CAS: 501684-93-1, stock 27.6g, assay 98.5%, MWt: 365.13, Formula: C14H9Cl2F3N2O2, Solubility: H2O : < 0.1 mg/mL (insoluble); DMSO : ≥ 300 mg/mL (821.63 mM), Clinical_Informat: No Development Reported, Pathway: Neuronal Signaling;Membrane Transporter/Ion Channel, Target: nAChR;nAChR, Biological_Activity: NS 1738 (NSC 213859) is a novel positive allosteric modulator of the α7 nAChR, with respect to positive modulation of α7 nAChR (EC50=3.4 μM in oocyte experiments).
IC50 & Target: EC50: 3.4 μM (α7 nAChR, in oocyte experiments)[1]
In Vitro: NS 1738 acts by increasing the peak amplitude of acetylcholine (ACh)-evoked currents at all concentrations; thus, it increased the maximal efficacy of ACh. Plotting peak current amplitude against the logarithm of the NS 1738 concentration used for preincubation reveals a sigmoidal concentration-response relationship that is well fit by the Hill equation (EC50=3.4 μM). Under similar experimental conditions, NS 1738 shows comparable efficacy and potency at the rat α7 nAChR (EC50=3.9 μM)[1].
In Vivo: To estimate the ability of NS 1738 to permeate the blood-brain barrier, rats are administered 10 mg/kg NS 1738 intraperitoneally. Peak brain concentrations are measured approximately 30 min after injection, and they amount to ~80 ng/mL (~200 nM) at this dose. The ratio between the amount of compound entering the brain and that in plasma is AUCbrain /AUCplasma=0.50. The half-life in plasma is estimated to 42 min. Incubation of NS1738 with isolated liver microsomes in vitro indicates that approximately 60 and 75% of NS 1738 is metabolized via the cytochrome P450 system in mouse and rat, respectively, within 1 h. Adult rats administered NS 1738 at 10 and 30 mg/kg i.p. immediately following the initial exposure to a juvenile rat (T1) display significant decreases in the investigative duration of a subsequent exposure to the same juvenile (T2) 2 h later (T2/T1 ratio of 0.69±0.13 and 0.61±0.07, respectively)[1].

Name: VU 0238429, CAS: 1160247-92-6, stock 6.5g, assay 98.5%, MWt: 351.28, Formula: C17H12F3NO4, Solubility: DMSO : ≥ 150 mg/mL (427.01 mM); H2O : < 0.1 mg/mL (insoluble), Clinical_Informat: No Development Reported, Pathway: Neuronal Signaling;GPCR/G Protein, Target: mAChR;mAChR, Biological_Activity: VU 0238429 is positive allosteric modulator of muscarinic acetylcholine receptor subtype 5 (mAChR5 or M5), with an EC50 of 1.16 μM.
IC50 & Target: EC50: 1.16 μM (mAChR5)[1].
In Vitro: VU 0238429 is positive allosteric modulator of mAChR5 (M5), with an EC50 of 1.16 μM, >30-fold selectivity versus M1 and M3, with no M2 or M4 potentiator activity[1].

Name: JNJ-5207852, CAS: 398473-34-2, stock 20.5g, assay 98%, MWt: 316.48, Formula: C20H32N2O, Solubility: DMSO : 77.5 mg/mL (244.88 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Immunology/Inflammation;GPCR/G Protein;Neuronal Signaling, Target: Histamine Receptor;Histamine Receptor;Histamine Receptor, Biological_Activity: JNJ-5207852 is a selective and potent histamine H3 receptor (H3R) antagonist, with pKis of 8.9, 9.24 for rat and human H3R, respectively.
IC50 & Target: pKi: 8.9 (rat H3R), 9.24 (human H3R)[1][2].
In Vivo: In mice and rats, JNJ-5207852 (1-10mg/kg s.c.) increases time spent awake and decreases REM sleep and slow-wave sleep, but fails to have an effect on wakefulness or sleep in H3 receptor knockout mice. No rebound hypersomnolence, as measured by slow-wave delta power, is observed. The wake promoting effects of this H3 receptor antagonist are not associated with hypermotility. A 4-week daily treatment of mice with JNJ-5207852 (10 mg/kg i.p.) does not lead to a change in body weight, possibly due to the compound being a neutral antagonist at the H3 receptor. JNJ-5207852 is extensively absorbed after oral administration and reaches high brain levels[1].

Name: Cenisertib AS-703569;R-763, CAS: 871357-89-0, stock 4.6g, assay 98.1%, MWt: 451.54, Formula: C24H30FN7O, Solubility: DMSO : 250 mg/mL (553.66 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Protein Tyrosine Kinase/RTK;Protein Tyrosine Kinase/RTK;Cell Cycle/DNA Damage;Epigenetics;PI3K/Akt/mTOR;JAK/STAT Signaling;Stem Cell/Wnt, Target: Bcr-Abl;FLT3;Aurora Kinase;Aurora Kinase;Akt;STAT;STAT, Biological_Activity: Cenisertib (AS-703569) is a multi-kinase inhibitor that blocks the activity of Aurora-kinase-A/B, ABL1, AKT, STAT5 and FLT3. Cenisertib induces major growth-inhibitory effects by blocking the activity of several different molecular targets in neoplastic mast cells (MC)[1]. Cenisertib inhibits tumor growth in xenograft models of pancreatic, breast, colon, ovarian, and lung tumors and leukemia[2].
IC50 & Target: Aurora-kinase-A/B, ABL1, AKT, STAT5 and FLT3[1]
In Vitro: Cenisertib (AS-703569) (1-1000 nM; for 48 hours) induces dose-dependent inhibition of proliferation in primary neoplastic mast cells (MC) [1]. 
Cenisertib (5-100 nM; for 24 hours) induces a substantial G2/M cell cycle arrest at low nanomolar concentrations in all MC lines[1]. 
Cenisertib (1-1000 nM; for 24 hours)induces apoptosis in HMC-1.1, HMC-1.2, C2, and NI-1 cells in a dose-dependent manner[1]. 
Cenisertib (5-500 nM; for 24 hours) induces cleavage of caspase 3 in both HMC-1 sub-clones as well as in C2 and NI-1 cells[1]. 
In Vivo: Cenisertib (AS-703569) (orally; 7 or 10 mg/kg/day; for 3 days) significantly suppresses tumor growth.

Name: AM211 AM211 free acid, CAS: 1175526-27-8, stock 39.8g, assay 98.7%, MWt: 500.51, Formula: C27H27F3N2O4, Solubility: H2O : < 0.1 mg/mL (insoluble); DMSO : ≥ 125 mg/mL (249.75 mM), Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein, Target: Prostaglandin Receptor, Biological_Activity: AM211 is a potent, selective and orally bioavailable prostaglandin D2 (PGD2) receptor type 2 (DP2) antagonist, with IC50s of 4.9 nM, 7.8 nM, 4.9 nM, 10.4 nM for human, mouse, guinea pig, and rat DP2, respectively.
IC50 & Target: IC50: 4.9 nM (Human DP2), 7.8 nM (Mouse DP2), 4.9 nM (Guinea pig DP2), 10.4 nM (Rat DP2)[1]
In Vitro: AM211 is a potent, selective and orally bioavailable prostaglandin D2 (PGD2) receptor type 2 (DP2) antagonist, with IC50s of 4.9 nM, 7.8 nM, 4.9 nM, 10.4 nM for human, mouse, guinea pig, and rat DP2, respectively. In the presence of 0.2% serum albumin, AM211 inhibits radiolabeled PGD2 binding to human, mouse, guinea pig, and rat DP2 with IC50 values of 12.2, 20.1, 22.9, and 34.2 nM, respectively. AM211 displays high selectivity for DP2 versus other receptors in the prostanoid family, with IC50 values for the inhibition of radioligand binding to human TP, IP, DP1, and FP of more than 100 μM. AM211 (100 μM) shows no activity at COX-1, COX-2 enzymes as well as PPAR family of nuclear receptors[1].
In Vivo: AM211 (1, 10, and 30 mg/kg, p.o.) dose-dependently decreases in the number of DK-PGD2-induced peripheral blood leukocytes, with a calculated ED50 of 0.85 mg/kg. AM211 (30 mg/kg) also decreases antigen-induced pulmonary inflammation in guinea pigs. AM211 (10 mg/kg, p.o.) causes significant decrease in ovalbumin (OVA)-induced sneezing in a mouse model of allergic rhinitis[1].

Name: Pyroxamide, CAS: 382180-17-8, stock 37.2g, assay 98.6%, MWt: 265.31, Formula: C13H19N3O3, Solubility: DMSO : 125 mg/mL (471.15 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Epigenetics;Cell Cycle/DNA Damage, Target: HDAC;HDAC, Biological_Activity: Pyroxamide is a potent inhibitor of histone deacetylase 1 (HDAC1) with an ID50 of 100 nM. Pyroxamide can induce apoptosis and cell cycle arrest in leukemia.
IC50 & Target: ID50: 100 nM[1]
In Vitro: Pyroxamide (1.25-20.0 μM; 24-72 hours) suppresses RD and RH30B cells growth, pyroxamide resulted in 44% dead cells for 72 h at 20.0 μM, results in 86% dead cells in culture[1].
Pyroxamide (10.0-20.0 μM; 48 hours) shows sub-G1 fractions of 45.0% and 72.3% at 10.0 and 20.0 μM, respectively[1].

Name: CP-547632, CAS: 252003-65-9, stock 30.9g, assay 98.1%, MWt: 532.40, Formula: C20H24BrF2N5O3S, Solubility: DMSO : ≥ 115 mg/mL (216.00 mM), Clinical_Informat: No Development Reported, Pathway: Protein Tyrosine Kinase/RTK;Protein Tyrosine Kinase/RTK, Target: VEGFR;FGFR, Biological_Activity: CP-547632 is a well-tolerated, orally-bioavailable inhibitor of the VEGFR-2 and basic fibroblast growth factor (FGF) kinases with IC50s of 11 nM and 9 nM, respectively. CP-547632 is an ATP-competitive kinase inhibitor and it is selective relative to epidermal growth factor receptor, platelet-derived growth factor β, and other related TKs. CP-547632 has antitumor efficacy[1].
IC50 & Target: IC50: 11 nM (VEGFR2), 9 nM (FGF2)[1]
In Vitro: CP-547632 (1-1000 nM; 1 hours) inhibits VEGF-stimulated VEGFR-2 phosphorylation in a dose-dependent fashion, with an IC50 value of 6 nM[1].
In Vivo: CP-547632 (p.o.; 6.25-100 mg/kg/day; for 10-24 days) causes a dose-dependent inhibition of growth in Colo-205, DLD-1, and MDA-MB-231 xenografts[1]. 
CP-547632 (oral; 50 mg/kg) of a single oral dose of 50 mg/kg yieldes plasma concentrations above 500 ng/ml for 12 hours[1].

Name: XL888, CAS: 1149705-71-4, stock 24.4g, assay 99%, MWt: 503.64, Formula: C29H37N5O3, Solubility: DMSO : ≥ 100 mg/mL (198.55 mM), Clinical_Informat: Phase 1, Pathway: Metabolic Enzyme/Protease;Cell Cycle/DNA Damage, Target: HSP;HSP, Biological_Activity: XL888 is a heat shock protein-90 (HSP90) inhibitor, with an IC50 of 24 nM.
IC50 & Target: IC50: 24 nM (HSP90)[3]
In Vitro: XL888 is a heat shock protein-90 (HSP90) inhibitor. Treatment with XL888 leads to dose dependent decreases in the growth of all the cell lines with no significant difference in IC50 values observed between the naive and resistance pairs of cell lines (t=0.25, p=0.82). Treatment of all of the vemurafenib resistant cell lines with XL888 (300 nM) induces high levels (>66%) of apoptosis, caspase-3 cleavage and loss of mitochondrial membrane potential (TMRM) in every cell line tested. Treatment of cell lines that are naïve, intrinsically resistant and with acquired vemurafenib resistance with XL888 (300 nM) leads to robust time-dependent increases in the expression of HSP70 isoform 1 (HSP71)[2].
In Vivo: Treatment of the established M245 tumors with XL888 (125 mg/kg 3× week) leads to a significant slowing of tumor growth (P=0.017) without any effect upon animal weights. Analysis of xenograft specimens by LC-MRM shows a marked increase in intratumoral HSP70 expression following XL888 treatment[1]. It is noted that the XL888 is well tolerated by the mice, with no significant alterations in body weigh observed over the study period. LC-MRM mediated analysis of xenograft samples following 15-days of XL888 treatment shows a robust (8.6-fold) increase in intratumoral HSP70 expression compare to controls[2].

Name: MRS 1754, CAS: 264622-58-4, stock 19.8g, assay 98.6%, MWt: 486.52, Formula: C26H26N6O4, Solubility: H2O : < 0.1 mg/mL (insoluble); DMSO : 15 mg/mL (30.83 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein, Target: Adenosine Receptor, Biological_Activity: MRS 1754 is a selective antagonist radioligand for A2B adenosine receptor with very low affinity for A1 and A3 receptors of both humans and rats[1].
IC50 & Target: A2B Adenosine Receptor[1]
In Vitro: The most potent displacer of [3H]MRS 1754 binding is MRS 1754. The Ki value for displacement of [3H]MRS 1754 binding to human A2B receptors expressed in HEK-293 cell membranes is 1.45±0.21 nM[1].

Name: Veliflapon BAY X 1005;DG-031, CAS: 128253-31-6, stock 8.5g, assay 98.1%, MWt: 361.43, Formula: C23H23NO3, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein;Metabolic Enzyme/Protease, Target: Leukotriene Receptor;Lipoxygenase, Biological_Activity: Veliflapon (BAY X 1005; DG-031) is an orally active inhibitor of the synthesis of the leukotrienes B4 and C4[1]. Veliflapon is shown to be a selective inhibitor of the formation of 5-lipoxygenase-derived metabolites in vitro, without effects on other routes of arachidonic acid metabolism[2].
In Vitro: Veliflapon (BAY X 1005; DG-031) effectively inhibits the synthesis of LTB4 in A23187-stimulated leukocytes from rats, mice and humans (IC50s of 0.026, 0.039 and 0.22 μM, respectively) as well as the formation of LTC4 (IC50 of 0.021 μM) in mouse peritoneal macrophages stimulated with opsonized zymosan[2]. 
In Vivo: Veliflapon (BAY X 1005; DG-031; diet; 18.8 mg/kg/day for 16 weeks ) inhibits atherogenesis[3]. 
Veliflapon after topical (18 μg/ear) and oral (48.7 mg/kg) administration has antiedematous effects in the arachidonic acid-induced mouse ear inflammation test[3]. 
Veliflapon is potent (11.8 and 6.7 mg/kg p.o. at 1 and 5 hours, respectively) and has a long duration of action (ED40 of 16 hours, 70 mg/kg p.o.) in the rat whole blood ex vivo leukotriene B4 inhibition assay[3].

Name: MRK-560, CAS: 677772-84-8, stock 15.3g, assay 98.6%, MWt: 517.92, Formula: C19H17ClF5NO4S2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Stem Cell/Wnt;Neuronal Signaling, Target: γ-secretase;γ-secretase, Biological_Activity: MRK-560 is a potent, orally bioavailable and brain-penetrant γ-secretase inhibitor[1].
IC50 & Target: γ-secretase[1]

Name: Begacestat GSI-953, CAS: 769169-27-9, stock 19.7g, assay 99%, MWt: 391.74, Formula: C9H8ClF6NO3S2, Solubility: 10 mM in DMSO, Clinical_Informat: Phase 1, Pathway: Stem Cell/Wnt;Neuronal Signaling, Target: γ-secretase;γ-secretase, Biological_Activity: Begacestat (GSI-953) is a selective thiophene sulfonamide inhibitor of amyloid precursor protein gamma-secretase (IC50Aβ40=15 nM) for the treatment of Alzheimer's disease[1].
IC50 & Target: IC50: 15 nM (Aβ40)[1].
In Vivo: Begacestat (5 mg/kg, p.o. in mice) treatment for 4 h significantly reduces the Aβ40 and Aβ42 in brain (37% lowering of brain Aβ40 and 25% lowering of Aβ40 observed)[1]. 
Begacestat (GSI-953: 0, 2.5, 5, or 10 mg/kg, oral gavage, 3 h) results in a dose-dependent reversal of contextual fear conditioning deficits when compound is orally administered 3 h before training. Significant deficits are observed after treatment with 2.5 mg/kg Begacestat, and there is some reversal of this at 5 mg/kg and full reversal at 10 mg/kg compared with vehicle-dosed Tg2576 mice[2]. 
A dosage-related trend of slightly lower percentages of SP CD4+ cells in males at all dosages (SP CD4+ cells=~11% in controls compared with ~7% to ~9% in Begacestat-dosed animals) and females at 2000 mg/kg/day (SP CD4+ cells=~10% in controls compared with ~8% in Begacestat-dosed animals) is observed[2].

Name: Compound E Compound E (secretase inhibitor)；DuPont E, CAS: 209986-17-4, stock 14.4g, assay 98.9%, MWt: 490.50, Formula: C27H24F2N4O3, Solubility: DMSO : 100 mg/mL (203.87 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Stem Cell/Wnt;Neuronal Signaling, Target: γ-secretase;γ-secretase, Biological_Activity: Compound E is a γ-secretase inhibitor. Compound E bloks β-amyloid(40), β-amyloid(42), and Notch γ-secretase cleavage with IC50s of 0.24, 0.37, 0.32 nM, respectively.
IC50 & Target: IC50: 0.24 nM (β-amyloid(40)), 0.37 nM (β-amyloid(42)), 0.24 nM (Notch)[1]
In Vitro: Compound E reduces the proliferation of T47D, and MCF-7 cell lines by less than 50% at a concentration of 50 μM[1].

Name: Zinterol MJ 9184, CAS: 37000-20-7, stock 11.1g, assay 98.8%, MWt: 378.49, Formula: C19H26N2O4S, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein;Neuronal Signaling, Target: Adrenergic Receptor;Adrenergic Receptor, Biological_Activity: Zinterol (MJ 9184) is a potent and selective β2-adrenoceptor agonist[1]. Zinterol increases ICa in a concentration-dependent manner with an EC50 of 2.2 nM[2].
IC50 & Target: β2-adrenoceptor[1]
In Vivo: Zinterol (2.5 μg/kg i.v. bolus over 5 s) leads to ventricular arrhythmias including premature ventricular complexes (PVCs) and runs of ventricular tachycardia (VT) in heart failure (HF) rabbits. Zinterol at a lower dose (1 μg/kg i.v, n=4) does not induce ventricular arrhythmias in HF rabbits[3].

Name: L-745870, CAS: 158985-00-3, stock 3.1g, assay 98.4%, MWt: 326.82, Formula: C18H19ClN4, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein;Neuronal Signaling, Target: Dopamine Receptor;Dopamine Receptor, Biological_Activity: L-745870 is a high-affinity, selective and orally active human dopamine D4 receptor antagonist with a Ki of 0.43 nM, and considerably weaker D2 (Ki of 960 nM) and D3 (Ki of 2300 nM) receptors affinity. L-745870 has excellent brain penetration[1][2][3].
IC50 & Target: Ki: 0.43 nM (Human dopamine D4 receptor), 960 nM (Human dopamine D2 receptor), 2300 nM (Human dopamine D3 receptor)[1][3]
In Vitro: In vitro pharmacological studies revealed that L-745870 is an antagonist at human D4 receptors, in that L-745870 is capable of antagonizing the ability of D4 receptors to inhibit agonist-induced stimulation of [35S]-GTPgS binding; blocking the inhibition of forskolin-stimulated adenylate cyclase activity in transfected human embryonic kidney (HEK293) and Chinese hamster ovary (CHO) cells; blocking dopamine-induced inhibition of Ca2+ currents in transfected GH4C1 pituitary cells; inhibiting D4 activation of cloned G protein-coupled inwardly rectifying K+ channels; and antagonizing dopamine-induced stimulation of extracellular acidification in transfected cells[1][2].
In Vivo: L-745870 has good pharmacokinetic properties (20-60% oral bioavailability and plasma t1/2 2.1-2.8 hours) in both rat and monkey, and excellent brain penetration with high brain to plasma ratios in rat[2]. 
Evaluation of L-745870 in surrogate marker assays demonstrates that this compound is freely available for biological activity in the brain and that at doses of 5 to 60 mg/kg p.o. L-745870 would occupy 50% D4 receptors in the brain. L-745870 has no effect on apomorphine-induced stereotypy in rats but does induce catalepsy in mice, albeit at a high dose of 100 mg/kg p.o. that is likely to occupy D2 receptors in vivo. High doses of L-745870 might also be expected to cause extrapyramidal symptoms in primates because the levels in the CNS at these doses would be sufficient to antagonize D2 receptors. Following oral administration to squirrel monkeys, L745870 (10 mg/kg p.o.) induces mild sedation and extrapyramidal motor symptoms, notably bradykinesia, became apparent at 30 mg/kg. Lower doses of L-745870 has no observable behavioural effects in monkeys[1][2].

Name: GSK-25, CAS: 874119-56-9, stock 2.5g, assay 98.8%, MWt: 513.33, Formula: C24H16Cl2F2N6O, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: TGF-beta/Smad;Stem Cell/Wnt;Cell Cycle/DNA Damage;MAPK/ERK Pathway, Target: ROCK;ROCK;ROCK;Ribosomal S6 Kinase (RSK), Biological_Activity: GSK-25 is a potent, selective and orally bioavailable ROCK1 inhibitor (IC50=7 nM). GSK-25 maintains good selectivity against a panel of 31 kinases (>100 fold), as well as RSK1 and p70S6K (RSK1: IC50=398 nM, p70S6K: IC50=1 μM). GSK-25 inhibits P450 profile (IC50s of 2.5, 5.2, 2.5 µM for CYP2C9, CYP2D6, CYP3A4, respectively)[1].
In Vivo: GSK-25 (Rat aorta IC50=256 nM) is profiled in a spontaneously hypertensive rat (SHR) model of hypertension. At 30 mg/kg (p.o.), GSK-25 induces a 25 mmHg (t=3 hours) drop in blood pressure[1]. 
GSK-25 has promising oral bioavailability (49% in male Sprague-Dawley rats and 19% in monkey), good half-life (1.8 hours in rat and 2.2 hours in monkey)[1].

Name: TUG-424, CAS: 1082058-99-8, stock 39.1g, assay 98.7%, MWt: 264.32, Formula: C18H16O2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein, Target: GPR40, Biological_Activity: TUG-424 is a potent and selective free fatty acid receptor 1 (FFA1/GPR40) agonist with an EC50 of 32 nM. TUG-424 significantly increases glucose-stimulated insulin secretion at 100 nM. TUG-424 may serve to explore the role of FFA1 in metabolic diseases such as diabetes or obesity[1].
IC50 & Target: EC50: 32 nM (FFA1/GPR40)[1]
In Vitro: Increasing concentrations (100 nM to 10 µM) of TUG-424 enhances glucose-stimulated insulin secretion significantly already at 100 nM and with a maximal effect at 3 µM. The approximately 2-fold stimulation of secretion by TUG-424 in the presence of 12 mM glucose is comparable to that induced by palmitate in the presence of the same glucose concentration. Basal insulin secretion at 2.8 mM glucose is slightly but significantly reduces by TUG-424[1].

Name: Emicerfont GW876008, CAS: 786701-13-1, stock 3.4g, assay 98.7%, MWt: 404.46, Formula: C22H24N6O2, Solubility: 10 mM in DMSO, Clinical_Informat: Phase 2, Pathway: GPCR/G Protein, Target: CRFR, Biological_Activity: Emicerfont is a corticotropin-releasing factor type 1 (CRF1) receptor antagonist with an IC50 of 66 nM.
IC50 & Target: IC50: 66 nM (CRF1 receptor)[1]
In Vitro: Emicerfont is a corticotropin-releasing factor type 1 (CRF1) receptor antagonist with an IC50 of 66 nM[1].
In Vivo: At concentration of 10 mg/kg, Emicerfont reduces i.c.v. CRF-induced gerbil forepaw treading and marmoset defensive postures. Emicerfont also reduces rat pup ultrasonic vocalization at concentration of 30 mg/kg[1].

Name: Elagolix sodium NBI-56418 sodium, CAS: 832720-36-2, stock 32.2g, assay 98.8%, MWt: 653.57, Formula: C32H29F5N3NaO5, Solubility: DMSO : 50 mg/mL (76.50 mM; Need ultrasonic); H2O : ≥ 50 mg/mL (76.50 mM), Clinical_Informat: Launched, Pathway: GPCR/G Protein, Target: GNRH Receptor, Biological_Activity: Elagolix sodium is a human GnRH receptor (GnRHR) antagonist with an IC50 and Ki of 0.25 and 3.7 nM, respectively.
IC50 & Target: IC50: 0.25 nM (GnRHR)[1]
Ki: 3.7 nM (GnRHR)[2]
In Vitro: Elagolix sodium is a human GnRH receptor (GnRHR) antagonist with an IC50 of 0.25 nM in Kinase assay. Elagolix sodium has advanced to phase 3 trials for the treatment of endometriosis and uterine fibroids. Elagolix sodium also shows NFAT inhibition with an IC50 of 5.4 nM and effectively blocks Ca2+ flux with an IC50 of 0.86 nM[1]. Kinase assay also demonstrates that Elagolix sodium is a human GnRH receptor (GnRHR) antagonist with a Ki value of 3.7 nM[2].

Name: GPP78 CAY10618, CAS: 1202580-59-3, stock 32.3g, assay 98.2%, MWt: 439.55, Formula: C27H29N5O, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease;Autophagy, Target: Nampt;Autophagy, Biological_Activity: GPP78 (CAY10618) is a potent Nampt inhibitor with an IC50 of 3.0 nM for nicotinamide adenine dinucleotide (NAD) depletion. GPP78 is cytotoxic to neuroblastoma cell line SH-SY5Y cells with an IC50 of 3.8 nM by inducing autophagy. GPP78 has anti-cancer and anti-inflammatory effects[1][2].
IC50 & Target: Nampt[1]; 
Autophagy[1]
In Vitro: GPP78 (Compound 8; 10 nM; 24-40 hours; SH-SY5Y cells) treatment with cells, punctate staining of LC3-II and the formation of autophagolysosomes are observable. LC3-II is membrane-bound and is present in autophagosomes[1]. 
GPP78 (Compound 8) inhibits the growth of most cell lines tested, with nanomolar potency (GI50) in cell lines derived from leukemia, lung, CNS, colon, melanoma, ovarian, renal, and prostate cancers. GPP78 appears truly cytotoxic in melanoma cell lines, while in the others it is mainly cytostatic[1].
In Vivo: GPP78 (10 mg/kg; intraperitoneal injection; daily; 1 hour or 6 hours after SCI; for 19 days; male adult CD1 mice) treatment reduces the severity of spinal cord trauma in SCI mice[2].

Name: SR8278, CAS: 1254944-66-5, stock 3.9g, assay 98.4%, MWt: 361.48, Formula: C18H19NO3S2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: SR8278 is a competitive nuclear heme receptor REV-ERB synthetic antagonist. SR8278 inhibits the REV-ERBα transcriptional repression activity with an EC50 of 0.47μM. SR8278 is used to regulate the metabolism in organisms and study biological rhythm[1][2].
IC50 & Target: REV-ERB[1]

Name: NB001 HTS 09836, CAS: 686301-48-4, stock 32.6g, assay 98.4%, MWt: 264.33, Formula: C12H20N6O, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein, Target: Adenylate Cyclase, Biological_Activity: NB001 (HTS 09836) is an adenylcyclase 1 (AC1) inhibitor which has effect on neural and non-neural pain by modulating AC1 activity[1].
IC50 & Target: AC1[1]

Name: GSK-269984A, CAS: 892664-04-9, stock 16.6g, assay 98.2%, MWt: 429.22, Formula: C20H14Cl2FNNaO3, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein, Target: Prostaglandin Receptor, Biological_Activity: GSK-269984A is a Prostaglandin E2 Receptor 1 (EP1) antagonist with a pIC50 of 7.9.
IC50 & Target: pIC50: 7.9 (Prostaglandin E2 Receptor 1 (EP1))[1]
In Vitro: Results from [3H]-PGE2 binding assay in CHO cells overexpressing the human EP1 receptor demonstrate that GSK-269984A is an antagonist of EP1 receptor with a pIC50 of 7.9. GSK-269984A is found to cause a concentration-dependent rightward shift of the PGE2 dose-response curve and Schild analysis shows that GSK-269984A is a competitive antagonist with pA2 8.1±0.3 and slope 1.0[1].
In Vivo: GSK-269984A demonstrates an ED50 of 2.6 mg/kg (po), with the 10 mg/kg dose showing equivalent reversal of hypersensitivity to the standard. GSK-269984A displays moderate blood clearance in the rat
and dog and high clearance in the monkey which is reflected in the half-life for each species[1].

Name: MDR-1339 DWK-1339, CAS: 1018946-38-7, stock 34.7g, assay 98.3%, MWt: 326.39, Formula: C20H22O4, Solubility: DMSO : ≥ 83.3 mg/mL (255.22 mM), Clinical_Informat: No Development Reported, Pathway: Neuronal Signaling, Target: Amyloid-β, Biological_Activity: MDR-1339 (DWK-1339) is an orally active and blood-brain-barrier-permeable Aβ-aggregation inhibitor, used in the research of Alzheimer's disease.
IC50 & Target: Amyloid-β[1]
In Vitro: MDR-1339 is an Aβ-aggregation inhibitor, and shows no significant inhibition a panel of CYP isozymes, while it slightly inhibits CYP2C8 (IC50, 31.4 μM). MDR-1339 (3.1-50 μM) dose-dependently blocks the formation of Aβ aggregates, and disaggregates Aβ fibrils. MDR-1339 (1.5-10 μM) also protects cells from this Aβ-induced toxicity[1].
In Vivo: MDR-1339 (0.1-10 mg/kg, p.o.) dose-dependently restores the passive avoidance responses in mice models of Alzheimer's disease (AD), with an ED50 of 0.19 mg/kg. MDR-1339 (30 and 100 mg/kg, p.o. daily for 8 weeks) significantly improves spontaneous alternation, and reduces the Aβ1-40 and Aβ1-42 levels in APP/PS1 mice[1].

Name: Aminopterin 4-Aminofolic acid; APGA, CAS: 54-62-6, stock 19.7g, assay 98.7%, MWt: 440.41, Formula: C19H20N8O5, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Cell Cycle/DNA Damage, Target: Antifolate, Biological_Activity: Aminopterin (4-Aminofolic acid), the 4-amino derivative of folic acid, is a folic acid antagonist. Aminopterin catalyses the reduction of folic acid to tetrahydrofolic acid, and competitively inhibits dihydrofolate reductase (DHFR) with a Ki of 3.7 pM. Aminopterin has anticancer and immunosuppressive activity. Aminopterin is used in treatment of pediatric leukemia[1][2].
In Vitro: The IC50 value of Aminopterin (4-Aminofolic acid) against CCRF-CEM cells during 72 h of exposure is 4.4 nM[2]. 
Aminopterin (4-Aminofolic acid) produces a marked inhibition of mitosis in low concentrations in human leukemic leukocytes[4].

Name: Lometrexol DDATHF, CAS: 106400-81-1, stock 18.3g, assay 98.9%, MWt: 443.45, Formula: C21H25N5O6, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Apoptosis;Cell Cycle/DNA Damage, Target: Apoptosis;Antifolate, Biological_Activity: Lometrexol (DDATHF), an antipurine antifolate, can inhibit the activity of glycinamide ribonucleotide formyltransferase (GARFT) by tightly binding with it. Lometrexol can further inhibit de novo purine synthesis, causing abnormal cell proliferation and apoptosis, even cell cycle arrest. Lometrexol has anticancer activity[1].
IC50 & Target: Antifolate and GARFT[1]
In Vitro: Lometrexol (DDATHF) induces abnormal proliferation and apoptosis exist in neural tube defects (NTDs)[1]. 
Lometrexol significantly reduces the expression of PH3[1]. 
In Vivo: Lometrexol (DDATHF; i.p.; 15-60 mg/kg; on gestation day 7.5) increases the rate of embryonic resorption and growth retardation in a dose-dependent manner[1]. 
Lometrexol (i.p.; 40 mg/kg) maximally inhibits GARFT activity after at 6 hours and thereafter gradually increases with time but remains significantly lower than control even at 96 hours. Levels of ATP, GTP, dATP and dGTP of NTDs embryonic brain tissue decreases significantly at 6 h, and more significantly over time[1].

Name: Osanetant SR142801, CAS: 160492-56-8, stock 2.2g, assay 98.1%, MWt: 606.62, Formula: C35H41Cl2N3O2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Neuronal Signaling;GPCR/G Protein, Target: Neurokinin Receptor;Neurokinin Receptor, Biological_Activity: Osanetant (SR142801) is a selective NK3 receptor antagonist. Osanetant produces anxiolytic- and antidepressant-like effects and is researched for the treatment of schizophrenia[1].
In Vivo: Osanetant (SR142801; po; 1-10 mg/kg; 60 min before testing) significantly increases social interaction time[1]. 
Osanetant (ip; 5 and 10 mg/kg; 30 min before testing) decreases immobility time[1].

Name: Dihydrexidine DAR-0100, CAS: 123039-93-0, stock 22.1g, assay 98.1%, MWt: 267.32, Formula: C17H17NO2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein;Neuronal Signaling, Target: Dopamine Receptor;Dopamine Receptor, Biological_Activity: Dihydrexidine (DAR-100) is a high potent, selective and full efficacy D1 dopamine receptor agonist with an IC50 of 10 nM, and displays some affinity for the D2 receptor. Dihydrexidine (DAR-100) exhibits potent antiparkinsonian activity[1][2][3].
IC50 & Target: IC50: 10 nM (D1 dopamine receptor)[1]

Name: Irosustat STX64;BN83495;667-Coumate, CAS: 288628-05-7, stock 35.9g, assay 98.1%, MWt: 309.34, Formula: C14H15NO5S, Solubility: DMSO : ≥ 150 mg/mL (484.90 mM), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Irosustat is a potent steroid sulfatase inhibitor, with an IC50 of 8 nM, and exhibits anti-breast cancer activity.
IC50 & Target: IC50: 8 nM (Steroid sulfatase)[1], 0.2 nM (Steroid sulfatase, MCF-7 cells)[2]
In Vitro: Irosustat (667 COUMATE) is a potent steroid sulfatase inhibitor, with an IC50 of 8 nM[1]. Irosustat (667 COUMATE) inhibits steroid sulphatase (STS) activity in MCF-7 cells with an IC50 of 0.2 nM, but has no effect on the morphology or proliferation of MCF-7 cells at 10 μM[2].
In Vivo: Irosustat potently inhibits rat liver, with inhibition of >90% when at a 1 mg/kg concentration. Irosustat (2 mg/kg, p.o. for 5 d) blocks the uterine growth stimulated by oestrone sulfate (E1S) in ovariectomized rats. In addition, Irosustat (2, 10 mg/kg, p.o.) plus E1S dose-dependently decreases the growth of NMU-induced mammary tumors in ovariectomized rats[1]. Irosustat (667 COUMATE; 10 mg/kg, p.o.) shows 97.9 ± 0.06% inhibition on steroid sulphatase (STS) activity in rat liver[2].

Name: Tectochrysin Techtochrysin;NSC 80687, CAS: 520-28-5, stock 14.2g, assay 98.3%, MWt: 268.26, Formula: C16H12O4, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: NF-κB, Target: NF-κB, Biological_Activity: Tectochrysin (Techtochrysin) is one of the major flavonoids of Alpinia oxyphylla Miquel. Tectochrysin (Techtochrysin) inhibits activity of NF-κB.
IC50 & Target: NF-κB p50[1]
In Vitro: Tectochrysin (Techtochrysin) inhibits activity of NF-κB. Tectochrysin (Techtochrysin) binds directly to the p50 unit. Tectochrysin (Techtochrysin) concentration-dependently inhibits the translocation of p50 and p65 into the nucleus through inhibition of the phosphorylation of IκB. To assess the inhibitory effect of Tectochrysin on cell growth of colon cancer cells (SW480, HCT116), cell viability is analyzed by MTT assay. The cells are treated with varying concentrations of Tectochrysin (Techtochrysin) (1, 5, 10 μg/mL) for 24 h. Tectochrysin (Techtochrysin) inhibits cell growth in colon cancer cells in a concentration-dependent manner. Tectochrysin (Techtochrysin) inhibits SW480 cells growth with IC50 value of 6.3 μg/mL and HCT116 cells growth with IC50 value of 8.4 μg/mL. Morphologic observation shows that the cells are reduced in size by the treatment of NSC 80687 (10 μg/mL) in SW480 cells and HCT116 cells. However, Tectochrysin (Techtochrysin) is not cytotoxic in the normal CCD-18co cells in the tested concentration by MTT assay. To delineate whether the induction of apoptotic cell death is critical for cell growth inhibition by NSC 80687, changes are evaluated in the chromatin morphology of cells using DAPI staining. To further characterize the apoptotic cell death by Tectochrysin (Techtochrysin), TUNEL staining assays are performed, and then the labeled cells are analyzed by fluorescence microscopy. Apoptotic cells number (DAPI-positive TUNEL stained cells) in SW480 cell is increased to 1 and 58 % by 0 and 10 μg/mL NSC 80687, respectively, and 1 and 54 % by 0 and 10 μg/mL Tectochrysin in HCT116[1].
In Vivo: To elucidate the antitumor effects of Tectochrysin in in vivo, the tumor growth in colon cancer xenograft-bearing nude mice following Tectochrysin (NSC 80687) treatments is investigated. In HCT116 xenograft studies, Tectochrysin (NSC 80687) is administrated i.p. twice per week for 3 weeks to mice with tumors ranging from 200 to 300 mm3 in volume. The mice are weighed twice per week. The changes in body weights between the control and the Tectochrysin (NSC 80687)-treated mice (n=10) are not remarkably different during the experiment. However, On day 21, the final tumor weights are recorded. Tumor weights and volumes in mice treated with Tectochrysin (NSC 80687) at 5 mg/kg doses are 57.9 % and 46.4 % of the vehicle group, respectively[1].

Name: (S)-Glutamic acid (+)-L-Glutamic acid, CAS: 56-86-0, stock 27.8g, assay 98.9%, MWt: 147.13, Formula: C5H9NO4, Solubility: H2O : 6.25 mg/mL (42.48 mM; Need ultrasonic); DMSO : 2 mg/mL (13.59 mM; ultrasonic and warming and heat to 60°C), Clinical_Informat: No Development Reported, Pathway: Membrane Transporter/Ion Channel;Neuronal Signaling;Apoptosis;Metabolic Enzyme/Protease, Target: iGluR;iGluR;Ferroptosis;Endogenous Metabolite, Biological_Activity: (S)-Glutamic acid acts as an excitatory transmitter and an agonist at all subtypes of glutamate receptors (metabotropic, kainate, NMDA, and AMPA). (S)-Glutamic acid shows a direct activating effect on the release of DA from dopaminergic terminals.
IC50 & Target: DA[1].

Name: Geraniol, CAS: 106-24-1, stock 13.9g, assay 98.2%, MWt: 154.25, Formula: C10H18O, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Anti-infection, Target: Fungal, Biological_Activity: Geraniol, an olefinic terpene, was found to inhibit growth of Candida albicans and Saccharomyces cerevisiae strains[1].

Name: Zingerone Vanillylacetone;Gingerone, CAS: 122-48-5, stock 34.3g, assay 98.5%, MWt: 194.23, Formula: C11H14O3, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: NF-κB, Target: NF-κB, Biological_Activity: Zingerone (Vanillylacetone) is a nontoxic methoxyphenol isolated from Zingiber officinale, with potent anti-inflammatory, antidiabetic, antilipolytic, antidiarrhoeic, antispasmodic and anti-tumor[3] properties[1]. Zingerone alleviates oxidative stress and inflammation, down-regulates NF-κB mediated signaling pathways[2]. Zingerone acts as an anti-mitotic agent, and inhibits the growth of neuroblastoma cells[3].
IC50 & Target: NF-κB[3]
In Vitro: Zingerone is a nontoxic methoxyphenol with potent anti-inflammatory, antidiabetic, antilipolytic, antidiarrhoeic, antispasmodic properties[1]. 
Zingerone (0-2 mM) decreases neruoblastoma cell survival[3]. 
Zingerone (0-2 mM) reduces cyclin D1 expression, increases cleavage of caspase-3 and PARP-1 in BE(2)-M17 cells[3]. 
In Vivo: Zingerone (50, 100  mg/kg, p.o. daily for 21 days) protects against alloxan-induced diabetes via alleviation of oxidative stress and inflammation in rat[2]. 
Zingerone (10 mg/kg, i.p.) inhibits tumor progression through mitotic arrest, failure of cell division, and stimulation of apoptosis[3].

Name: Quarfloxin CX-3543, CAS: 865311-47-3, stock 5.6g, assay 98.9%, MWt: 604.67, Formula: C35H33FN6O3, Solubility: 10 mM in DMSO, Clinical_Informat: Phase 2, Pathway: Cell Cycle/DNA Damage, Target: DNA/RNA Synthesis, Biological_Activity: Quarfloxin (CX-3543), a fluoroquinolone derivative with antineoplastic activity, targets and inhibits RNA pol I activity, with IC50 values in the nanomolar range in neuroblastoma cells. Quarfloxin disrupts the interaction between the nucleolin protein and a G-quadruplex DNA structure in the ribosomal DNA (rDNA) template[1].
IC50 & Target: RNA pol I[1].
In Vitro: Quarfloxin (CX-3543) effectively inhibits the growth of neuroblastoma cells in vitro. MNA (or high c-Myc) and wt-TP53 cell lines are found to be more sensitive to Quarfloxin. Quarfloxin and induces DNA damage, p53 signaling, cell death, and cell cycle arrest in neuroblastoma cell lines[1].
Solution in vitro: Quarfloxin is resuspended in DMSO to a stock of 10 mM[1].

Name: Radiprodil RGH-896, CAS: 496054-87-6, stock 37g, assay 98.5%, MWt: 397.40, Formula: C21H20FN3O4, Solubility: DMSO : 250 mg/mL (629.09 mM; Need ultrasonic), Clinical_Informat: Phase 2, Pathway: Membrane Transporter/Ion Channel;Neuronal Signaling, Target: iGluR;iGluR, Biological_Activity: Radiprodil (RGH-896) is an orally active and selective NMDA NR2B antagonist. A potential therapeutic agent in treatment of neuropathic pain and possibly other chronic pain conditions[1].
IC50 & Target: NMDA NR2B[1].
In Vitro: Preincubation with Radiprodil (10 nM) restores long-term potentiation (LTP) in the presence of Aβ1-42, 3NTyr10-Aβ and Aβ1-40, but not AβpE3[2]. 
As for LTP, Radiprodil (10 nM) reverses the synaptic toxicity of 3NTyr-AβAβ1-40 and Aβ1-42 but not that AβpE3-42[2]. 
In Vivo: Radiprodil could block NMDA currents in Mg2+ insensitive variants, with potencies similar to those obtained without Mg2+[3]. 
Radiprodil's potency is higher at pH 7.0 than at pH 7.6, suggesting that radiprodil may retain its ability to block glutamate-induced NMDA currents even under acidic conditions that manifest under long term seizures[3].

Name: Tosedostat CHR-2797, CAS: 238750-77-1, stock 18.5g, assay 98.1%, MWt: 406.47, Formula: C21H30N2O6, Solubility: DMSO : 25 mg/mL (61.51 mM; Need ultrasonic and warming), Clinical_Informat: Phase 2, Pathway: Metabolic Enzyme/Protease, Target: Aminopeptidase, Biological_Activity: Tosedostat is an aminopeptidase inhibitor.
IC50 & Target: Aminopeptidase[1]
In Vitro: Treatment of HL-60 cells with Tosedostat (CHR-2797) leads to an increase in the secretion of Stanniocalcin 2 (STC2) protein into the growth medium. Increases in SLC7A11 expression are detectable at 60 nM Tosedostat and as early as 2 h posttreatment. The IC50s for inhibition of proliferation by Tosedostat in U-937 and HuT 78 cell lines are 10 nM and >10 μM, respectively. Tosedostat treatment increases expression of amino acid deprivation response (AADR) genes in U-937 cells but not in HuT 78 cells[1]. By 24 h with 0.01 μM Tosedostat the mean MCA production is reduced to 77.8% of the untreated control cells; similarly the MCA production is reduced to 51.3% with 1 μM, 38.5% with 5 μM, and 35.3% with 10 μM Tosedostat[2].
In Vivo: Tosedostat (CHR-2797) is active as an anticancer agent in vivo in rodent cancer models, and a dose-response relationship has been shown in two models. The effect of Tosedostat is less apparent when the tumor burden is higher before treatment[1].

Name: Karenitecin Cositecan;BNP 1350, CAS: 203923-89-1, stock 13.8g, assay 98.3%, MWt: 448.59, Formula: C25H28N2O4Si, Solubility: 10 mM in DMSO, Clinical_Informat: Phase 3, Pathway: Cell Cycle/DNA Damage, Target: Topoisomerase, Biological_Activity: Karenitecin (Cositecan) is a topoisomerase I inhibitor, with potent anti-cancer activity.
IC50 & Target: Topoisomerase I[1]
In Vitro: Karenitecin is a topoisomerase I inhibitor, with potent anti-cancer activity. Karenitecin inhibits cell growth of A253 cells with IC10, IC50, and IC90 values of 0.01, 0.07, and 0.7 μM after 2 h treatment. Karenitecin induces DNA damage (0.01, 0.07, and 0.7 μM), and increases cyclin E and cdk2 protein expression in A253 cells (0.07, and 0.7 μM). Karenitecin markedly enhances the cyclin B/cdc2-associated kinase activity at low concentration, but slightly suppresses this kinase activity at higher concentration[1]. Karenitecin inhibits several human colon cancer cell lines such as COLO205, COLO320, LS174T, SW1398 and WiDr cells, with IC50s of 2.4 nM, 1.5 nM, 1.6 nM, 2.9 nM, and 3.2 nM, respectively[2].
In Vivo: Karenitecin shows maximum growth inhibition of 61% on COLO320 cells and 54% on COLO205 colon cancer cells via i.p. administration of 1 mg/kg in mice. Karenitecin (1.0 mg/kg daily × 5 i.p.) significantly suppresses growth inhibition both in the parental Pgp-negative xenografts and in the Pgp-positive xenografts[2].

Name: (E/Z)-4-Hydroxytamoxifen, CAS: 68392-35-8, stock 37.3g, assay 98.1%, MWt: 387.51, Formula: C26H29NO2, Solubility: H2O : < 0.1 mg/mL (insoluble); DMSO : 83.33 mg/mL (215.04 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Others, Target: Estrogen Receptor/ERR, Biological_Activity: (E/Z)-4-Hydroxytamoxifen is a racemic compound of (Z)-4-Hydroxytamoxifen and (E)-4-Hydroxytamoxifen isomers. (E/Z)-4-Hydroxytamoxifen is an estrogen receptor modulator.

Name: Sograzepide Netazepide;YF 476;YM-220, CAS: 155488-25-8, stock 22.9g, assay 98.2%, MWt: 498.58, Formula: C28H30N6O3, Solubility: DMSO : ≥ 100 mg/mL (200.57 mM), Clinical_Informat: Phase 1, Pathway: GPCR/G Protein;Neuronal Signaling, Target: Cholecystokinin Receptor;Cholecystokinin Receptor, Biological_Activity: Sograzepide (Netazepide; YF 476; YM-220) is an extremely potent , highly selective and orally active Gastrin/CCK-B antagonist with an IC50 value of 0.1 nM, has inhibitory effect on Gastrin/CCK-A activity with an IC50 of 502 nM[1]. Sograzepide (Netazepide; YF 476; YM-220) replaces the specific binding of [125I]CCK-8 to the rat brain, cloned canine and cloned human Gastrin/CCK-B receptors, with Ki values of 0.068, 0.62 and 0.19 nM, respectively[2].
IC50 & Target: IC50: 0.1 nM (Gastrin/CCK-B); 501 nM (Gastrin/CCK-A)[1]
In Vivo: Sograzepide (Netazepide; YF 476; YM-220) (0.1 μmol/kg; intravenous injection) has an inhibition effect on pentagastrin-induced gastric acid secretion in anethsetized rats with an ED50 of 87 nmol/kg[1].
Sograzepide (Netazepide; YF 476; YM-220) (intravenous injection; 10 μM/kg) inhibits pentagastrin-induced acid secretion with an ED50 value of 0.0086 μM/kg, but does not affect histamine- and bethanechol-induced acid secretion[2].Sograzepide (Netazepide; YF 476; YM-220) (intravenous injection; oral administration) in Heidenhain pouch dogs, inhibits pentagastrin-stimulated gastric acid secretion in a dose-dependent manner with ED50 values of 0.018 and 0.020 μM/kg, respectively [2].

Name: Tecarfarin ATI-5923, CAS: 867257-26-9, stock 20.5g, assay 98.2%, MWt: 460.32, Formula: C21H14F6O5, Solubility: 10 mM in DMSO, Clinical_Informat: Phase 3, Pathway: Others, Target: Others, Biological_Activity: Tecarfarin (ATI-5923) is an orally active and non-competitive vitamin K epoxide reductase (VKOR) antagonist, and impairs the activation of the vitamin K-dependent clotting factors II, VII, IX and X[1]. Tecarfarin has the antithrombotic activity [2].
IC50 & Target: VKOR[1]

Name: Derenofylline SLV 320, CAS: 251945-92-3, stock 15.2g, assay 98.7%, MWt: 308.38, Formula: C18H20N4O, Solubility: 10 mM in DMSO, Clinical_Informat: Phase 2, Pathway: GPCR/G Protein, Target: Adenosine Receptor, Biological_Activity: Derenofylline (SLV 320) is a potent, selective and orally active adenosine A1 receptor antagonist, with Ki values of 1 nM, 200 nM and 398 nM for human A1, A3 and A2A receptors respectively. Derenofylline suppresses cardiac fibrosis and attenuates albuminuria without affecting blood pressure in rats[1].
IC50 & Target: Ki: 1 nM (adenosine A1 receptor)[1].

Name: Mapracorat ZK-245186;BOL-303242X, CAS: 887375-26-0, stock 25.9g, assay 98.6%, MWt: 462.48, Formula: C25H26F4N2O2, Solubility: DMSO : ≥ 33.6 mg/mL (72.65 mM), Clinical_Informat: Phase 3, Pathway: GPCR/G Protein, Target: Glucocorticoid Receptor, Biological_Activity: Mapracorat is a novel non-steroidal selective glucocorticoid receptor agonist.
In Vitro: Mapracorat concentration dependently inhibited TNFα secretion from activated canine PBMC with IC50 value of approximately 0.2 nM.
In Vivo: Intradermal injection of compound 48/80 (50 μg in 50 μL saline) resulted in a clear wheal and flare reaction over the 60 min observation period. Topical pre-treatment with mapracorat (0.1%) leads to significant reduction in the wheal and flare responses compared to vehicle (acetone) treated areas.

Name: Tonapofylline BG 9928, CAS: 340021-17-2, stock 24.9g, assay 98.8%, MWt: 416.51, Formula: C22H32N4O4, Solubility: 10 mM in DMSO, Clinical_Informat: Phase 3, Pathway: GPCR/G Protein, Target: Adenosine Receptor, Biological_Activity: Tonapofylline (BG 9928) is an orally active and selective adenosine A1 receptor antagonist with a Ki of 7.4 nM for human adenosine A1 receptor (hA1), which displays 915-fold selectivity versus human adenosine A2A receptor and 12-fold selectivity versus human adenosine A2B receptor and is used in development for the treatment of heart failure[1][2].
IC50 & Target: Ki: 7.4 nM (Human adenosine A1 receptor)[1]
In Vivo: Tonapofylline (BG 9928) (1 mg/kg; p.o., b.i.d, days 0-6) produces sustained reductions in post-Cisplatin serum creatinine and blood urea nitrogen levels, improves body weight recovery and significant attenuation of Cisplatin-induced (5.5 mg/kg) kidney pathology scores[3].

Name: Fedovapagon, CAS: 347887-36-9, stock 36.8g, assay 98.6%, MWt: 462.58, Formula: C27H34N4O3, Solubility: DMSO : ≥ 125 mg/mL (270.22 mM), Clinical_Informat: Phase 3, Pathway: Others, Target: Others, Biological_Activity: Fedovapagon is a selective vasopressin V2 receptor (V2R) agonist with an EC50 of 24 nM, which is being developed for the treatment of nocturia[1].
IC50 & Target: EC50：24 nM (V2R)[1]

Name: Gemigliptin LC15-0444, CAS: 911637-19-9, stock 4.2g, assay 98.3%, MWt: 489.36, Formula: C18H19F8N5O2, Solubility: DMSO : 50 mg/mL (102.17 mM; Need ultrasonic), Clinical_Informat: Phase 4, Pathway: Metabolic Enzyme/Protease, Target: Dipeptidyl Peptidase, Biological_Activity: Gemigliptin is a highly selective dipeptidyl peptidase 4 (DPP4) inhibitor with a KD of 7.25 nM.
IC50 & Target: Ki: 7.25 nM (DPP4)[1]
In Vitro: In in vitro assay, gemigliptin dose-dependently inhibits methylglyoxal-modified AGE-bovine serum albumin (BSA) formation (IC50=11.69 mM). AGE-collagen cross-linking assays shows that gemigliptin has a potent inhibitory effect (IC50=1.39 mM) on AGE-BSA cross-links to rat tail tendon collagen. In addition, gemigliptin directly traps methylglyoxal in a concentration-dependent manner[1]. Gemigliptin is a reversible and competitive inhibitor with a Ki value of 7.25±0.67 nM. Gemigliptin shows at least >23,000-fold selectivity for DPP-4 over various proteases and peptidases, including DPP-8, DPP-9, and fibroblast activation protein (FAP)-α[2].
In Vivo: Administration of gemigliptin supressed elevated serum levels of advanced glycation end products (AGE) in type 2 diabetic db/db mice. In mice and dogs, gemigliptin prevents the degradation of active glucagon-like peptide-1 by DPP-4 inhibition, which improves glucose tolerance by increasing insulin secretion and reducing glucagon secretion during an oral glucose tolerance test[2].

Name: Verubulin MPC 6827, CAS: 827031-83-4, stock 0.7g, assay 98.1%, MWt: 279.34, Formula: C17H17N3O, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Cell Cycle/DNA Damage;Cytoskeleton;Apoptosis, Target: Microtubule/Tubulin;Microtubule/Tubulin;Apoptosis, Biological_Activity: Verubulin (MPC-6827) is a microtubule-disrupting agent with potent and broad-spectrum in vitro and in vivo cytotoxic activities, and acts as a promising candidate for the treatment of multiple cancer types[1].
IC50 & Target: Microtubule[1]

Name: Lapaquistat T-91485, CAS: 189059-71-0, stock 37.2g, assay 98%, MWt: 603.10, Formula: C31H39ClN2O8, Solubility: DMSO : 25 mg/mL (41.45 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: Lapaquistat (T-91485), a cholesterol biosynthesis inhibitor, is the active metabolite of TAK-475. Lapaquistat can decrease statin-induced myotoxicity in lipid-lowering therapy[1].
IC50 & Target: Cholesterol biosynthesis[1]

Name: Volinanserin MDL100907;M 100907, CAS: 139290-65-6, stock 12.7g, assay 98.1%, MWt: 373.46, Formula: C22H28FNO3, Solubility: DMSO : 106.6 mg/mL (285.44 mM; Need ultrasonic), Clinical_Informat: Phase 3, Pathway: Neuronal Signaling;GPCR/G Protein, Target: 5-HT Receptor;5-HT Receptor, Biological_Activity: Volinanserin is a potent and selective antagonist of 5-HT2 receptor, with a Ki of 0.36 nM, and shows 300-fold selectivity for 5-HT2 receptor over 5-HT1c, alpha-1 and DA D2 receptors. Volinanserin has antipsychotic activity.
IC50 & Target: Ki: 0.36 nM (5-HT2 receptor)[1]
In Vitro: Volinanserin (MDL 100907) is a potent antagonist at the 5-HT2 receptor, with a Ki of 0.36 nM, and shows 300-fold selectivity for 5-HT2 receptor over 5-HT1c receptor, alpha-1 and DA D2 receptors. Volinanserin has antipsychotic activity[1].
In Vivo: Volinanserin (MDL 100907; 0.008-2.0 mg/kg, i.p.) significantly decreases d-amphetamine-stimulated locomotor activity in mice, with an ED50 of 0.3 mg/kg, but shows no obvious reduction in the base-line locomotor activity in mice. Volinanserin produces atalepsy with an ED50 of 10-50 mg/kg in rats. Volinanserin does not reduces apomorphine-induced stereotypies or produces catalepsy in rats[1]. Volinanserin (M100907) combined with MK-801 significantly decreases reinforcers at 1 μg/kg, but dose-dependently (10, 100 μg/kg) antagonizes the disruptive effect of MK-801 in rats via i.p. administration. Volinanserin (6.25 μg/kg) enhances the antidepressant-like action of desipramine in rats performing under a DRL 72-s schedule, and elevates the antidepressant-like effect of tranylcypromine[2].

Name: Elacytarabine CP 4055, CAS: 188181-42-2, stock 20.4g, assay 98.4%, MWt: 507.66, Formula: C27H45N3O6, Solubility: DMSO : 125 mg/mL (246.23 mM; Need ultrasonic), Clinical_Informat: Phase 3, Pathway: Others, Target: Others, Biological_Activity: Elacytarabine (CP 4055) is a lipid-conjugated derivative of the nucleoside analog cytarabine. Elacytarabine (CP 4055) is an antineoplastic drug with cytotoxicity in solid tumors.

Name: Ozenoxacin T-3912, CAS: 245765-41-7, stock 15.1g, assay 98.6%, MWt: 363.41, Formula: C21H21N3O3, Solubility: DMSO : 6 mg/mL (16.51 mM; Need ultrasonic and warming), Clinical_Informat: Launched, Pathway: Anti-infection, Target: Bacterial, Biological_Activity: Ozenoxacin is a nonfluorinated quinolone antibacterial, which shows potent activities against the main microorganisms isolated from skin and soft tissue infections.
IC50 & Target: Bacterial[1]
In Vitro: Ozenoxacin (OZN) shows potent antibacterial activities against clinical isolates of Gram-positive microorganisms, with MICs ranging from 0.008 to 4 mg/L. Ozenoxacin shows good activities against strains of MRSA, MSSA, MSSE, and MRSE with 2, 3, or 4 mutations in the gyrA and grlA (parC) genes[1]. Ozenoxacin inhibits MSSA strains and S. agalactiae strains, with the rates of resistance of >10−10 and 5.3 × 10−10, respectively. The maximum MIC value for mutant strains is 8 mg/L for ozenoxacin[2].

Name: SCH79797 (dihydrochloride), CAS: 1216720-69-2, stock 28.7g, assay 98.3%, MWt: 444.40, Formula: C23H27Cl2N5, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein;Apoptosis, Target: Protease-Activated Receptor (PAR);Apoptosis, Biological_Activity: SCH79797 dihydrochloride is a highly potent, selective nonpeptide protease activated receptor 1 (PAR1) antagonist. SCH79797 dihydrochloride inhibits binding of a high-affinity thrombin receptor-activating peptide to PAR1 with an IC50 of 70 nM and a Ki of 35 nM. SCH79797 dihydrochloride inhibits thrombin-induced platelet aggregation with an IC50 of 3 μM. SCH79797 dihydrochloride has antiproliferative and pro-apoptotic effects, and limits myocardial ischemia/reperfusion injury in rat hearts. SCH79797 dihydrochloride also potently prevents PAR1 activation in vascular smooth muscle cells, endothelial cells, and astrocytes[1][2][3][4].
IC50 & Target: Protease activated receptor 1 (PAR1)[1]; Apoptosis[3]
In Vitro: SCH79797 inhibits high-affinity thrombin receptor-activating peptide ([3H]haTRAP) binding in a competitive manner. SCH79797 inhibits α-thrombin- and haTRAP-induced aggregation of human platelets, but does not inhibit human platelet aggregation induced by the tethered ligand agonist for protease-activated receptor-4 (PAR-4), γ-thrombin, ADP, or collagen. Thrombin produces transient increases in cytosolic free Ca2+ concentration ([Ca2+]i) in hCASMC. SCH79797 effectively inhibits this increase in [Ca2+]i. SCH79797 completely inhibits Thrombin- and TK-stimulated [3H]thymidine incorporation [1]. 
SCH79797 is able to interfere with the growth of several human and mouse cell lines, in a concentration-dependent manner. The ED50 for growth inhibition iss 75 nM, 81 nM and 116 nM for NIH 3T3, HEK 293 and A375 cells, respectively. In NIH 3T3 cells, SCH79797 inhibits serum-stimulated activation of p44/p42 mitogen-activated protein kinases (MAPK) at low concentrations and induces apoptosis at higher concentrations[2].
In Vivo: SCH79797 (2.5-250 μg/kg; intravenous injection; male Sprague Dawley rats) treatment immediately before or during ischemia reduces myocardial necrosis following I/R in the intact rat heart in two rat models of myocardial ischemia/reperfusion (I/R) injury. This response is dose-dependent with the optimal dose being 25 μg/kg[4].

Name: Fuscoside OPC-21268, CAS: 131631-89-5, stock 10.1g, assay 98.6%, MWt: 449.54, Formula: C26H31N3O4, Solubility: DMSO : 50 mg/mL (111.22 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein, Target: Vasopressin Receptor, Biological_Activity: Fuscoside (OPC-21268) is an orally effective, nonpeptide, vasopressin V1 receptor antagonist with an IC50 of 0.4 μM.
IC50 & Target: IC50: 0.4 μM (vasopressin V1)
Ki: 0.14 μM (vasopressin V1)[1]
In Vitro: The concentration of Fuscoside (OPC-21268) that displaces 50% of specific AVP binding (IC50) is 0.4 μM for VI receptors and 100 μM for V2 receptors. The inhibition constant (Ki) of Fuscoside (OPC-21268) for V1 receptors (0.14 μM)[1].
In Vivo: Fuscoside (OPC-21268) competitively and specifically antagonizes pressor responses to AVP in vivo. Oral administration of Fuscoside (OPC-21268) (10 mg/kg) inhibits the vasoconstriction induced by exogenous AVP in a dose- and time-dependent manner and the effect lasts for more than 8 hours at 30 mg/kg[1]. Fuscoside (OPC-21268) predominantly exerts a protective effect in areas where the maximum amount of blood-brain barrier breakdown occurs, and it is effective in the treatment of cold-induced vasogenic brain edema. Fuscoside (OPC-21268) treatment at the dosages of 200 and 300 mg/kg significantly reduces brain water content in both hemispheres. Swelling of the traumatized hemispheres is also significantly reduced at 200 and 300 mg/kg dosages[2].

Name: L-371,257, CAS: 162042-44-6, stock 22.4g, assay 98.6%, MWt: 507.58, Formula: C28H33N3O6, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein;GPCR/G Protein, Target: Vasopressin Receptor;Oxytocin Receptor, Biological_Activity: L-371,257 is an orally bioavailable, non-blood-brain barrier penetrant, selective and competitive antagonist of oxytocin receptor (pA2=8.4) with high affinity at both the oxytocin receptor (Ki=19 nM) and vasopressin V1a receptor (Ki=3.7 nM)[1][2].
IC50 & Target: Ki: 19 nM (oxytocin receptor), 3.7 nM (vasopressin V1a receptor)[2]

Name: SSR240612, CAS: 464930-42-5, stock 29.4g, assay 98.1%, MWt: 793.41, Formula: C42H53ClN4O7S, Solubility: DMSO : ≥ 100 mg/mL (126.04 mM), Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein, Target: Bradykinin Receptor, Biological_Activity: SSR240612 is a potent, and orally active specific non-peptide bradykinin B1 receptor antagonist, with Kis of 0.48 nM and 0.73 nM for B1 kinin receptors of human fibroblast MRC5 and HEK cells expressing human B1 receptors, 481 nM and 358 nM for B2 receptors of guinea pig ileum membranes and CHO cells expressing human B1 receptor, respectively.
IC50 & Target: Ki: 0.48 nM (bradykinin B1 receptor, Human MRC5), 0.73 nM (bradykinin B1 receptor, Human HEK-B1), 481 nM (bradykinin B2 receptor, guinea pig ileum membranes), 358 nM (bradykinin B2 receptor, Human CHO-B2)[1]
In Vitro: SSR240612 is a potent bradykinin B1 receptor antagonist, with Kis of 0.48 nM and 0.73 nM for B2 kinin receptors of human fibroblast MRC5 and HEK cells expressing human B1 receptors, 481 nM and 358 nM for B1 receptors of guinea pig ileum membranes and CHO cells expressing human B1 receptor, respectively. SSR240612 inhibits inositol phosphate 1 formation with an IC50 of 1.9 nM, but shows no obvious effect on inositol phosphate-1 formation induced by BK (3 nM) activation of B2 receptor in human fibroblast MRC5[1].
In Vivo: SSR240612 (10 mg/kg p.o. or 0.3, 1 mg/kg i.p.) obviously blocks the des-Arg9-BK-induced paw edema in the mice. SSR240612 (10 and 30 mg/kg) reduces the duration of the late phase of paw licking in a dose dependent manner in the formalin model of inflammation in mice. SSR240612 (0.3, 3, and 30 mg/kg, p.o.) treatment before capsaicin potently and non-concentration-dependently reduces the ear edema. SSR240612 (0.3 mg/kg, i.v.) also suppresses the tissue destruction and neutrophil accumulation in the rat intestine, after splanchnic artery occlusion/reperfusion. Moreover, SSR240612 (1 and 3 mg/kg p.o.) dramacally increases the withdrawal latencies in the thermal hyperalgesia induced by UV irradiation in rats[1]. SSR240612 inhibits tactile and cold allodynia at 3 h in glucose-fed rats but had no effect in control rats with ID50s of 5.5 and 7.1 mg/kg, respectively. SSR240612 shows no effect on plasma glucose and insulin, insulin resistance (HOMA index) and aortic superoxide anion production in glucose-fed rats at 10 mg/kg[2].

Name: INO-1001, CAS: 501364-82-5, stock 6.5g, assay 98.2%, MWt: 439.53, Formula: C23H25N3O4S, Solubility: DMSO : 31.25 mg/mL (71.10 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Epigenetics;Cell Cycle/DNA Damage, Target: PARP;PARP, Biological_Activity: INO-1001 is a potent and selective poly (ADP-ribose) polymerase (PARP) inhibitor. INO-1001 is a potent enhancer of radiation sensitivity and enhances radiation-induced cell killing by interfering with DNA repair mechanisms, resulting in necrotic cell death[1]. INO-1001 has anti-tumor effects[2].
In Vitro: INO-1001 has an IC50 of 0.05 μM in Chinese hamster ovary AA8 (CHO) cells[1].

Name: NBQX FG9202, CAS: 118876-58-7, stock 4.8g, assay 98%, MWt: 336.28, Formula: C12H8N4O6S, Solubility: DMSO : ≥ 75 mg/mL (223.03 mM); H2O : < 0.1 mg/mL (insoluble), Clinical_Informat: No Development Reported, Pathway: Membrane Transporter/Ion Channel;Neuronal Signaling, Target: iGluR;iGluR, Biological_Activity: NBQX is a highly selective and competitive AMPA receptor antagonist.
IC50 & Target: AMPA receptor[1]
In Vitro: NBQX has a high affinity for AMPA and kainate binding sites with little or no affinity for the glutamate recognition site on the NMDA receptor complex[1].
In Vivo: NBQX is neuroprotective in a focal ischaemia model in the rat when given as an i.v. bolus dose of 30 mg/kg at the time of MCA occlusion and again at 1 h post occlusion[1]. NBQX provides potent anticonvulsant protection against AMPA. The ED50 values for the protection against AMPA-induced seizures by NBQX (30 min, i.p.) is 23.6 (11.6- 48.0)[2].

Name: MKT-077 FJ-776, CAS: 147366-41-4, stock 23.2g, assay 98.1%, MWt: 432.00, Formula: C21H22ClN3OS2, Solubility: DMSO : 41.67 mg/mL (96.46 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease;Cell Cycle/DNA Damage, Target: HSP;HSP, Biological_Activity: MKT-077 is a rhodacyanine dye and also a heat shock protein 70 (Hsp70) inhibitor which exhibits significant antitumor activity.
IC50 & Target: Hsp70[1]
In Vitro: MKT-077 is a rhodacyanine dye and also a heat shock protein 70 (Hsp70) inhibitor which exhibits significant antitumor activity. MKT-077 treatment (0.1 to 10 µM dose ranges) for 48 hours can effectively decrease TT cell viability. MKT-077 treatment results in accumulation of cells in the G0/G1 phase in a dose-dependent manner, and also increases sub-G0/G1 phase population in TT cell culture in a dose-dependent manner. MKT-077 also downregulates cellular levels of the proliferation marker, Ki67, and the S-phase transcription factor, E2F-1, in TT and MZ-CRC-1 cells. Moreover, flow cytometry using different doses of MKT-077 reveales that TT cells can uptake and retain MKT-077 at significantly higher levels than MZ-CRC-1 cells[1]. MKT-077 has EC50 values of 1.4±0.2 and 2.2±0.2 μM against MDA-MB-231 and MCF7 breast cancer cells, respectivelyl[2].
In Vivo: Systemic administration of MKT-077 significantly delays the growth of TT xenografts in mice throughout the treatment. At the end of MKT-077 treatment, it is found that tumor weights are about two-times less in MKT-077-treated group than in control group. MKT-077 treatment also results in weight loss and general toxicity in animals[1]. Results show that the succinate-induced, ADP-stimulated respiratory rate in mitochondria isolated from the liver of rats treated with a bolus i.v. injection of 15 mg MKT-077 1kg body weight each day for 5 days is significantly lower than that of untreated controls[3].

Name: MK-0429 L-000845704, CAS: 227963-15-7, stock 37.1g, assay 98.1%, MWt: 439.51, Formula: C23H29N5O4, Solubility: DMSO : 250 mg/mL (568.82 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Cytoskeleton, Target: Integrin, Biological_Activity: MK-0429 (L-000845704) is an orally active, potent, selective and nonpeptide αvβ3 integrin antagonist with an IC50 of 80 nM.
IC50 & Target: IC50: 80 nM (αvβ3 integrin)[1]
In Vivo: MK-0429 (100 or 300 mg/kg, p.o., twice daily b.i.d., 2 weeks) reduces metastatic tumor colony formation and area in the lungs. MK-0429 is safe and efficacious in significantly decreasing melanoma metastasis in the lungs[1].

Name: L-Theanine L-Glutamic Acid γ-ethyl amide;Nγ-Ethyl-L-glutamine, CAS: 3081-61-6, stock 2.7g, assay 98.4%, MWt: 174.20, Formula: C7H14N2O3, Solubility: H2O : 150 mg/mL (861.08 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Apoptosis, Target: Apoptosis, Biological_Activity: L-Theanine (L-Glutamic Acid γ-ethyl amide）is a non-protein amino acid contained in green tea leaves, which blocks the binding of L-glutamic acid to glutamate receptors in the brain, and with neuroprotective and anti-oxidative activities. L-Theanine causes anti-stress effects via the inhibition of cortical neuron excitation by oral intake[1][2][3].

Name: DL-O-Phosphoserine, CAS: 17885-08-4, stock 36.5g, assay 98.8%, MWt: 185.07, Formula: C3H8NO6P, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: DL-O-Phosphoserine, a normal metabolite in human biofluid, is an ester of serine and phosphoric acid.

Name: Guadecitabine sodium SGI-110 sodium;S-110 sodium, CAS: 929904-85-8, stock 30.2g, assay 98.1%, MWt: 579.39, Formula: C18H23N9NaO10P, Solubility: DMSO : 50 mg/mL (86.30 mM; Need ultrasonic); H2O, Clinical_Informat: Phase 3, Pathway: Epigenetics, Target: DNA Methyltransferase, Biological_Activity: Guadecitabine sodium (SGI-110 sodium; S-110 sodium) is a dinucleotide consisting of 5-Aza-CdR followed by a deoxyguanosine which shows to be an effective DNA methylation inhibitor.
IC50 & Target: Target: DNA methylation inhibitor[1]
In Vitro: After HCT116 colorectal carcinoma cells are treated for 6 days, a dose-dependent increase in p16expression is observed with Guadecitabine sodium (SGI-110 sodium). In addition, T24 and HCT116 cells treated with Guadecitabine sodium or 5-aza-CdR for 3 days show a dose-dependent increase in the level of p16 protein, showing the competence of Guadecitabine sodium to inhibit DNA methylation and induce p16 at both mRNA and protein levels as well as 5-aza-CdR. Thus, Guadecitabine sodium is able to inhibit DNA methylation at 5′-region and induce the expression of the p16 gene in T24 and HCT116 cells at concentrations comparable to 5-aza-CdR, and the induction of p16 expression by both agents correlates with the demethylation at the 5′-end region of the gene in both cell lines. Guadecitabine sodium is slightly less toxic than 5-aza-CdR at the doses tested up to 1 μM concentration but displaying similar toxicity at 10 μM concentration[1].
In Vivo: Guadecitabine sodium (SGI-110 sodium) at 10mg/kg is an effective dose at reducing DNA methylation and retarding tumor growth, and caused roughly the same level of toxicity as 5-Aza-CdR. Guadecitabine sodium is effective in vivo at reactivating the expression of the p16 gene, which is heavily methylated in the parent EJ6 cells. Guadecitabine sodium is effective in reducing the level of DNA methylation in vivo at the p16 promoter region. Guadecitabine sodium is better tolerated than 5-Aza-CdR in vivo, suggesting that it can be an attractive alternative for potential clinical use[2].

Name: SL 0101-1 SL0101, CAS: 77307-50-7, stock 18.3g, assay 98.1%, MWt: 516.45, Formula: C25H24O12, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: MAPK/ERK Pathway, Target: Ribosomal S6 Kinase (RSK), Biological_Activity: SL 0101-1 (SL0101), a kaempferol glycoside, isolated from the tropical plant F. refracta, is a cell-permeable, selective, reversible, ATP-competitive p90 Ribosomal S6 Kinase (RSK) inhibitor, with an IC50 of 89 nM. Shows proliferation inhibition in human breast cancer cell line MCF-7 and produces a cell cycle block in G1 phase[1].
IC50 & Target: IC50: 89 nM (RSK)[1].

Name: L-798106 CM9;GW671021, CAS: 244101-02-8, stock 0.2g, assay 98.4%, MWt: 536.44, Formula: C27H22BrNO4S, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein, Target: Prostaglandin Receptor, Biological_Activity: L-798106 is potent and highly selective prostanoid EP3 receptor antagonist (Ki=0.3 nM), it also has micromolar activities at the EP4, EP1 and EP2 receptors with Ki values of 916 nM, >5000 nM and >5000 nM at EP4, EP1 and EP2, respectively[1].
IC50 & Target: Ki values: 0.3 nM (EP3 receptor); 916 nM (EP4 receptor); > 5000 nM (EP1/2 receptor)[1]

Name: NVP-TAE 684 TAE 684, CAS: 761439-42-3, stock 30.9g, assay 98.8%, MWt: 614.20, Formula: C30H40ClN7O3S, Solubility: DMSO : 7.69 mg/mL (12.52 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Apoptosis;Protein Tyrosine Kinase/RTK, Target: Apoptosis;ALK, Biological_Activity: NVP-TAE 684 is a highly potent and selective ALK inhibitor, which blocks the growth of ALCL-derived and ALK-dependent cell lines with IC50 values between 2 and 10 nM.
In Vitro: TAE684 inhibits the proliferation of Ba/F3 NPM-ALK cells with an ICsub>50 of 3 nM, without affecting the survival of parental Ba/F3 cells at concentrations up to 1 μM. TAE684 inhibits STAT3 and STAT5 phosphorylation in a dose-dependent manner in both Ba/F3 NPM-ALK and Karpas-299 cells. TAE684 induces apoptosis and G1 phase arrest in NPM-ALK-expressing Ba/F3 cells and ALCL patient cell lines[1]. NVP-TAE684 markedly reduces cell survival in both sensitive H3122 and H3122 CR cells, but has little to no effect on the viability of other, non-ALK-dependent cancer cell lines. NVP-TAE684 treatment of H3122 CR cells suppresses phosphorylation of ALK, AKT, and ERK and induces marked apoptosis. TAE684 potently suppresses the survival of Ba/F3 cells expressing the EML4-ALK L1196M mutant[2]. Neurite outgrowth induced by expression of the mALKR1279Q mutant is completely inhibited at 30 nM NVP-TAE684, which is comparable with the response seen with activated wt mALK[3].
In Vivo: NVP-TAE684 suppresses lymphomagenesis in two independent models of ALK-positive ALCL and induces regression of established Karpas-299 lymphomas. TAE684 displays appreciable bioavailability and half-life in vivo. TAE684 (1, 3, and 10 mg/kg. p.o.) significantly delays in lymphoma development and shows 100- to 1,000-fold reduction in luminescence signal. The TAE684- (10 mg/kg) treated group appeares healthy and does not display any signs of compound- or disease-related toxicity[1].

Name: SB-265610, CAS: 211096-49-0, stock 12.8g, assay 98.8%, MWt: 357.16, Formula: C14H9BrN6O, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein;Immunology/Inflammation, Target: CXCR;CXCR, Biological_Activity: SB-265610 is a selective, competitive, nonpeptide and allosteric CXCR2 antagonist. SB-265610 blocks rat cytokine-induced neutrophil chemoattractant-1 (CINC-1)-induced calcium mobilization and neutrophil chemotaxis with IC50s of 3.7 nM and 70 nM, respectively[1][2].
In Vitro: In vitro, SB-265610 antagonizes rat cytokine-induced neutrophil chemoattractant-1 (CINC-1)-induced calcium mobilization, IC50 of 3.7 nM, and rat neutrophil chemotaxis in a concentration-dependent manner, IC50 of 70 nM. SB-265610 reduces the antiapoptotic effect of CINC-1 to the levels of those untreated with CINC-1[1].
In Vivo: SB-265610 (100 mg/kg/day; oral administration; daily; for 5 days; CXCR2 wild type mice) treatment during the wound repair process markedly delays healing parameters in CXCR2 wild type mice[2].

Name: AZD3988, CAS: 892489-52-0, stock 21.2g, assay 98.6%, MWt: 456.44, Formula: C23H22F2N4O4, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Acyltransferase, Biological_Activity: AZD3988 is a diacylglycerol acyl transferase-1 (DGAT-1) inhibitor with IC50s of 6, 5, 11 nM for human, rat, mouse, respectively[1].
IC50 & Target: IC50: 6 nM (h DGAT-1), 5 nM (Rat DGAT-1), 11 nM (Mouse DGAT-1)[1]

Name: Lestaurtinib CEP-701;KT-5555, CAS: 111358-88-4, stock 22.9g, assay 98.3%, MWt: 439.46, Formula: C26H21N3O4, Solubility: DMSO : 50 mg/mL (113.78 mM; Need ultrasonic), Clinical_Informat: Phase 3, Pathway: Protein Tyrosine Kinase/RTK;Epigenetics;Stem Cell/Wnt;JAK/STAT Signaling;Protein Tyrosine Kinase/RTK;Neuronal Signaling, Target: FLT3;JAK;JAK;JAK;Trk Receptor;Trk Receptor, Biological_Activity: Lestaurtinib (CEP-701;KT-5555) is a multi-kinase inhibitor with potent activity against the Trk family of receptor tyrosine kinases. Lestaurtinib inhibits JAK2, FLT3 and TrkA with IC50s of 0.9, 3 and less than 25 nM, respectively.
IC50 & Target: IC50: 0.9 nM (JAK2), 3 nM (FLT3), 25 nM (TrkA)[1]

Name: A-769662, CAS: 844499-71-4, stock 39.3g, assay 98.3%, MWt: 360.39, Formula: C20H12N2O3S, Solubility: DMSO : 100 mg/mL (277.48 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Epigenetics;PI3K/Akt/mTOR, Target: AMPK;AMPK, Biological_Activity: A-769662 is a potent, reversible AMPK activator with EC50 of 0.8 μM, and has little effect on GPPase/FBPase activity.
IC50 & Target: EC50: 0.8 μM (AMPK)
In Vitro: A-769662 is equally potent in activating the baculovirus expressed α1,β1,γ1 recombinant isoform of AMPK (EC50=0.7 μM). A-769662 and A-592107 activate AMPK purified from multiple tissues and species in a dose-responsive manner with modest variations in observed EC50s. EC50s determined for A-769662 using partially purified AMPK extracts from rat heart, rat muscle, or human embryonic kidney cells (HEKs) are 2.2 μM, 1.9 μM, or 1.1 μM, respectively[1]. A-769662 activates endogenous AMPK in LKB1-expressing (HEK293) and LKB1-deficient (CCL13) cells. A-769662 allosterically activates AMPK complexes containing γ1 harboring a substitution of arginine residue 298 to glycine (R298G). A-769662 inhibits dephosphorylation of Thr-172 in the mutant γ1-containing complexes to a similar degree as seen in the wild-type complexes[2]. A769662 (300 μM) has toxic effects on MEF cells. A769662 reversibly inhibits the proteasomal activity[3].
In Vivo: A-769662 (30 mg/kg, i.p.) significantly reduced the respiratory exchange ratio (RER) in the SD rat. There are 33% and 58% reductions of malonyl CoA levels in livers of animals treated with 30 mg/kg A-769662 (0.905 nmol/g) or 500 mg/kg metformin (0.574 nmol/g), respectively. A-769662 (30 mg/kg, b.i.d.) significantly decreases fed plasma glucose (30%-40% reduction), while the lower doses (3 and 10 mg/kg) of A-769662 had no effect on the in diabetic ob/ob mice[1].

Name: BIO-acetoxime BIA, CAS: 667463-85-6, stock 14.9g, assay 98.9%, MWt: 398.21, Formula: C18H12BrN3O3, Solubility: DMSO : 20.83 mg/mL (52.31 mM; Need ultrasonic); H2O : < 0.1 mg/mL (insoluble), Clinical_Informat: No Development Reported, Pathway: Stem Cell/Wnt;PI3K/Akt/mTOR;Apoptosis;Anti-infection, Target: GSK-3;GSK-3;Apoptosis;HSV, Biological_Activity: BIO-acetoxime (BIA) is a potent and selective GSK-3 inhibitor, with IC50s of both 10 nM for GSK-3α/β. BIO-acetoxime has anticonvulsant and anti-infection activity.
IC50 & Target: IC50: 10 nM (GSK-3α/β)
In Vitro: BIO-acetoxime (BIA; Compound 13) is a potent and selective GSK-3α/β inhibitor, with IC50s of both 10 nM. BIO-acetoxime (BIA) shows weak effect on CDK5/p35 (IC50, 2.4 μM), CDK2/cyclin A (IC50, 4.3 μM), and CDK1/cyclin B (IC50, 63 μM)[1]. BIO-acetoxime (BIA) (5 μM and 10 μM) increases the viability of HSV-1-infected cells but shows little effect on morphology and viability of mockin-fected cells. Moreover, BIO-acetoxime (BIA) (0.625, 1.25, 2.5, 5, and 10 μM) significantly reduces the release of HSV-1 particles in OC3 cells, with an EC50 of 0.68 ± 0.28 μM. BIO-acetoxime (BIA) inhibits the expression of HSV-1 genes, and may not affect the nuclear targeting of HSV-1 capsids. In addition, delayed addition of BIO-acetoxime (BIA) also inhibits HSV-1 infection[2].
In Vivo: BIO-acetoxime (BIA) shows anticonvulsant effects in the focal pilocarpine rat model at 0.5 mg/kg, and in 6-Hz fully kindled FVB/N mice at 0.5, 2.5, and 5 mg/kg via i.p. administration[3].

Name: CP-466722, CAS: 1080622-86-1, stock 13.5g, assay 99%, MWt: 349.35, Formula: C17H15N7O2, Solubility: DMSO : 7 mg/mL (20.04 mM; Need warming), Clinical_Informat: No Development Reported, Pathway: Cell Cycle/DNA Damage;PI3K/Akt/mTOR, Target: ATM/ATR;ATM/ATR, Biological_Activity: CP-466722 is a rapidly reversible inhibitor of ATM, with an IC50 of 4.1 μM, and has no effects on PI3K or closely related PI3K-like protein kinase (PIKK) family members.
IC50 & Target: IC50: 4.1 μM (ATM)[2]
In Vitro: CP-466722 (CP466722, 6-10 μM) inhibits IR-induced ATM kinase activity, and the inhibition can be rapidly and completely reversed. CP466722 (6, 10 μM) inhibits p53 induction and ATM-dependent phosphorylation in mouse cells, but CP466722 fails to inhibit ATR activity and ATR-dependent phosphorylation of Chk1. CP466722 (6 μM) disrupts ATM-dependent cell cycle checkpoints in cells[1]. CP466722 (1 µM) completely inhibits ATM-dependent phosphorylation in MCF7 cells. CP466722 (10 µM) reduces pKAP1 phosphorylation in MCF7 cells, with an IC50 of 0.41 µM. CP466722 (10 µM) inhibits both pATM and pKAP1 signals[2]. CP-466722 (CP466722, 5-50 μM) inhibits proliferation of SKBr-3 cancer cells more strongly than MCF-7 cancer cells. CP466722 (10 µM) also slightly increases proportions of MCF-7 and SKBr-3 cells in the G1 phase after treatment for 48 hours[3].

Name: FPA-124, CAS: 902779-59-3, stock 38g, assay 98.5%, MWt: 381.73, Formula: C11H9Cl2CuN3O2S, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Apoptosis;PI3K/Akt/mTOR, Target: Apoptosis;Akt, Biological_Activity: FPA-124, a cell-permeable copper complex, is a selective Akt inhibitor with an IC50 of 0.1 μM. FPA-124 interacts with both the pleckstrin homology (PH) and the kinase domains of Akt. FPA-124 induces apoptosis[1][2].
In Vitro: FPA-124 exhibits dose-dependent growth inhibitory effects with IC50s of 7, 10, 34, and 55 μM in BT20, PC-3, COLO 357 and BxPC-3 cancer cell lines, respectively[1].
In Vivo: FPA-124 exhibits PKB (Akt protein) inhibitory activities and causes NF-κB inactivation in a well-established orthotopic pancreatic tumor model using COLO 357 cells[1].

Name: GW 6471, CAS: 880635-03-0, stock 14.4g, assay 98.3%, MWt: 619.67, Formula: C35H36F3N3O4, Solubility: H2O : < 0.1 mg/mL (insoluble); DMSO : 125 mg/mL (201.72 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Cell Cycle/DNA Damage, Target: PPAR, Biological_Activity: GW 6471 is a potent PPARα antagonist.
IC50 & Target: PPARα[1]
In Vitro: In a cell-based reporter assay, GW 6471 completely inhibits GW409544-induced activation of PPARα with an IC50 of 0.24 μM[1]. The functional role of PPARα is evaluated on renal cell carcinoma (RCC) cell viability by MTT assay. Both Caki-1 (VHL wild type) and 786-O (VHL mutated) cells are incubated separately with a specific PPARα agonist, WY14,643, or a specific PPARα antagonist, GW 6471 at concentrations from 12.5 to 100 µM for 72 hours, and cell viability is assessed. While WY14,643 either has no affect on, or slightly increased, cell viability, GW 6471 significantly and dose-dependently inhibits cell viability (up to approximately 80%) in both cell lines[2].
In Vivo: To test the antitumor activity of PPARα antagonism in vivo, a subcutaneous xenograft mouse model is used. Caki-1 cells are implanted subcutaneously in nude (Nu/Nu) mice. After tumor masses reach ∼5 mm in diameter, GW 6471 is administrated intraperitoneally every other day for 4 wk at a dose (20 mg/kg mouse body wt) that is described to be effective in an in vivo dose-response study and confirmed here to be efficacious. There are significant differences in tumor growth between vehicle- and GW 6471-treated animals. No toxicity is observed at the doses of GW 6471 based on weights of the animals, and laboratory values, including kidney and liver function tests, are not adversely affected. To demonstrate on-target effects of GW 6471, c-Myc levels are evaluated in the tumors, which show significant decreases in the GW 6471-treated animals[3].

Name: Anitrazafen LY 122512, CAS: 63119-27-7, stock 19.7g, assay 98.6%, MWt: 307.35, Formula: C18H17N3O2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Anitrazafen is a topically effective antiinflammatory agent.
In Vivo: Anitrazafen is a topically effective antiinflammatory agent. The disposition of 14C in normal and in bile-duct cannulated rats after oral administration of a single dose of 25 mg/kg of [3-14C]Anitrazafen shows the drug to be well absorbed from the gastro-intestinal tract and biliary excretion to be the major route of elimination of drug and/or metabolites. Plasma concentrations of total 14C after subcutaneous administration of [3-14C]Anitrazafen in corn oil solution are about one half those found after oral administration[1].

Name: FTY720 (S)-Phosphate (S)-FTY720P;(S)-FTY720 phosphate, CAS: 402616-26-6, stock 22.4g, assay 98.7%, MWt: 387.45, Formula: C19H34NO5P, Solubility: H2O : < 0.1 mg/mL (insoluble), Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein, Target: LPL Receptor, Biological_Activity: FTY720 (S)-Phosphate is an agonist of S1P receptor 1 (S1PR1), used in the research of acute inflammatory diseases such as acute lung injury.
IC50 & Target: S1PR1[1]
In Vitro: FTY720 (S)-Phosphate is an agonist of S1PR1. FTY720 (S)-Phosphate (Tys, 1 µM) maintains S1PR1 protein expression, enhances the human pulmonary artery endothelial cells barrier via S1PR1, but shows no effect on inducing ubiquitination of S1PR1. FTY720 (S)-Phosphate (0.01-50 µM) also reduces β-arrestin recruitment to S1PR1[1].
In Vivo: FTY720 (S)-Phosphate (0.5 mg/kg, i.p.) preserves S1PR1 expression in mouse lungs, is protective in bleomycin-induced acute lung injury (ALI) and attenuates lung tissue leukocyte infiltration in bleomycin-injured mice[1].

Name: NE 10790 3-PEHPC, CAS: 152831-36-2, stock 21.2g, assay 98.5%, MWt: 247.14, Formula: C8H10NO6P, Solubility: H2O : 5 mg/mL (20.23 mM; ultrasonic and adjust pH to 6 with NaOH), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: NE 10790, a poor farnesyl pyrophosphate synthase inhibitor, is a phosphonocarboxylate analogue of the potent bisphosphonate risedronate and is a weak antiresorptive agent.
IC50 & Target: FPP synthase[1].
In Vitro: NE 10790 inhibits incorporation of [14C]mevalonic acid into Rab6, but not into H-Ras or Rap1, proteins that are modified by FTase and GGTase I, respectively. NE 10790 reduces viability in J774 cells. NE 10790 prevents prenylation of 22-26-kDa proteins that are not modified by FTase or GGTase I[1].

Name: A-385358, CAS: 406228-55-5, stock 20.2g, assay 98.5%, MWt: 639.83, Formula: C32H41N5O5S2, Solubility: DMSO : 125 mg/mL (195.36 mM; Need ultrasonic and warming), Clinical_Informat: No Development Reported, Pathway: Apoptosis, Target: Bcl-2 Family, Biological_Activity: A-385358 is a selective inhibitor of Bcl-XL with Kis of 0.80 and 67 nM for Bcl-XL and Bcl-2, respectively.
IC50 & Target: Ki: 0.80 nM (Bcl-XL), 67 nM (Bcl-2)
In Vitro: A-385358 is a selective inhibitor of Bcl-XL with Kis of 0.80 and 67 nM for Bcl-XL and Bcl-2, respectively, in fluorescence polarization assays. Treatment of IL-3-deprived FL5.12/Bcl-XL cells for 24 hours with A-385358 results in cell killing with an EC50 of 0.47±0.05 μM (n=68). This effect is accompanied by an increase in caspase-3 activity. Consistent with the greater affinity for the Bcl-XL versus Bcl-2 hydrophobic grooves, the EC50 of A-385358 for IL-3-depleted FL5.12/Bcl-2 cells (1.9±0.1 μM; n=55) is 4-fold higher relative to the cytokine-deprived FL5.12/Bcl-XL cells. In addition, A-385358 is more effective at stimulating cytochrome c release from mitochondria isolated from FL5.12/Bcl-XL versus Bcl-2 cells[1].
In Vivo: The combination of A-385358 given at 100 mg/kg/d plus the lower dose of paclitaxel produces a significant reduction in tumor growth (%T/C) compare with paclitaxel monotherapy. This combination also yields a >100% increase in time for tumors to reach 900 mm3 (%ILS) compare with vehicle control. Maximal efficacy is observed during the dosing period for A-385358, with slow but steady increase in the tumor growth after termination of treatment. The combination of A-385358 at 75 mg/kg/d plus paclitaxel at 30 mg/kg/d is also well tolerated and inhibits tumor growth rate by nearly 80%. Significant effects on tumor growth relative to paclitaxel monotherapy are observed with doses as low as 50 mg/kg/d[1].

Name: Carboxyamidotriazole L 651582;CAI, CAS: 99519-84-3, stock 1.2g, assay 98%, MWt: 424.67, Formula: C17H12Cl3N5O2, Solubility: 10 mM in DMSO, Clinical_Informat: Phase 3, Pathway: Membrane Transporter/Ion Channel;Neuronal Signaling, Target: Calcium Channel;Calcium Channel, Biological_Activity: Carboxyamidotriazole (L 651582) is a blocker of non-voltage dependent calcium channel[1]. Carboxyamidotriazole (L 651582) is a non-cytotoxic anti-tumor drug, which also shows anti-inflammatory activity[2].
IC50 & Target: Calcium channel[1]

Name: DMAPT Dimethylamino Parthenolide, CAS: 870677-05-7, stock 8.9g, assay 98.3%, MWt: 293.40, Formula: C17H27NO3, Solubility: DMSO : 125 mg/mL (426.04 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: NF-κB, Target: NF-κB, Biological_Activity: DMAPT (Dimethylamino Parthenolide), a water soluble analogue of Parthenolide (PTL), is an oral active NF-κB inhibitor, with a LD50 of 1.7 μM for cell population in AML cells. Has potential anti-cancer and anti-metastatic effect[1].
IC50 & Target: NF-κB[1].
In Vitro: DMAPT treatment decreased constitutive NF-κB binding activity, inhibits cell proliferation and viability of PC-3 and DU145 cells[2].
Treatment of PC-3 and DU145 cells with 5 and 4 μM DMAPT, respectively, increases the population doubling times of PC-3 prostate cancer cells from 23.0 ± 5.0 h to 42.0 ± 3.0 h and of the DU145 cells from 20.4 ± 2.2 h to 72.5 ± 24.8 h[2].
In Vivo: Treatment with DMAPT (100 mg/kg, Oral gavage daily for 7 days) increases sensitivity of PC-3 tumor xenografts to X-rays[2]. 
DMAPT (100 mg/kg, Oral gavage thrice weekly from 42 to 300 days since birth) treatment slows normal tumor development in TRAMP mice, extending the time-to-palpable prostate tumor by 20%[3]. 
DMAPT further reduces the metastatic area below that of the water vehicle treatment group in lung tissues (0.10% ± 0.15 SD, 92% reduction, p = 0.0028) in TRAMP mice[3].

Name: Ethynylcytidine ECyD;TAS-106;3'-C-Ethynylcytidine, CAS: 180300-43-0, stock 18.7g, assay 98.2%, MWt: 267.24, Formula: C11H13N3O5, Solubility: DMSO : 250 mg/mL (935.49 mM; Need ultrasonic), Clinical_Informat: Phase 2, Pathway: Cell Cycle/DNA Damage, Target: Nucleoside Antimetabolite/Analog, Biological_Activity: Ethynylcytidine is a new nucleoside antimetabolite.
IC50 & Target: nucleoside antimetabolite[1]
In Vitro: The IC50 values of Ethynylcytidine in the five human tumors with 4, 24 and 72 h exposure range from 0.114 to 1.032 μM, 0.015 to 0.067 μM, and 0.008 to 0.058 μM, respectively. These results suggest that the cytotoxicity of Ethynylcytidine tends to become stronger as the exposure time becomes longer. The differences in IC50 values between the 24 and 72 h exposure times are not large, and Ethynylcytidine appeares to show sufficiently potent cytotoxicity at the 24 h exposure time in all 5 human tumors. Even at the 4 h exposure time, Ethynylcytidine clearly shows potent cytotoxicity with IC50 values at submicromolar concentrations in 4 of the 5 human tumors[1].
In Vivo: In both OCUM-2MD3 and LX-1 xenografts, tumor regression is noted and a very potent antitumor effect with an tumor growth inhibition rate (IR) on day 15 of approximately 90% or even higher is observed at the minimum toxic doses of Ethynylcytidine (TAS-106) on all three administration schedules. In particular, administration of Ethynylcytidine at 6 mg/kg once weekly exhibits a marked tumor shrinking effect with an IR of 98% against the LX-1 tumor. While Ethynylcytidine treatment on an either 3 or 5 times weekly schedule has a potent antitumor effect with an IR of approximately 85%, the IR of Ethynylcytidine once weekly is less than 60% and its antitumor effect is rather weak[1].

Name: FR194738, CAS: 204067-52-7, stock 6.6g, assay 98.6%, MWt: 476.11, Formula: C27H38ClNO2S, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: FR194738 is a squalene epoxidase inhibitor. FR194738 inhibits squalene epoxidase activity in HepG2 cell homogenates with an IC50 of 9.8 nM.
IC50 & Target: IC50: 9.8 nM (squalene epoxidase, in HepG2 cell homogenates)[1]
In Vitro: In intact HepG2 cells<, FR194738 concentration-dependently inhibits the incorporation of [14C]acetate into free cholesterol and cholesteryl ester, with IC50s of 4.9 and 8.0 nM, respectively. FR194738 induces intracellular [14C]squalene accumulation. FR194738 increases the incorporation of [14C]acetate into squalene, an intermediate of cholesterol synthesis[1]. FR194738 potently inhibits squalene epoxidase (SE) in HepG2 cell homogenate and liver microsomes in dogs and rats. The inhibitory effect of FR194738 in comparison to the HMG-CoA reductase inhibitors, Simvastatin, Fluvastatin and Pravastatin, on cholesterol biosynthesis in HepG2 cells is examined. Among these compounds, FR194738 is the most potent, with an IC50 of 2.1 nM. The IC50s of Simvastatin, Fluvastatin and Pravastatin are 40, 28 and 5100 nM, respectively[2]. FR194738 inhibits hamster liver microsomal squalene epoxidase activity in a concentration-dependent manner with an IC50 of 14 nM[3].
In Vivo: Serum lipid levels in hamsters after daily administration of FR194738 and Pravastatin for 10 d are measured. FR194738 reduces the serum levels of total, non high density lipoprotein (HDL) and HDL cholesterol, and triglyceride. Treatment of hamsters with FR194738 increases HMG-CoA reductase activity by 1.3-fold at 32 mg/kg compared to the control group and does not significantly change that at 100 mg/kg[3].

Name: FX-11 LDHA Inhibitor FX11, CAS: 213971-34-7, stock 13.4g, assay 99%, MWt: 350.41, Formula: C22H22O4, Solubility: DMSO : 250 mg/mL (713.45 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Lactate Dehydrogenase, Biological_Activity: FX-11 (LDHA Inhibitor FX11) is a potent lactate dehydrogenase A (LDHA) inhibitor with an IC50 of 23.3 μM for HeLa cell，a Ki value of 8 μM.
IC50 & Target: IC50: 23.3 μM (LDHA, HeLa cell) [1].

Name: Gadoxetate (Disodium) Gd-EOB-DTPA (Disodium);ZK 139834, CAS: 135326-22-6, stock 17.9g, assay 98%, MWt: 725.71, Formula: C23H28GdN3Na2O11, Solubility: 10 mM in DMSO, Clinical_Informat: Launched, Pathway: Others, Target: Others, Biological_Activity: Gadoxetate Disodium (Gd-EOB-DTPA Disodium) is a contrast agent in magnetic resonance imaging (MRI) of the hepatobiliary system, which accumulates in normal, functioning hepatocytes. Gadoxetate Disodium (Gd-EOB-DTPA Disodium) is used to evaluate focal liver lesions, such as hepatocellular carcinoma or liver metastasis on T1-weighted imaging[1][2][3].

Name: GGTI-2418, CAS: 501010-06-6, stock 21.5g, assay 99%, MWt: 441.52, Formula: C23H31N5O4, Solubility: DMSO : 125 mg/mL (283.11 mM; Need ultrasonic), Clinical_Informat: Phase 1, Pathway: Others, Target: Others, Biological_Activity: GGTI-2418 is a highly potent, competitive, and selective geranylgeranyltransferase I (GGTase I) inhibitor. GGTI-2418 inhibits GGTase I and FTase activities with IC50s of 9.5 nM and 53 μM, respectively. GGTI-2418 also increases p27(Kip1) and induces significant regression of breast tumors[1].
IC50 & Target: IC50: 9.5 nM (GGTase I), 53 μM (FTase)[1]
In Vitro: GGTI-2418 inhibits GGTase I and FTase activities with IC50s of 9.5±2.0 nM and 53±11 μM, respectively, a 5,600-fold selectivity toward inhibition of GGTase I versus FTase. GGTI-2418 demonstrates competitive inhibition of GGTase I against the H-Ras-CVLL protein with a Ki of 4.4±1.6 nM[1]. 
GGTi-2418 (10-15 μM; 16 hours) treatment delocalizes FBXL2 and stabilizes IP3R3[2].
In Vivo: GGTI-2418 (100 mg/kg daily or 200 mg/kg every third day; 15 days) significantly inhibits the growth of breast tumor xenografts in nude mice with MDA-MB-231 xenografts[1]. 
GGTI-2418 (100 mg/kg daily; 5 days) induces regression of ErbB2-driven mammary tumors in ErbB2 transgenic mice[1]. 
GGTI-2418 inhibits the geranylgeranylation of Rap1 and causes a dramatic decrease in S473 phosphorylation of Akt. GGTI-2418 also upregulates p27 levels in vivo[1].

Name: Darusentan Lu-135252, CAS: 171714-84-4, stock 15.7g, assay 98.7%, MWt: 410.42, Formula: C22H22N2O6, Solubility: DMSO : ≥ 125 mg/mL (304.57 mM); H2O : < 0.1 mg/mL (insoluble), Clinical_Informat: Phase 3, Pathway: GPCR/G Protein, Target: Endothelin Receptor, Biological_Activity: Darusentan is a selective endothelin A (ETA) receptor antagonist. Darusentan competes for radiolabeled endothelin binding in rat aortic vascular smooth muscle cells (RAVSMs) membranes with single-site kinetics, exhibiting a Ki=13 nM[1].

Name: Lapaquistat acetate TAK-475, CAS: 189060-13-7, stock 28.5g, assay 99%, MWt: 645.14, Formula: C33H41ClN2O9, Solubility: DMSO : 46 mg/mL (71.30 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Farnesyl Transferase, Biological_Activity: Lapaquistat acetate (TAK-475) is a squalene synthase inhibitor, blocking the conversion of farnesyl diphosphate (FPP) to squalene[1]. Lapaquistat acetate (TAK-475) is originally intended use to Mevalonate Kinase Deficiency (MKD), it is effective at lowering low-density lipoprotein cholesterol, but it might cause liver damage[2].
IC50 & Target: Squalene synthase[1]

Name: Metipranolol hydrochloride, CAS: 36592-77-5, stock 19.5g, assay 98.3%, MWt: 345.86, Formula: C17H28ClNO4, Solubility: DMSO : 100 mg/mL (289.13 mM; Need ultrasonic); H2O : ≥ 100 mg/mL (289.13 mM), Clinical_Informat: Launched, Pathway: GPCR/G Protein;Neuronal Signaling, Target: Adrenergic Receptor;Adrenergic Receptor, Biological_Activity: Metipranolol hydrochloride is a non-selective β adrenergic receptor blocking agent.
IC50 & Target: β adrenergic receptor [1].
In Vitro: Metipranolol is used systemically for the treatment of arterial hypertension and topically for the management of glaucoma[1].

Name: Minodronic acid YM-529, CAS: 180064-38-4, stock 30.7g, assay 98.3%, MWt: 322.15, Formula: C9H12N2O7P2, Solubility: DMSO : < 1 mg/mL (insoluble or slightly soluble); H2O : 5 mg/mL (15.52 mM; Need ultrasonic and warming), Clinical_Informat: No Development Reported, Pathway: Apoptosis;Membrane Transporter/Ion Channel, Target: Apoptosis;P2X Receptor, Biological_Activity: Minodronic acid (YM-529) is a third-generation bisphosphonate that directly and indirectly prevents proliferation, induces apoptosis, and inhibits metastasis of various types of cancer cells. Minodronic acid (YM-529) is an antagonist of purinergic P2X2/3 receptors involved in pain[1][2].
IC50 & Target: P2X2/3[2]

Name: RP-64477, CAS: 135239-65-5, stock 37.1g, assay 98%, MWt: 498.72, Formula: C29H42N2O3S, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Acyltransferase, Biological_Activity: RP-64477 is a potent inhibitor of the cholesterol esterifying enzyme Acyl-coenzyme A:cholesterol O-acyltransferase (ACAT).
IC50 & Target: ACAT[1]
In Vitro: RP-64477 is a potent inhibitor of the cholesterol esterifying enzyme Acyl-coenzyme A:cholesterol O-acyltransferase (ACAT). Inhibitory potencies of RP-64477 in vitro in tissue preparations are obtained from a range of species and in human cell cultures. For animal tissues, IC50 values in the range 6 to 283 nM are recorded, with no obvious species/tissue differences apparent. Potent inhibitory activity of RP-64477 is also recorded in human cell lines of hepatic (HepGZ), intestinal (CaCo-2), and monocytic (THP-1) origin with IC50s of 503, 113, and 180 nM, respectively. No inhibitory activity is recorded against rat PCEH or LCAT at test concentrations up to 200 μM and 20 μM, respectively[1].
In Vivo: Administration of RP-64477 (0.01% and 0.03% w/w by diet) reduces significantly plasma cholesterol levels in cholesterol/cholic acid-fed rats by 29% and 61%, respectively. Food consumption is not affected by dietary incorporation of RP-64477. Animals receiving RP-64477 (10 and 30 mg/kg b.i.d.) over this period exhibit significantly lower plasma cholesterol levels on both days 4 and 7 when compare to values recorded from vehicle treated animals fed the cholesterol-containing diet. Compare to cholesterol-fed controls, after 7 days of dosing, plasma cholesterol levels are 35% and 53% lower in animals receiving 10 and 30 mg/kg b.i.d. doses of RP-64477, respectively[1].

Name: Sapacitabine CS682;CYC682, CAS: 151823-14-2, stock 34.6g, assay 98.4%, MWt: 490.64, Formula: C26H42N4O5, Solubility: DMSO : 25 mg/mL (50.95 mM; Need ultrasonic and warming), Clinical_Informat: Phase 3, Pathway: Cell Cycle/DNA Damage, Target: Nucleoside Antimetabolite/Analog, Biological_Activity: Sapacitabine is an orally available nucleoside analog prodrug that is structurally related to cytarabine.
IC50 & Target: nucleoside analog[1]
In Vitro: Concentrations of Sapacitabine required to achieve an IC50 range from 3±0.6 μM for the colon cancer cell line HCT116 to 67±14 μM for the breast cancer cell line MDA-MB-435. Cell cycle analysis shows that 35% Sapacitabine-treated cells are arrested in late-S phase and 41% in G2/M phase. L1210 cells with deoxycytidine kinase (dCK) activity are sensitive to Sapacitabine, (IC50 20±6 μM). In the docetaxel/Sapacitabine combinations, synergistic effects (CI<1) are observed when docetaxel is given before Sapacitabine in both cell lines[1].
In Vivo: On Day 14, the Sapacitabine (5 mg/kg)+vorinostat (33 mg/kg) group has a mean tumour volume of 245 mm3 and a tumour growth inhibition (TGI) of 92%, whereas the Sapacitabine (15 mg/kg)+vorinostat (33 mg/kg) group has a mean tumour volume of 107 mm3 and a TGI of 112%[2].

Name: SAR125844, CAS: 1116743-46-4, stock 39.1g, assay 98.2%, MWt: 550.63, Formula: C25H23FN8O2S2, Solubility: DMSO : 45 mg/mL (81.72 mM; Need ultrasonic), Clinical_Informat: Phase 2, Pathway: Protein Tyrosine Kinase/RTK;Apoptosis, Target: c-Met/HGFR;Apoptosis, Biological_Activity: SAR125844 is a potent, highly selective, reversible and ATP-competitive MET receptor tyrosine kinase (RTK) inhibitor, with an IC50 of 4.2 nM. Shows inhibition of MET autophosphorylation in cell-based assays[1].
IC50 & Target: IC50: 4.2 nM (MET RTK)[1].

Name: SB 204990, CAS: 154566-12-8, stock 36.3g, assay 98.4%, MWt: 389.27, Formula: C18H22Cl2O5, Solubility: H2O : 10 mg/mL (25.69 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: ATP Citrate Lyase, Biological_Activity: SB 204990 is a potent and specific inhibitor of ATP citrate lyase (ACLY) enzyme.
IC50 & Target: ACLY[1].
In Vitro: SB204990 (SB) is a specific inhibitor of ACLY enzyme. SB204990 treatment leads to a decrease in cytosolic Ac-CoA level and is thus expected to decrease acetylated and active β-catenin levels[1].
In Vivo: SB 204990, when administered orally to rats, is absorbed into the systemic circulation. When administered in the diet (0.05-0.25%, w/w) for 1 week, SB 204990 causes a dose-related decrease in plasma cholesterol (by up to 46%) and triglyceride levels (by up to 80%) in rats. SB 204990 (25 mg/kg per day) also decreases plasma cholesterol levels (by up to 23%) and triglyceride levels (by up to 38%) in the dog, preferentially decreasing low-density lipoprotein compared with high-density lipoprotein cholesterol levels[2].

Name: Teglicar, CAS: 250694-07-6, stock 16.1g, assay 98.9%, MWt: 399.61, Formula: C22H45N3O3, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: Teglicar is a selective and reversible inhibitor of liver isoform of carnitine palmitoyl-transferase 1 (L-CPT1). Teglicar reduces ketogenesis and glucose production, decreases gluconeogenesis and improves glucose homeostasis. Teglicar has a potential antihyperglycemic propert[1].
IC50 & Target: IC50: L-CPT1[1]

Name: Transcrocetinate disodium Disodium trans-crocetinate, CAS: 591230-99-8, stock 25.8g, assay 98.2%, MWt: 372.37, Formula: C20H22Na2O4, Solubility: 10 mM in DMSO, Clinical_Informat: Phase 2, Pathway: Membrane Transporter/Ion Channel;Neuronal Signaling, Target: iGluR;iGluR, Biological_Activity: Transcrocetinate disodium, extracted from saffron (Crocus sativus L.), acts as an NMDA receptor antagonist with high affinity.
IC50 & Target: NMDA receptor[1]
In Vitro: Transcrocetinate (Transcrocetin, trans-Crocetin), a saffron metabolite originating from the crocin apocarotenoids, has been shown to exert strong NMDA receptor affinity and is thought to be responsible for the CNS activity of saffron.To ensure unchanged viability of Caco-2 cells throughout the transport experiments, cellular mitochondrial dehydrogenase activity of Caco-2 cells is measured by MTT assay after a 24 h incubation period with the test compounds: Hydroalcoholic saffron extract saffron extract (SE, 0.5-1 mg/mL) and crocin-1 (250-1000 µM) reveal no negative significant changes in cellular viability. Transcrocetinate at 10 µM level does not change viability while higher concentrations (40-160 µM) reduces significantly cellular viability[1].

Name: Upamostat WX-671, CAS: 590368-25-5, stock 26.8g, assay 98.3%, MWt: 629.81, Formula: C32H47N5O6S, Solubility: DMSO : ≥ 250 mg/mL (396.95 mM), Clinical_Informat: Phase 2, Pathway: Metabolic Enzyme/Protease, Target: Ser/Thr Protease, Biological_Activity: Upamostat is a serine protease inhibitor. Upamostat is the orally available prodrug of the WX-UK1, which is a urokinase plasminogen activator (uPA) inhibitor.
IC50 & Target: Serine protease, uPA[1]
In Vitro: Upamostat is the urokinase plasminogen activator (uPA) inhibitor. Upamostat is the oral pro-drug of the active metabolite WX-UK1, a novel uPA inhibitor[1]. Upamostat inhibits the urokinase-type plasminogen activator (uPA) system, which plays a major role in tumor invasion and metastasis. Upamostat is the orally available amidoxime- (i.e. hydroxyamidine-) prodrug of the pharmacologically active form, WX-UK1[2].
In Vivo: The validated method is used to evaluate the pharmacokinetics of Upamostat (Mesupron) in rats. The mean plasma concentrations of Upamostat after a single intravenous injection of 2 mg/kg in five rats are measured. The substance decays in a mono-phasic pattern with a terminal half-life of 0.5 h; its volume of distribution is 2.0 L/kg, and clearance is about 2.7 L/h/kg[3].

Name: YF-2 (hydrochloride), CAS: 1312005-62-1, stock 6.4g, assay 98.7%, MWt: 467.31, Formula: C20H23Cl2F3N2O3, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Epigenetics, Target: Histone Acetyltransferase, Biological_Activity: YF-2 hydrochloride is a highly selective, blood-brain-barrier permeable histone acetyltransferase activator, acetylates H3 in the hippocampus, with EC50s of 2.75 μM, 29.04 μM and 49.31 μM for CBP, PCAF, and GCN5, respectively, shows no effect on HDAC. Anti-cancer and anti-Alzheimer's disease[1].
IC50 & Target: EC50: 2.75 μM (CBP), 29.04 μM (PCAF), 49.31 μM (GCN5)[1]
In Vitro: YF-2 (0.03, 0.1, 0.25, 0.5, 1, 2.5, 5, 15, 40 and 80 μM, 72 hours) inhibits the preliferation of U251, CCRF-CEM, Hs578T, NCI-ADR-RES cells[1].
In Vivo: YF-2 (20 mg/kg, 2 hours befor electric shock or 5 mg/kg, 30 min before the electric shock, i.p.) rescues the defect in contextual memory in mice, and shows no effect on contextual memory alone at 20 mg/kg in mice[1].

Name: YF-2, CAS: 1311423-89-8, stock 27.2g, assay 98.4%, MWt: 430.85, Formula: C20H22ClF3N2O3, Solubility: DMSO : ≥ 125 mg/mL (290.12 mM); H2O : < 0.1 mg/mL (insoluble), Clinical_Informat: No Development Reported, Pathway: Epigenetics, Target: Histone Acetyltransferase, Biological_Activity: YF-2 is a highly selective, blood-brain-barrier permeable histone acetyltransferase activator, acetylates H3 in the hippocampus, with EC50s of 2.75 μM, 29.04 μM and 49.31 μM for CBP, PCAF, and GCN5, respectively, shows no effect on HDAC. Anti-cancer and anti-Alzheimer's disease[1].
IC50 & Target: EC50: 2.75 μM (CBP), 29.04 μM (PCAF), 49.31 μM (GCN5)[1]
In Vitro: YF-2 (0.03, 0.1, 0.25, 0.5, 1, 2.5, 5, 15, 40 and 80 μM, 72 hours) inhibits the preliferation of U251, CCRF-CEM, Hs578T, NCI-ADR-RES cells[1].
In Vivo: YF-2 (20 mg/kg, 2 hours befor electric shock or 5 mg/kg, 30 min before the electric shock, i.p.) rescues the defect in contextual memory in mice, and shows no effect on contextual memory alone at 20 mg/kg in mice[1].

Name: D159687, CAS: 1155877-97-6, stock 12.2g, assay 98.2%, MWt: 366.84, Formula: C21H19ClN2O2, Solubility: DMSO : 150 mg/mL (408.90 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Phosphodiesterase (PDE), Biological_Activity: D159687 is a selective PDE4D inhibitor[1].
IC50 & Target: PDE4D[1]
In Vitro: D159687 (1 μM, 0-24 hours) induces a transient increase in CREB phosphorylation which peaked at 6 hours after treatment[1]. 
D159687 (0.01-1 μM, 6 hours) causes optimal CREB phosphorylation at 1 μM[1].
In Vivo: D159687 (0.05-5 mg/kg; oral daily for a week) shows a potential recruitment or enhancement of synaptic function with increased task difficulty in female Cynomolgus macaques[2].

Name: 1-Azakenpaullone 1-Akp, CAS: 676596-65-9, stock 4.4g, assay 98.8%, MWt: 328.16, Formula: C15H10BrN3O, Solubility: DMSO : 62.5 mg/mL (190.46 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Stem Cell/Wnt;PI3K/Akt/mTOR, Target: GSK-3;GSK-3, Biological_Activity: 1-Azakenpaullone (1-Akp) is a highly selective and ATP-competitive inhibitor of glycogen synthase kinase-3 β (GSK-3β), with an IC50 value of 18 nM[1].
IC50 & Target: IC50: 18 nM (GSK-3β), 2 μM (CDK1/cyclin B), 4 μM (CDK5/p25)[1].

Name: Riviciclib hydrochloride P276-00, CAS: 920113-03-7, stock 15.1g, assay 98.6%, MWt: 438.30, Formula: C21H21Cl2NO5, Solubility: DMSO : 50 mg/mL (114.08 mM; Need ultrasonic), Clinical_Informat: Phase 2, Pathway: Apoptosis;Cell Cycle/DNA Damage, Target: Apoptosis;CDK, Biological_Activity: Riviciclib hydrochloride (P276-00) is a potent cyclin-dependent kinase (CDK) inhibitor, which inhibits CDK9-cyclinT1, CDK4-cyclin D1, and CDK1-cyclinB with IC50s of 20 nM, 63 nM, and 79 nM, respectively[1][2].
Riviciclib hydrochloride (P276-00) shows antitumor activity on cisplatin-resistant cells[3].
IC50 & Target: IC50: 0.020 μM (Cdk9-T1); 0.063 ± 0.018 μM (Cdk4-D1); 0.079 μM (Cdk1-B); 0.224 μM (Cdk2-A); 2.540 ± 0.409 μM (Cdk2-E); 0.396 μM (Cdk6-D3); 2.900 μM (Cdk9-H);
In Vitro: Riviciclib hydrochloride (1.5-5 μM; 72 hours) shows no detectable cells in G1 and G2 in promyelocytic leukemia cells and arrest of cells in G1 in synchronized human non-small cell lung carcinoma (H-460) and human normal lung fibroblast (WI-38) cells[3]. 
Riviciclib hydrochloride (3-24 hours; 1.5 μM) reduces cyclin D1, Cdk4, and Rb levels in H-460 cells. Rb (retinoblastoma) phosphorylation at Ser780 decrease at 3 h[2]. 
Riviciclib hydrochloride shows activity in human cancer cell lines, such as colon carcinoma, osteosarcomal, cervical carcinoma, and bladder carcinoma cells[2].
In Vivo: Riviciclib hydrochloride (administered i.p.; 35 kg/mg daily for 10 days, in human xenograft mode with severe combined immunodeficient mice) shows significant inhibition in the growth of human colon carcinoma HCT-116 xenograft[3]. 
Riviciclib hydrochloride (administered via i.p.; 50 mg/kg once daily; 30 mg/kg twice daily for 18 treatments, in human xenograft mode with severe combined immunodeficient mice) significantly inhibited growth[3].

Name: Biphenylindanone A BINA;, CAS: 866823-73-6, stock 4.7g, assay 98.9%, MWt: 454.56, Formula: C30H30O4, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein;Neuronal Signaling, Target: mGluR;mGluR, Biological_Activity: Biphenylindanone A (BINA) is a selective human mGluR2 (hmGluR2) potentiator for the treatment of many neurological disorders[1].
In Vitro: Biphenylindanone A (BINA) shows activity on glutamate-induced scintillation proximity assay [3H]IP1 hydrolysis on WT mGluR2 (EC50=1.57 μM) in the absence or presence of 5 μM glutamate[1].

Name: CE-224535 PF-04905428, CAS: 724424-43-5, stock 28.9g, assay 99%, MWt: 480.94, Formula: C22H29ClN4O6, Solubility: 10 mM in DMSO, Clinical_Informat: Phase 2, Pathway: Membrane Transporter/Ion Channel, Target: P2X Receptor, Biological_Activity: CE-224535 is a selective P2X7 receptor antagonist.
IC50 & Target: P2X7 receptor[1]
In Vitro: CE-224535 is developed as a disease-modifying antirheumatic drugs (DMARD) and is a selective antagonist of the human P2X7 receptor. CE-224535 can reduce leukocyte secretion of IL-1 and IL-18, thereby providing a novel therapeutic approach for treatment of rheumatoid arthritis (RA)[1].
In Vivo: In rats, CE-224535 has low CLp (11 mL/min/kg) and a large Vdss of 7.6 L/kg, which results in a half-life of 2.4 h. Upon oral administration to rats at 5 mg/kg, CE-224535 provides maximal plasma exposure (Cmax) that is ~90 fold over its IC90 in human blood (Cmax=0.21 μg/mL or 0.44 μM). The oral bioavailability of CE-224535 is low in rats (F=2.6%), but this is believed to be a rat specific phenomenon since corresponding oral bioavailability in both dog (59%) and monkey (22%) is adequate[2].

Name: AG-13958 AG-013958, CAS: 319460-94-1, stock 37.7g, assay 98.4%, MWt: 467.50, Formula: C26H22FN7O, Solubility: DMSO : 5 mg/mL (10.70 mM; ultrasonic and warming and heat to 60°C), Clinical_Informat: No Development Reported, Pathway: Protein Tyrosine Kinase/RTK, Target: VEGFR, Biological_Activity: AG-13958 (AG-013958), a potent VEGFR tyrosine kinase inhibitor, is used for treatment of choroidal neovascularization associated with age-related macular degeneration (AMD)[1].

Name: RWJ-67657 JNJ 3026582, CAS: 215303-72-3, stock 31.1g, assay 98.7%, MWt: 425.50, Formula: C27H24FN3O, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: MAPK/ERK Pathway, Target: p38 MAPK, Biological_Activity: RWJ 67657 (JNJ 3026582) is an orally active and selective p38α and p38β MAPK inhibitor with IC50s of 1 and 11 μM, respectively. RWJ 67657 displays no activity at p38γ and p38δ, and exhibits cardio protective. Anti-inflammatory and anti-tumor activity[1].
In Vitro: RWJ 67657 inhibits the release of TNF-α by lipopolysaccharide (LPS)-treated human peripheral blood mononuclear cells with an IC50 of 3 nM, as well as the release of TNF-α from peripheral blood mononuclear cells treated with the superantigen staphylococcal enterotoxin B, with an IC50 value of 13 nM[2]. 
RWJ67657 (10 μM; 24 hours) decreases colony formation in MCF-7 cells[3].
In Vivo: RWJ 67657 inhibits TNF-alpha production in lipopolysaccharide-injected mice (87% inhibition at 50 mg/kg) and in rats (91% inhibition at 25 mg/kg) after oral administration[2]. 
RWJ-67657 (50 mg/kg; administered orally; once per day for 7 consecutive days) displays a potent anti-inflammatory effect. By both improving the functioning of endothelial progenitor cells (EPCs) and reducing inflammation, EPC transplantation plus RWJ-67657 administration synergistically promotes angiogenesis and neurogenesis after diabetic stroke[4].

Name: 2-Hydroxy-4-methoxybenzoic acid 4-Methoxysalicylic Acid, CAS: 2237-36-7, stock 14.9g, assay 98.4%, MWt: 168.15, Formula: C8H8O4, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: 2-Hydroxy-4-methoxybenzoic acid is a derivative of methoxybenzoic. 2-Hydroxy-4-methoxybenzoic is a potential biomarker.

Name: Thapsigargin Thapsigargin (TG), CAS: 67526-95-8, stock 39.7g, assay 98.1%, MWt: 650.75, Formula: C34H50O12, Solubility: DMSO : 250 mg/mL (384.17 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Apoptosis;Membrane Transporter/Ion Channel;Neuronal Signaling, Target: Apoptosis;Calcium Channel;Calcium Channel, Biological_Activity: Thapsigargin is an inhibitor of microsomal Ca2+-ATPase. Thapsigargin is a well characterized Endoplasmic Reticulum (ER) stress inducing agent[1][2][3][4].
IC50 & Target: Ca2+-ATPase[1]
In Vitro: Thapsigargin (0.001- 1 μM; for 2 and 4 days) arrests cell proliferations in MH7A human rheumatoid arthritis synovial cells in a time- and dose-dependent manner[2]. 
Thapsigargin (0.001- 1 μM; for 2 and 4 days) induces cell apoptosis in MH7A cells in a time- and dose-dependent manner[2]. 
Thapsigargin (0.001- 1 μM; for 2 and 4 days) impairs mTOR activity and leads to cyclin D1 expressions in MH7A cells[2]. 
Thapsigargin inhibits Ca2+ entry into human neutrophil granulocytes[1]. 
Thapsigargin inhibits the carbachol-evoked [Ca2+]i-transients with (IC50=0.353 nM) or without (IC50=0.448 nM) a KCl-prestimulation, but an additional small component, with a much lower sensitivity (IC50=4814 nM), is observed in the absence of a KCl-prestimulation. In contrast, the KCl-evoked [Ca2+]i-transients displayed only one component with a very low sensitivity to Thapsigargin in both absence (IC50=3343 nM) and presence (IC50=6858 nM) of a carbachol-prestimulation[3]. 
In Vivo: Thapsigargin (Injection; 0.25ug/g, 0.5ug/g and 1ug/g; 24 hours) significant increases of 2 to 5-fold in chemokine and pro-inflammatory expression. Thapsigargin is more sensitive to inducing a systemic immune response[4].

Name: Calcimycin (hydrate) A23187 (hydrate), CAS: 52665-69-7, stock 28g, assay 98.1%, MWt: 528.14, Formula: C29H37N3O6.1/4H2O, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Apoptosis;Autophagy, Target: Apoptosis;Autophagy, Biological_Activity: Calcimycin hydrate (A23187 hydrate) is an antibiotic and a unique divalent cation ionophore (like calcium and magnesium). Calcimycin hydrate induces Ca2+-dependent cell death by increasing intracellular calcium concentration. Calcimycin hydrate inhibits the growth of Gram-positive bacteria and some fungi. Calcimycin hydrate also inhibits the activity of ATPase and uncouples oxidative phosphorylation of mammalian cells. Calcimycin hydrate induces apoptosis[1][2][3][4].

Name: SR144528, CAS: 192703-06-3, stock 8.1g, assay 98.2%, MWt: 476.05, Formula: C29H34ClN3O, Solubility: DMSO : 50 mg/mL (105.03 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein;Neuronal Signaling, Target: Cannabinoid Receptor;Cannabinoid Receptor, Biological_Activity: SR144528 is a potent and selective CB2 receptor antagonist with a Ki of 0.6 nM.
IC50 & Target: Ki: 0.6 nM (CB2 receptor)[1]
In Vitro: SR144528 is a potent and selective CB2 receptor antagonist with a Ki of 0.6 nM. SR144528 alone is able to stimulate in a concentration-dependent manner (EC50=26±6 nM, two experiments) the forskolin-sensitive adenylyl cyclase activity in CHO-CB2 cells with a maximum effect at 1 μM (4-fold stimulation) whereas at this concentration it has no significant effect on CHO-CB1 cells (15% inhibition)[1]. Raw 264.7 macrophages supplemented with SR144528 display reduced caspase-3 activity. SR144528 inhibits microsomal acyl-coenzymeA:cholesterol acyltransferase (ACAT) activity in a concentration-dependent manner with an IC50 value of 3.6±1.1 μM. At 10 μM, SR144528 inhibits ACAT activities ~68%[2].
In Vivo: No effect on the binding of [3H]-CP 55,940 to its specific sites in the brain is observed after either oral (up to 10 mg/kg) or i.c.v. (10 μg/animal) administration of SR144528 in mice. The occupancy by SR144528 of the spleen cannabinoid receptor is time-dependent and significant for at least 18 hours after oral administration at 3 mg/kg[1]. SR144528 does not induce any significant effect on gastrointestinal (GI) motility when given alone. SR144528 does not block but enhances delayedgastric emptying[3].

Name: CID-1067700, CAS: 314042-01-8, stock 16.1g, assay 98.5%, MWt: 390.48, Formula: C18H18N2O4S2, Solubility: DMSO : 75 mg/mL (192.07 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein, Target: Ras, Biological_Activity: CID-1067700 is a pan GTPase inhibitor, and competitively inhibits Ras-related in brain 7 (Rab7) with a Ki of 13 nM.
IC50 & Target: Ki: 13 nM (Rab7)[1]
In Vitro: CID-1067700 is a pan GTPase inhibitor, and competitively inhibits Rab7 with a Ki of 13 nM. CID-1067700 shows inhibitory activity against nucleotide binding by Rab7, with Kds of 100 nM and 40 nM for BODIPY-GTP and BODIPY-GDP, respectively. With increasing concentration, CID-1067700 causes strong inhibition on binding of the BODIPY-linked nucleotides, with EC50 values of 11.22 ± 1.34 nM for BODIPY-GTP and 20.96 ± 1.34 nM for BODIPY-GDP and calculated Ki values of 12.89 nM and 19.70 nM respectively. CID-1067700 (10 μM) has no effect on the rate of release of bound BODIPY-linked nucleotide by wild type Rab7 under equilibrium binding conditions[1]. CID-1067700 (0-40 μM) inhibits Rab7 activity, NF-κB activation as well as AID induction in B cells. Furthermore, CID-1067700 binds Rab7 with a high affinity (EC50: 10-20 nM), and blocks Class switch DNA recombination (CSR) in B cells via targeting Rab7[2].
In Vivo: CID-1067700 (16 mg/kg, i.p.) prevents disease development in lupus-prone mice by Rab7 inhibition, and reduces IgG-IC deposition in MRL/Faslpr/lpr mice. CID-1067700 also targets B cells and specifically impairs the CSR machinery in vivo[2].

Name: Benzyl isothiocyanate, CAS: 622-78-6, stock 7g, assay 98.8%, MWt: 149.21, Formula: C8H7NS, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Apoptosis;Anti-infection, Target: Apoptosis;Bacterial, Biological_Activity: Benzyl isothiocyanate is a member of natural isothiocyanates with antimicrobial activity[1][2]. Benzyl isothiocyanate potent inhibits cell mobility, migration and invasion nature and matrix metalloproteinase-2 (MMP-2) activity of murine melanoma cells[2].

Name: Tozasertib VX 680;MK-0457, CAS: 639089-54-6, stock 35.3g, assay 98.9%, MWt: 464.59, Formula: C23H28N8OS, Solubility: DMSO : ≥ 106.67 mg/mL (229.60 mM), Clinical_Informat: Phase 2, Pathway: Cell Cycle/DNA Damage;Epigenetics;Autophagy, Target: Aurora Kinase;Aurora Kinase;Autophagy, Biological_Activity: Tozasertib (VX 680; MK-0457) is an inhibitor of Aurora A/B/C kinases with Kis of 0.6, 18, 4.6 nM, respectively.
IC50 & Target: Ki: 0.6 nM (Aurora A), 18 nM (Aurora B), 4.6 nM (Aurora C)[1]
In Vitro: Tozasertib induces similar cytotoxicity with IC50 of approximately 300 nM and exhibits an AUR B-like inhibitory phenotype of G2/M arrest, endoreduplication and apoptosis in BaF3 cells transfected with ABL or FLT-3 (mutant and wild type) kinases. Tozasertib prevents the CAL-62 proliferation in a time-dependent manner. Tozasertib treatment for 14 days significantly decreases the number and size of colonies by approximately 70% in the 8305C and 90% in the CAL-62, 8505C and BHT-101. Treatment of the different ATC cells with Tozasertib inhibits proliferation with the IC50 between 25 and 150 nM. The Tozasertib significantly impairs the ability of the different cell lines to form colonies in soft agar. Analysis of caspase-3 activity indicates that Tozasertib induces apoptosis in the different cell lines. CAL-62 cells exposed for 12 hours to Tozasertib show an accumulation of cells with ≥ 4N DNA content. Time-lapse analysis demonstrates that Tozasertib-treated CAL-62 cells exit metaphase without dividing. Moreover, histone H3 phosphorylation is abrogated following Tozasertib treatment[2]. Tozasertib has significant inhibitory activity against BCR-Abl bearing the T315I mutation in patient-derived samples[3].

Name: AM-1638, CAS: 1142214-62-7, stock 24.8g, assay 98.6%, MWt: 514.63, Formula: C33H35FO4, Solubility: DMSO : 250 mg/mL (485.79 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein, Target: GPR40, Biological_Activity: AM-1638 is a potent and orally bioavailable GPR40/FFA1 full agonist with an EC50 of 0.16 μM.
IC50 & Target: IC50: 0.16 μM (GPR40/FFA1)[1]
In Vivo: AM-1638 exhibits moderate cross-species plasma clearance and volume of distribution, resulting in plasma half-lives suitable for evaluation of its antidiabetic properties in mouse, rat, and cynomologus monkey. Moreover, oral administration of full agonist AM-1638 demonstrates excellent oral bioavailability (mouse, >100%; rat, 72%; and cyno, 71%). AM-1638
exhibits antidiabetic activity in BDF/DIO mice[1].

Name: KW-2478, CAS: 819812-04-9, stock 10.5g, assay 98.7%, MWt: 574.66, Formula: C30H42N2O9, Solubility: DMSO : ≥ 83.3 mg/mL (144.96 mM), Clinical_Informat: Phase 2, Pathway: Metabolic Enzyme/Protease;Cell Cycle/DNA Damage, Target: HSP;HSP, Biological_Activity: KW-2478 is an inhibitor of Hsp90α, with an IC50 of 3.8 nM, and has antitumor activity against various human hematological tumor cells.
IC50 & Target: IC50: 3.8 nM (Hsp90α)[1]
In Vitro: KW-2478 is an inhibitor of Hsp90, with an IC50 of 3.8 nM for Hsp90α. KW-2478 shows anti-proliferative activity against multiple myeloma (MM) and non-Hodgkin’s lymphoma (NHL), with GI50s of 0.30 μM (OPM-2/GFP), 0.34 μM (KMS-11), 0.39 μM (RPMI 8226), 0.12 μM (NCI-H929), 0.36 μM (Raji), 0.098 μM (SR), and 0.33 μM μM (SC-1). KW-2478 also inhibits the transcription of c-Maf and Cyclin D1 genes by mainly suppressing the function of Cdk9[1].
In Vivo: KW-2478 (25-200 mg/kg, i.v.) inhibits tumor growth in combined immunodeficiency (SCID) mice bearing NCI-H929 cells, without body weight loss. KW-2478 (100 mg/kg, i.v.) causes degradation of the Hsp90 client proteins (IGF-1Rβ, c-Raf-1, Cdk9) levels and dephosphorylated Erk1/2 proteins in NCI-H929 tumors of mice[1].

Name: Oridonin NSC-250682; Isodonol, CAS: 28957-04-2, stock 33.7g, assay 98.4%, MWt: 364.43, Formula: C20H28O6, Solubility: DMSO : ≥ 150 mg/mL (411.60 mM), Clinical_Informat: No Development Reported, Pathway: Anti-infection;PI3K/Akt/mTOR, Target: Bacterial;Akt, Biological_Activity: Oridonin (NSC-250682), a diterpenoid isolated from Rabdosia rubescens, acts as an inhibitor of AKT, with IC50s of 8.4 and 8.9 μM for AKT1 and AKT2; Oridonin possesses anti-tumor, anti-bacterial and anti-inflammatory effects.
IC50 & Target: IC50: 8.4 μM (AKT1), 8.9 μM (AKT2)[1]
In Vitro: Oridonin is an ATP-competitive inhibitor of AKT with IC50s of 8.4 and 8.9 μM for AKT1 and AKT2, respectively. Oridonin (5, 10 or 20 μM) obviously inhibits the growth of KYSE70, KYSE410 and KYSE450 ESCC cells via targeting AKT1/2. Oridonin (10 or 20 μM) causes G2/M phase cell cycle arrest in KYSE70, KYSE410 and KYSE450 cells, and induces apoptosis in these three cell lines at 20 μM. In addition, Oridonin (5, 10 or 20 μM) in combination with cisplatin or 5-FU enhances the inhibition of esophageal squamous cell carcinoma (ESCC) cell growth[1]. Oridonin (0.1 and 1 μM) preferentially suppresses AKT/mTOR signaling. Oridonin (1 μM) also selectively suppresses growth of breast cancer cells with hyperactivation of AKT signaling[2].
In Vivo: Oridonin (160 mg/kg, p.o.) shows significant reduction in the tumor growth without obvious weigh loss in SCID mice bearing EG9 and HEG18 tumor cells. Oridonin treatment also suppresses the expression of Ki-67, phosphorylated AKT, GSK-3β or mTOR in mice[1]. Oridonin (15 mg/kg, i.p.) impairs cell growth in breast cancer with hyperactivation of AKT signaling in nude mice[2].

Name: Vitexin, CAS: 3681-93-4, stock 7.7g, assay 98.3%, MWt: 432.38, Formula: C21H20O10, Solubility: DMSO : 83.33 mg/mL (192.72 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Vitexin is a c-glycosylated flavone, and is found in various medicinal plants species such as Ficus deltoid and Spirodela polyrhiza. Vitexin has a wide range of pharmacological effects, including anti-oxidant, anti-cancer, anti-inflammatory, anti-hyperalgesic, and neuroprotective effects[1][2].
In Vivo: Vitexin exerts neuroprotective effect against pentylenetetrazole-induced seizures, scopolamine-induced memory impairment, and glutamate-induced neuronal excitotoxicity[1].

Name: Cistanoside A, CAS: 93236-42-1, stock 8.5g, assay 98.3%, MWt: 800.75, Formula: C36H48O20, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Cistanoside A is a phenylethanoid isolated from Cistanche deserticola, reduces NO accumulation, but shows no effect on iNOS mRNA, iNOS protein levels or iNOS activity. Anti-inflammatory effect[1].

Name: 2'-Acetylacteoside, CAS: 94492-24-7, stock 33.6g, assay 98.8%, MWt: 666.62, Formula: C31H38O16, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: 2'-Acetylacteoside is a phenylethanoid glycoside isolated from Brandisia hancei, inhibits free radical-induced hemolysis of red blood cells and exhibits free radical scavenging activity[1].

Name: Polyphyllin I, CAS: 50773-41-6, stock 32.2g, assay 98.3%, MWt: 855.02, Formula: C44H70O16, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: MAPK/ERK Pathway;Apoptosis;PI3K/Akt/mTOR;PI3K/Akt/mTOR;PI3K/Akt/mTOR;Autophagy, Target: JNK;Apoptosis;mTOR;Akt;PDK-1;Autophagy, Biological_Activity: Polyphyllin I is a bioactive constituent extracted from Paris polyphylla, has strong anti-tumor activity. Polyphyllin I is an activator of the JNK signaling pathway and is an inhibitor of PDK1/Akt/mTOR signaling. Polyphyllin I induces autophagy, G2/M phase arrest and apoptosis[1][2][3].
IC50 & Target: JNK signaling[2] 
PDK1/Akt/mTOR signaling[3]

Name: Ferulic acid Coniferic acid, CAS: 1135-24-6, stock 6.2g, assay 98.7%, MWt: 194.18, Formula: C10H10O4, Solubility: DMSO : 100 mg/mL (514.99 mM; Need ultrasonic), Clinical_Informat: Launched, Pathway: Protein Tyrosine Kinase/RTK;Metabolic Enzyme/Protease, Target: FGFR;Endogenous Metabolite, Biological_Activity: Ferulic acid is a novel fibroblast growth factor receptor 1 (FGFR1) inhibitor with IC50s of 3.78 and 12.5 μM for FGFR1 and FGFR2, respectively.
IC50 & Target: IC50: 3.78 μM (FGFR1), 12.5 μM (FGFR2)[1]
In Vitro: Ferulic acid (FA) is a novel fibroblast growth factor receptor 1 (FGFR1) inhibitor with IC50s of 3.78 and 12.5 μM for FGFR1 and FGFR2, respectively. Ferulic acid exhibits great inhibitory activity on FGFR1 with an inhibitory rate of 92% at 1 µM. The proliferation of HUVEC stimulated by FGF1 is markedly decreased after Ferulic acid treatment ranging from 5 to 40 μM for 24 h. Ferulic acid does not exert significant cell viability up to 20 μM, but over 30 μM Ferulic acid exhibits a cytotoxic effect in HUVEC compare to the control. Ferulic acid inhibits FGF1-induced HUVEC migration and invasion in a dose-dependent manner. Ferulic acid markedly suppresses the FGF1-induced phosphorylation of PI3K and Akt. Ferulic acid treatments significantly inhibit MMP-2 and MMP-9 expression stimulated by FGF1[1].
In Vivo: Treatment with Ferulic acid (FA) potently inhibits FGF1-induced neovascularization. It is found that intragastric administration of Ferulic acid markedly inhibits tumor volume and tumor weight, as compare to the counterparts treated with DMSO. Furthermore, Ferulic acid treatment is well tolerated, and there is no significant difference in weight between the vehicle group and the FA-treated groups[1]. Ferulic acid (0.01, 0.1, 1 or 10 mg/kg) given by oral route decreases significantly the immobility time in the forced swimming test (FST) and tail suspension test (TST), whereas produces no effect in the open-field test. Results demonstrate that the administration of Ferulic acid (0.001 mg/kg, p.o.) boosts the antidepressant-like effect of fluoxetine (5 mg/kg, p.o.) in the TST[2].

Name: Ethyl ferulate, CAS: 4046-02-0, stock 19.5g, assay 98.9%, MWt: 222.24, Formula: C12H14O4, Solubility: DMSO : ≥ 100 mg/mL (449.96 mM), Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease;NF-κB;Immunology/Inflammation, Target: Reactive Oxygen Species;Reactive Oxygen Species;Reactive Oxygen Species, Biological_Activity: Ethyl ferulate, a naturally lipophilic derivative of ferulic acid originally derived from giant fennel (F. communis), induces heme oxygenase-1 (HO-1) and protects rat neurons against oxidative stress[1]. Ethyl ferulate also protects neurons against amyloid β peptide (1-42)-induced oxidative stress and neurotoxicity[2].

Name: Angoroside C, CAS: 115909-22-3, stock 4.3g, assay 98.7%, MWt: 784.75, Formula: C36H48O19, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Angoroside C, a phenylpropanoid glycoside isolated from Radix Scrophulariae, has beneficial effects against ventricular remodeling[1].
In Vivo: Angoroside C has beneficial effects against ventricular remodeling. The mechanism is likely to be related to decreasing the level of Ang Ⅱ, attenuating the mRNA expressions of ET-1 and TGF-β1[1].

Name: Crotonoside Isoguanosine, CAS: 1818-71-9, stock 7.8g, assay 98.5%, MWt: 283.24, Formula: C10H13N5O5, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Protein Tyrosine Kinase/RTK;Epigenetics;Cell Cycle/DNA Damage, Target: FLT3;HDAC;HDAC, Biological_Activity: Crotonoside is isolated from Chinese medicinal herb, Croton. Crotonoside inhibits FLT3 and HDAC3/6, exhibits selective inhibition in acute myeloid leukemia (AML) cells. Crotonoside could be a promising new lead compound for the treatment of AML[1].
In Vitro: Crotonoside (0-200 μM;) selectively inhibits the viability of AML cell line MV4-11, MOLM-13 (with FLT3-ITD mutant) and KG-1 (without FLT3-ITD mutant) in a dose-dependent manner with an IC50 of 11.6 μM, 12.7 μM and 17.2 μM, respectively[1].
Crotonoside (0-100μM; 7 hours) inhibits the phosphorylation of FLT3 Erk1/2, Akt/mTOR and STAT5 is strongly inhibited by crotonoside at higher concentration of 12.5 μM in a concentration-dependent manner[1].
Crotonoside (0-100 μM; 12 hours) exhibits a dose-dependent increase in the percentage of G0/G1 phase and a dose-dependent decrease in the percentage of G2/M and S phases cells[1].
Crotonoside (0-100 μM; 24 hours) leads to concentration-dependent changes in the number of apoptotic MV4-11 cells, results in a dose-dependent decrease in the level of pro-caspase-3 and a dose-dependent increase in the level of the cleaved caspase-3 fragments[1].
In Vivo: Crotonoside(intraperitoneal and intravenous injection; 70 mg/kg, 35 mg/kg; once daily) induces a significant antitumor activity and inhibited xenograft tumor progress as compared to treatment with vehicle[1].

Name: Brazilin, CAS: 474-07-7, stock 17.8g, assay 98.5%, MWt: 286.28, Formula: C16H14O5, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Apoptosis;Autophagy, Target: Apoptosis;Autophagy, Biological_Activity: Brazilin is a red dye precursor obtained from the heartwood of several species of tropical hardwoods. Brazilin inhibits the cells proliferation, promotes apoptosis, and induces autophagy through the AMPK/mTOR pathway. Brazilin shows chondroprotective and anti-inflammatory activities[1][2][3].

Name: Byakangelicol, CAS: 26091-79-2, stock 22g, assay 98.5%, MWt: 316.31, Formula: C17H16O6, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Immunology/Inflammation, Target: COX, Biological_Activity: Byakangelicol, isolated from Angelica dahurica, inhibits interleukin-1beta (IL-1beta) -induced prostaglandin E2 (PGE2) release in A549 cells mediated by suppression of cyclooxygenase-2 (COX-2) expression and the activity of COX-2 enzyme. Byakangelicol has therapeutic potential as an anti-inflammatory drug on airway inflammation[1].

Name: Praeruptorin C, CAS: 72463-77-5, stock 1.4g, assay 98.4%, MWt: 428.47, Formula: C24H28O7, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Membrane Transporter/Ion Channel;Neuronal Signaling, Target: Calcium Channel;Calcium Channel, Biological_Activity: Praeruptorin C is a main bioactive constituent of Peucedanum praeruptorum (also known as Bai-Hua Qian Hu). Praeruptorin C is a calcium antagonist with pD2′ value of 5.7[1].

Name: (±)-Praeruptorin A, CAS: 73069-25-7, stock 37.9g, assay 98.1%, MWt: 386.40, Formula: C21H22O7, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Membrane Transporter/Ion Channel;Neuronal Signaling, Target: Calcium Channel;Calcium Channel, Biological_Activity: (±)-Praeruptorin A is the di-esterified product of cis-khellactone (CKL) and the major active ingredient in Peucedani Radix which consists of the dried roots of Peucedanum praeruptorumDunn (Apiaceae). (±)-Praeruptorin A has been widely employed as one of the famous traditional Chinese medicines (TCMs) for the treatment of cough with thick sputum and dyspnea, nonproductive cough and upper respiratory infections for centuries in China. (±)-Praeruptorin A has dramatically therapeutic effects on hypertension mainly through acting as a Ca2+-influx blocker[1].

Name: Praeruptorin B Praeruptorin D, CAS: 73069-28-0, stock 2.9g, assay 98.6%, MWt: 426.46, Formula: C24H26O7, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Fatty Acid Synthase (FAS), Biological_Activity: Praeruptorin B is an inhibitor of sterol regulatory element-binding proteins (SREBPs).
IC50 & Target: SREBP[1].
In Vitro: Praeruptorin B inhibits the SREBPs activity and decreases intracellular lipid levels. Praeruptorin B is found to powerfully decrease the SRE-luciferase activity, and this effect is dose dependent. Praeruptorin B shows negligible cytotoxicity, even at the higher concentration. Praeruptorin B also significantlytly down-regulates the expression of SREBP-1c and SREBP-2[1]. Praeruptorin B also exhibits significant inhibition on the activity of UGT1A9[2].
In Vivo: The mice treated with Praeruptorin B (50 mg/kg) are significantly lighter than the vehicle treated mice, although they are still heavier than the chow diet-fed mice, suggesting that Praeruptorin B can ameliorate diet-induced obesity (DIO). More importantly, the fat/lean and fat/body-weight ratios are obviously dropped at the same dosage of Praeruptorin B treated mice. It is also showed that the serum TC and TG levels of Praeruptorin B treated mice are significantly lower than those of the HFD-fed mice. Praeruptorin B increases HDL-c and decreases LDL-c similar as lovastatin. In addition, compared with vehicle treated mice, Praeruptorin B significantly lowers the level of TC and TG in liver, comparable to lovastatin. The staining results reveal that Praeruptorin B-treated mice exhibit less lipid accumulation than that of vehicle treated mice. The elevated fasting blood glucose and insulin in HFD-fed mice are significantly reduced by Praeruptorin B[1].

Name: Epothilone A Epo A, CAS: 152044-53-6, stock 32.2g, assay 98.6%, MWt: 493.66, Formula: C26H39NO6S, Solubility: DMSO : 125 mg/mL (253.21 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Cell Cycle/DNA Damage;Cytoskeleton;Apoptosis, Target: Microtubule/Tubulin;Microtubule/Tubulin;Apoptosis, Biological_Activity: Epothilone A is a competitive inhibitor of the binding of [3H] paclitaxel to tubulin polymers, with a Ki of 0.6-1.4 μM.
In Vitro: Epothilone A is a competitive inhibitor of the binding of [3H] paclitaxel to tubulin polymers. The apparent Ki value for Epothilone A is 1.4 μM by Hanes analysis and 0.6 μM by Dixon analysis[1]. Epothilone A, is noted to be highly cytotoxic (IC50=0.05 μM) in vitro when applied to the human T-24 bladder carcinoma cell line. The binding affinity of Epothilone A to tubulin is of the same order of magnitude as the binding affinity of paclitaxel to tubulin based on competition assays. The IC50 for displacement of 100 nM of (3H) paclitaxel from the tubulin binding site is 3.6 μM for paclitaxel, 2.3 μM for Epothilone A, and 3.3 μM for patupilone[2].

Name: CCG-50014, CAS: 883050-24-6, stock 10.6g, assay 98.9%, MWt: 316.35, Formula: C16H13FN2O2S, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein, Target: RGS Protein, Biological_Activity: CCG-50014 is the most potent against the regulator of G-protein signaling protein type 4 (RGS4) (IC50 =30 nM) and is >20-fold selective for RGS4 over other RGS proteins. CCG-50014 binds covalently to the RGS, forming an adduct on two cysteine residues located in an allosteric regulatory site[1]. CCG50014, reduces nociceptive responses and enhances opioid-mediated analgesic effects in the mouse formalin test[2].
In Vivo: CCG50014 (10, 30, or 100 nM) attenuates the nociceptive responses during the late phase in a dose-dependent manner[2].

Name: Aloperine, CAS: 56293-29-9, stock 23g, assay 98.4%, MWt: 232.36, Formula: C15H24N2, Solubility: DMSO : 31.25 mg/mL (134.49 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Apoptosis;Autophagy;Anti-infection;Anti-infection, Target: Apoptosis;Autophagy;Filovirus;HIV, Biological_Activity: Aloperine is an alkaloid in sophora plants such as Sophora alopecuroides L, which has shown anti-cancer, anti-inflammatory and anti-virus properties[1].
Aloperine is widely used to treat patients with allergic contact dermatitis eczema and other skin inflammation in China[2]. Aloperine induces apoptosis and autophagy in HL-60 cells[1].
In Vitro: Aloperine (1-20 mM; 24 hours) gives growth-inhibitory IC50 values in cancer cells ranges from 0.04 to 1.36 mM, the IC50 values in HL-60, U937, K562, EC109, A549 and HepG2 cells are 0.04, 0.27, 0.36, 1.11, 1.18 and 1.36 mM,respectively[1].
Aloperine (1-20 mM; 24 hours) induces apoptosis and decreases bcl-2 expression in HL-60 cells[1].
Aloperine (20–100 mM; 18 hours) induces autophagy and formation of acidic vacuole in HL-60 cells[1].

Name: Crustecdysone 20-Hydroxyecdysone, CAS: 5289-74-7, stock 24.3g, assay 98.2%, MWt: 480.63, Formula: C27H44O7, Solubility: DMSO : 125 mg/mL (260.08 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Apoptosis;Autophagy, Target: Caspase;Autophagy, Biological_Activity: Crustecdysone (20-Hydroxyecdysone) is a naturally occurring ecdysteroid hormone isolated from Cyanotis arachnoides C.B.Clarke which controls the ecdysis (moulting) and metamorphosis of arthropods, it inhibits caspase activity and induces autophagy via the 20E nuclear receptor complex, EcR-USP[1].
Crustecdysone exhibits regulatory or protective roles in the cardiovascular system[2].

Name: AS-604850, CAS: 648449-76-7, stock 22.6g, assay 98.3%, MWt: 285.22, Formula: C11H5F2NO4S, Solubility: DMSO : 250 mg/mL (876.52 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: PI3K/Akt/mTOR, Target: PI3K, Biological_Activity: AS-604850 is a potent, selective and ATP-competitive PI3Kγ inhibitor with an IC50 value of 0.25 μM and a Ki value of 0.18 μM. AS-604850 shows isoform selective inhibitor of PI3Kγ with over 30-fold selectivity for PI3Kδ and β, and 18-fold selectivity over PI3Kα, respectively[1].
In Vitro: AS-604850 inhibits C5a-mediated PKB phosphorylation with an IC50 of 10 μM in RAW264 mouse macrophages[1]. 
AS-604850 blocks PKB phosphorylation induced by MCP-1 and has little or no effect after stimulation with CSF-1 in in primary monocytes from Pik3cg+/+ or Pik3cg–/– mice[1]. 
AS-604850 (0-30 μM; 15 minutes; primary monocytes from Pik3cg+/+ mice) treatment inhibits MCP-1-mediated phosphorylation of PKB and its downstream substrates GSK3α andβ in a concentration-dependent manner. MCP-1-induced phosphorylation of p44/42 ERK (ERK1/2) MAPKs is also reduced, in a concentration dependent manner in primary monocytes from Pik3cg+/+ mice[1].
In Vivo: AS-604850 (10-100 mg/kg; oral administration; for 4.5 or 4.25 hours; Balb/C or C3H mice) treatment reduces RANTES-induced peritoneal neutrophil recruitment with an ED50 value of 42.4 mg/kg. In the thioglycollate-induced peritonitis model, oral administration of 10 mg/kg AS-604850 results in a 31% reduction of neutrophil recruitment[1].

Name: Cepharanthine, CAS: 481-49-2, stock 7.1g, assay 98.5%, MWt: 606.71, Formula: C37H38N2O6, Solubility: DMSO : 125 mg/mL (206.03 mM; Need ultrasonic), Clinical_Informat: Launched, Pathway: Apoptosis;Autophagy;Anti-infection, Target: Apoptosis;Autophagy;HIV, Biological_Activity: Cepharanthine, an alkaloid derived from Stephania cepharantha Hayata, with possesses anti-inflammatory and antioxidative activities[1][2][3]. Cepharanthine attenuates muscle and kidney injuries induced by limb ischemia/reperfusion (I/R)[3]. Cepharanthine induces autophagy, apoptosis and cell cycle arrest in breast cancer cells[4]. Cepharanthine inhibits the HIV-1 entry process by reducing plasma membrane fluidity[5].

Name: Tretazicar CB 1954, CAS: 21919-05-1, stock 35.6g, assay 98.6%, MWt: 252.18, Formula: C9H8N4O5, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Cell Cycle/DNA Damage, Target: DNA Alkylator/Crosslinker, Biological_Activity: Tretazicar (CB 1954), an antitumor prodrug, is highly selective against the Walker 256 rat tumour line. Tretazicar is enzymatically activated to generate a bifunctional agent, which can form DNA-DNA interstrand cross-links. Tretazicar in rat cells involves the reduction of its 4-nitro group to a 4-hydroxylamine by the enzyme NAD(P)H:quinone oxidoreductase 1 (NQO1)[1][2].
In Vitro: Tretazicar (CB 1954) (0.1-1000 μM; 3 days) has sensitivity for retrovirally transduced AB22 (AB22-nr) cells with an IC50 of 3 μM[3]. 
DNA cross-link formation in affected cells is a result of the bioactivation of the drug by the enzyme DT diaphorase (NAD(P)H dehydro-genase (quinone)) in the Walker cells which reduces the 4-nitro group of Tretazicar. The product of this reaction is a difunctional alkylating agent, 5-aziridin-1-yl-4-hydroxylamino-2-nitrobenzamide[4].
In Vivo: Tretazicar (CB 1954) (80 mg/kg; i.p. on days 2 and 9) results in a significant increase in survival[3].

Name: Beraprost (sodium), CAS: 496807-11-5, stock 19.2g, assay 98%, MWt: 420.47, Formula: C24H29NaO5, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein, Target: Prostaglandin Receptor, Biological_Activity: Beraprost sodium, a prostacyclin analog, is a stable and orally active prodrug of PGI2. Beraprost sodium is a potent vasodilator, has the potential for pulmonary arterial hypertension treatment through expanding renal vessels, improving microcirculation[1].
IC50 & Target: prodrug of PGI2; Vasodilator[1]
In Vitro: Beraprost sodium (0.1, 1.0, and 10.0 μM; 24 hours) treatment leads to a significant increase in the number of tube formation, BPS plays an important role on angiogenic activity[1]. Beraprost sodium (0.1, 1.0, and 10.0 μM; 24 hours) treatment let VE-cadherin at regions of cell–cell contact becomes more abundant and the morphology of endothelial cells tends to be normal compared with those cultured under hypoxia conditions[1].
In Vivo: Beraprost sodium (oral adminstration; 0.6 mg/kg; once daily; 3 or 7 days) can mitigate the development of renal interstitial fibrosis, decrease renal oxidative stress through its potential vasodilation effect, and further prevent renal interstitial fibrosis[1].

Name: BI-9627, CAS: 1204329-34-9, stock 36.7g, assay 98.4%, MWt: 356.34, Formula: C16H19F3N4O2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Membrane Transporter/Ion Channel, Target: Sodium Channel, Biological_Activity: BI-9627 is a sodium-hydrogen exchanger isoform 1 (NHE1) inhibitor with an EC50 of 31 nM[1].
IC50 & Target: EC50: 31 nM (Sodium-hydrogen exchanger isoform 1)[1]

Name: SA 47, CAS: 792236-07-8, stock 15.6g, assay 98.4%, MWt: 334.41, Formula: C17H26N4O3, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Neuronal Signaling;Metabolic Enzyme/Protease;Autophagy, Target: FAAH;FAAH;Autophagy, Biological_Activity: SA 47 is a selective and potent inhibitor of fatty acid amide hydrolase (FAAH) and carbamate[1].
IC50 & Target: FAAH, Carbamate[1].

Name: PF 750, CAS: 959151-50-9, stock 13.6g, assay 98.4%, MWt: 345.44, Formula: C22H23N3O, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Neuronal Signaling;Metabolic Enzyme/Protease;Autophagy, Target: FAAH;FAAH;Autophagy, Biological_Activity: PF 750 is a selective and covalent fatty acid amide hydrolase (FAAH) inhibitor, with IC50s varied from 16.2-595 nM in different pre-incubation times. Covalently modifies the enzyme’s active site serine nucleophile[1].
IC50 & Target: IC50: 16.2-595 nM (FAAH)[1].

Name: MDL-28170 Calpain Inhibitor III, CAS: 88191-84-8, stock 10.7g, assay 98.2%, MWt: 382.45, Formula: C22H26N2O4, Solubility: DMSO : 30 mg/mL (78.44 mM; Need ultrasonic and warming), Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Proteasome, Biological_Activity: MDL-28170 (Calpain Inhibitor III) is a potent, selective and membrane-permeable cysteine protease inhibitor of calpain that rapidly penetrates the blood-brain barrier following systemic administration[1][2]. MDL-28170 also block γ-secretase[4].
IC50 & Target: Calpain[1].
In Vitro: MDL-28170 significantly and time-dependently improves the recovery of synaptic responses in hippocampal slices following prolonged, moderate hypoxia without hypoxic depolarization[1]. 
MDL-28170 dose-dependently inhibits brain cysteine proteinase activity (in vitro Ki= 0.01 μM)[2].
In Vivo: Treatment with MDL-28170 (50 mg/kg, i.p.) completely prevents the striatal damage in four animals in each of the two treatment groups. The numbers of necrotic neurons are reduced by 85% and 68% in animals in which MDL-28170 injections are initiated at 0.5 and 3 h of recirculation, respectively[2]. 
MDL-28170 (30 mg/kg, i.p.) reduces the functional and structural deterioration of corpus callosum following fluid percussion injury[3]. 
MDL-28170 (10 mg/kg, i.p.) significantly improves nerve function parameters in diabetic rats. MDL-28170 (3 and 10 mg/kg, i.p.) improves nociceptive behavior in diabetic rats[5].

Name: PF-04995274, CAS: 1331782-27-4, stock 19.1g, assay 98.2%, MWt: 432.51, Formula: C23H32N2O6, Solubility: DMSO : 100 mg/mL (231.21 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Neuronal Signaling;GPCR/G Protein, Target: 5-HT Receptor;5-HT Receptor, Biological_Activity: PF-04995274 is a potent, high-affinity, orally active and partial serotonin 4 receptor (5-HT4R) agonist. PF-04995274 has an EC50 range of 0.26-0.47 nM for human 5-HT4A/4B/4D/4E (Ki range of 0.15-0.46 nM), and has an EC50 range of 0.59-0.65 nM for rat 5-HT4S/4L/4E (Ki of 0.30 nM for rat 5-HT4S). PF-04995274 is brain penetrant and can be used to treat for cognitive disorders associated with Alzheimer＇s disease[1][2][3].
IC50 & Target: 5-HT4 receptor[1][2][3]
In Vitro: PF-04995274 has EC50 values of 0.47 nM, 0.36 nM, 0.37 nM, 0.26 nM, 0.59 nM, 0.65 nM and 0.62 nM for human 5-HT4A/4B/4D/4E and rat 5-HT4S/4L/4E, respectively. PF-04995274 has Ki values of 0.36 nM, 0.46 nM, 0.15 nM, 0.32 nM and 0.3nM for human 5-HT4A/4B/4D/4E and rat 5-HT4S, respectively[3].
In Vivo: PF-04995274 (3-10 mg/kg; intravenous injection; for 17 days; male 129S6/SvEv mice) treatment results in prophylactic efficacy by attenuating learned fear and decreasing stress-induced depressive-like behavior[1].

Name: Rolitetracycline, CAS: 751-97-3, stock 9.4g, assay 98.7%, MWt: 527.57, Formula: C27H33N3O8, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Anti-infection, Target: Bacterial, Biological_Activity: Rolitetracycline, a derivative of tetracycline, is a broad-spectrum antibiotic[1][2]. Rolitetracyclin has a role as a protein synthesis inhibitor, an antiprotozoal drug and a prodrug[3].

Name: CCT241736, CAS: 1402709-93-6, stock 6.4g, assay 98.6%, MWt: 456.37, Formula: C22H23Cl2N7, Solubility: H2O : < 0.1 mg/mL (insoluble); DMSO : 75 mg/mL (164.34 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Protein Tyrosine Kinase/RTK;Cell Cycle/DNA Damage;Epigenetics, Target: FLT3;Aurora Kinase;Aurora Kinase, Biological_Activity: CCT241736 is a potent and orally bioavailable dual FLT3 and Aurora kinase inhibitor, which inhibits Aurora kinases (Aurora-A Kd, 7.5 nM, IC50, 38 nM; Aurora-B Kd, 48 nM), FLT3 kinase (Kd, 6.2 nM), and FLT3 mutants including FLT3-ITD (Kd, 38 nM) and FLT3(D835Y) (Kd, 14 nM).
IC50 & Target: IC50: 38 nM (Aurora-A)[1] 
Kd: 7.5 nM (Aurora-A), 48 nM (Aurora-B), 6.2 nM (FLT3), 38 nM (FLT3-ITD), 14 nM (FLT3(D835Y))[1]
In Vitro: CCT241736 (Compound 27e) is a potent and orally bioavailable dual FLT3 and Aurora kinase inhibitor, which inhibits Aurora kinases (Aurora-A Kd, 7.5 nM, IC50, 38 nM, Aurora-B Kd, 48 nM), FLT3 kinase (Kd, 6.2 nM), and FLT3 mutants including FLT3-ITD (Kd, 38 nM) and FLT3(D835Y) (Kd, 14 nM). CCT241736 exhibits antiproliferative activity in a range of human tumor cell lines, such as HCT116 human colon carcinoma (GI50, 0.300 μM), the human FLT3-ITD positive AML cell lines MOLM-13 (GI50, 0.104 μM) and MV4-11 (GI50, 0.291 μM). CCT241736 also inhibits both the autophosphorylation of Aurora-A at T288 (a biomarker for Aurora-A inhibition: IC50, 0.030 μM) and histone H3 phosphorylation at S10 (a biomarker for Aurora-B inhibition: IC50, 0.148 μM), consistent with potent cellular activity versus both Aurora-A and -B. CCT241736 suppresses Aurora-A in MOLM-13 cells with concomitant inhibition of FLT3 signaling[1].
In Vivo: CCT241736 (50, 100 mg/kg, b.i.d, p.o.) dose-dependently suppresses the growth of MV4-11 human tumor xenografts, and completely abolishes the tumors at 100 mg/kg via p.o. administration twice a day[1].

Name: Longdaysin, CAS: 1353867-91-0, stock 6g, assay 98.4%, MWt: 335.33, Formula: C16H16F3N5, Solubility: H2O : < 0.1 mg/mL (insoluble); DMSO : 125 mg/mL (372.77 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Stem Cell/Wnt;MAPK/ERK Pathway;Cell Cycle/DNA Damage;Stem Cell/Wnt;Cell Cycle/DNA Damage, Target: ERK;ERK;CDK;Casein Kinase;Casein Kinase, Biological_Activity: Longdaysin is a inhibitor of the Wnt/β-catenin signaling pathway, which exerts antitumor effect through blocking CK1δ/ε-dependent Wnt signaling. Longdaysin inhibits CK1α, CK1δ, CDK7, and ERK2 with IC50s of 5.6 µM, 8.8 µM, 29 µM, and 52 µM, respectively[1][2].
IC50 & Target: IC50: 5.6 µM (CK1α), 8.8 µM (CK1δ), 29 µM (CDK7), 52 µM (ERK2)[2]

Name: MRT-83, CAS: 1263131-92-5, stock 6.9g, assay 98.2%, MWt: 538.59, Formula: C31H30N4O5, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Stem Cell/Wnt, Target: Smo, Biological_Activity: MRT-83 is a potent antagonist of Smo, with an IC50 in the nanomolar range. MRT-83 also blocks Hedgehog (Hh) signaling.
IC50 & Target: Smo[1].
In Vitro: MRT-83 displays full antagonist properties with an IC50 (~3 nM) for inhibiting ShhN (3 nM)-induced proliferation of rat GCPs. MRT-83 also blocks SAG (0.01 μM)-induced proliferation of GCPs (IC50 ~6 nM). MRT-83 blocks BC binding to HEK-hSmo cells in a dose-dependent manner with an IC50 of 4.6 nM. MRT-83 abrogates BC binding to cells expressing mouse Smo with an IC50 of 14 nM, which is in good correlation with its IC50 in the Shh-light2 and alkaline phosphatase assays[1].
In Vivo: Animals treated with ShhN in the presence of MRT-83 are as healthy as those of the other groups but up-regulation of Ptc transcription in the SVZ of these animals is no longer observed in agreement with a complete inhibition of ShhN-mediated effects (8.7±2.4 Ptc+ cells/section, n=9) and is not different from vehicle-mediated effects. MRT-83 but not MRT-36 antagonizes the up-regulation of Ptc transcription induced by ShhN in vivo in the SVZ of the LV[1].

Name: AZD8329, CAS: 1048668-70-7, stock 29.1g, assay 98.2%, MWt: 421.53, Formula: C25H31N3O3, Solubility: DMSO : 62.5 mg/mL (148.27 mM; Need ultrasonic), Clinical_Informat: Phase 1, Pathway: Others, Target: Others, Biological_Activity: AZD8329 is a potent 11β-Hydroxysteroid dehydrogenase type 1 (11β-HSD1) inhibitor with an IC50 of 9 nM for human 11β-HSD1, displays excellent selectivity versus 11β-HSD2, 17β-HSD1 and 17β-HSD3[1].
IC50 & Target: IC50: 9 nM (Human 11β-HSD1)[1]
In Vitro: AZD8329 shows IC50s of 0.009, 0.0086, 0.008, 0.024, 0.002 and 6.1 μM for human enzyme, rat enzyme, dog enzyme, cyno enzyme, human adipocyte and mouse enzyme, respectively[1].

Name: Erteberel LY500307, CAS: 533884-09-2, stock 38.1g, assay 98.9%, MWt: 282.33, Formula: C18H18O3, Solubility: 10 mM in DMSO, Clinical_Informat: Phase 2, Pathway: Others, Target: Estrogen Receptor/ERR, Biological_Activity: Erteberel (LY500307) is a potent and selective estrogen receptor beta (ERβ) agonist with Ki and EC50 of 1.54 nM and 3.61 nM, respectively[1]. Anti-tumor activities[2].
IC50 & Target: Ki: 1.54 nM (ERβ)[1]
EC50: 3.61 nM[1]
In Vitro: Treatment with Erteberel (0.25-10 μM, 72 hours) significantly reduces the proliferation of GBM cells with no activity on normal astrocytes in vitro[2].
Erteberel promotes apoptosis of GBM cells. Erteberel modulated several pathways related to apoptosis, cell cycle, and DNA damage response[2].
Erteberel (0-1000 μM) sensitizes GBM cells to several FDA-approved chemotherapeutic drugs including cisplatin, lomustine and temozolomide[2].
In Vivo: Erteberel (5 mg/Kg body weight/day, oral, 28 days) treatment significantly reduces tumor growth and promotes apoptosis of GBM tumors in an orthotopic model[2].
Erteberel (5 mg/Kg body weight/day, oral, 40-50 days) treatment improves the overall survival of tumor-bearing mice in the GL26 syngeneic glioma model[2].

Name: AKT-IN-1, CAS: 1357158-81-6, stock 13.8g, assay 98%, MWt: 343.42, Formula: C22H21N3O, Solubility: DMSO : 25 mg/mL (72.80 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: PI3K/Akt/mTOR, Target: Akt, Biological_Activity: AKT-IN-1 is an allosteric AKT inhibitor with an IC50 of 1.042 μM.
IC50 & Target: IC50: 1.042 μM (AKT)[1]
In Vitro: AKT-IN-1 is able to potently inhibit phosphorylation of AKT in cells at both Thr308 and Ser473, with IC50s of 0.422 and 0.322 μM, respectively. AKT-IN-1 inhibits the phosphorylation of ribosomal protein S6, a downstream effector of the PI3K-AKT pathway. AKT-IN-1 potently inhibits the phosphorylation of PRAS40[1].
In Vivo: The effects of AKT-IN-1 (Compound 26) in vivo are characterized by measuring the pharmacodynamic activity of AKT-IN-1 in a BT474c breast adenocarcinoma xenograft model. Following acute doses of 100 and 200 mg/kg, AKT-IN-1 potently inhibits the phosphorylation of its downstream substrate GSK3β as well as the phosphorylation of AKT (Ser473), with a potency consistent with its pharmacokinetic profile. The in vivo activity of AKT-IN-1 is further characterized by measuring the effects on the growth of tumor cell xenografts. Continuous (daily) oral dosing of AKT-IN-1 (100 and 200 mg/kg) to nude mice bearing BT474c breast adenocarcinoma xenografts results in inhibition of tumor growth in a dose-dependent manner. When dosed at 200 mg/kg daily, AKT-IN-1 causes significant tumor growth inhibition[1].

Name: Crolibulin EPC2407, CAS: 1000852-17-4, stock 0.7g, assay 98.9%, MWt: 417.26, Formula: C18H17BrN4O3, Solubility: DMSO : 125 mg/mL (299.57 mM; Need ultrasonic and warming), Clinical_Informat: Phase 2, Pathway: Cell Cycle/DNA Damage;Cytoskeleton, Target: Microtubule/Tubulin;Microtubule/Tubulin, Biological_Activity: Crolibulin is a small molecule tubulin polymerization inhibitor.
IC50 & Target: tubulin polymerization[1]

Name: Bisindolylmaleimide X (hydrochloride) BIM-X (hydrochloride);Ro31-8425 (hydrochloride), CAS: 145317-11-9, stock 9.8g, assay 98.7%, MWt: 460.96, Formula: C26H25ClN4O2, Solubility: DMSO : 20.83 mg/mL (45.19 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: TGF-beta/Smad;Epigenetics;Cell Cycle/DNA Damage, Target: PKC;PKC;CDK, Biological_Activity: Bisindolylmaleimide X hydrochloride (BIM-X hydrochloride) is a potent and selective protein kinase C (PKC) inhibitor. Bisindolylmaleimide X hydrochloride is a potent cyclin-dependent kinase 2 (CDK2) antagonist with an IC50 of 200 nM[1].

Name: (R)-CR8 CR8, (R)-Isomer, CAS: 294646-77-8, stock 19.1g, assay 99%, MWt: 431.53, Formula: C24H29N7O, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Apoptosis;Cell Cycle/DNA Damage, Target: Apoptosis;CDK, Biological_Activity: (R)-CR8 (CR8), a second-generation analog of Roscovitine, is a potent CDK1/2/5/7/9 inhibitor. (R)-CR8 (CR8) inhibits CDK1/cyclin B (IC50=0.09 μM), CDK2/cyclin A (0.072 μM), CDK2/cyclin E (0.041 μM), CDK5/p25 (0.11 μM), CDK7/cyclin H (1.1 μM), CDK9/cyclin T (0.18 μM) and CK1δ/ε (0.4 μM). (R)-CR8 (CR8) induces apoptosis and has neuroprotective effect[1][2].
In Vitro: (R)-CR8 (CR8) (0.1-100 μM; 48 hours) is a potent inducer of apoptotic cell death with an IC50 of 0.49 μM for SH-SY5Y cell line[1]. 
(R)-CR8 (0.25-10 μM) induces a dose-dependent induction of poly-(ADP-ribose)polymerase (PARP) cleavage[1].
In Vivo: (R)-CR8 (5 mg/Kg; i.p.) results in a significant reduction in lesion size at 28 days in histological assessment[2].

Name: Diflunisal MK-647, CAS: 22494-42-4, stock 15.1g, assay 98.2%, MWt: 250.20, Formula: C13H8F2O3, Solubility: DMSO : 50 mg/mL (199.84 mM; Need ultrasonic), Clinical_Informat: Launched, Pathway: Immunology/Inflammation, Target: COX, Biological_Activity: Diflunisal (MK-647) is a salicylate derivative with nonsteroidal anti-inflammatory and uricosuric properties, which is used alone as an analgesic and in rheumatoid arthritis patients. The mechanism of action of diflunisal is as a Cyclooxygenase (COX) Inhibitor.
IC50 & Target: Target: Cyclooxygenase
In Vivo: Administration of increasing doses of Diflunisal to rats shows that the effect of the dose on the pharmacokinetics of Diflunisal is quite complicated. The plasma concentrations of Diflunisal decline exponentially with time, albeit with a half-life that increases with increasing dose. The CLP is reduced considerably when the dose increases from 3 to 10 mg/kg and then remains relatively constant over the dose range of 10 to 60 mg/kg. Diflunisal has been shown to be highly bound to rat plasma protein and dependent on concentration. The fraction of unbound Diflunisal is increased about 10-fold over the concentration range of 5 to 300 μg/mL[1]. Diflunisal exhibits activity after oral administration with potency about 25 times greater than that of aspirin, about 3 times that of glafenine and twice that of zomepirac[2].

Name: Indotecan LMP-400; NSC-724998, CAS: 915303-09-2, stock 21.7g, assay 98.8%, MWt: 478.49, Formula: C26H26N2O7, Solubility: 10 mM in DMSO, Clinical_Informat: Phase 1, Pathway: Cell Cycle/DNA Damage, Target: Topoisomerase, Biological_Activity: Indotecan (LMP-400) is a potent topoisomerase 1(Top1) inhibitor with IC50 values of 300, 1200, 560 nM for P388, HCT116, MCF-7 cell lines, respectively.
IC50 & Target: IC50：300, 1200, 560 nM for P388, HCT116, MCF-7 cell lines, respectively[1].

Name: Saridegib IPI-926;Patidegib, CAS: 1037210-93-7, stock 21.5g, assay 98.5%, MWt: 504.77, Formula: C29H48N2O3S, Solubility: 10 mM in DMSO, Clinical_Informat: Phase 3, Pathway: Stem Cell/Wnt, Target: Smo, Biological_Activity: Saridegib is a potent and specific inhibitor of Smoothened (Smo), a key signaling transmembrane protein in the Hedgehog (Hh) pathway.
IC50 & Target: Smo[1].
In Vivo: Evidence from a genetically engineered mouse model of pancreatic cancer demonstrates that Saridegib (IPI-926) can deplete tumor-associated stromal tissue and increase intratumoral mean vessel density. These changes result in enhanced delivery of concurrently administered systemic agents, leading to a decreased tumor burden and prolonged survival in this mouse model[1].

Name: Oligomycin A MCH 32, CAS: 579-13-5, stock 35.7g, assay 98.2%, MWt: 791.06, Formula: C45H74O11, Solubility: DMSO : 125 mg/mL (158.02 mM; Need ultrasonic); H2O : < 0.1 mg/mL (insoluble), Clinical_Informat: No Development Reported, Pathway: Membrane Transporter/Ion Channel, Target: ATP Synthase, Biological_Activity: Oligomycin A, created by Streptomyces, acts as a mitochondrial F0F1-ATPase inhibitor, with a Ki of 1 μM; Oligomycin A shows anti-fungal activity.
IC50 & Target: Ki: 1 μM (F0F1-ATPase)[1]
In Vitro: Oligomycin A is a mitochondrial F0F1-ATPase inhibitor with a Ki of 1 μM. Oligomycin A shows cytotoxic to the NCI-60 cell lines, with GI50 of 10 nM. Oligomycin A also inhibits the activity of Triton X-100-solubilized ATPase with a Ki of 0.1 μM. Furthermore, Oligomycin A has anti-fungal activity[1]. Oligomycin A (2.4 µM) inhibits the ability of spermatozoa to achieve feasible in vitro capacitation (IVC), and also suppresses progesterone-induced in vitro acrosome exocytosis (IVAE) as well as the concomitant peaks of O2 consumption and ATP levels[2].

Name: Encequidar (mesylate) HM30181 (mesylate);HM30181A (mesylate), CAS: 849675-87-2, stock 17.3g, assay 98.9%, MWt: 784.83, Formula: C39H40N6O10S, Solubility: H2O, Clinical_Informat: No Development Reported, Pathway: Membrane Transporter/Ion Channel, Target: P-glycoprotein, Biological_Activity: Encequidar mesylate (HM30181 mesylate; HM30181A mesylate) is a competitive and potent P-glycoprotein inhibitor.
IC50 & Target: P-glycoprotein[1][2].
In Vitro: Compared with control (0 nM Encequidar (HM30181)), paclitaxel potently inhibits the survival of K1735 cells by about 65% at 100 nM and 72% at 1000 nM in a dose-dependent manner. Encequidar (HM30181) does not make any significant changes in the survival of K1735 cells. In contrast, bEnd.3 cells do not show any decreases in survival by the paclitaxel treatment without Encequidar (HM30181). However, treatment of 0.1 or 1 nM Encequidar (HM30181) lead to 20 and 42% inhibition of survival at the 100 nM and 1000 nM paclitaxel treatment, respectively[2].
In Vivo: The plasma concentrations of Encequidar (HM30181) are higher for the simultaneous administration with the microcapsule than with the powder; providing significant differences from 1 to 2 h. The microcapsule has about a 1.7-fold faster Tmax and a 1.6-fold higher AUC value compared with the powder (2.5±0.6 vs. 4.3±0.9 h; 107.7±20.1 vs. 64.3±18.0 h ng/mL). The faster and overall improved absorption of Encequidar (HM30181) in microcapsule form might be due to the remarkable enhancement of the aqueous solubility and dissolution resulting from its crystalline conversion to the amorphous form and particle size reduction[1].

Name: Indibulin ZIO 301;D 24851, CAS: 204205-90-3, stock 18.4g, assay 98.3%, MWt: 389.83, Formula: C22H16ClN3O2, Solubility: DMSO : 50 mg/mL (128.26 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Cell Cycle/DNA Damage;Cytoskeleton;Apoptosis, Target: Microtubule/Tubulin;Microtubule/Tubulin;Apoptosis, Biological_Activity: Indibulin (ZIO 301), an orally applicable inhibitor of tubulin assembly, shows potent anticancer activity with a minimal neurotoxicity. Indibulin reduces inter-kinetochoric tension, produces aberrant spindles, activates mitotic checkpoint proteins Mad2 and BubR1, and induces mitotic arrest and apoptosis[1].
IC50 & Target: Tubulin[1]
In Vitro: Indibulin (300-2100 nM; 48 hours) inhibits the proliferation of MCF-7 cells with an IC50 of 150 nM[1]. 
Indibulin (300, 600 nM; 48 hours) blockes the cells in the G2/M phase indicating that indibulin blockes the progression of the cell cycle at mitosis[1]. 
Indibulin (150-600 nM; 24 hours) induces apoptosis in MCF-7 cells[1]. 
Indibulin (150-600 nM; 48 hours) with 300 and 600 nM generates cleaved fragments of PARP protein the treatment of MCF-7 cells[1].

Name: N-Acetyl-L-leucine, CAS: 1188-21-2, stock 10.4g, assay 98.8%, MWt: 173.21, Formula: C8H15NO3, Solubility: , Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity:

Name: Indisulam E 7070, CAS: 165668-41-7, stock 34.9g, assay 98.9%, MWt: 385.85, Formula: C14H12ClN3O4S2, Solubility: DMSO : 130 mg/mL (336.92 mM; Need ultrasonic), Clinical_Informat: Phase 2, Pathway: Metabolic Enzyme/Protease, Target: Carbonic Anhydrase, Biological_Activity: Indisulam (E 7070) is a carbonic anhydrase inhibitor with anticancer activity. Indisulam (E 7070) is a sulfonamide agent that targets the G1 phase of the cell cycle. Indisulam (E 7070) causes a blockade in the G1/S transition through inhibition of the activation of both CDK2 and cyclin E. Indisulam (E 7070) targets splicing by inducing RBM39 degradation via recruitment to DCAF15[1][2].
IC50 & Target: Carbonic anhydrase[1].

Name: Nilutamide Nilandron;RU 23908, CAS: 63612-50-0, stock 1.9g, assay 98.4%, MWt: 317.22, Formula: C12H10F3N3O4, Solubility: DMSO : ≥ 250 mg/mL (788.10 mM), Clinical_Informat: Launched, Pathway: Others, Target: Androgen Receptor, Biological_Activity: Nilutamide (Nilandron) is a non-steroidal anti-androgen drug proposed in the treatment of metastatic prostatic carcinoma[1][2].

Name: Nimustine (hydrochloride) ACNU, CAS: 55661-38-6, stock 28.9g, assay 98.3%, MWt: 309.15, Formula: C9H14Cl2N6O2, Solubility: DMSO : 62.5 mg/mL (202.17 mM; Need ultrasonic), Clinical_Informat: Launched, Pathway: Apoptosis;Cell Cycle/DNA Damage, Target: Apoptosis;DNA/RNA Synthesis, Biological_Activity: Nimustine hydrochloride (ACNU) is a DNA cross-linking and DNA alkylating agent, which induces DNA replication blocking lesions and DNA double-strand breaks and inhibits DNA synthesis, commonly used in chemotherapy for glioblastomas[1][2][3].

Name: CAY10471 Racemate TM30089 Racemate, CAS: 844639-57-2, stock 39.2g, assay 98.5%, MWt: 416.47, Formula: C21H21FN2O4S, Solubility: DMSO : 150 mg/mL (360.17 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein, Target: Prostaglandin Receptor, Biological_Activity: CAY10471 Racemate (TM30089 Racemate) is a potent and highly selective prostaglandin D2 receptor CRTH2 antagonist, with a Ki of 0.6 nM for hCRTH2, selective over human thromboxane A2 receptor TP (Ki, >10000 nM) or PGD2 receptor DP (Ki, 1200 nM). CAY10471 Racemate also has effect on mouse and rat orthologs of CRTH2[1].
IC50 & Target: Ki: 0.6 nM (CRTH2), 1200 nM (DP)[1]
In Vitro: CAY10471 Racemate (Compound 13) inhibits PGD2-induced inositol phosphate or cAMP formation, suppresses β-arrestin translocation with IC50s of 12 and 3 nM, respectively[1].

Name: Tin(IV) mesoporphyrin IX (dichloride) Stannsoporfin, CAS: 106344-20-1, stock 22.9g, assay 98.7%, MWt: 754.29, Formula: C34H36Cl2N4O4Sn, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Tin(IV) mesoporphyrin IX dichloride (Stannsoporfin) is a heme oxygenase (HO) inhibitor being developed for the prevention of hyperbilirubinemia in infants at risk of developing jaundice, extracted from patent WO2011103196A1[1].
IC50 & Target: HO[1]

Name: Norepinephrine Levarterenol;L-Noradrenaline, CAS: 51-41-2, stock 39g, assay 98.9%, MWt: 169.18, Formula: C8H11NO3, Solubility: H2O : 5 mg/mL (29.55 mM; Need ultrasonic); DMSO : 5 mg/mL (29.55 mM; ultrasonic and warming and heat to 60°C), Clinical_Informat: Launched, Pathway: GPCR/G Protein;Autophagy;Metabolic Enzyme/Protease;Neuronal Signaling, Target: Adrenergic Receptor;Autophagy;Endogenous Metabolite;Adrenergic Receptor, Biological_Activity: Norepinephrine (Levarterenol; L-Noradrenaline) is a β1-selective adrenergic receptor agonist with EC50 of 5.37 μM.
IC50 & Target: EC50: 5.37 μM (β1-selective adrenergic receptor)[1]
In Vitro: Norepinephrine (NE) bitartrate monohydrate is generally considered to be a β1-subtype selective adrenergic agonist. Norepinephrine(NE) also has direct activity at the β2-adrenoceptor in higher concentrations[1].Adipocytes from the inguinal fat pad (iWA) or the interscapular fat pad (BA) are isolated from neonatal wild-type C57BL/6J mice and cultured. To examine the effect of activating AT2 upon β-adrenergic signaling, cAMP production is first assessed in response to Norepinephrine (NE, 10 µM) with or without CGP (10 nM) co-treatment.Norepinephrine (NE) increases cAMP as expected in iWA, and CGP does not alter this effectNorepinephrine (NE) is also known to induce lipolysis, and liberated fatty acids are required to functionally activate UCP1 protein and to stimulate heat production. CREB phosphorylation at Ser133 is increased after Norepinephrine (NE) treatment and significantly attenuated with CGP co-treatment in mouse iWA[2].

Name: Phenoxodiol Idronoxil;Dehydroequol;Haginin E, CAS: 81267-65-4, stock 23.8g, assay 98.8%, MWt: 240.25, Formula: C15H12O3, Solubility: 10 mM in DMSO, Clinical_Informat: Phase 3, Pathway: Apoptosis;Apoptosis;Cell Cycle/DNA Damage, Target: Apoptosis;Caspase;Topoisomerase, Biological_Activity: Phenoxodiol, a synthetic analog of Genestein, activates the mitochondrial caspase system, inhibits XIAP (an apoptosis inhibitor), and sensitizes the cancer cells to Fas-mediated apoptosis. This agent also inhibits DNA topoisomerase II by stabilizing the cleavable complex. Phenoxodiol induces cell cycle arrest in the G1/S phase of the cell cycle and upregulates p21WAF1 via a p53 independent manner[1][2].
IC50 & Target: Caspase, DNA topoisomerase II[1][2].

Name: HPPH Photochlor, CAS: 149402-51-7, stock 14.2g, assay 98.4%, MWt: 636.82, Formula: C39H48N4O4, Solubility: H2O : < 0.1 mg/mL (insoluble); DMSO : 50 mg/mL (78.52 mM; Need ultrasonic), Clinical_Informat: Phase 2, Pathway: Others, Target: Others, Biological_Activity: HPPH (Photochlor) is a second generation photosensitizer, which acts as a photodynamic therapy (PDT) agent.
In Vitro: Fluorescence image of 4T1 cells incubated with 0.49 µg/mL GO-PEG, 1 μM HPPH (free HPPH) or equivalent amount of GO-PEG-HPPH (1 µM HPPH and 0.49 µg/mL GO-PEG) after 24 h. The cellular uptake of GO-PEG-HPPH and HPPH is investigated with 4T1 murine mammary cancer cells. The cells are incubated with GO-PEG-HPPH and free HPPH at equivalent HPPH concentration (1 µM) for 24 h and then observed with a confocal microscope. Cells treated with GO-PEG-HHPH shows stronger fluorescence signal than those treated with free HPPH. In fact, the fluorescence of HPPH is rather weak[1].
In Vivo: Tumors are treated with an immune-enhancing PDT regimen followed by a tumor-controlling PDT regimen can leads to enhancement of anti-tumor immunity, while retaining effective control of primary tumor growth. To test this hypothesis, a combination treatment regimen is devised in which Colo26-HA tumor-bearing BALB/c mice are treated with a HPPH-PDT regimen known to lead to enhanced anti-tumor immunity (0.4 μmoles/kg HPPH followed 18 h later by illumination with 665 nm light for a total dose of 48 J/cm2). Following illumination, mice are rested for 9 days; on the ninth day, mice are injected with HPPH. On day 10 following the first treatment, tumors are treated with a tumor control treatment regimen (illumination with 665 nm light for a total dose of 132 J/cm2 given)[2].

Name: Rubitecan RFS 2000;9-Nitrocamptothecin, CAS: 91421-42-0, stock 32.9g, assay 98.3%, MWt: 393.35, Formula: C20H15N3O6, Solubility: DMSO : 125 mg/mL (317.78 mM; Need ultrasonic), Clinical_Informat: Phase 3, Pathway: Cell Cycle/DNA Damage, Target: Topoisomerase, Biological_Activity: Rubitecan (RFS 2000), a Camptothecin derivative, is an orally active topoisomerase I inhibitor with broad antitumor activity, and induces protein-linked DNA single-strand breaks, thereby blocking DNA and RNA synthesis in dividing cells[1][2][3].
IC50 & Target: Topoisomerase I[1]
In Vitro: Rubitecan (RFS 2000) inhibits U-CH1, U-CH2, and CCL4 cells with IC50s 0.32, 0.83, and 7.7 µM, respectively[4].

Name: Sardomozide CGP 48664;SAM-486A, CAS: 149400-88-4, stock 8.3g, assay 98.4%, MWt: 230.27, Formula: C11H14N6, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Sardomozide is an S-adenosylmethionine decarboxylase (SAMDC) inhibitor with an IC50 of 5 nM.
IC50 & Target: IC50: 5 nM (SAMDC)[1]
In Vitro: Sardomozide is a S-adenosylmethionine decarboxylase (SAMDC) inhibitor with an IC50 of 5 nM in cell assay. Following treatment for 48 h with 3 μM Sardomozide, intracellular SAMDC activity is reduced to 10% of control[1]. When the CHO/664 cells are grown in the presence of Sardomozide and during treatment with DENSPM, vacuole formation is not observed, and these cells are growth-inhibited and contain levels of DENSPM similar to the parental CHO cells[2].

Name: Semustine, CAS: 13909-09-6, stock 1.5g, assay 98.7%, MWt: 247.72, Formula: C10H18ClN3O2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Cell Cycle/DNA Damage, Target: DNA Alkylator/Crosslinker, Biological_Activity: Semustine is a DNA alkylator, binds to DNA, and acts as a cancer chemotherapeutic agent[1].

Name: Tetrandrine NSC-77037；d-Tetrandrine, CAS: 518-34-3, stock 34.4g, assay 98.6%, MWt: 622.75, Formula: C38H42N2O6, Solubility: H2O : < 0.1 mg/mL (insoluble); DMSO : 5 mg/mL (8.03 mM; Need ultrasonic and warming), Clinical_Informat: Launched, Pathway: Membrane Transporter/Ion Channel;Membrane Transporter/Ion Channel;Neuronal Signaling, Target: Calcium Channel;Potassium Channel;Calcium Channel, Biological_Activity: Tetrandrine (NSC-77037; d-Tetrandrine) is a bis-benzyl-isoquinoline alkaloid, which inhibits voltage-gated Ca2+ current (ICa) and Ca2+-activated K+ current.
IC50 & Target: Ca2+ current[1] 
K+ current[1]
In Vitro: The effects of Tetrandrine (NSC-77037), a bis-benzyl-isoquinoline alkaloid, on voltage-gated Ca2+ currents (ICa) and on Ca2+-activated K+ current (IK(Ca)) and channels in isolated nerve terminals of the rat neurohypophysis are investigated using patch-clamp techniques. The non-inactivating component of ICa is inhibited by external Tetrandrine (NSC-77037) in a voltage- and dose-dependent manner, with an IC50=10.1μM. Tetrandrine (NSC-77037) decreases the channel-open probability, within bursts, with an IC50=0.21 μM[1]. To evaluate the effects of Tetrandrine on HCC cells, Huh7, HCCLM9 and Hep3B cells are treated with 0 (DMSO), 0.5, 1, 2 or 4 μM of Tetrandrine for 24 h. The cell proliferation assay indicates that Tetrandrine exhibits almost no effect on the inhibition of HCC cell proliferation at 0.5-2 μM. However, Tetrandrine (NSC-77037) inhibits HCC cell migration in a dose-dependent manner. Furthermore, a wound-healing and transwell assay shows that 2 μM Tetrandrine significantly inhibits HCC cell migration and invasion[2].
In Vivo: To evaluate the effect of Tetrandrine (NSC-77037) on the inhibition of tumor metastasis in vivo, HCCLM9 subcutaneous tumor xenograft models is established with athymic nude mice. When the tumor volume reach approximately 50 mm3, nude mice are orally administered vehicle or Tetrandrine (NSC-77037) (30 mg/kg) every other day for 37 days. Tetrandrine (NSC-77037) treatment inhibits tumor growth by reducing the tumor volume and weight[2].

Name: AZ-23 AZ23;AZ 23, CAS: 915720-21-7, stock 5.8g, assay 98.1%, MWt: 391.83, Formula: C17H19ClFN7O, Solubility: DMSO : 125 mg/mL (319.02 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Protein Tyrosine Kinase/RTK;Neuronal Signaling, Target: Trk Receptor;Trk Receptor, Biological_Activity: AZ-23 is an ATP-competitive and orally bioavailable Trk kinase A/B/C inhibitor with IC50s of 2 nM (TrkA), 8 nM (TrkB), 24 nM (FGFR1), 52 nM (Flt3), 55 nM (Ret), 84 nM (MuSk), 99 nM (Lck), respectively.
IC50 & Target: IC50: 2 nM (TrkA), 8 nM (TrkB), 24 nM (FGFR1), 52 nM (Flt3), 55 nM (Ret), 84 nM (MuSk), 99 nM (Lck)[1]
In Vitro: AZ-23 potently and selectivity inhibits Trk phosphorylation in cells. AZ-23 potently inhibits Trk-mediated survival (EC50 of 2 nM). AZ-23 Inhibits Trk-Dependent Survival in MCF10ATrkA-Δ and TF-1 Cell Lines[1].
In Vivo: AZ-23 shows in vivo TrkA kinase inhibition and efficacy in mice following oral administration in a TrkA-driven allograft model and significant tumor growth inhibition in a Trk-expressing xenograft model of neuroblastoma[1].

Name: Hypoxanthine Purin-6-ol; Sarcine, CAS: 68-94-0, stock 36.3g, assay 98.1%, MWt: 136.11, Formula: C5H4N4O, Solubility: DMSO : 10 mg/mL (73.47 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: Hypoxanthine, a purine derivative, is a potential free radical generator and could be used as an indicator of hypoxia.
In Vitro: Hypoxanthine is a potential free radical generator. Hypoxanthine seems to play a role in posthypoxic reoxygenation cell injury through oxygen radical production and is therefore involved in the pathogenesis of a number of diseases. Hypoxanthine also modulates a number of other processes because it reacts with benzodiazepine receptors and inhibits phosphodiesterase in the brain. Hypoxanthine inhibits the effect of several cytotoxic drugs and may therefore influence treatment with such drugs[1].
In Vivo: In pigs, a linear increase of plasma hypoxanthine with duration of hypoxemia is found, and there is no difference between arterial and venous plasma. There are good correlations between hypoxanthine and lactate, base deficit and pH. There is also a direct relationship between survival time and increase in plasma hypoxanthine. Survival time correlates negatively with the rate of hypoxanthine increase (r=-0.62).All animals die when hypoxanthine exceeds 125 pM/liter. The increase of hypoxanthine therefore reflected the prognosis of acute hypoxia in contrast to base deficit[1].

Name: Sophocarpine, CAS: 6483-15-4, stock 2.8g, assay 98.3%, MWt: 246.35, Formula: C15H22N2O, Solubility: DMSO : 250 mg/mL (1014.82 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: PI3K/Akt/mTOR;Apoptosis;PI3K/Akt/mTOR;Autophagy, Target: PI3K;Apoptosis;Akt;Autophagy, Biological_Activity: Sophocarpine is one of the significant alkaloid extracted from the traditional herb medicine Sophora flavescens which has many pharmacological properties such as anti-virus, anti-tumor, anti-inflammatory. Sophocarpine significantly inhibits the growth of gastric cancer (GC) cells through multiple mechanisms such as induction of autophagy, activation of cell apoptosis and down-regulation of cell survival PI3K/AKT signaling pathway. Sophocarpine has been demonstrated to have anti-tumor activity in various cancer cells, including hepatocellular carcinoma, prostate cancer and colorectal cancer[1].

Name: Cyclovirobuxine D, CAS: 860-79-7, stock 10.6g, assay 98.8%, MWt: 402.66, Formula: C26H46N2O, Solubility: Ethanol : 13 mg/mL (32.29 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Apoptosis;PI3K/Akt/mTOR;PI3K/Akt/mTOR;Autophagy, Target: Apoptosis;mTOR;Akt;Autophagy, Biological_Activity: Cyclovirobuxine D (CVB-D) is the main active component of the traditional Chinese medicine Buxus microphylla. Cyclovirobuxine D induces autophagy and attenuates the phosphorylation of Akt and mTOR[1]. Cyclovirobuxine D inhibits cell proliferation of gastric cancer cells through suppression of cell cycle progression and inducement of mitochondria-mediated apoptosis[2]. Cyclovirobuxine D is beneficial for heart failure induced by myocardial infarction[3].
In Vitro: Cyclovirobuxine D (0-240 µM ;24-72 hours) shows a concentration- and time-dependent reduced cell viability after CVB-D treatment, only 10% MGC-803 cells and 20% MKN28 cells are alive at 72 h after treatment with 240 µM[2].
Cyclovirobuxine D (0-120 µM; 48 hours) arrests the cell cycle of gastric cancer cells at S phase in a concentration-dependent manner[2].
Cyclovirobuxine D (0-120 µM; 48 hours) leads to apoptosis in gastric cancer cells in a concentration-dependent manner, especially early stage apoptosis.
Cyclovirobuxine D (0-120 µM; 48 hours) causes apoptosis via up-regulation of the apoptosis- related proteins, cleaved Caspase-3 and ratio of Bax/Bcl-2, in gastric cancer cells[2].

Name: Physcion Parietin;Rheochrysidin, CAS: 521-61-9, stock 3.6g, assay 99%, MWt: 284.26, Formula: C16H12O5, Solubility: DMSO : 5 mg/mL (17.59 mM; Need ultrasonic and warming); H2O : < 0.1 mg/mL (insoluble), Clinical_Informat: No Development Reported, Pathway: Anti-infection, Target: Bacterial, Biological_Activity: Physcion (Parietin) is an anthraquinone isolated from traditional Chinese medicine Radix et Rhizoma Rhei, acts as an inhibitor of 6-phosphogluconate dehydrogenase, with an IC50 and a Kd of 38.5 μM and 26.0 μM, respectively[1][2]. Physcion (Parietin) exhibits laxative, hepatoprotective, anti-inflammatory, anti-microbial, anti-proliferative and anti-tumor effects[2].
IC50 & Target: IC50: 38.5 μM (6-phosphogluconate dehydrogenase)[1] 
Kd: 26.0 μM (6-phosphogluconate dehydrogenase)[1]

Name: Coenzyme Q10 CoQ10;Ubiquinone-10, CAS: 303-98-0, stock 26.4g, assay 98.7%, MWt: 863.34, Formula: C59H90O4, Solubility: DMF : 7.14 mg/mL (8.27 mM; Need ultrasonic); DMSO : < 1 mg/mL (insoluble or slightly soluble), Clinical_Informat: Launched, Pathway: Apoptosis;Metabolic Enzyme/Protease;Metabolic Enzyme/Protease;NF-κB;Immunology/Inflammation, Target: Ferroptosis;Endogenous Metabolite;Reactive Oxygen Species;Reactive Oxygen Species;Reactive Oxygen Species, Biological_Activity: Coenzyme Q10 is an essential cofactor of the electron transport chain and a potent antioxidant agent.
IC50 & Target: Antioxidant[1]
In Vitro: Coenzyme Q10 is an obligatory member of the respiratory chain in the mitochondria of all cells. Therefore, it is an essential ingredient in the formation of adenosine triphosphate (ATP), the source of energy in most cellular processes. Coenzyme Q10 is located in the mitochondria, lysosomes, and Golgi and plasma membranes, and provides an antioxidant action either by direct reaction with free radicals or by regeneration of tocopherol and ascorbate from their oxidised state[1]. Coenzyme Q10 is a popular dietary supplement because of its recognition by the public as an important nutrient in supporting human health. The rationale for the use of Coenzyme Q10 as a therapeutic agent in several cardiovascular and degenerative neurologic and neuromuscular diseases is based upon its fundamental role in mitochondrial function and cellular bioenergetics[2].
In Vivo: Because of its hydrophobicity and large molecular weight, absorption of dietary Coenzyme Q10 is slow and limited. In the case of dietary supplements, solubilized Coenzyme Q10 formulations show enhanced bioavailability. The Tmax is around 6 h, with an elimination half-life of about 33 h. The reference intervals for plasma Coenzyme Q10 range from 0.40 to 1.91 mM in healthy subjects. With Coenzyme Q10 supplements there is reasonable correlation between increase in plasma Coenzyme Q10 and ingested dose up to a certain point. Animal data show that Coenzyme Q10 in large doses is taken up by all tissues including heart and brain mitochondria[2]. In 12-month-old rats administration of coenzyme Q10 results in significant increases in cerebral cortex mitochondrial concentrations of coenzyme Q10. Oral administration of coenzyme Q10 markedly attenuates striatal lesions produced by systemic administration of 3-nitropropionic acid and significantly increases life span in a transgenic mouse model of familial amyotrophic lateral sclerosis[3].

Name: Hordenine Ordenina;Peyocactine, CAS: 539-15-1, stock 35.8g, assay 98.3%, MWt: 165.23, Formula: C10H15NO, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Hordenine, an alkaloid found in plants, inhibits melanogenesis by suppression of cyclic adenosine monophosphate (cAMP) production[1].

Name: (S)-(-)-Phenylethanol, CAS: 1445-91-6, stock 4.3g, assay 98.7%, MWt: 122.16, Formula: C8H10O, Solubility: , Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity:

Name: TS-011, CAS: 339071-18-0, stock 6.2g, assay 99%, MWt: 255.70, Formula: C11H14ClN3O2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: TS-011 is a selective inhibitor of 20-Hydroxyeicosatetraenoic acid synthesis.
In Vivo: TS-011 is a selective inhibitor of 20-Hydroxyeicosatetraenoic acidsynthesis. TS-011 at a dose of 0.3 mg/kg inhibits the reduction in the blood flow velocities at 1 and 7 h after reperfusion (P<0.001). In addition, TS-011 inhibits the increase in the blood flow velocity at 24 h after reperfusion (P<0.01). TS-011 protects the microvascular perfusion area from the loss observed in vehicle-treated mice. TS-011, at a dose of 0.3 mg/kg, also reduces the infarct volume by almost 40% (P<0.05)[1]. In 9 dogs with delayed vasospasm, acute blockade of the synthesis of 20-HETE with TS-011 (1 mg/kg IV) significantly increases the diameter of the basilar artery by 39%[2].

Name: 5-Hydroxytryptophan 5-HTP;DL-5-Hydroxytryptophan, CAS: 56-69-9, stock 16.1g, assay 98.8%, MWt: 220.22, Formula: C11H12N2O3, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: 5-Hydroxytryptophan, a tryptophan metabolite, is a direct 5-hydroxytryptamine (5-HT) precursor and an L-aromatic amino acid decarboxylase substrate. [1][2][3].

Name: Shikimic acid, CAS: 138-59-0, stock 26.9g, assay 98.6%, MWt: 174.15, Formula: C7H10O5, Solubility: H2O : 130 mg/mL (746.48 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: Shikimic acid is a key metabolic intermediate of the aromatic amino acid biosynthesis pathway, found in microbes and plants.
In Vitro: Shikimic acid is an important metabolic intermediate with various applications. Shikimic acid is an industrially important compound that acts as a precursor in the synthesis of many chemical substances like oseltamivir phosphate[1].

Name: Synephrine Oxedrine, CAS: 94-07-5, stock 16.9g, assay 98.7%, MWt: 167.21, Formula: C9H13NO2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein;Metabolic Enzyme/Protease;Neuronal Signaling, Target: Adrenergic Receptor;Endogenous Metabolite;Adrenergic Receptor, Biological_Activity: Synephrine (Oxedrine) is an α-adrenergic and β-adrenergic agonist derived from the Citrus aurantium, it has sympathomimetic and structural similarities to ephedra and ephedrine alkaloids[1][2].
IC50 & Target: α-adrenergic and β-adrenergic[1]
In Vivo: Synephrine (1 mg/kg; oral gavage; for 8 days; PVL and BDL rats) significantly ameliorates the hyperdynamic state in both PVL and BDL rats. The portal venous pressure in PVL and BDL rats, portal tributary blood flow and cardiac index are significantly reduced, while mean arterial pressure and systemic as well as portal territory vascular resistance are enhanced by treatment of Synephrine[2].

Name: BIBF0775, CAS: 334951-90-5, stock 7.6g, assay 98.6%, MWt: 494.63, Formula: C31H34N4O2, Solubility: DMSO : 62.5 mg/mL (126.36 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: TGF-beta/Smad, Target: TGF-β Receptor, Biological_Activity: BIBF0775 is a potent and selective transforming growth factor β (TGFβ) type I receptor (Alk5) inhibitor with an IC50 of 34 nM.
IC50 & Target: IC50: 34 nM (Alk5)[1]

Name: Quercetin (dihydrate), CAS: 6151-25-3, stock 38.8g, assay 98.2%, MWt: 338.27, Formula: C15H14O9, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: PI3K/Akt/mTOR;Apoptosis, Target: PI3K;Apoptosis, Biological_Activity: Quercetin (dihydrate), a natural flavonoid, is a stimulator of recombinant SIRT1 and a PI3K inhibitor with IC50s of 2.4 μM, 3.0 μM and 5.4 μM for PI3K γ, PI3K δ and PI3K β, respectively[1].
IC50 & Target: IC50:PI3K γ (2.4 μM)，PI3K δ (3.0 μM)，PI3K β (5.4 μM)(Quercetin dihydrate)[1]
In Vitro: Quercetin (dihydrate) is a type of plant-based chemical, or phytochemical, used as an ingredient in supplements, beverages or foods. In several studies, it may have anti-inflammatory and antioxidant properties, and it is being investigated for a wide range of potential health benefits[1].
Quercetin (dihydrate) is a PI3K inhibitor with IC50s of 2.4-5.4 μM. Quercetin dihydrate (Sophoretin dihydrate) strongly abrogates PI3K and Src kinases, mildly inhibits Akt1/2, and slightly affected PKC, p38 and ERK1/2[1].
Quercetin (dihydrate) inhibits TNF-induced LDH% release, EC-dependent neutrophils adhesion to bovine pulmonary artery endothelial cells (BPAEC), and BPAEC DNA synthesis and proliferation[2].

Name: Monensin sodium salt Monensin A sodium salt, CAS: 22373-78-0, stock 20g, assay 98.2%, MWt: 692.85, Formula: C36H61NaO11, Solubility: Ethanol : 25 mg/mL (36.08 mM; Need ultrasonic); DMSO : < 1 mg/mL (insoluble or slightly soluble); H2O : < 0.1 mg/mL (insoluble), Clinical_Informat: No Development Reported, Pathway: Anti-infection, Target: Bacterial, Biological_Activity: Monensin sodium salt is an antibiotic secreted by the bacteria Streptomyces cinnamonensis.
IC50 & Target: bacterial[1]
In Vitro: Monensin sodium salt is an antibiotic secreted by the bacteria Streptomyces cinnamonensis. Untreated cells display 2.5% apoptosis; 48 hours treatment with 1 μM Monensin sodium salt shows 4.5% apoptosis whereas 5 μM Monensin sodium salt for 48 hours induces a greater apoptotic response (16.4%). Pretreatment with either 1 or 5 μM Monensin sodium salt for 24 hours followed by 10 μM erlotinib treatment for another 24 hours results in a marked increases in apoptotic events (14.6% and 38.7%, respectively) when compare with either Monensin sodium salt or erlotinib treatments alone. Combination of 5 μM Monensin sodium salt with 10 μM erlotinib shows the highest percentage of apoptosis (38.7%)[1].
In Vivo: Although the numbers of tumors do not change substantially, a significant (P=0.0144) reduction in the average size of lesions is observed in Monensin sodium salt-treated Apc+/Min mice when compare with control animals (mean 0.199 mm2 vs. 0.299 mm2). The total tumor area estimated in one animal is decreased in individuals receiving Monensin sodium salt (mean 10.16 mm2 vs. 16.46 mm2; P=0.0125). Monensin sodium salt treatment increases the numbers of apoptotic cells and cells expressing the p21 cell-cycle inhibitor at the surface area of the neoplastic outgrowths. No changes in the cell proliferation, differentiation, and tissue architecture in the healthy parts of mucosa are noted after exposure to Monensin sodium salt[2].

Name: Rhamnose (monohydrate) L-Rhamnose (monohydrate), CAS: 10030-85-0, stock 33.5g, assay 98.9%, MWt: 182.17, Formula: C6H14O6, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Rhamnose monohydrate (L-Rhamnose monohydrate) is a monosaccharide found in plants and bacteria. Rhamnose monohydrate-conjugated immunogens is used in immunotherapies[1]. Rhamnose monohydrate crosses the epithelia via the transcellular pathway and acts as a marker of intestinal absorption[2].

Name: Gramine Donaxine, CAS: 87-52-5, stock 9.5g, assay 98.9%, MWt: 174.24, Formula: C11H14N2, Solubility: DMSO : ≥ 125 mg/mL (717.40 mM), Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein;GPCR/G Protein;Anti-infection;Neuronal Signaling, Target: Adrenergic Receptor;Adiponectin Receptor;Reverse Transcriptase;Adrenergic Receptor, Biological_Activity: Gramine (Donaxine) is a natural alkaloid isolated from giant reed[2], acts as an active adiponectin receptor (AdipoR) agonist, with IC50s of 3.2 and 4.2 µM for AdipoR2 and AdipoR1, respectively[1]. Gramine is also a human and mouse β2-Adrenergic receptor (β2-AR) agonist[2]. Gramine (Donaxine) has anti-tumor, anti-viral and anti-inflammatory properties[1].
IC50 & Target: IC50: 3.2 µM (AdipoR2), 4.2 µM (AdipoR1)[1]
In Vitro: Gramine is an active adiponectin receptor (AdipoR) agonist, with IC50s of 3.2 and 4.2 µM for AdipoR2 and AdipoR1, respectively[1]. Gramine is a potential β2-AR agonist[2]. 
Gramine (20 µM to 1.2 nM) dose-dependently inhibits the growth of AdipoR1/adipoR2-positive cancer cell lines (MDA-MB-231 and MCF-7 cells), with IC50s of 9.6±0.9 and 0.1±0.1 µM, respectively[1].

Name: Hyodeoxycholic acid HDCA, CAS: 83-49-8, stock 29.9g, assay 98.6%, MWt: 392.57, Formula: C24H40O4, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein;Metabolic Enzyme/Protease, Target: GPCR19;Endogenous Metabolite, Biological_Activity: Hyodeoxycholic acid is a secondary bile acid formed in the small intestine by the gut flora, and acts as a TGR5 (GPCR19) agonist, with an EC50 of 31.6 µM in CHO cells.
IC50 & Target: EC50: 31.6 µM (TGR5, in CHO cells)[1]
In Vitro: Hyodeoxycholic acid is a secondary hydrophilic bile acid formed in the small intestine by the gut flora, and acts as an agonist of TGR5, with an EC50 of 31.6 µM in CHO cells[1]. Hyodeoxycholic acid (50, 100 μM) increases the expression of genes (Abca1, Abcg1, and Apoe) involved in cholesterol efflux in RAW 264.7 cells[2].
In Vivo: Hyodeoxycholic acid (HDCA; 1.25% (wt/wt)) obviously decreases fat mass and increases lean mass but does not raise the serum levels of any organ toxicity markers in LDLRKO mice. Hyodeoxycholic acid inhibits atherosclerotic lesion formation in LDLRKO at multiple sites, improves plasma lipoprotein profiles, decreases plasma glucose level and intestinal cholesterol absorption efficiency and increases daily cholesterol excretion through fecal output. Hyodeoxycholic acid also improves HDL function as measured by a cholesterol efflux assay[2].

Name: Cinchonidine α-Quinidine, CAS: 485-71-2, stock 4.8g, assay 98.2%, MWt: 294.39, Formula: C19H22N2O, Solubility: DMSO : 33.33 mg/mL (113.22 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Neuronal Signaling;Anti-infection, Target: Serotonin Transporter;Parasite, Biological_Activity: Cinchonidine (α-Quinidine) is a cinchona alkaloid found in Cinchona officinalis and Gongronema latifolium. A building block used in asymmetric synthesis in organic chemistry. Weak inhibitor of serotonin transporter (SERT) with Kis of 330, 4.2, 36, 196, 15 μM for dSERT, hSERT, hSERT I172M, hSERT S438T, hSERT Y95F, respectively. Antimalarial activities[1].
IC50 & Target: Ki: 330 μM (dSERT), 4.2 μM (hSERT), 36 μM (hSERT I172M), 196 μM (hSERT S438T), 15 μM (hSERT Y95F) [1]
In Vitro: Cinchonidine (α-Quinidine) is a cinchona alkaloid found in Cinchona officinalis and Gongronema latifolium. A building block used in asymmetric synthesis in organic chemistry. Weak inhibitor of serotonin transporter (SERT) with Kis of 330, 4.2, 36, 196, 15 μM for dSERT, hSERT, hSERT I172M, hSERT S438T, hSERT Y95F, respectively[1].

Name: Cytisinicline Cytisine; Sophorine; Baptitoxine, CAS: 485-35-8, stock 11.7g, assay 98.2%, MWt: 190.24, Formula: C11H14N2O, Solubility: DMSO : 125 mg/mL (657.06 mM; Need ultrasonic), Clinical_Informat: Launched, Pathway: Neuronal Signaling;Membrane Transporter/Ion Channel, Target: nAChR;nAChR, Biological_Activity: Cytisinicline (Cytisine) is an alkaloid that occurs naturally in several plant genera, such as Laburnum and Cytisus. Cytisinicline (Cytisine) is a partial agonist of α4β2 nAChRs[1], and partial to full agonist at β4 containing receptors and α7 receptors[2]. Has been used medically to help with smoking cessation[3].
IC50 & Target: α4β2 nAChRs[1].
In Vitro: Cytisinicline (Cytisine) (2.5, 5 and 10 mM) is capable of inducing apoptosis in HepG2 cells[4]. 
Treatment with Cytisinicline (Cytisine) increases the percentage of cells in the sub-G1 phase (P<0.01). The preincubation of HepG2 cells with Cytisinicline (Cytisine) (2.5, 5 and 10 mM) significantly increases the sub-G1 cell population[4].
In Vivo: Cytisinicline (Cytisine) (5 mg/kg, i.p.) eat less and gain less weight than those that receive the vehicle[2]. 
Total pellet intake increases during Cytisinicline (Cytisine) substitution relative to nicotine and animals self-administered Cytisine significantly less than nicotine[2].

Name: Ergosterol Ergosterin; Provitamin D; Provitamin D2, CAS: 57-87-4, stock 30g, assay 98.2%, MWt: 396.65, Formula: C28H44O, Solubility: Ethanol : 2.6 mg/mL (6.55 mM; ultrasonic and warming and heat to 80°C), Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: Ergosterol is the primary sterol found in fungi, with antioxidative, anti-proliferative, and anti-inflammatory effects.
In Vitro: Ergosterol is a sterol isolated from Grifola frondosa, which can be used in the research of mast cell-dependent allergic diseases. Ergosterol (10, 20, 50 μM) inhibits the antigen-induced release of β-hexosaminidase and histamine in antigen-stimulated RBL-2H3 cells. Ergosterol (20 and 50 μM) significantly reduces the mRNA levels of of IL-4 and TNF-α. Ergosterol (50 μM) inhibits the antigen-induced aggregation of FcεRI[1].
In Vivo: Ergosterol (25, 50 mg/kg, p.o.) significantly mitigates the reduced cardiac performance in rats induced by LPS, increases SOD activity and decreases the formation of MDA, CK-MB, and LDH in LPS-induced sepsis rats[2].

Name: (+)-Usnic acid, CAS: 7562-61-0, stock 0.5g, assay 98.9%, MWt: 344.32, Formula: C18H16O7, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: PI3K/Akt/mTOR, Target: mTOR, Biological_Activity: (+)-Usnic acid is isolated from isolated from lichens, binds at the ATP-binding pocket of mTOR, and inhibits mTORC1/2 activity. (+)-Usnic acid inhibits the phosphorylation of mTOR downstream effectors: Akt (Ser473), 4EBP1, S6K, induces autophay, with anti-cancer activity[1].
IC50 & Target: mTORC1/2[1]

Name: Esculin, CAS: 531-75-9, stock 26.2g, assay 98.8%, MWt: 340.28, Formula: C15H16O9, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: MAPK/ERK Pathway, Target: p38 MAPK, Biological_Activity: Esculin, a fluorescent coumarin glucoside, is an active ingredient of ash bark[1]. Esculin ameliorates cognitive impairment in experimental diabetic nephropathy (DN), and exerts anti‑oxidative stress and anti‑inflammatory effects, via the MAPK signaling pathway[2].

Name: Asiatic acid, CAS: 464-92-6, stock 10.9g, assay 98.2%, MWt: 488.70, Formula: C30H48O5, Solubility: DMSO : 62.5 mg/mL (127.89 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Apoptosis;Anti-infection, Target: Apoptosis;Parasite, Biological_Activity: Asiatic acid, a pentacyclic triterpene found in Centella asiatica, induces apoptosis in melanoma cells. Asiatic acid can be used to treat skin cancer[1]. Asiatic acid also has anti-inflammatory activities[2].

Name: Blebbistatin, CAS: 674289-55-5, stock 35.1g, assay 99%, MWt: 292.33, Formula: C18H16N2O2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Cytoskeleton, Target: Myosin, Biological_Activity: Blebbistatin is a selective non-muscle myosin II (NMII) inhibitor, promotes directional migration of corneal endothelial cells (CECs) and accelerates wound healing, and better preserves cell junctional integrity and barrier function[1].
IC50 & Target: Non-muscle myosin II (NMII)[1]
In Vitro: The therapeutic potential of targeting NMII to enhance CEC migration is investigated using bovine corneal endothelial cells (BCECs). Blebbistatin, a direct myosin motor inhibitor, promotes migration and directional persistence in CECs through decreasing actin retrograde flow and increasing lamellipodial protrusion persistence to accelerate wound healing in vitro[1].
In Vivo: Blebbistatin (0.05 mL, 20 μM; intracameral injection; daily; for 6 days; New Zealand white rabbits) treatment promotes wound healing in rabbit corneal endothelial scraping model[1].

Name: ELQ-300, CAS: 1354745-52-0, stock 8.8g, assay 98.1%, MWt: 475.84, Formula: C24H17ClF3NO4, Solubility: H2O : < 0.1 mg/mL (insoluble); DMSO : 15.62 mg/mL (32.83 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Anti-infection, Target: Parasite, Biological_Activity: ELQ-300 is a potent and orally bioavailable antimalarial agent, acts as an inhibitor of the reductive (Qi) site of the cytochrome bc1 complex (cyt bc1)[1].
IC50 & Target: ELQ-300 sensitizes P. falciparum Dd2, Tm90-C2B, and D1 strains with IC50s of 6.6, 4.6 and 160 nM, respectively[1].

Name: GSK-1070916 GSK-1070916A, CAS: 942918-07-2, stock 19.8g, assay 98%, MWt: 507.63, Formula: C30H33N7O, Solubility: DMSO : ≥ 26.5 mg/mL (52.20 mM), Clinical_Informat: Phase 1, Pathway: Apoptosis;Cell Cycle/DNA Damage;Epigenetics, Target: Apoptosis;Aurora Kinase;Aurora Kinase, Biological_Activity: GSK-1070916 is a potent and selective ATP-competitive inhibitor of aurora B and aurora C with Kis of 0.38 and 1.5 nM, respectively, and is >250- fold selective over Aurora A.
IC50 & Target: Ki: 0.38 nM (Aurora B), 1.5 nM (Aurora C)[1]
In Vitro: GSK-1070916 potently inhibits Aurora B/INCENP and Aurora C/INCENP kinases with Kis of 0.38±0.29 and 1.45±0.35 nM, respectively, but is less potent against Aurora A/ TPX2 with a Ki of 492±61 nM. GSK-1070916 also inhibits FLT1, TIE2, SIK, FLT4, and FGFR1 with IC50 values of 42, 59, 70, 74, and 78 nM, respectively. Treatment of A549 human lung cancer cells with GSK-1070916 results in a potent antiproliferative effect (EC50=7 nM)[1]. GSK-1070916 inhibits a panel of tumor cell lines and is shown o inhibits the phosphorylation of HH3- S10 in all cell lines with average EC50 values ranging from 8 to 118 nM[2].
In Vivo: In nude mice implanted with human colon tumor (HCT116) xenografts, a single dose of GSK-1070916 administered i.p. inhibits HH3-S10 phosphorylation in a dose-dependent manner. Repeated i.p. administration of GSK-1070916 produces complete or partial antitumor activity in 4 of 8 tumor types [lung, A549; colon, HCT116; acute myelogenous leukemia (AML), HL60; and chronic myelogenous leukemia, K562], stable disease in 3 of 8 (colon, Colo205; lung, H460; and breast, MCF-7), and tumor growth delay in 1 of 8 tumor types (colon, SW620). Daily administration of GSK-1070916 is generally well-tolerated[2].

Name: N-Methylisatoic anhydride NMIA, CAS: 10328-92-4, stock 15.8g, assay 98.1%, MWt: 177.16, Formula: C9H7NO3, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: N-Methylisatoic anhydride (NMIA) is a 2'-OH selective acylation agent of RNAs, and is widely used for
resolving secondary RNA structures using the SHAPE (Selective 2'-Hydroxyl Acylation Analyzed by Primer Extension) technology[1].

Name: GKA50, CAS: 851884-87-2, stock 22.6g, assay 99%, MWt: 464.51, Formula: C26H28N2O6, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Glucokinase, Biological_Activity: GKA50 is a potent glucokinase activator (EC50=33 nM at 5 mM glucose). GKA50 stimulates insulin release from mouse islets of Langerhans and MIN6 cells. GKA50 shows significant glucose lowering in high fat fed female rats[1][2].
In Vitro: GKA50 (0.01-100 μM; 24 hours) enhances INS-1 cell proliferation with EC50values ranging from 1 to 2 μM[2]. 
GKA50 (1.2 μM+40 μM glucose; 2-4 days) treatment reduces apoptosis induced by chronic high glucose in INS-1 cells[2]. 
GKA50 activates human glucokinase enzymatic activity with an EC50 of 0.022 μM. GKA50 stimulates insulin secretion in the pancreatic insulinoma cell line, INS-1, with an EC50 of 0.065 μM. GKA50 reduces chronic-high-glucose-induced apoptosis via modulation of glucokinase and apoptotic protein BAD[2].
In Vivo: GKA50 (1-30 mg/kg; p.o.) gives significant glucose lowering in an oral glucose tolerance test[1].

Name: Tesaglitazar, CAS: 251565-85-2, stock 2.5g, assay 98.2%, MWt: 408.47, Formula: C20H24O7S, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Cell Cycle/DNA Damage, Target: PPAR, Biological_Activity: Tesaglitazar is a dual peroxisome proliferator-activated receptor (PPAR) alpha/gamma agonist that is more potent on PPARγ than on PPARα, with EC50s of 13.4 μM and 3.6 μM for rat PPARα and human PPARα, respectively, and approximately 0.2 μM for both rat and human PPARγ. Tesaglitazar induces interstitial mesenchymal cell DNA synthesis and fibrosarcomas in subcutaneous tissues in rats[1].
IC50 & Target: EC50: 13.4 μM (rat PPARα), 3.6 μM (human PPARα), 0.2 μM (PPARγ)[1]

Name: Ardisiacrispin A Deglucocyclamin; LTS-4; Saxifragifolin B, CAS: 23643-61-0, stock 6.3g, assay 98.1%, MWt: 1061.21, Formula: C52H84O22, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Ardisiacrispin A (Deglucocyclamin) is a common triterpenoid saponin from Ardisia species. Ardisiacrispin A has similar biological properties with some triterpenoid saponins in A. crenata which is one of the species of genus Ardisia and exhibits cytotoxic effect on tumor cells, immunomodulatory and antiviral activities[1].

Name: Patchouli alcohol, CAS: 5986-55-0, stock 23.7g, assay 98.4%, MWt: 222.37, Formula: C15H26O, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Anti-infection, Target: Bacterial, Biological_Activity: Patchouli alcohol is a natural tricyclic sesquiterpene extracted from Pogostemon cablin (Blanco) Benth, and exhibits anti-Helicobacter pylori and anti-inflammatory properties[1].

Name: Kaempferol-3-O-glucorhamnoside, CAS: 40437-72-7, stock 21.3g, assay 98.9%, MWt: 612.53, Formula: C27H32O16, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Kaempferol-3-O-glucorhamnoside, a flavonoid derived from plant Thesium chinense Turcz, inhibits inflammatory responses via MAPK and NF-κB pathways in vitro and in vivo[1].

Name: Cyasterone, CAS: 17086-76-9, stock 33.3g, assay 98.1%, MWt: 520.65, Formula: C29H44O8, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: JAK/STAT Signaling;Protein Tyrosine Kinase/RTK, Target: EGFR;EGFR, Biological_Activity: Cyasterone, a natural EGFR inhibitor, mainly isolated from Ajuga decumbens Thunb (Labiatae).
Cyasterone manifests anti-proliferation effect by induced apoptosis and cell cycle arrests. Cyasterone may serves as a clinical therapeutic anti-tumor agent against human tumors[1].
In Vitro: Cyasterone (0-100μM; 24hours) inhibits cell growth in a concentration-and time-dependent manner, IC50 values are 38.50 mg/mL, 32.96 mg/mL in A549 and MGC823 cells ,respectively[1].

Name: Benzoic acid, CAS: 65-85-0, stock 33.5g, assay 98.9%, MWt: 122.12, Formula: C7H6O2, Solubility: 10 mM in DMSO, Clinical_Informat: Launched, Pathway: Anti-infection;Anti-infection, Target: Fungal;Bacterial, Biological_Activity: Benzoic acid is an aromatic alcohol existing naturally in many plants and is a common additive to food, drinks, cosmetics and other products. It acts as preservatives through inhibiting both bacteria and fungi.

Name: Dauricine, CAS: 524-17-4, stock 32.1g, assay 98.9%, MWt: 624.77, Formula: C38H44N2O6, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Apoptosis;NF-κB, Target: Apoptosis;NF-κB, Biological_Activity: Dauricine, a bisbenzylisoquinoline alkaloid in Asiatic Moonseed Rhizome, possesses anti-inflammatory activity. Dauricine inhibits cell proliferation and invasion, and induces apoptosis by suppressing NF-κB activation in a dose- and time-dependent manner in colon cancer[1].

Name: Avicularin, CAS: 572-30-5, stock 11g, assay 98.5%, MWt: 434.35, Formula: C20H18O11, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Avicularin is a bio-active flavonoid from plants, anti-inflammatory, anti-allergic, anti-oxidant, hepatoprotective, and anti-tumor activities. Avicularin exhibits anti-inflammatory activity through the suppression of ERK signaling pathway in LPS-stimulated RAW 264.7 macrophage cells. Avicularin ameliorates human hepatocellular carcinoma via the regulation of NF κB (p65), COX 2 and PPAR γ activities[1][2].

Name: Epigoitrin, CAS: 1072-93-1, stock 15.6g, assay 99%, MWt: 129.18, Formula: C5H7NOS, Solubility: DMSO : 8.33 mg/mL (64.48 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Anti-infection, Target: Influenza Virus, Biological_Activity: Epigoitrin is a natural alkaloid from Isatis indigotica, with antiviral activities. Epigoitrin reduces susceptibility to influenza virus via mitochondrial antiviral signaling[1][2].

Name: 7-epi-Taxol 7-epi-Paclitaxel, CAS: 105454-04-4, stock 30.3g, assay 98.6%, MWt: 853.91, Formula: C47H51NO14, Solubility: DMSO : ≥ 106.6 mg/mL (124.84 mM), Clinical_Informat: No Development Reported, Pathway: Cell Cycle/DNA Damage;Cytoskeleton, Target: Microtubule/Tubulin;Microtubule/Tubulin, Biological_Activity: 7-epi-Taxol is an active metabolite of taxol, with activity comparable to that of taxol against cell replication, promoting microtubule bundle formation and against microtubule depolymerization.
IC50 & Target: Microtubule/Tubulin[2]
In Vitro: 7-epi-Taxol (7-Epitaxol) is a metabolite of taxol[1]. 7-epi-Taxol has activity comparable to that of taxol on cell replication, microtubule bundle formation and in vitro microtubule polymerization[2].

Name: Scoparone, CAS: 120-08-1, stock 9.4g, assay 98.8%, MWt: 206.19, Formula: C11H10O4, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Scoparone is isolated from Artemisia capillaris, has anticoagulant, vasorelaxant antioxidant, anti-inflammatory activities[1].
In Vitro: Scoparone (0-0.4 nM; 24-48 hours) produces the most inhibition on PSC proliferation at 0.4 nM[1].
In Vivo: Scoparone (oral administration; 30 mg/kg, 60 mg/kg; 4 weeks) greatly ameliorates the pancreatic weight loss induced by DBTC in pancreatitis rats[1].

Name: Herbacetin, CAS: 527-95-7, stock 26.8g, assay 98.5%, MWt: 302.24, Formula: C15H10O7, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Herbacetin is a natural flavonoid from flaxseed, exerts various pharmacological activities, including antioxidant, anti-inflammatory and anticancer effects[1]. Herbacetin is an Ornithine decarboxylase (ODC) allosteric inhibitor, directly binds to Asp44, Asp243, and Glu384 on ODC. Ornithine decarboxylase (ODC) is a rate-limiting enzyme in the first step of polyamine biosynthesis[2].
IC50 & Target: IC50: Ornithine decarboxylase[2]
In Vivo: Herbacetin (orally administration; 20mg/kg) significantly reduces the body weight, plasma glucose, plasma insulin, and HOMA-IR activity in obesity associated insulin resistant mice (OIR). (Herbacetin dissolves in 0.5% DMSO)[1].
Herbacetin (intraperitoneal injection; 0.4, 2, 10 or 20 mg/kg; B.W.) decreases the number and size of polyps in APCMin+ mice with no overt toxicity[2].

Name: Rhodionin, CAS: 85571-15-9, stock 18.6g, assay 98.6%, MWt: 448.38, Formula: C21H20O11, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Neuronal Signaling, Target: AChE, Biological_Activity: Rhodionin, isolated from the root of Rhodiola crenulata, is a specific non-competitive cytochrome P450 2D6 inhibitor with an IC50 of 0.761 μM and a Ki of 0.769 μM[1]. Rhodionin exhibits potent, dose-dependent inhibitory effects on acetylcholinesterase (AChE) with IC50 ranged from 57.50 to 2.43 μg/mL[2]. Rhodionin exhibits potent DPPH free radical scavenging activities, with an IC50 of 19.49 μM[3].
IC50 & Target: IC50: 0.761 μM (cytochrome P450 2D6)[1]；57.50-2.43 μg/mL (AChE)[2]；19.49 μM (DPPH free radical scavenging)[3]

Name: Fraxinellone, CAS: 28808-62-0, stock 24.6g, assay 99%, MWt: 232.28, Formula: C14H16O3, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: JAK/STAT Signaling;Stem Cell/Wnt;Metabolic Enzyme/Protease;Immunology/Inflammation, Target: STAT;STAT;HIF/HIF Prolyl-Hydroxylase;PD-1/PD-L1, Biological_Activity: Fraxinellone is isolated from the root bark of the Rutaceae plant, Dictamnus dasycarpus. Fraxinellone is a PD-L1 inhibitor and inhibits HIF-1α protein synthesis without affecting HIF-1α protein degradation. Fraxinellone has the potential to be a valuable candidate for cancer treatment by targeting PD-L1[1].
In Vitro: Fraxinellone (0-100 μM；12 hours) decreases the percent of PD-L1 positive cells from 20.4% to 11.4% in A549 cells[1].
In Vivo: Fraxinellone (oral gavage; 30 and 100 mg/kg; every three days; 30 days) significantly suppresses tumor growth, reduces HIF-1α, pTyr705 STAT3, PD-L1 and VEGF staining compared with the control group in female athymic BALB/c nude mice[1].

Name: Theaflavin-3-gallate, CAS: 30462-34-1, stock 25.5g, assay 98.3%, MWt: 716.60, Formula: C36H28O16, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Theaflavin-3-gallate, a black tea theaflavin monomer, is regarded as the biologically important active component of black tea and provides health benefits. Theaflavin-3-gallate acts as prooxidants and induces oxidative stress in the carcinoma cells. Theaflavin-3-gallate reacts directly with reduced glutathione (GSH) in a time- and concentration-dependent manner[1].

Name: Saikosaponin A, CAS: 20736-09-8, stock 33.2g, assay 98.2%, MWt: 780.98, Formula: C42H68O13, Solubility: DMSO : 250 mg/mL (320.11 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Anti-infection;Metabolic Enzyme/Protease, Target: Bacterial;LXR, Biological_Activity: Saikosaponin A is an active component of Bupleurum falcatum, up-regulates LXRα expression, with potent anti-inflammatory activity[1].

Name: Saikosaponin B1, CAS: 58558-08-0, stock 19.2g, assay 98.5%, MWt: 780.98, Formula: C42H68O13, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Saikosaponin B1 is a component of Saiko, enhances the effect of cancer chemotherapy[1].

Name: Saikosaponin B2, CAS: 58316-41-9, stock 23.1g, assay 98.1%, MWt: 780.98, Formula: C42H68O13, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Anti-infection, Target: HCV, Biological_Activity: Saikosaponin B2 is an active component from Bupleurum kaoi root, acts as an entry inhibitor against HCV infection[1]. Anti-cancer activity[2].

Name: Saikosaponin C, CAS: 20736-08-7, stock 14.7g, assay 98.8%, MWt: 927.12, Formula: C48H78O17, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Neuronal Signaling, Target: Amyloid-β, Biological_Activity: Saikosaponin C is a bioactive component found in radix bupleuri, targets amyloid beta and tau in Alzheimer's disease. Saikosaponin C inhibits the secretion of both Aβ1-40 and Aβ1-42, and suppresses abnormal tau phosphorylation, but shows no effect on BACE1 activity and expression[1].

Name: Saikosaponin D, CAS: 20874-52-6, stock 39g, assay 98.1%, MWt: 780.98, Formula: C42H68O13, Solubility: H2O : < 0.1 mg/mL (insoluble); DMSO : 50 mg/mL (64.02 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Others;Anti-infection;JAK/STAT Signaling;Stem Cell/Wnt;NF-κB, Target: Estrogen Receptor/ERR;Bacterial;STAT;STAT;NF-κB, Biological_Activity: Saikosaponin D is a triterpene saponin isolated from Bupleurum, with anti-inflammatory, anti-bacterial, anti-tumor, and anti-allergic activities; Saikosaponin D inhibits selectin, STAT3 and NF-kB and activates estrogen receptor-β.
IC50 & Target: Selectin[1], STAT3, NF-kB[2], Estrogen receptor-β[3]
In Vitro: Saikosaponin D (Compound 3) is a triterpene saponin, which inhibits E-selectin, L-selectin and P-selectin binding to THP-1 cells, with IC50s of 1.8 µM, 3.0 µM and 4.3 µM, and such effects are not due to cytotoxic action. Saikosaponin D (1, 5, 10 µM) dose-dependently inhibits the THP-1 adhesion to the HUVECs monolayer activated by TNF-α. Saikosaponin D (30 μM) also inhibits the expression of P-selectin ligand (CD162) in THP-1 cells[1]. Saikosaponin D (5 μM) suppresses the proliferation of HSC-T6 cells induced by H2O2 treatment, reduces the expression levels of α-SMA, TGF-β1, Hyp, COL1 and TIMP-1, and increases MMP-1 expressioon, thus inhibiting H2O2-induced excessive extracellular matrix (ECM) formation, with similar effects to estradiol (E2), and these effects are blocked by ER antagonists. Saikosaponin D also inhibits oxidative stress-induced ROS generation and down reduates MAPK signaling pathway, and the inhibition is also suppressed by ER antagonists[3].
In Vivo: Saikosaponin D (2 mg/kg/day, i.p.) shows a protective effect on overdose of acetaminophen (APAP)-induced liver injury of mice. Saikosaponin D affects APAP metabolism, increases GSH levels but does not alter PPARα activation. Saikosaponin D (2 mg/kg/day, i.p.) also suppresses APAP-induced increases in the expression of STAT3 target genes and pro-inflammatory cytokines and inhibits APAP-induced activation of STAT3 and NF-kB[2].

Name: Vincristine Leurocristine;NSC-67574;22-Oxovincaleukoblastine, CAS: 57-22-7, stock 16.4g, assay 98.3%, MWt: 824.96, Formula: C46H56N4O10, Solubility: 10 mM in DMSO, Clinical_Informat: Launched, Pathway: Cell Cycle/DNA Damage;Cytoskeleton, Target: Microtubule/Tubulin;Microtubule/Tubulin, Biological_Activity: Vincristine (Leurocristine) is a microtubule-destabilizing agent (MDA). Vincristine (Leurocristine) binds to tubulin and inhibits the formation of microtubules, thereby inhibiting mitosis of the cancer cell. Vincristine (Leurocristine) is used to treat hematologic cancers, such as leukemia and lymphoma, and childhood sarcomas[1][2].

Name: Epimedin A1 Hexandraside F, CAS: 140147-77-9, stock 38.1g, assay 98.9%, MWt: 838.80, Formula: C39H50O20, Solubility: DMSO : 150 mg/mL (178.83 mM; Need ultrasonic and warming), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Epimedin A1 is a flavonoid extracted from Herba Epimedii which is one of commonly used Chinese medicines.

Name: Aurantio-obtusin, CAS: 67979-25-3, stock 4.5g, assay 98.3%, MWt: 330.29, Formula: C17H14O7, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Aurantio-obtusin is an anthraquinone isolated from Semen Cassiae, with anti-Inflammatory, anti-oxidative, anti-coagulating and anti-hypertension activities[1][2][3]. Aurantio-obtusin relaxes systemic arteries through endothelial PI3K/AKT/eNOS-dependent signaling pathway in rats, thus acts as a new potential vasodilator[2]. Aurantio-obtusin inhibits allergic responses in IgE-mediated mast cells and anaphylactic models and is potential for treatment for allergy-related diseases[3].

Name: Toosendanin, CAS: 58812-37-6, stock 10.6g, assay 98.8%, MWt: 574.62, Formula: C30H38O11, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Toosendanin, a triterpenoid extracted from the bark of fruit of Melia toosendan Sieb et Zucc, possesses analgesic, insecticidal and anti-inflammatory activities[1].
In Vivo: Toosendanin (0.5 and 1 mg/kg, Intraperitoneal injection daily for 7 days) alleviates DSS-induced experimental colitis by inhibiting M1 macrophage polarization and regulating NLRP3 inflammasome and Nrf2/HO-1 signaling, and may provide a novel Chinese patent medicine for the treatment of murine colitis[1].

Name: Asperosaponin VI, CAS: 39524-08-8, stock 18.7g, assay 98%, MWt: 929.10, Formula: C47H76O18, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Apoptosis, Target: Apoptosis, Biological_Activity: Asperosaponin VI, A saponin component from Dipsacus asper wall, induces osteoblast differentiation through BMP‐2/p38 and ERK1/2 pathway[1]. Asperosaponin Ⅵ inhibits apoptosis in hypoxia-induced cardiomyocyte by increasing the Bcl-2/Bax ratio and decreasing active caspase-3 expression, as well as enhancing of p-Akt and p-CREB[2].

Name: Irisflorentin, CAS: 41743-73-1, stock 5.7g, assay 98.7%, MWt: 386.35, Formula: C20H18O8, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Immunology/Inflammation, Target: NO Synthase, Biological_Activity: Irisflorentin, a naturally occurring isoflavone, is an abundant active constituent in Rhizoma Belamcandae. Irisflorentin markedly reduces the transcriptional and translational levels of inducible nitric oxide synthase (iNOS) as well as the production of NO. Anti-inflammatory activity[1].
In Vitro: Irisflorentin does not affect the LPS-stimulated RAW 264.7 macrophages viability up to a concentration of 40 μM[1]. 
Irisflorentin (10-40 μM) inhibits the LPS-induced production of NO in a concentration-dependent manner without affecting the iNOS activity in RAW 264.7 macrophages[1]. 
Irisflorentin (10-40 μM) concentration dependently inhibits the LPS (10 ng/mL)-induced increase in iNOS mRNA expression in LPS stimulated RAW 264.7 macrophages. Irisflorentin (10-40 μM) concentration-dependently suppresses the production of TNF-α, IL-1β and IL-6 in LPS stimulated RAW 264.7 macrophages[1]. 
Irisflorentin (10-40 μM) concentration dependently inhibits the LPS (10 ng/mL)-induced increase in iNOS protein levels. Irisflorentin (10-40 μM) concentration-dependently suppresses LPS-induced p38 and ERK1/2 phosphorylation in a concentration-dependent manner, but slightly affects JNK phosphorylation[1].

Name: Echinatin, CAS: 34221-41-5, stock 24.7g, assay 98.1%, MWt: 270.28, Formula: C16H14O4, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Echinatin is a chalcone isolated from the Chinese herbal medicine Gancao with hepatoprotective and anti-inflammatory effects. Echinatin may undergo an electron transfer (ET) and a proton transfer (PT) to cause the antioxidant action in aqueous solution[1]. Echinatin can be quickly absorbed and eliminated and extensively distributed with an absolute bioavailability of approximately 6.81% in Rat[2].

Name: NSC 13138 Cinchoninic acid (6CI,7CI,8CI); 4-Carboxyquinoline, CAS: 486-74-8, stock 11g, assay 98.3%, MWt: 173.17, Formula: C10H7NO2, Solubility: , Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity:

Name: Cinnamyl Alcohol, CAS: 104-54-1, stock 39.1g, assay 98.5%, MWt: 134.18, Formula: C9H10O, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Cell Cycle/DNA Damage, Target: PPAR, Biological_Activity: Cinnamyl Alcohol is an active component from chestnut flower, inhibits increased PPARγ expression, with anti-obesity activity[1].

Name: 3,4,5-Trimethoxybenzoic acid Eudesmic acid;Trimethylgallic Acid, CAS: 118-41-2, stock 27.4g, assay 98.9%, MWt: 212.20, Formula: C10H12O5, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: 3,4,5-Trimethoxybenzoic acid (Eudesmic acid;Trimethylgallic Acid) is a benzoic acid derivative. A building block in medicine and organic synthesis.

Name: 2-Naphthol, CAS: 135-19-3, stock 12.7g, assay 98.6%, MWt: 144.17, Formula: C10H8O, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: 2-Naphthol is a metabolite of naphthalene, catalyzed by cytochrome P450 (CYP) isozymes (CYP 1A1, CYP 1A2, CYP 2A1, CYP 2E1 and CYP 2F2).
In Vitro: 2-Naphthol is a metabolite of naphthalene, catalyzed by cytochrome P450 (CYP) isozymes (CYP 1A1, CYP 1A2, CYP 2A1, CYP 2E1 and CYP 2F2). 2-Naphthol (10, 25, 50 and 100 μM) causes no cytotoxic effect and the inhibition of peripheral-blood mononuclear cells proliferation[1].

Name: Cinchonine (8R,9S)-Cinchonine; LA40221, CAS: 118-10-5, stock 26.5g, assay 98.5%, MWt: 294.39, Formula: C19H22N2O, Solubility: DMSO : 4.76 mg/mL (16.17 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Apoptosis;Anti-infection, Target: Apoptosis;Parasite, Biological_Activity: Cinchonine is a natural compound present in Cinchona bark. Cinchonine activates endoplasmic reticulum stress-induced apoptosis in human liver cancer cells[1].

Name: Thymol, CAS: 89-83-8, stock 20.7g, assay 98.9%, MWt: 150.22, Formula: C10H14O, Solubility: DMSO : 125 mg/mL (832.11 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Thymol is the main monoterpene phenol occurring in essential oils isolated from plants belonging to the Lamiaceae family, and other plants such as those belonging to the Verbenaceae, Scrophulariaceae, Ranunculaceae and Apiaceae families. Thymol has antioxidant, anti-inflammatory, antibacterial and antifungal effects[1].

Name: Benzoyleneurea, CAS: 86-96-4, stock 13.3g, assay 98.9%, MWt: 162.15, Formula: C8H6N2O2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Anti-infection, Target: Bacterial, Biological_Activity: Benzoyleneurea possesses anti-bacterial activity. Benzoyleneurea scaffold can be used in the synthesis of novel protein geranylgeranyltransferase-I (PGGTase-I) inhibitors[1].

Name: KSD 2405, CAS: 620-24-6, stock 11.2g, assay 98.3%, MWt: 124.14, Formula: C7H8O2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity:

Name: Estetrol, CAS: 15183-37-6, stock 4.8g, assay 98.9%, MWt: 304.38, Formula: C18H24O4, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others;Metabolic Enzyme/Protease, Target: Estrogen Receptor/ERR;Endogenous Metabolite, Biological_Activity: Estetrol, a natural estrogen synthesized exclusively during pregnancy by the human fetal liver, is a selective nuclear estrogen receptor modulator. Estetrol exerts estrogenic actions on the endometrium or the central nervous system but presents antagonistic effects on the breast[1][2].
IC50 & Target: Estrogen receptor[1]

Name: Roniciclib BAY 1000394, CAS: 1223498-69-8, stock 33.3g, assay 98.2%, MWt: 430.44, Formula: C18H21F3N4O3S, Solubility: DMSO : ≥ 250 mg/mL (580.80 mM), Clinical_Informat: Phase 2, Pathway: Cell Cycle/DNA Damage, Target: CDK, Biological_Activity: Roniciclib is an orally bioavailable pan-cyclin dependent kinase (CDK) inhibitor, with IC50s of 5-25 nM for CDK1, CDK2, CDK3, CDK4, CDK7 and CDK9.
IC50 & Target: IC50: 5-25 nM (CDK)[1].
In Vitro: Roniciclib (BAY 1000394) inhibits the kinase activity of the cell-cycle CDKs CDK1/cyclin B, CDK2/cyclin E, and CDK4/cyclinDwith IC50 values of 7, 9, and 11 nM, respectively. The transcriptional CDKs CDK9/cyclin T1 and CDK7/cyclin H/MAT1 are inhibited in a similar range (5 and 25 nM)[1]. Roniciclib potently inhibits the proliferation of various human and murine tumor cell lines with a very balanced profile (mean IC50 on human tumor cells: 16 nM)[2].
In Vivo: Tumor growth is strongly inhibited in a dose-dependent manner with T/C values of 0.19 at the lower dose and of 0.02 (tumor regression) at the higher dose. Furthermore, Roniciclib strongly inhibits growth of HeLa-MaTu tumors that have been grown to a size of approximately 50mm2 before start of treatment (day 8 after inoculation). Treatment with Roniciclib at doses of 1.5 and 1 mg/kg slow tumor growth to T/C values of 0.15 and 0.62, respectively. Addition of Roniciclib to cisplatin result in a strong tumor growth inhibition with T/C values of 0.01 (1.0 mg/kg Roniciclib) and -0.02 (1.5 mg/kg Roniciclib)[1]. Roniciclib has low blood clearance rates in mouse, rat, and dog (0.51, 0.78, and 0.50 Lh-1kg-1, respectively) [2].

Name: CGP37157, CAS: 75450-34-9, stock 35.4g, assay 98.9%, MWt: 324.22, Formula: C15H11Cl2NOS, Solubility: DMSO : ≥ 125 mg/mL (385.54 mM), Clinical_Informat: No Development Reported, Pathway: Membrane Transporter/Ion Channel, Target: Na+/Ca2+ Exchanger, Biological_Activity: CGP37157 is a potent, selective inhibitor of Na+/Ca2+ exchanger, inhibiting the Na+-induced Ca2+-release from guinea-pig heart mitochondria, with an IC50 of 0.8 μM.
IC50 & Target: IC50: 0.8 μM (Na+/Ca2+ exchanger)[1]
In Vitro: CGP37157 (Compound XVI) is a potent, selective inhibitor of Na+/Ca2+ exchanger, inhibiting the Na+-induced Ca2+-release from guinea-pig heart mitochondria, with an IC50 of 0.8 μM[1]. CGP37157 (10 μM) shows inhibitory effect on mitochondrial Na+/Ca2+ exchanger in cortical neurons, modulates intracellular Ca2+ levels via suppresssing voltage-gated calcium channels, and reduces NMDA-induced cytosolic and mitochondrial Ca2+ overloads. CGP37157 (10 μM) also reduces NMDA-induced excitotoxicity, and such an effect is via attenuating mitochondrial damage and calpain activity in neurons[2]. CGP37157 (10 μM) in combination with salinomycin significantly attenuates cell viability and increases apoptosis of FaDu and HLaC79 cells. Moreover, CGP37157 has no inhibitory effect on salinomycin tumor toxicity[3].

Name: PD0166285, CAS: 185039-89-8, stock 8.7g, assay 98.5%, MWt: 512.43, Formula: C26H27Cl2N5O2, Solubility: H2O : < 0.1 mg/mL (insoluble); DMSO : 65 mg/mL (126.85 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Apoptosis;Cell Cycle/DNA Damage, Target: Apoptosis;Wee1, Biological_Activity: PD0166285 is a WEE1 inhibitor and a weak Myt1 inhibitor with IC50s of 24 and 72 nM, respectively.
IC50 & Target: IC50: 24 nM (WEE1), 72 nM (Myt1)[1]
In Vitro: PD0166285 is a pyridopyrimidine class of molecule. At the cellular level, 0.5 μM PD0166285 dramatically inhibits irradiation-induced Cdc2 phosphorylation at the Tyr-15 and Thr-14 in seven of seven cancer cell lines. PD0166285 sensitizes radiation-induced cell killing in p53 mutant HT29 cells and in the E6-transfected, p53-null ovarian cancer cell line PA-1 but to a lesser extent in p53 wild-type PA-1 cells. PD0166285 abrogates irradiation-induced G2 arrest and significantly increases mitotic cell populations. Biologically, PD0166285 acts as a radiosensitizer to sensitize cells to radiation-induced cell death with a sensitivity enhancement ratio of 1.23[1].

Name: Isocarboxazid, CAS: 59-63-2, stock 31.4g, assay 99%, MWt: 231.25, Formula: C12H13N3O2, Solubility: 10 mM in DMSO, Clinical_Informat: Launched, Pathway: Neuronal Signaling, Target: Monoamine Oxidase, Biological_Activity: Isocarboxazid is a non-selective and irreversible inhibitor of monoamine oxidase, with an IC50 of 4.8 μM for rat brain monoamine oxidase in vitro[1].
IC50 & Target: IC50: 4.8 μM (rat brain monoamine oxidase)[1].
In Vivo: Isocarboxazid (1, 3 mg/kg, i.p., 60 min) pretreatment in mice shows the significant increased number of head twitches at 15 and 30 min after 5-HTP[2]. 
Isocarboxazid (1, 3 mg/kg, i.p., 60 min) treatment in mice together with 5-HTP administration causes 43% 5-HT concentration increased and 22% of 5-HIAA decreased compared to brain concentrations in mice given 5-HTP alone[2].

Name: Methyl-Hesperidin, CAS: 11013-97-1, stock 7.2g, assay 98.7%, MWt: 624.59, Formula: C29H36O15, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Methyl-Hesperidin is a vasodilating agent[1].

Name: Caffeic acid phenethyl ester, CAS: 104594-70-9, stock 21.7g, assay 98.1%, MWt: 284.31, Formula: C17H16O4, Solubility: DMSO : 150 mg/mL (527.59 mM; Need ultrasonic and warming), Clinical_Informat: No Development Reported, Pathway: Apoptosis;NF-κB, Target: Apoptosis;NF-κB, Biological_Activity: Caffeic acid phenethyl ester is a NF-κB inhibitor.
IC50 & Target: NF-κB[1]
In Vitro: Caffeic acid phenethyl ester is a NF-κB inhibitor. Cell survival and proliferation of CRPC cell lines are all significantly suppressed by Caffeic acid phenethyl ester (CAPE) treatment dose-dependently. The growth inhibitory effect of Caffeic acid phenethyl ester is evident within 24 hours of treatment but the suppressive effect accumulates over time. The IC50 of 24, 48, 72, and 96 h Caffeic acid phenethyl ester treatment on LNCaP 104-R1 cells is 64.0, 30.5, 20.5, and 18.0 μM, respectively. Colony formation assay reveals that treatment with 10 μM Caffeic acid phenethyl ester reduces colony formation of LNCaP 104-R1 cells by 90% while treatment with 20 μM Caffeic acid phenethyl ester completely blocks the formation of LNCaP 104-R1 colonies. Flow cytometric analysis reveals a reduction of cells in the S phase and G2/M phase but an increase of cells in the G1 phase population in LNCaP 104-R1 cells under Caffeic acid phenethyl ester treatment. Caffeic acid phenethyl ester treatment also significantly decreases protein levels of fatty acid synthase (FAS), retinoblastoma protein (Rb), phospho-Rb Ser807/811, c-Myc, p70S6kinase, phospho-p70S6kinase Thr421/Ser424, Skp2, p90RSK, and NF-κB p65[1].

In Vivo: Administration of Caffeic acid phenethyl ester (CAPE) by gavage (10 mg/kg body weight per day) for eight weeks results in 50% reduction of tumor volume, suggesting that Caffeic acid phenethyl ester treatment retards the growth of LNCaP 104-R1 xenografts. Caffeic acid phenethyl ester gavage slows down the tumor growth of LNCaP 104-R1 cells, which is consistent with our observation that Caffeic acid phenethyl ester treatment induces cell cycle arrest but not apoptosis[1].

Name: (±)-10-Hydroxycamptothecin (±)-10-HCPT, CAS: 64439-81-2, stock 35.8g, assay 98.8%, MWt: 364.35, Formula: C20H16N2O5, Solubility: DMSO : ≥ 37.5 mg/mL (102.92 mM), Clinical_Informat: No Development Reported, Pathway: Cell Cycle/DNA Damage, Target: Topoisomerase, Biological_Activity: (±)-10-Hydroxycamptothecin, an indole alkaloid isolated from Camptotheca acuminate, inhibits the activity of topoisomerase I and has a broad spectrum of anticancer activity.
IC50 & Target: Topoisomerase I[1]
In Vitro: (±)-10-Hydroxycamptothecin (10-OH-camptothecin) is an inhibitor of topo I[1]. (±)-10-Hydroxycamptothecin (10-HCPT, 5-20 nM) markedly inhibits the proliferation of Colo 205 cells in a dose-dependent manner. (±)-10-Hydroxycamptothecin (5-20 nM) arrests Colo 205 cells in the G2 phase of the cell cycle and triggers apoptosis through a caspase-3-dependent pathway[2]. (±)-10-Hydroxycamptothecin (HPT, 0.01-10 μg/mL) causes cell shrinage, nuclear fragmentation and condensed chromosomes and induces apoptosis of human urinary bladder cancer cell line (T24)[3].
In Vivo: (±)-10-Hydroxycamptothecin (10-HCPT, 2.5-7.5 mg/kg/2 days, p.o.) significantly suppresss tumor growth in mouse xenografts. (±)-10-Hydroxycamptothecin (1-7.5 mg/kg, p.o., once per 2 or 4 days) causes no obvious acute toxicity in nude mice[2].

Name: Cardamonin Cardamomin; Alpinetin chalcone, CAS: 18956-16-6, stock 25g, assay 98.2%, MWt: 270.28, Formula: C16H14O4, Solubility: DMSO : 130 mg/mL (480.98 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Immunology/Inflammation;Immunology/Inflammation, Target: NOD-like Receptor (NLR);Aryl Hydrocarbon Receptor, Biological_Activity: Cardamonin (Cardamomin), a natural flavone isolated from Alpinia katsumadai Hayata, acts as an aryl hydrocarbon receptor (AhR) activator. Cardamonin alleviates inflammatory bowel disease by the inhibition of NLRP3 inflammasome activation via an AhR/Nrf2/NQO1 pathway[1].

Name: Daphnetin 7,8-Dihydroxycoumarin, CAS: 486-35-1, stock 17.2g, assay 98.5%, MWt: 178.14, Formula: C9H6O4, Solubility: DMSO : 150 mg/mL (842.03 mM; Need ultrasonic and warming), Clinical_Informat: Launched, Pathway: Stem Cell/Wnt;Protein Tyrosine Kinase/RTK;TGF-beta/Smad;Epigenetics;JAK/STAT Signaling;Protein Tyrosine Kinase/RTK;Autophagy;Anti-infection, Target: PKA;PKA;PKC;PKC;EGFR;EGFR;Autophagy;Parasite, Biological_Activity: Daphnetin (7,8-dihydroxycoumarin), one coumarin derivative isolated from plants of the Genus Daphne, is a protein kinase inhibitor, with IC50s of 7.67 μM, 9.33 μM and 25.01 μM for EGFR, PKA and PKC in vitro, respectively[1][2]. Daphnetin (7,8-dihydroxycoumarin) is a secondary metabolite of plants used in folk medicine to counter inflammatory and allergic diseases, also has been clinically used in the treatment of coagulation disorders, rheumatoid arthritis with anti-malarian and anti-pyretic properties[3].

Name: Esculetin, CAS: 305-01-1, stock 25g, assay 99%, MWt: 178.14, Formula: C9H6O4, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: PI3K/Akt/mTOR;PI3K/Akt/mTOR, Target: PI3K;Akt, Biological_Activity: Esculetin is an active ingredient extracted mainly from the bark of Fraxinus rhynchophylla. Esculetin inhibits platelet-derived growth factor (PDGF)-induced airway smooth muscle cells (ASMCs) phenotype switching through inhibition of PI3K/Akt pathway. Esculetin has antioxidant, antiinflammatory, and antitumor activities[1].

Name: Oleuropein, CAS: 32619-42-4, stock 30.9g, assay 98.1%, MWt: 540.51, Formula: C25H32O13, Solubility: DMSO : 250 mg/mL (462.53 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Cell Cycle/DNA Damage;Apoptosis;Others, Target: PPAR;Apoptosis;Aromatase, Biological_Activity: Oleuropein, found in olive leaves and oil, exerts antioxidant, anti-inflammatory and anti-atherogenic effects through direct inhibition of PPARγ transcriptional activity[1]. Oleuropein induces apoptosis in breast cancer cells via the p53-dependent pathway and through the regulation of Bax and Bcl2 genes. Oleuropein also inhibits aromatase[2].
In Vitro: Aromatase, a cytochrome P450 enzyme, is an important pharmacological target in breast cancer therapy[2].

Name: Hederasaponin B, CAS: 36284-77-2, stock 17.9g, assay 98.7%, MWt: 1205.38, Formula: C59H96O25, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Anti-infection, Target: Enterovirus, Biological_Activity: Hederasaponin B, isolated from Hedera helix, has broad-spectrum antiviral activity against various subgenotypes of Enterovirus 71 (EV71).

Name: Ciwujianoside B, CAS: 114902-16-8, stock 34.6g, assay 99%, MWt: 1189.34, Formula: C58H92O25, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Apoptosis, Target: Bcl-2 Family, Biological_Activity: Ciwujianoside B is isolated from Eleutherococcus senticosus leaf, is able to penetrate and work in the brain after the oral administration. Ciwujianoside B significantly enhances object recognition memory[1].
Ciwujianoside B shows radioprotective effects on the hematopoietic system in mice, which is associated with changes in the cell cycle, reduces DNA damage and down-regulates the ratio of Bax/Bcl-2 in bone marrow cells exposed to radiation[2].

Name: Soyasaponin Ba, CAS: 114590-20-4, stock 32.3g, assay 98%, MWt: 959.12, Formula: C48H78O19, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Soyasaponin Ba is a soyasaponin isolated from Phaseolus vulgaris, acts as an aldose reductase inhibitors (ARI)[1].

Name: Soyasaponin Bb, CAS: 51330-27-9, stock 2g, assay 98.9%, MWt: 943.12, Formula: C48H78O18, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: soyasaponin Bb is a soyasaponin isolated from Phaseolus vulgaris, acting as an aldose reductase differential inhibitor (ARDI)[1].

Name: Emodin-8-glucoside, CAS: 23313-21-5, stock 1.3g, assay 98.1%, MWt: 432.38, Formula: C21H20O10, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Emodin-8-glucoside is an anthraquinone derivative isolated from Aloe vera, binds to minor groove of DNA[1].

Name: Euphol, CAS: 514-47-6, stock 38.3g, assay 98.3%, MWt: 426.72, Formula: C30H50O, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Euphol is a tetracyclic triterpene alcohol isolated from the sap of Euphorbia tirucalli with anti-mutagenic, anti-inflammatory and immunomodulatory effects, orally active. Euphol inhibits the monoacylglycerol lipase (MGL) activity via a reversible mechanism (IC50=315 nM). MGL inhibition in the periphery modulates the endocannabinoid system to block the development of inflammatory pain[1].
IC50 & Target: IC50: 315 nM (monoacylglycerol lipase activity)[1]
In Vitro: Euphol (0.01-0.3 mM; 24-72 hours) markedly inhibits T47D cells proliferation, the IC50 values of euphol treatment for 24, 48 and 72 h were 0.26, 0.22 and 0.13 mM, respectively[2].
Euphol (0.03 mM; 48 or 72 hours) leads to cell cycle arrest by regulating expression of cell cycle-associated proteins[2].

Name: Allicin Diallyl thiosulfinate, CAS: 539-86-6, stock 16.4g, assay 98.3%, MWt: 162.27, Formula: C6H10OS2, Solubility: DMSO : 5 mg/mL (30.81 mM; Need ultrasonic); H2O : < 0.1 mg/mL (insoluble), Clinical_Informat: Phase 2, Pathway: Anti-infection, Target: Bacterial, Biological_Activity: Allicin (diallyl thiosulfinate) is isolated from garlic including Diallyl monosulfide, Diallyl disulfide, Diallyl trisulfide, Diallyl tetrasulfide, and Methyl allyl disulphide etc. They accounts for 98% of the extract. Allicin (diallyl thiosulfinate) has highly potent antimicrobial activity, and inhibits growth of a variety of microorganisms, among them antibiotic-resistant strains[1][2].
In Vitro: Allicin exhibits comparable MICs (32-64 μg/mL) toward methicillin-resistant S. aureus ATCC 43300, the type strain S. aureus DSM 20231, E. coli DSM 30083, A. baumannii DSM 30007, and C. albicans DSM 1386[1].

Name: Salvianolic acid A, CAS: 96574-01-5, stock 8.1g, assay 98.1%, MWt: 494.45, Formula: C26H22O10, Solubility: DMSO : 125 mg/mL (252.81 mM; Need ultrasonic), Clinical_Informat: Phase 1, Pathway: Metabolic Enzyme/Protease, Target: MMP, Biological_Activity: Salvianolic acid A could protect the blood brain barrier through matrix metallopeptidase 9 (MMP-9) inhibition and anti-inflammation.
In Vivo: A significant beneficial effect of Salvianolic acid A (SAA) is observed in the Salvianolic acid A treatment groups. Salvianolic acid A (20 mg/kg) could significantly prolonged the retention time of rats on the plate. While compared with sham operation group, the brain water content in model group significantly increases, which is attenuated significantly by Salvianolic acid A (10 and 20 mg/kg). Compared with the model group, Salvianolic acid A (5, 10, and 20 mg/kg) could maintain the normal structures of neurons and increase neurons number. It is also found that Salvianolic acid A (20 mg/kg) could significantly reduce I/R induced MMP-9 upregulation. While the MMP-2 expression is not significantly affected by Salvianolic acid A. Tissue inhibitors of metalloproteinases (TIMPs) could inhibit the activity of MMPs through high affinity binding to MMPs catalytic domain[1].

Name: Salvianolic acid C, CAS: 115841-09-3, stock 5.1g, assay 98.6%, MWt: 492.43, Formula: C26H20O10, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Cytochrome P450, Biological_Activity: Salvianolic acid C is a noncompetitive Cytochrome P4502C8 (CYP2C8) inhibitor and a moderate mixed inhibitor of Cytochrome P45022J2 (CYP2J2), with Kis of 4.82 μM and 5.75 μM for CYP2C8 and CYP2J2, respectively.
IC50 & Target: Ki: 4.82 μM (CYP2C8), 5.75 μM (CYP2J2)[1].
In Vitro: Salvianolic acid C is a noncompetitive CYP2C8 inhibitor and a moderate mixed inhibitor of CYP2J2, with Kis of 4.82, 5.75 μM for CYP2C8 and CYP2J2, respectively[1]. 1 and 5 μM Salvianolic acid C (SalC) could significantly inhibit the NO production induced by LPS. Salvianolic acid C decreases the expression of iNOS significantly. Salvianolic acid C inhibits LPS-induced TNF-α, IL-1β, IL-6 and IL-10 overproduction. Salvianolic acid C inhibits LPS-induced NF‑κB activation. Salvianolic acid C also increases the expression of Nrf2 and HO-1 in BV2 microglial cells[2].
In Vivo: Salvianolic acid C (20 mg/kg) treatment could significantly decrease the escape latency. In addition, SalC (10 and 20 mg/kg) treatment significantly increase the platform crossing number compared with the LPS model group. Systemic administration of Salvianolic acid C down regulates the brain TNF-α, IL-1β and IL-6 levels compared with the model group. The iNOS and COX-2 levels in rat brain cortex and hippocampus are higher than that in the control group, while Salvianolic acid C treatment significantly down regulates the cortex and hippocampus regions. Salvianolic acid C (5, 10 and 20 mg/kg) treatment dose-dependently increases the p-AMPK, Nrf2, HO-1 and NQO1 levels in rat brain cortex and hippocampus[2].

Name: Salvianolic acid D, CAS: 142998-47-8, stock 33.5g, assay 98.9%, MWt: 418.35, Formula: C20H18O10, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Salvianolic acid D, isolated from Salvia miltiorrhiza, is a potential antiplatelet activity compound[1][2].

Name: Bilirubin, CAS: 635-65-4, stock 21.4g, assay 98.7%, MWt: 584.66, Formula: C33H36N4O6, Solubility: H2O : < 0.1 mg/mL (insoluble); H2O : 1 mg/mL (1.71 mM; ultrasonic and adjust pH to 11 with NaOH); DMSO : 6 mg/mL (10.26 mM; Need ultrasonic), Clinical_Informat: Phase 3, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: Bilirubin is a yellow breakdown product of heme catabolism[1]. Bilirubin exhibits antioxidant and antimutagenic effects[2].
In Vitro: Unconjugated Bilirubin inhibits the cleavage of F485-rVWF73-H, D633-rVWF73-H, and GST-rVWF71-11K by ADAMTS13 in a concentration-dependent manner with a half-maximal inhibitory concentration (IC50) of ~13 μM, ~70 μM, and ~17 μM, respectively. Unconjugated Bilirubin also dose-dependently inhibits the cleavage of multimeric VWF by ADAMTS13 under denaturing conditions[1]. Bilirubin exhibits antioxidant and antimutagenic effects in vitro[2].

Name: Lobetyolin, CAS: 129277-38-9, stock 35.3g, assay 98.4%, MWt: 396.43, Formula: C20H28O8, Solubility: Methanol : ≥ 125 mg/mL (315.31 mM), Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease;NF-κB;Immunology/Inflammation, Target: Reactive Oxygen Species;Reactive Oxygen Species;Reactive Oxygen Species, Biological_Activity: Lobetyolin is derived from Codonopsis pilosula and has antioxidative effect.
In Vitro: Lobetyolin is derived from Codonopsis pilosula and has antioxidative effect. MUC5AC gene expression induced by phorbol 12-myristate 13-acetate (PMA) from NCI-H292 cells is inhibited by pretreatment with Lobetyolin, lobetyol or methyl linoleate. Lobetyolin does not affect PMA-induced MUC5AC production from NCI-H292 cells. The amounts of mucin in the cells of Lobetyolin-treated cultures are 100±25%, 487±33%, 524±38%, 411±24%, and 402±45% for control, 10 ng/mL of PMA alone, PMA plus Lobetyolin 1 μM, PMA plus Lobetyolin 10 μM, and PMA plus Lobetyolin 100 μM, respectively[1].

Name: Deltaline, CAS: 6836-11-9, stock 29.8g, assay 98.5%, MWt: 507.62, Formula: C27H41NO8, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Deltaline is a diterpenoid alkaloid and isolated from plants of the genus Delphinium delavayi Franch. Deltaline itself has analgesic properties, and plants of the genus Delphinium delavayi Franch have also been therapeutically used to treat rheumaticpain, paralysis due to stroke, rheumatoid arthritis[1].

Name: Ziyuglycoside I, CAS: 35286-58-9, stock 5.8g, assay 98%, MWt: 766.96, Formula: C41H66O13, Solubility: DMSO : 250 mg/mL (325.96 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Apoptosis;Apoptosis, Target: Apoptosis;MDM-2/p53, Biological_Activity: Ziyuglycoside I isolated from S. officinalis root, has anti-wrinkle activity, and increases the expression of type I collagen. Ziyuglycoside I could be used as an active ingredient for cosmetics[1].
Ziyuglycoside I triggers cell cycle arrest and apoptosis mediated by p53, it can be a potential drug candidate for treating triple-negative breast cancer (TNBC)[2].
In Vitro: Ziyuglycoside I (5-160 µM; 24 hours) reveals a marked anti-proliferation activity with an IC50 value of 13.96 µM in MDA-MB-231 cells[2].
Ziyuglycoside I (5-20 µM; 24 hours) induces MDA-MB-231 cell apoptosis by increasing the percentage of apoptotic cells from 2.43% to 44.76% at 20 µM[2].
Ziyuglycoside I (5-20 µM; 24 hours) induces the cleavage of caspas-8, caspase-9, and caspase-3, up-regulates the pro-apoptotic protein Bax, and down-regulates anti-apoptotic protein Bal-2, dose-dependently reduces the level of mito-cyto c expression[2].

Name: Ziyuglycoside II, CAS: 35286-59-0, stock 3.5g, assay 98.4%, MWt: 604.81, Formula: C35H56O8, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Apoptosis;Metabolic Enzyme/Protease;NF-κB;Immunology/Inflammation, Target: Apoptosis;Reactive Oxygen Species;Reactive Oxygen Species;Reactive Oxygen Species, Biological_Activity: Ziyuglycoside II is a triterpenoid saponin compound extracted from Sanguisorba officinalis L.. Ziyuglycoside II induces reactive oxygen species (ROS) production and apoptosis. Anti-inflammation and anti-cancer effect[1].
In Vitro: Ziyuglycoside II (10-60 μM; 24 h and 48 h) inhibits MDA-MB-435 cells growth in a dose-dependent manner. The IC50 of Ziyuglycoside II at 24 h and 48 h is 5.92 μM and 4.74 μM, respectively[1]. 
Ziyuglycoside II (5-25 μM) induces G0/G1 and S phase arrest in MDA-MB-435 cells at 24 h[1]. 
Ziyuglycoside II (5-25 μM; 24 hours) significantly increases apoptotic rate of MDA-MB-435 cells[1]. 
Ziyuglycoside II (5-25 μM; 24 hours) increases expressions of both p53 and p21 in MDA-MB-435 cells, which effect is dose-dependent[1].

Name: (+)-Magnoflorine Magnoflorine;α-Magnoflorine;Thalictrine, CAS: 2141-09-5, stock 32.5g, assay 98.7%, MWt: 342.41, Formula: C20H24NO4+, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Anti-infection, Target: Fungal, Biological_Activity: (+)-Magnoflorine (Magnoflorine) is an aporphine alkaloid found in Acoruscalamus, with anti-fungal activity, reduces the formation of C. albicans’ biofilm[1]. Anti-antidiabetic
and anti-oxidative activity[2].
IC50 & Target: Fungal[1]

Name: Indigo, CAS: 482-89-3, stock 27.1g, assay 98.2%, MWt: 262.26, Formula: C16H10N2O2, Solubility: 10 mM in H2O, Clinical_Informat: Phase 4, Pathway: Others, Target: Others, Biological_Activity: Indigo is a deep and rich color dye for indole stain, isolated from the plant Indigofera tinctoria and related species[1].

Name: 3-Butylidenephthalide Butylidenephthalide, CAS: 551-08-6, stock 19.2g, assay 98.3%, MWt: 188.22, Formula: C12H12O2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: 3-Butylidenephthalide (Butylidenephthalide) is a phthalic anhydride derivative identified in Ligusticum chuanxiong Hort, and has larvicidal activity (LC50 of 1.56 mg/g for Spodoptera litura larvae)[1].

Name: (-)-Syringaresnol-4-O-β-D-apiofuranosyl-(1→2)-β-D-glucopyranoside, CAS: 136997-64-3, stock 27.5g, assay 98.9%, MWt: 712.69, Formula: C33H44O17, Solubility: DMSO : 250 mg/mL (350.78 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: (-)-Syringaresnol-4-O-β-D-apiofuranosyl-(1→2)-β-D-glucopyranoside is isolated from the bark of Albizzia myriophylla[1].

Name: Syringic acid, CAS: 530-57-4, stock 25.6g, assay 98.3%, MWt: 198.17, Formula: C9H10O5, Solubility: DMSO : 62.5 mg/mL (315.39 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Anti-infection;Metabolic Enzyme/Protease, Target: Bacterial;Endogenous Metabolite, Biological_Activity: Syringic acid is correlated with high antioxidant activity and inhibition of LDL oxidation.
In Vitro: Syringic acid is a phenol present in some distilled alcohol beverages. It is also a product of microbial (gut) metabolism of anthocyanins and other polyphenols that have been consumed[1]. Research suggests that phenolics from wine may play a positive role against oxidation of low-density lipoprotein (LDL), which is a key step in the development of atherosclerosis. Syringic acid is correlated with high antioxidant activity and inhibition of LDL oxidation[2].

Name: Helicid Helicide; Helicidum;4-Formylphenyl-β-D-allopyranoside, CAS: 80154-34-3, stock 33.4g, assay 99%, MWt: 284.26, Formula: C13H16O7, Solubility: 10 mM in DMSO, Clinical_Informat: Launched, Pathway: Others, Target: Others, Biological_Activity: Helicid (Helicide) is a major constituent of Helicia nilgirica Bedd. Helicid has been used to treat psychoneurosis for its sedative-hypnotic and analgesic properties[1].
In Vivo: Helicid (8-32 mg/kg; given i.g.; once daily for 6 weeks) significantly reverses chronic unpredictable mild stress (CUMS)-induced depression-like behaviors in rats[1].

Name: Farrerol, CAS: 24211-30-1, stock 11.6g, assay 98.3%, MWt: 300.31, Formula: C17H16O5, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Farrerol is a bioactive constituent of Rhododendron, with broad activities such as anti-oxidative, anti-inflammatory, anti-tumor, neuroprotective and hepatoprotective effects[1][2][3][4][5][6].
In Vitro: Farrerol observably reduces the production of inflammatory mediators including IL-1β, IL-6, TNF-α, COX-2, and iNOS in LPS-induced RAW264.7 cells via suppressing AKT, ERK1/2, JNK1/2, and NF-κB p65 phosphorylation[1]. 
Farrerol attenuates β-amyloid-induced oxidative stress and inflammation through Nrf2/Keap1 pathway in a microglia cell line[2]. 
Farrerol inhibits angiogenesis through Akt/mTOR, Erk and Jak2/Stat3 signal pathway[3]. 
Farrerol overcomes the invasiveness of lung squamous cell carcinoma cells by regulating the expression of inducers of epithelial mesenchymal transition[4]. 
Farrerol ameliorates acetaminophen-induced hepatotoxicity via activation of Nrf2 and autophagy[6]. 
In Vivo: Farrerol protects dopaminergic neurons in a rat model of lipopolysaccharide-induced Parkinson's disease by suppressing the activation of the AKT and NF-κB signaling pathways[5].

Name: Anthraquinone, CAS: 84-65-1, stock 4.7g, assay 98.6%, MWt: 208.21, Formula: C14H8O2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Anti-infection, Target: Virus Protease, Biological_Activity: Anthraquinone is used as a precursor for dye formation.

Name: (+)-Catechin hydrate, CAS: 225937-10-0, stock 36.7g, assay 98.9%, MWt: 1000, Formula: C15H14O6.xH2O, Solubility: DMSO : 150 mg/mL (Need ultrasonic and warming), Clinical_Informat: Phase 4, Pathway: Immunology/Inflammation, Target: COX, Biological_Activity: (+)-Catechin hydrate inhibits cyclooxygenase-1 (COX-1) with an IC50 of 1.4 μM.
IC50 & Target: IC50: 1.4 uM (COX-1)[1]
In Vitro: (+)-Catechin exhibits >95% inhibitory activity at 70 μg/mL against cyclooxygenase-1 (COX-1) with an IC50 of 1.4 μM[1]. A dose-dependent reduction in color is observed after 24 hours of treatment with (+)-Catechin, and 54.76% of the cells are dead at the highest concentration of (+)-Catechin tested (160 μg/mL) whereas the IC50 of (+)-Catechin is achieved at 127.62 μg/mL (+)-Catechin. A dose- and time-dependent increase in the induction of apoptosis is observed when MCF-7 cells are treated with (+)-Catechin. When compare to the control cells at 24 hours, 40.7 and 41.16% of the cells treated with 150 μg/mL and 300 μg/mL (+)-Catechin, respectively, undergo apoptosis. The expression levels of Caspase-3, -8, and -9 and p53 in MCF-7 cells treated with 150 μg/mL (+)-Catechin for 24 h increase by 5.81, 1.42, 3.29, and 2.68 fold, respectively, as compare to the levels in untreated control cells[2].
In Vivo: Animals treated with (+)-Catechin at the lowest tested dose, i.e., 50 mg/kg, p.o. have spent comparatively more time in exploring the novel object in the choice trial, however, the difference is not statistically significant. (+)-Catechin prevents the time-induced episodic memory deficits in a dose-dependent manner, the most effective being 200 mg/kg, p.o.. Treatment with (+)-Catechin prevents the rise in MPO level compare to DOX alone treatment group (21.98±9.44 and 36.76±4.39% in the hippocampus and the frontal cortex respectively)[3].

Name: 3,29-Dibenzoyl rarounitriol, CAS: 873001-54-8, stock 9.8g, assay 98.9%, MWt: 666.93, Formula: C44H58O5, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: 3,29-Dibenzoyl rarounitriol is one major bioactive compound of multiflorane triterpene esters Trichosanthes kirilowii, can be chosen as the marker for quantitation of Trichosanthes kirilowii[1].

Name: 1,4-Dicaffeoylquinic acid 1,4-DCQA, CAS: 1182-34-9, stock 18g, assay 98.8%, MWt: 516.45, Formula: C25H24O12, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: 1,4-Dicaffeoylquinic acid (1,4-DCQA) is a phenylpropanoid from Xanthii fructus, inhibits LPS-stimulated TNF-α production[1].

Name: Dihydrocapsaicin, CAS: 19408-84-5, stock 22.4g, assay 98.1%, MWt: 307.43, Formula: C18H29NO3, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Membrane Transporter/Ion Channel;Neuronal Signaling, Target: TRP Channel;TRP Channel, Biological_Activity: Dihydrocapsaicin is a natural capsaicin, acts as a selective TRPV1 agonist, and also increases p-Akt levels. Dihydrocapsaicin enhances the hypothermia-induced neuroprotection[1][2].

Name: (+)-Columbianetin (S)-Columbianetin, CAS: 3804-70-4, stock 3.8g, assay 98.7%, MWt: 246.26, Formula: C14H14O4, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: (+)-Columbianetin is an isomer of Columbianetin. Columbianetin is a phytoalexin associated with celery (Apium graveolens) resistance to pathogens during storage. Columbianetin exhibits excellent anti-fungal and anti-inflammatory activity[1][2].

Name: Sennoside A, CAS: 81-27-6, stock 36.1g, assay 98.7%, MWt: 862.74, Formula: C42H38O20, Solubility: DMSO : 125 mg/mL (144.89 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Anti-infection, Target: HIV, Biological_Activity: Sennoside A is an anthraquinone glycoside, found in large quantities in leaves and pods of Senna (Cassia angustifolia)[1]. Sennoside A is a HIV-1 inhibitor effective on HIV-1 replication[2].

Name: Sennoside B, CAS: 128-57-4, stock 19.4g, assay 98.2%, MWt: 862.74, Formula: C42H38O20, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Protein Tyrosine Kinase/RTK, Target: PDGFR, Biological_Activity: Sennoside B is an anthraquinone glycoside, found in large quantities in leaves and pods of Senna (Cassia angustifolia)[1]. Sennoside B can inhibit PDGF-stimulated cell proliferation by binding to PDGF-BB and its receptor and by down-regulating the PDGFR-beta signaling pathway[2].

Name: Linalool, CAS: 78-70-6, stock 39.9g, assay 98%, MWt: 154.25, Formula: C10H18O, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Apoptosis;Membrane Transporter/Ion Channel;Neuronal Signaling, Target: Apoptosis;iGluR;iGluR, Biological_Activity: Linalool is natural monoterpene in essential olis of coriander, acts as a competitive antagonist of Nmethyl d-aspartate (NMDA) receptor, with anti-tumor, anti-cardiotoxicity activity[1].Linalool is a PPARα ligand that reduces plasma TG levels and rewires the hepatic transcriptome and plasma metabolome[2].

Name: Fangchinoline, CAS: 436-77-1, stock 13.5g, assay 98.9%, MWt: 608.72, Formula: C37H40N2O6, Solubility: DMSO : 50 mg/mL (82.14 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Apoptosis;Autophagy;Anti-infection;Protein Tyrosine Kinase/RTK, Target: Apoptosis;Autophagy;HIV;FAK, Biological_Activity: Fangchinoline is isolated from Stephania tetrandra with extensive biological activities, such as enhancing immunity, anti-inflammatory sterilization and anti-atherosclerosis. Fangchinoline, a novel HIV-1 inhibitor, inhibits HIV-1 replication by impairing gp160 proteolytic processing[1]. Fangchinoline targets Focal adhesion kinase (FAK) and suppresses FAK-mediated signaling pathway in tumor cells which highly expressed FAK[2]. Fangchinoline induces apoptosis and adaptive autophagy in bladder cancer[3].
IC50 & Target: HIV-1 replication[1]; Focal adhesion kinase (FAK)[2]; apoptosis; autophagy[3]
In Vitro: Fangchinoline (2.5-40 µM; 24-96 hours) inhibits both T24 and 5637 cells in dose-dependent manner, the IC50 values of Fangchinoline in T24 cells are 19.0 µM (24 h), 12.0 µM (48 h) and 7.57 µM (72 h), and 11.9 µM (24 h), 9.92 µM (48 h) and 7.13 µM (72 h) in 5637 cells[1].
Fangchinoline (5 µM; 24 hours) induces a significant increase in the LC3-II/LC3-I ratio and a decrease in p62 in both T24 and 5637 cells, and causes a significant increase in the cleavage of caspase-3[1].

Name: Licochalcone B, CAS: 58749-23-8, stock 29.1g, assay 98.5%, MWt: 286.28, Formula: C16H14O5, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Neuronal Signaling, Target: Amyloid-β, Biological_Activity: Licochalcone B is an extract from the root of Glycyrrhiza inflate. Licochalcone B inhibits amyloid β (Aβ42) self-aggregation (IC50=2.16 μM) and disaggregate pre-formed Aβ42 fibrils, reduce metal-induced Aβ42 aggregation through chelating metal ions[1].

Name: Licochalcone C, CAS: 144506-14-9, stock 37g, assay 98.1%, MWt: 338.40, Formula: C21H22O4, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Glucosidase, Biological_Activity: Licochalcone C could inhibit α-glucosidase, with IC50s of <100 nM and 92.43 μM for α-glucosidase and protein tyrosine phosphatase 1B (PTP1B), respectively.
IC50 & Target: IC50: <100 nM (α-glucosidase), 92.43 μM (PTP1B)[1].
In Vitro: Licochalcone C could inhibit α- glucosidase, with IC50s of <100 nM and 92.43 μM for α- glucosidase and PTP1B, respectively[1]. It is also indicated that Licochalcone C induces T24 cell apoptosis in a concentration‑dependent manner. Licochalcone C treatment reduces the levels of the anti‑apoptotic mRNAs (Bcl-2, Bcl-w and Bcl-XL) and increases expression of the pro-apoptotic mRNAs (Bax and Bim). The Bcl-2 family inhibitor (ABT-737) reduces apoptosis induced by licochalcone C in T24 cells[2].

Name: Liquiritin, CAS: 551-15-5, stock 33g, assay 98.4%, MWt: 418.39, Formula: C21H22O9, Solubility: DMSO : 150 mg/mL (358.52 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease;NF-κB;Immunology/Inflammation, Target: Reactive Oxygen Species;Reactive Oxygen Species;Reactive Oxygen Species, Biological_Activity: Liquiritin, a flavonoid isolated from Glycyrrhiza, is a potent and competitive AKR1C1 inhibitor with IC50s of 0.62 μM, 0.61 μM, and 3.72μM for AKR1C1, AKR1C2 and AKR1C3, respectively. Liquiritin efficiently inhibits progesterone metabolism mediated by AKR1C1 in vivo[1]. Liquiritin acts as an antioxidant and has neuroprotective, anti-cancer and anti-inflammatory activity[2].
IC50 & Target: IC50: 0.62 μM (AKR1C1), 0.61 μM (AKR1C2) and 3.72μM (AKR1C3)[1]
In Vitro: Liquiritin can target the residues Ala-27, Val-29, Ala-25, and Asn-56 of AKR1C1[1]. 
Liquiritin (50 μM; 6 hours) results in 85.00% of reduction in progesterone metabolism, which is mediated by Aldo-keto reductase family 1 member C1 (AKR1C1) enzymatic activity in HEC-1-B cells[1]. 
Liquiritin (100 µM) increases glucose-6-phosphate dehydrogenase expression on B65 neuroblastoma cells[2].

Name: D-Mannose, CAS: 3458-28-4, stock 22.4g, assay 98.9%, MWt: 180.16, Formula: C6H12O6, Solubility: H2O : ≥ 50 mg/mL (277.53 mM); DMSO : 50 mg/mL (277.53 mM; Need ultrasonic), Clinical_Informat: Phase 4, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: D-Mannose is a carbohydrate, which plays an important role in human metabolism, especially in the glycosylation
of specific proteins.

Name: Homovanillic acid Vanilacetic acid, CAS: 306-08-1, stock 9.2g, assay 98.9%, MWt: 182.17, Formula: C9H10O4, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: Homovanillic acid is a dopamine metabolite found to be associated with aromatic L-amino acid decarboxylase deficiency, celiac disease, growth hormone deficiency, and sepiapterin reductase deficiency.

Name: Gomisin J, CAS: 66280-25-9, stock 28.2g, assay 98.8%, MWt: 388.45, Formula: C22H28O6, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Membrane Transporter/Ion Channel;Epigenetics;PI3K/Akt/mTOR;Neuronal Signaling, Target: Calcium Channel;AMPK;AMPK;Calcium Channel, Biological_Activity: Gomisin J is a small molecular weight lignan found in Schisandra chinensis and has been demonstrated to have vasodilatory activity[1]. Gomisin J suppresses lipid accumulation by regulating the expression of lipogenic and lipolytic enzymes and inflammatory molecules through activation of AMPK, LKB1 and Ca2+/calmodulin-dependent protein kinase II and inhibition of fetuin-A in HepG2 cells. gomisin J has potential benefits in treating nonalcoholic fatty liver disease[2].
IC50 & Target: AMPK, LKB1, Ca2+/calmodulin-dependent protein kinase II, fetuin-A[2]

Name: Griffonilide, CAS: 61371-55-9, stock 27.4g, assay 98.9%, MWt: 168.15, Formula: C8H8O4, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Griffonilide is a butenolide, isolated from the roots of Semiaquilegia adoxoides, and often occurs alongside lithospermoside[1][2].

Name: Gelsemine, CAS: 509-15-9, stock 31.5g, assay 98.6%, MWt: 322.40, Formula: C20H22N2O2, Solubility: DMSO : ≥ 125 mg/mL (387.72 mM), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Gelsemine, an alkaloid from the Chinese herb Gelsemium elegans, is effective in mitigating chronic pain. Antinociceptive and hypnotic effects.
In Vivo: Gelsemine is an effective agent for treatment of both neuropathic pain and sleep disturbance in partial sciatic nerve ligation (PSNL) mice. Gelsemine (4 mg/kg) exerts analgesic effects on PSNL-induced mechanical allodynia and thermal hyperalgesia. In PSNL mice, Gelsemine (2 and 4 mg/kg) increases the mechanical threshold for 4 h and prolonged the thermal latencies for 3 h. Furthermore, Gelsemine (4 mg/kg, administered at 6:30 AM) increases non-rapid eye movement (non-REM, NREM) sleep, decreases wakefulness, but does not affect rapid eye movement (REM) sleep during the first 3 h in PSNL mice[1]. 
Immunohistochemical study shows that PSNL increases c-Fos expression in the neurons of the anterior cingulate cortex, and Gelsemine (4 mg/kg) decreases c-Fos expression by 58%[1].

Name: Polygalasaponin F, CAS: 882664-74-6, stock 9.4g, assay 98.1%, MWt: 1091.24, Formula: C53H86O23, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: PI3K/Akt/mTOR;PI3K/Akt/mTOR;Immunology/Inflammation;NF-κB, Target: PI3K;Akt;Toll-like Receptor (TLR);NF-κB, Biological_Activity: Polygalasaponin F, an oleanane-type triterpenoid saponin extracted from Polygala japonica, decreases the release of the inflammatory cytokine tumor necrosis factor a (TNFa). Polygalasaponin F reduces neuroinflammatory cytokine secretion through the regulation of the TLR4-PI3K/AKT-NF-kB signaling pathway [1].
IC50 & Target: TLR4-PI3K/AKT-NF-kB[1]

Name: Glabridin, CAS: 59870-68-7, stock 10g, assay 98.6%, MWt: 324.37, Formula: C20H20O4, Solubility: DMSO : 150 mg/mL (462.43 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Cell Cycle/DNA Damage;Metabolic Enzyme/Protease;NF-κB;Immunology/Inflammation, Target: PPAR;Reactive Oxygen Species;Reactive Oxygen Species;Reactive Oxygen Species, Biological_Activity: Glabridin is a natural isoflavan from Glycyrrhiza glabra, binds to and activates PPARγ, with an EC50 of 6115 nM. Glabridin exhibits antioxidant, anti-bacterial, anti-nephritic, anti-diabetic, anti-fungal, antitumor, anti-inflammatory, antiosteoporotic, cardiovascular protective, neuroprotective and radical scavenging activities[1][2].
In Vitro: Glabridin binds to and activates PPARγ, with an EC50 of 6115 nM[1]. 
Glabridin (40, 80 μM) inhibits the proliferation of SCC-9 and SAS cell lines in a dose- and time-dependent manner after treatment for 24 and 48 h[2]. 
Glabridin (0-80 μM) also induces apoptosis, causes Sub-G1 cell cycle arrest in SCC-9 and SAS cell lines[2]. 
Glabridin (0, 20, 40, and 80 μM) dose-dependently activates caspase-3, −8, and −9 and increases PARP cleavage, significantly phosphorylates ERK1/2, JNK1/2, and p-38 MAPK in SCC-9 cells[2].
In Vivo: Glabridin (50 mg/kg, p.o. once daily) shows potent anti-inflammatory activity, ameliorates the inflammatory alterations induced by Dextran sodium sulphate (DSS) in rats[3].

Name: L-Cystine, CAS: 56-89-3, stock 19.2g, assay 98.7%, MWt: 240.30, Formula: C6H12N2O4S2, Solubility: 10 mM in DMSO, Clinical_Informat: Launched, Pathway: Apoptosis;Metabolic Enzyme/Protease, Target: Ferroptosis;Endogenous Metabolite, Biological_Activity: L-Cystine is an amino acid and intracellular thiol, which plays a critical role in the regulation of cellular processes.

Name: Harpagoside, CAS: 19210-12-9, stock 27.7g, assay 98.6%, MWt: 494.49, Formula: C24H30O11, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Immunology/Inflammation;Immunology/Inflammation, Target: COX;NO Synthase, Biological_Activity: Harpagoside is isolated from Harpagophytum procumbens (Hp). Harpagoside has inhibitory effects on COX-1 and COX-2 activity and inhibits NO production[1].
IC50 & Target: COX-1; COX-2; NO production[1]

Name: Harpagide, CAS: 6926-08-5, stock 9.4g, assay 98.7%, MWt: 364.35, Formula: C15H24O10, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Anti-infection, Target: Parasite, Biological_Activity: Harpagide is a class of iridoid glycoside isolated from Scrophularia cryptophila and has antiparasitic activity, which exhibits good in vitro trypanocidal activities against African trypanosomes (T.b. rhodesiense) with an IC50 of 21 μg/mL. Harpagide exerts significant antileishmanial activity against L. donovani with an IC50 value of 2.0 μg/mL. Harpagide also possess significant anti-inflammatory activities[1][2].
In Vitro: Harpagide shows cytotoxic activity over 50% in a concentration of 90 μg/mL, Harpagide on the A431 and HeLa cell lines. The cytotoxic effect of Harpagide on the MCF7 cell line in a concentration of 90 μg/mL[3].

Name: Sec-O-Glucosylhamaudol, CAS: 80681-44-3, stock 6.7g, assay 98.1%, MWt: 438.43, Formula: C21H26O10, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein;Neuronal Signaling, Target: Opioid Receptor;Opioid Receptor, Biological_Activity: Sec-O-Glucosylhamaudol is a natural compound extracted from Peucedanum japonicum Thunb, decreases levels of μ-opioid receptor, with analgesic effect[1].

Name: Wogonoside, CAS: 51059-44-0, stock 20.9g, assay 98.2%, MWt: 460.39, Formula: C22H20O11, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Autophagy, Target: Autophagy, Biological_Activity: Wogonoside, a flavonoid glycoside isolated from Huangqin, possesses anti-inflammatory effects. Wogonoside induces autophagy in breast cancer cells by regulating MAPK-mTOR pathway[1][2].

Name: 2"-O-beta-L-galactopyranosylorientin, CAS: 861691-37-4, stock 10.4g, assay 98.1%, MWt: 610.52, Formula: C27H30O16, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: 2"-O-beta-L-galactopyranosylorientin is extracted from the flowers of Trollius ledebouri. 2"-O-beta-L-galactopyranosylorientin involves transporter mediated efflux in addition to passive diffusion and is the substrate of multidrug resistance protein 2 (MRP2)[1][2].

Name: Picroside I 6'-Cinnamoylcatalpol, CAS: 27409-30-9, stock 34.4g, assay 98.8%, MWt: 492.47, Formula: C24H28O11, Solubility: H2O : 125 mg/mL (253.82 mM; Need ultrasonic); DMSO : 250 mg/mL (507.65 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: JAK/STAT Signaling;Stem Cell/Wnt, Target: STAT;STAT, Biological_Activity: Picroside I is the major ingredient of Picrorhiza kurroa. Picrorhiza kurroa is a high value medicinal herb due to rich source of hepatoprotective metabolites, Picroside-I and Picroside-II[1]. Picroside I is a promising agent for the management of asthma. Picroside I reduces the inflammation significantly at its higher dose. Picroside I also downregulates pSTAT6 and GATA3 expressions. Picroside I dose-dependently increases the serum levels of IFN-γ[2].

Name: Picroside II, CAS: 39012-20-9, stock 20.7g, assay 98.6%, MWt: 512.46, Formula: C23H28O13, Solubility: DMSO : 100 mg/mL (195.14 mM; Need ultrasonic); Methanol : 125 mg/mL (243.92 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Apoptosis;NF-κB;Metabolic Enzyme/Protease;NF-κB;Immunology/Inflammation, Target: Apoptosis;NF-κB;Reactive Oxygen Species;Reactive Oxygen Species;Reactive Oxygen Species, Biological_Activity: Picroside II, an iridoid compound extracted from Picrorhiza, exhibits anti-inflammatory and anti-apoptotic activities.
picroside II alleviates the inflammatory response in sepsis and enhances immune function by inhibiting the activation of NLRP3 inflammasome and NF-κB pathways[1].
Picroside II is an antioxidant, exhibits a significant neuroprotective effect through reducing ROS production and protects the blood-brain barrier (BBB) after cerebral ischemia-reperfusion (CI/R) injury[2].

Name: Picroside III, CAS: 64461-95-6, stock 22.2g, assay 98.2%, MWt: 538.50, Formula: C25H30O13, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Picroside III is an iridoid glycoside isolated from Picrorhiza scrophulariiflora (PS), a traditional Chinese medicine[1].

Name: Hupehenine, CAS: 98243-57-3, stock 35.4g, assay 98.3%, MWt: 415.65, Formula: C27H45NO2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Hupehenine, a bioactive isosteroidal alkaloid, is a main antitussive components present in most of Fritillariae Bulbus[1].

Name: Trigonelline Trigenolline, CAS: 535-83-1, stock 2.9g, assay 98.4%, MWt: 137.14, Formula: C7H7NO2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Apoptosis;Metabolic Enzyme/Protease, Target: Ferroptosis;Endogenous Metabolite, Biological_Activity: Trigonelline, an alkaloid with potential antidiabetic activity, is present in considerable amounts in coffee.
In Vitro: It is found that Trigonelline (TG) significantly rescues the morphology of the H9c2 cells. Treatment of cells with Trigonelline attenuates H2O2 induced cell deaths and improves the antioxidant activity. In addition, Trigonelline regulates the apoptotic gene caspase-3, caspase-9 and anti-apoptotic gene Bcl-2, Bcl-XL during H2O2 induced oxidative stress in H9c2 cells. For evident, flow cytometer results also confirms that Trigonelline significantly reduces the H2O2 induced necrosis and apoptosis in H9c2 cells. However,
further increment of Trigonelline concentration against H2O2 can induce the necrosis and apoptosis along with H2O2[1].
In Vivo: Trigonelline decreases bone mineralization and tends to worsen bone mechanical properties in streptozotocin-induced diabetic rats. In nicotinamide/streptozotocin-treated rats, Trigonelline significantly increases bone mineral density (BMD) and tends to improve cancellous bone strength. Trigonelline differentially affects the skeletal system of rats with streptozotocin-induced metabolic disorders, intensifying the osteoporotic changes in streptozotocin-treated rats and favorably affecting bones in the non-hyperglycemic (nicotinamide/streptozotocin-treated) rats[2].

Name: Succinic acid Wormwood acid, CAS: 110-15-6, stock 15.8g, assay 98.2%, MWt: 118.09, Formula: C4H6O4, Solubility: H2O : 30 mg/mL (254.04 mM; Need ultrasonic); DMSO : 100 mg/mL (846.81 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: Succinic acid is an intermediate product of the tricarboxylic acid cycle, as well as one of fermentation products of anaerobic metabolism.

Name: Sophocarpine (monohydrate), CAS: 145572-44-7, stock 32.8g, assay 98.3%, MWt: 264.36, Formula: C15H24N2O2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: PI3K/Akt/mTOR;Apoptosis;PI3K/Akt/mTOR;Autophagy, Target: PI3K;Apoptosis;Akt;Autophagy, Biological_Activity: Sophocarpine (monohydrate) is one of the significant alkaloid extracted from the traditional herb medicine Sophora flavescens which has many pharmacological properties such as anti-virus, anti-tumor, anti-inflammatory. Sophocarpine (monohydrate) significantly inhibits the growth of gastric cancer (GC) cells through multiple mechanisms such as induction of autophagy, activation of cell apoptosis and down-regulation of cell survival PI3K/AKT signaling pathway. Sophocarpine (monohydrate) has been demonstrated to have anti-tumor activity in various cancer cells, including hepatocellular carcinoma, prostate cancer and colorectal cancer[1].

Name: Sophoricoside, CAS: 152-95-4, stock 17.6g, assay 98.1%, MWt: 432.38, Formula: C21H20O10, Solubility: DMSO : ≥ 150 mg/mL (346.92 mM), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Sophoricoside is an isoflavone glycoside isolated from Sophora japonica and has anti-inflammatory, anti-cancer and immunosuppressive effects.
In Vitro: Sophoricoside is an isoflavone glycoside isolated from Sophora japonica and has anti-inflammatory, anti-cancer and immunosuppressive effects. The results show that Sophoricoside (50 μM) significantly inhibits the PMACI-induced histamine release. The inhibition rate reaches up to 30.24%. The maximal rates of TNF-α, IL-8 and IL-6 inhibition by Sophoricoside (50 μM) are approximately 31.42%, 43.43% and 34.24%, respectively. The rates of the levels of Rel/p65 inhibition in nuclear by Sophoricoside (50 μM) is approximately 50.14%. Results show that the enhanced caspase-1 activity induced by PMACI is significantly reduced by Sophoricoside in a dose-dependent manner[1].
In Vivo: When the Sophoricoside is orally administered 1 h before compound 48/80 injections, the scratching behaviors is reduced. The inhibition rate of Sophoricoside (2 mg/kg) is approximately 41.21%. Orally administered Sophoricoside inhibits the scratching behaviors by 47.31%. When mice are treated for 2 weeks with Sophoricoside, the atopic dermatitis is recovered to a significant extent[1].

Name: Phellodendrine, CAS: 6873-13-8, stock 18.9g, assay 98.2%, MWt: 342.41, Formula: C20H24NO4, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: PI3K/Akt/mTOR;NF-κB, Target: Akt;NF-κB, Biological_Activity: Phellodendrine, a isoquinoline alkaloid, is one of important characteristic ingredients in the Phellodendri chinensis cortex. phellodendrine is against AAPH-induced oxidative stress through regulating the AKT/NF-κB pathway. Phellodendrine has good antioxidant, and anti-inflammatory effect [1].

Name: Obacunone, CAS: 751-03-1, stock 15.2g, assay 98.7%, MWt: 454.51, Formula: C26H30O7, Solubility: DMSO : 250 mg/mL (550.04 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Apoptosis, Target: Apoptosis, Biological_Activity: Obacunone, isolated from seeds of Marsh White grapefruit, exhibits anti-tumor activity by the induction of apoptosis[1].

Name: Diosbulbin B, CAS: 20086-06-0, stock 36.1g, assay 99%, MWt: 344.36, Formula: C19H20O6, Solubility: DMSO : 16 mg/mL (46.46 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Diosbulbin B is a diterpene lactone isolated from D. bulbifera L., with anti-tumor activity. Diosbulbin B can induce liver injury[1][2].

Name: Engeletin, CAS: 572-31-6, stock 5g, assay 98.3%, MWt: 434.39, Formula: C21H22O10, Solubility: DMSO : ≥ 83.3 mg/mL (191.76 mM), Clinical_Informat: No Development Reported, Pathway: NF-κB, Target: NF-κB, Biological_Activity: Engeletin is a flavanonol glycoside isolated from hymenaea martiana, inhibits NF-κB signaling-pathway activation, and possesses anti-inflammatory, analgesic, diuresis, detumescence, and antibiosis effects.
IC50 & Target: NF-κB[1]
In Vitro: Engeletin is a flavanonol glycoside isolated from hymenaea martiana, inhibits NF-κB signaling-pathway activation[1].
In Vivo: Engeletin (25, 50, 100 mg/kg, i.p.) markedly reduces LPS-increased myeloperoxidase activity in mice, activates NF-κB-pathway activation, decreases the production of inflammatory mediators (iNOS and COX-2), and suppresses the expression of TLR4-signaling downstream molecules such as MyD88, IRAK1, TRAF6, and TAK1 proteins[1].

Name: Pimpinellin, CAS: 131-12-4, stock 24.9g, assay 98.1%, MWt: 246.22, Formula: C13H10O5, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Apoptosis, Target: Apoptosis, Biological_Activity: Pimpinellin is a constituent of Cyrtomium fortumei (J.). Pimpinellin inhibits the growth of tumor cells via the induction of tumor cell apoptosis[1].
In Vitro: Pimpinellin has potent cytotoxic activities against the three tumor cells MGC-803, PC3, and A375, with the IC50 values of 14.4±0.3 μM, 20.4±0.5 μM, and 29.2±0.6 μM, respectively. Pimpinellin inhibits the growth of MGC-803 cells via the induction of tumor cell apoptosis, with apoptosis ratio of 27.44% after 72 h of treatment at 20 μM[1].

Name: Asiaticoside Madecassol, CAS: 16830-15-2, stock 17.5g, assay 98.1%, MWt: 959.12, Formula: C48H78O19, Solubility: DMSO : 50 mg/mL (52.13 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Apoptosis;Stem Cell/Wnt;TGF-beta/Smad;Metabolic Enzyme/Protease;NF-κB;Immunology/Inflammation, Target: Apoptosis;TGF-beta/Smad;TGF-beta/Smad;Reactive Oxygen Species;Reactive Oxygen Species;Reactive Oxygen Species, Biological_Activity: Asiaticoside, a trisaccaride triterpene from Centella asiatica, suppresses TGF-β/Smad signaling through inducing Smad7 and inhibiting TGF-βRI and TGF-βRII in keloid fibroblasts; Asiaticoside shows antioxidant, anti-inflammatory, and anti-ulcer properties.
IC50 & Target: TGF-beta/Smad[1]
In Vitro: Asiaticoside (0, 100, 250, and 500 mg/L) dose-dependently inhibits keloid fibroblasts proliferation. Asiaticoside (100, 250, and 500 mg/L) decreases the expression of collagen protein and mRNA, reduces the expression of TGF-bRI, TGF-bRII protein, and mRNA, increases the expression of Smad7, but does not affect Smad2, Smad3, Smad4, phosphorylated Smad2, and phosphorylated Smad3 in keloid fibroblasts[1]. Asiaticoside (12.5 and 50, and 25 and 50 µg/mL) prevents endothelial cells from hypoxia-induced inhibition of cell viability and NO production. Asiaticoside (50 µg/mL) also protects endothelial cells from hypoxia-induced apoptosis and upregulates and phosphorylation of AKT/eNOS in hypoxia-exposed HPAECs[2].
In Vivo: Asiaticoside (50 mg/kg daily) blocks the development of hypoxic pulmonary hypertension (PH), cardiovascular remodeling and endothelial cell injury in rats with pulmonary hypertension[2]. Asiaticoside (5, 15 or 45 mg/kg, p.o.) improves the learning and memory deficit, protects hippocampi against the impairment, decreases Aβ deposits in the hippocampus, and ameliorates impaired subcellular structure in rats treated with Aβ oligomers[3].

Name: Germacrone, CAS: 6902-91-6, stock 14.7g, assay 99%, MWt: 218.33, Formula: C15H22O, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Anti-infection, Target: Influenza Virus, Biological_Activity: Germacrone is extracted from Rhizoma Curcuma. Germacrone inhibits influenza virus infection[1].
IC50 & Target: Influenza virus[1]

Name: N-Methylcytisine Caulophylline, CAS: 486-86-2, stock 13.9g, assay 98.3%, MWt: 204.27, Formula: C12H16N2O, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Neuronal Signaling;Membrane Transporter/Ion Channel, Target: nAChR;nAChR, Biological_Activity: N-Methylcytisine (Caulophylline), a tricyclic quinolizidine alkaloid, exerts hypoglycaemic, analgesic and anti-inflammatory activities. N-methylcytisine is a selective ligand of nicotinic receptors of acetylcholine in the central nervous system and has a high affinity (Kd = 50 nM) to nicotinic acetylcholine receptors (nAChR) from squid optical ganglia[1][2].
IC50 & Target: kd: 50 nM (nicotinic acetylcholine receptors)[2]

Name: 8-Gingerol, CAS: 23513-08-8, stock 2.7g, assay 98.4%, MWt: 322.44, Formula: C19H30O4, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Membrane Transporter/Ion Channel;Neuronal Signaling, Target: TRP Channel;TRP Channel, Biological_Activity: 8-Gingerol, found in the rhizomes of ginger (Z. officinale) with oral bioavailability, activates TRPV1, with an EC50 of 5.0 µM. 8-Gingerol inhibits COX-2, and inhibits the growth of H. pylori in vitro[1][2].

Name: 10-Gingerol, CAS: 23513-15-7, stock 2g, assay 98.7%, MWt: 350.49, Formula: C21H34O4, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: 10-Gingerol is a major pungent constituent in the ginger oleoresin from fresh rhizome, with anti-inflammatory, antioxidant and anti-proliferative activities. 10-Gingerol inhibits the proliferation of MDA-MB-231 tumor cell line with an IC50 of 12.1 μM[1][2].

Name: Hyperoside, CAS: 482-36-0, stock 17g, assay 98.6%, MWt: 464.38, Formula: C21H20O12, Solubility: 10 mM in DMSO, Clinical_Informat: Launched, Pathway: Others, Target: Others, Biological_Activity: Hyperoside, a natural flavonoid, isolated from Camptotheca acuminate, possesses antifungal, anti-inflammatory, anti-viral, anti-oxidative and anti-apoptotic activities[1].

Name: DL-Arginine, CAS: 7200-25-1, stock 2.9g, assay 98.6%, MWt: 174.20, Formula: C6H14N4O2, Solubility: H2O : ≥ 150 mg/mL (861.08 mM), Clinical_Informat: Launched, Pathway: Others, Target: Others, Biological_Activity: DL-Arginine is used in physicochemical analysis of amino acid complexation dynamics and crystal structure formations.

Name: Catharanthine (Tartrate) (+)-3,4-Didehydrocoronaridine (Tartrate), CAS: 4168-17-6, stock 14.5g, assay 98.3%, MWt: 486.51, Formula: C25H30N2O8, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Membrane Transporter/Ion Channel;Neuronal Signaling, Target: Calcium Channel;Calcium Channel, Biological_Activity: Catharanthine Tartrate is an alkaloid isolated from Madagascar periwinkle, inhibits voltage-operated L-type Ca2+ channel, with anti-cancer and blood pressure-lowering activity[1].

Name: 1-Caffeoylquinic acid, CAS: 1241-87-8, stock 8.8g, assay 98.3%, MWt: 354.31, Formula: C16H18O9, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: NF-κB, Target: NF-κB, Biological_Activity: 1-Caffeoylquinic acid is an effective NF-κB inhibitor, shows significant binding affinity to the RH domain of p105 with Ki of 0.002 μM and binding energy of 1.50 Kcal/mol[1]. 1-Caffeoylquinic acid has anti-oxidative stress ability[2]. 1-Caffeoylquinic acid inhibits PD-1/PD-L1 interact[3].
IC50 & Target: Ki: 0.002 μM (1-Caffeoylquinic acid)[1]

Name: Corilagin, CAS: 23094-69-1, stock 10.9g, assay 98.6%, MWt: 634.45, Formula: C27H22O18, Solubility: DMSO : 125 mg/mL (197.02 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Anti-infection;Anti-infection, Target: Bacterial;Reverse Transcriptase, Biological_Activity: Corilagin, a gallotannin, is isolated from Caesalpinia coriaria (Jacq.) Willd. Corilagin inhibits activity of reverse transcriptase of RNA tumor viruses. Corilagin inhibits the growth of Staphylococcus aureus with a MIC of 25 μg/mL. Corilagin shows good anti-tumor activity on hepatocellular carcinoma and ovarian cancer. Corilagin shows a low level of toxicity toward normal cells and tissues[1].

Name: Blinin, CAS: 125675-09-4, stock 36g, assay 98.4%, MWt: 392.49, Formula: C22H32O6, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Blinin is a neoclerodane diterpene, isolated from the whole plant of Conyza blinii[1].

Name: D-(-)-Quinic acid, CAS: 77-95-2, stock 12.7g, assay 98.1%, MWt: 192.17, Formula: C7H12O6, Solubility: H2O : 125 mg/mL (650.47 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: D-(-)-Quinic acid is a cyclohexanecarboxylic acid and is implicated in the perceived acidity of coffee.

Name: Geraniin, CAS: 60976-49-0, stock 38.6g, assay 98.4%, MWt: 952.64, Formula: C41H28O27, Solubility: DMSO : 100 mg/mL (104.97 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Apoptosis, Target: TNF Receptor, Biological_Activity: Geraniin is a TNF-α releasing inhibitor with numerous activities including anticancer, anti-inflammatory, and anti-hyperglycemic activities, with an IC50 of 43 μM.
IC50 & Target: IC50: 43 μM (TNF-α)[1].
In Vitro: The IC50 value of TNF-α release inhibition is 43 μM for Geraniin[1]. Geraniin has long been used as a medicinal herb and possesses numerous activities including anticancer, anti-inflammatory, and anti-hyperglycemic activities. Geraniin significantly decreases the viability of OVCAR3 and SKOV3 cells in a concentration-dependent fashion. The IC50 value for Geraniin treatment is 34.5±2.8 μM in OVCAR3 cells and 23.6±1.9 μM in SKOV3 cells. However, Geraniin up to the maximal concentration used (80 μM) has no significant impact on the viability of normal human ovarian surface epithelial cells. Treatment with 10 and 40 μM of Geraniin for 48 h causes a significant increase in apoptosis (16.8±1.2% and 22.6±1.4%, respectively), compared with control OVCAR3 cells (3.9±1.1%). Similar results are observed in SKOV3 cells[2].
In Vivo: Treatment with Geraniin prior to application of okadaic acid delays development of tumors compared with control group, reduces the percentage of tumor bearing mice from 80.0% to 40.0%, and reduces the average numbers of tumor per mouse from 3.8 to 1.1 in week 20. It is also showed that oral administration of Geraniin to rats (50 mg/kg/d or 100 mg/kg/d) inhibit the elevation of serum total cholesterol, lipid peroxide, free fatty acid, triglyceride, glutamic oxaloacetic transaminase and glutamic pyruvic transaminase induced by treatment with peroxidized oil[1].

Name: ZM-447439, CAS: 331771-20-1, stock 15.2g, assay 98.7%, MWt: 513.59, Formula: C29H31N5O4, Solubility: DMSO : ≥ 100 mg/mL (194.71 mM), Clinical_Informat: No Development Reported, Pathway: Apoptosis;Cell Cycle/DNA Damage;Epigenetics, Target: Apoptosis;Aurora Kinase;Aurora Kinase, Biological_Activity: ZM-447439 is an aurora kinase inhibitor with IC50s of 110 and 130 nM for aurora A and B, respectively.
IC50 & Target: IC50: 110 nM (Aurora A), 130 nM (Aurora B)[1]
In Vitro: Cells treated with ZM-447439 progress through interphase, enter mitosis normally, and assemble bipolar spindles. However, chromosome alignment, segregation, and cytokinesis all fail. ZM-447439 inhibits cell division and inhibit mitotic phosphorylation of histone H3. ZM-447439 prevents chromosome alignment and segregation. ZM-447439 compromises spindle checkpoint function. ZM-447439 inhibits kinetochore localization of BubR1, Mad2, and Cenp-E[1]. Inhibition of Aurora kinase by ZM-447439 reduces histone H3 phosphorylation at Ser10 in Hep2 carcinoma cells. Multipolar spindles are induced in these ZM-treated G2/M-arrested cells with accumulation of 4N/8N DNA, similar to cells with genetically suppressed Aurora-B. ZM-447439 treatment induces cell apoptosis. ZM-447439 inhibition of Aurora kinase is potently in association with decrease of Akt phosphorylation at Ser473 and its substrates GSK3α/β phosphorylation at Ser21 and Ser9[2].

Name: Roburic acid, CAS: 6812-81-3, stock 28.9g, assay 98.6%, MWt: 440.70, Formula: C30H48O2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Immunology/Inflammation, Target: COX, Biological_Activity: Roburic acid, a tetracyclic triterpenoid found in Gentiana macrophylla, acts as an inhibitor of COX, with IC50s of 5 and 9 μM for COX-1 and COX-2, respectively[1].
IC50 & Target: IC50: 5 μM (COX-1), 9 μM (COX-2)[1]

Name: Phillyrin, CAS: 487-41-2, stock 3.7g, assay 98.3%, MWt: 534.55, Formula: C27H34O11, Solubility: DMSO : 260 mg/mL (486.39 mM; Need ultrasonic), Clinical_Informat: Launched, Pathway: Metabolic Enzyme/Protease, Target: Cytochrome P450, Biological_Activity: Phillyrin is isolated from Forsythia suspensa Vahl (Oleaceae), has antibacterial and anti-inflammatory activities. Phillyrin has potential inductive effects on rat CYP1A2 and CYP2D1 activities, without affecting CYP2C11 and CYP3A1/2 activities[1].
IC50 & Target: CYP1A2; CYP2D1[1]
In Vitro: Phillyrin (1–5 μM; pretreatment 1 hour; 24 hours) inhibits high glucose-induced FAS protein significantly in HepG2 cells[1].
Phillyrin (1–5 μM; pretreatment 1 hour; 24 hours) inhibits high glucose-induced FAS mRNA expression by suppressing SREBP-1c activation in human HepG2 hepatocytes[1].

Name: Liensinine (Diperchlorate), CAS: 5088-90-4, stock 17.4g, assay 98.3%, MWt: 811.66, Formula: C37H44Cl2N2O14, Solubility: DMSO : 100 mg/mL (123.20 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Autophagy;Autophagy, Target: Autophagy;Mitophagy, Biological_Activity: Liensinine Diperchlorate is a major isoquinoline alkaloid, extracted from the seed embryo of Nelumbo nucifera Gaertn. Liensinine Diperchlorate inhibits late-stage autophagy/mitophagy through blocking autophagosome-lysosome fusion. Liensinine Diperchlorate has a wide range of biological activities, including anti-arrhythmias, anti-hypertension, anti-pulmonary fibrosis, relaxation on vascular smooth muscle, etc[1].

Name: Gentiopicroside Gentiopicrin, CAS: 20831-76-9, stock 4.2g, assay 98.7%, MWt: 356.32, Formula: C16H20O9, Solubility: DMSO : ≥ 150 mg/mL (420.97 mM), Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease;Anti-infection, Target: Cytochrome P450;HCV, Biological_Activity: Gentiopicroside, a naturally occurring iridoid glycoside, inhibits P450 activity, with an IC50 and a Ki of 61 µM and 22.8 µM for CYP2A6; Gentiopicroside has antianti-inflammatoryand antioxidative effects.
IC50 & Target: IC50: 61 µM (CYP2A6)[1] 
Ki: 22.8 µM (CYP2A6)[1]
In Vitro: Gentiopicroside inhibits P450 activity, with an IC50 and a Ki of 61 µM and 8.12 µM for CYP2A6, also slightly inhibits CYP2E1 activity with an IC50 of 1.6 mM, but shows no inhibition on CYP1A2 and CYP3A4[1]. Gentiopicroside (12.5, 25 and 50 μM) inhibits RANKL-induced osteoclast formation from mouse bone marrow macrophages (BMMs) in a dose-dependent manner, blocks the expression of osteoclast-related proteins, prevents receptor activator of nuclear factor-κB ligand (RANKL)-triggered JNK and NF-κB activation. Gentiopicroside (50 μM) also inhibits RANKL-induced bone resorption[3].
In Vivo: Gentiopicroside (20, 40, and 80 mg/kg, p.o.) significantly reduces gastric ulcerindex in mice. Gentiopicroside (20, 40, and 80 mg/kg) also ovbiously decreases the levels of HSP-70, TNF-α, IL-6, MDA and increases ncreased GSH level and SOD activity. In addition, Gentiopicroside normalizes EGF and VEGF level in mice[2].

Name: Ruscogenin, CAS: 472-11-7, stock 27.3g, assay 98.4%, MWt: 430.62, Formula: C27H42O4, Solubility: DMSO : 125 mg/mL (290.28 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Immunology/Inflammation, Target: NOD-like Receptor (NLR), Biological_Activity: Ruscogenin, an important steroid sapogenin derived from Ophiopogon japonicus, attenuates cerebral ischemia-induced blood-brain barrier dysfunction by suppressing TXNIP/NLRP3 inflammasome activation and the MAPK pathway and exerts significant anti-inflammatory and anti-thrombotic activities[1][2].

Name: Parmodulin 2 ML161, CAS: 423735-93-7, stock 33.9g, assay 98.1%, MWt: 361.23, Formula: C17H17BrN2O2, Solubility: DMSO : 100 mg/mL (276.83 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein, Target: Protease-Activated Receptor (PAR), Biological_Activity: Parmodulin 2 (ML161),a probe, is an allosteric inhibitor of protease-activated receptor 1 (PAR1) with an IC50 of 0.26 μM. Parmodulin 2 inhibits platelet aggregation induced by a PAR1 peptide agonist or by thrombin and has shown cytoprotective effects[1, 2].
IC50 & Target: PAR1[1]

Name: Cyanidin (Chloride) IdB 1027, CAS: 528-58-5, stock 35.8g, assay 98.1%, MWt: 322.70, Formula: C15H11ClO6, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Cyanidin Chloride (IdB 1027), a subclass of anthocyanin, displays antioxidant and anti-carcinogenesis properties. Cyanidin Chloride (IdB 1027) inhibits osteoclast formation, hydroxyapatite resorption, and receptor activator of NF-κB ligand (RANKL)-induced osteoclast marker gene expression[1].
In Vitro: Cyanidin Chloride (IdB 1027) inhibits receptor activator of NF-κB ligand (RANKL)-induced NF-κB activation, suppresses the degradation of IκB-α and attenuates the phosphorylation of extracellular signal-regulated kinases (ERK). Cyanidin Chloride (IdB 1027) abrogates RANKL-induced calcium oscillations, the activation of nuclear factor of activated T cells calcineurin-dependent 1 (NFATc1), and the expression of c-Fos[1].
In Vivo: Cyanidin Chloride (IdB 1027) protects against OVX-induced bone loss in OVX-induced osteoporosis mouse model[1].

Name: Mogroside III, CAS: 130567-83-8, stock 1.4g, assay 98.5%, MWt: 963.15, Formula: C48H82O19, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Mogroside III, a triterpenoid glycoside isolated from the extracts of Luo Han Guo, is a nonsugar sweetener. Mogrosides are sweeter than sucrose. Mogrosides exhibit antioxidant, antidiabetic and anticancer activities[1].

Name: Astilbin, CAS: 29838-67-3, stock 20.9g, assay 98.8%, MWt: 450.39, Formula: C21H22O11, Solubility: DMSO : ≥ 60 mg/mL (133.22 mM), Clinical_Informat: No Development Reported, Pathway: Apoptosis;NF-κB;NF-κB, Target: TNF Receptor;Keap1-Nrf2;NF-κB, Biological_Activity: Astilbin, a flavonoid compound, is isolated from the rhizome of Smilax glabra. Astilbin enhances NRF2 activation. Astilbin also suppresses TNF-α expression and NF-κB activation.
IC50 & Target: NRF2,TNF-α,NF-κB[1]
In Vitro: Astilbin is a common dietary flavonoid that can be found in various kinds of herbs and foods such as Smilax Glabra, Sarcandra glabra, grape and red wine. Astilbin markedly inhibits cisplatin-induced cell apoptosis and recovers cell growth. Astilbin significantly decreases reactive oxygen species (ROS) accumulation and alleviates ROS-induced activation of p53, MAPKs and AKT signaling cascades, which in turn attenuates cisplatin-induced HEK-293 cell apoptosis. Astilbin effectively enhances NRF2 activation and transcription of its targeting antioxidant genes to reduce ROS accumulation in cisplatin-induced HEK-293 cells. Astilbin obviously suppresses tumor necrosis factor alpha (TNF-α) expression and NF-κB activation, and also inhibits the expression of induced nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2). To measure the effects of Astilbin on the growth of CDDP-treated renal cells, HEK-293 cells are treated with CDDP (100 μM) and/or Astilbin (200 μM). Astilbin treatment significantly improvescell growth in CDDP-induced HEK-293 cells[1].
In Vivo: To explore whether Astilbin improves CDDP-induced nephrotoxicity in vivo, an acute cisplatin nephrotoxic mouse model is established. Single injection of CDDP with 8 mg/kg dose results in notable weight loss compared with control group. However, the phenomenon is significantly alleviated by Astilbin at dose of 50 mg/kg. The mice fed Astilbin alone do not show any obvious alteration in body weight. Similarly, serum creatinine (SCr) and blood urea nitrogen (BUN) are higher in CDDP-treated mice than in control group. Treatment with Astilbin also decreases SCr and BUN levels. To examine the protective effect of Astilbin on CDDP-induced renal histopathological damage, the mouse kidney sections are stained with H&E. The mice in control group and Astilbin treated group have normal kidney morphology, while kidneys in CDDP group show severe damage with tubular degeneration, necrosis and cystic dilatation of the tubules with focal hemorrhages. Administration of Astilbin mitigated kidney injury, resulting in lower histopathological score compared to CDDP group. The apoptosis of renal cells is also detected using TUNEL staining to determine whether Astilbin treatment decreased renal cell apoptosis in CDDP-induced acute nephrotoxic mice[1].

Name: Aristolochic acid A Aristolochic acid I;TR 1736, CAS: 313-67-7, stock 36.2g, assay 98.5%, MWt: 341.27, Formula: C17H11NO7, Solubility: DMSO : 50 mg/mL (146.51 mM; Need ultrasonic); H2O : < 0.1 mg/mL (insoluble), Clinical_Informat: No Development Reported, Pathway: NF-κB, Target: NF-κB, Biological_Activity: Aristolochic acid A (Aristolochic acid I; TR 1736) is the main component of plant extract Aristolochic acids, which are found in various herbal plants of genus Aristolochia and Asarum. Aristolochic acid A significantly reduces both activator protein 1 (AP-1) and NF-κB activities. Aristolochic acid A reduces BLCAP gene expression in human cell lines[1].
In Vitro: Aristolochic acid A (150, 200 μM, 24 hours) inhibits the cell viabilities of kidney cells HEK293 and HK-2[1]. 
Aristolochic acid A (100, 200 μM, 24 hours) causes a concentration-dependent decrease in bladder cancer-associated protein (BLCAP) mRNA levels in kidney cells (HEK 293 and HK-2) , and bladder cancer cell line (HT-1376)[1]. 
Aristolochic acid A (100, 200 μM, 24 hours) weakens the BLCAP protein signals in a dose-dependent manner in both HEK293 and HT-1376 cells[1].

Name: Aristolochic acid B, CAS: 475-80-9, stock 34.9g, assay 98.8%, MWt: 311.25, Formula: C16H9NO6, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Aristolochic acid B is one of the major components of Aristolochic acids (AA) which are natural products derived from taxa in the Aristolochiaceae. Aristolochic acid is known to be a potent mutagen and carcinogen. Aristolochic acid B showes more carcinogenic risk than Aristolochic acid A in vivo[1].

Name: Casticin Vitexicarpin, CAS: 479-91-4, stock 11.6g, assay 98.6%, MWt: 374.34, Formula: C19H18O8, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: JAK/STAT Signaling;Stem Cell/Wnt, Target: STAT;STAT, Biological_Activity: Casticin is a methyoxylated flavonol isolated from Viticis Fructus, with antimitotic and anti-inflammatory effect. Casticin inhibits the activation of STAT3.
IC50 & Target: STAT3[3]
In Vitro: Casticin (0.2-1.0 μM) dose-dependently inhibits the proliferation of KB cells, with an IC50 of 0.23 μM on day 3, while shows no significant inhibition on 3T3 Swiss Albino and TIG-103 cells. Casticin (0.6 μM) alters spindle morphology with partial mitotic spindle breakdown or with disordered spindles[1]. Casticin (0-40 μM) dose-dependently inhibits the proliferation of LX2 cells. Casticin (40 μM) suppresses L02 cells proliferation and induces apoptosis. Casticin inhibits fibrotic effects of TGF-β1 on ECM deposition in LX2 cells by evaluating the mRNA levels of TGF-β, collagen α1(I), MMP-2, MMP-9, TIMP-1 and TIMP-2[2]. Casticin (0-8 μM) reduces the viability of 786-O, YD-8, and HN-9 cells, but shows no significant effect on that of the normal HEL 299 cells. Casticin (5 μM) increases cleavage caspase-3 and PPAR, diminishes the levels of B-cell lymphoma-extra large (Bcl-xl), Bcl-2, IAP-1/-2, vascular endothelial growth factor (VEGF), matrix metallopeptidase 9 (MMP-9), and cyclooxygenase 2 (COX-2) proteins in 786-O, YD-8, and HN-9 cells. Casticin (5 μM) also promotes apoptotic cell death, inhibits constitutively active STAT3 in tumor cells, modulates STAT3 activation by altering the activity of upstream STAT3 regulators, and abrogates IL-6-induced STAT3 activation. In addition, Casticin (2.5 μM) enhances the effect of ionizing radiation in 786-O cells and potentiates the therapeutic effect of radiotherapy[3].
In Vivo: Casticin (20 mg/kg, p.o.) has toxic effect on the liver in mice with CCl4-and BDL-induced hepatic injury. Casticin attenuates liver fibrosis induced by CCl4 or BDL in vivo. Casticin inhibits HSC activation and collagen matrix expression by blocking TGF-β/Smad signaling in vivo[2].

Name: Erianin, CAS: 95041-90-0, stock 13.7g, assay 98.8%, MWt: 318.36, Formula: C18H22O5, Solubility: DMSO : 125 mg/mL (392.64 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Anti-infection, Target: Bacterial, Biological_Activity: Erianin, often used as an antipyretic and analgesic agent, could inhibit IDO-induced tumor angiogenesis.
In Vitro: Erianin is often used as antipyretic and analgesic agent. Erianin belongs to bibenzyl derivatives in structure, with the activity of anti-virus, anti-bacterial, as well as anti-benign prostatic hyperplasia. Erianin has obvious damage on 2LL-IDO cells, Erianin basically has no cytotoxicity on human normal liver cell line L02, and cell viability is maintained at around 85%[1]. Erianin inhibits the growth of HeLa cells and induces apoptosis in a dose‑ and time‑dependent manner, inducing cell cycle arrest at the G2/M stage. Erianin treatment also increases the expression of Bax and caspase‑3, but decreases levels of Bcl‑2 and phosphorylated‑ERK1/2[2].

Name: Ethyl gallate, CAS: 831-61-8, stock 33.3g, assay 98.1%, MWt: 198.17, Formula: C9H10O5, Solubility: DMSO : 150 mg/mL (756.93 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Anti-infection, Target: Bacterial, Biological_Activity: Ethyl gallate is a nonflavonoid phenolic compound and also a scavenger of hydrogen peroxide.
In Vitro: Ethyl gallate is a nonflavonoid phenolic compound and also a scavenger of hydrogen peroxide. After treatment for 24 h or 48 h with Ethyl gallate, HL-60 cells show changes in morphology, including shrinkage of the cell membrane and the development of apoptotic bodies. Consistent with these effects, the viability of Ethyl gallate-treated cells decreases in a time- and dose-dependent manner, demonstrating that Ethyl gallate has a cytotoxic effect on HL-60 cells. Ethyl gallate treatment increases the proportion of cells in subG1 phase in a concentration- and time-dependent manner. Treatment of cells for 24 h or 48 h with 50 μM or 75 μM Ethyl gallate increases the percentage of cells in the subG1 phase from a baseline of 2.9% to 26.5% or 52.6%, respectively. It is found that Ethyl gallate treatment of HL-60 cells decreases the expression of Bcl-2 at 75 μM Ethyl gallate, and increases Bax and truncated Bid (tBid) expression at 24 h[1].
In Vivo: No significant difference in the serum total protein, albumin, globulin and glucose is found between the rats fed with A. nilotica (L.) leaf extract on ethyl gallate equivalent basis and those fed with Ethyl gallate alone. Significant differences in total bilirubin level, however, exist between the rats that receive A. nilotica (L.) leaf extract, 500 mg/kg body weight (ethyl gallate equivalent of 10 mg/kg, 0.34±0.01 mg/dL) and those receiving 10 mg/kg body weight of Ethyl gallate (0.26±0.01 mg/dL). Significant difference is found for ALT between groups fed with 500 and 1000 mg/kg body weight of A. nilotica (L.) leaf extract (26.52±1.23 and 30.05±1.38 U/L) and 10 and 20 mg/kg of Ethyl gallate (20.50±0.94 and 24.67±1.13 U/L)[2].

Name: 2"-O-Galloylhyperin, CAS: 53209-27-1, stock 4.9g, assay 98.3%, MWt: 616.48, Formula: C28H24O16, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: 2"-O-Galloylhyperin, an active compound isolated from Pyrola incarnate Fisch., possesses anti-oxidative and anti-inflammatory activities. 2"-O-Galloylhyperin has hepatoprotective effect against oxidative stress-induced liver damage[1][2].

Name: Dryocrassin ABBA Dryocrassin, CAS: 12777-70-7, stock 31.1g, assay 98.2%, MWt: 820.83, Formula: C43H48O16, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Anti-infection;Anti-infection, Target: Bacterial;Influenza Virus, Biological_Activity: Dryocrassin ABBA (Dryocrassin) is a flavonoid natural product derived from Dryopteris crassirhizoma, with antiviral and antibacterial activities[1][2]. Dryocrassin ABBA exhibits antiviral activity against H5N1 avian influenza virus[1]. Dryocrassin ABBA inhibits the coagulase activity of Staphylococcus aureus vWbp[3]. Dryocrassin ABBA suppresses immunostimulatory function of dendritic cells and prolongs skin allograft survival[4].
IC50 & Target: H5N1 avian influenza virus[1]

Name: Morroniside, CAS: 25406-64-8, stock 26.2g, assay 98.6%, MWt: 406.38, Formula: C17H26O11, Solubility: DMSO : 125 mg/mL (307.59 mM; Need ultrasonic); H2O : 50 mg/mL (123.04 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Apoptosis;Metabolic Enzyme/Protease, Target: Apoptosis;MMP, Biological_Activity: Morroniside has neuroprotective effect by inhibiting neuron apoptosis and MMP2/9 expression.
In Vivo: Morroniside reduces the expression of MMP2 and MMP9 in an I/R injury model. Treatment with Morroniside significantly reduces I/R‑associated neuron apoptosis in a dose dependent manner. The results demonstrate that active caspase‑3 and Bax are significantly upregulated in the model group compared with the control group, while Bcl‑2 is significantly downregulated. The expression of active caspase‑3 and Bax is significantly downregulated by Morroniside treatment in a dose‑dependent manner, while the expression of Bcl‑2 is significantly upregulated[1]. Morroniside has an ameliorative effect on diabetes-induced alterations such as oxidative stress, inflammation, and apoptosis in the liver of type 2 diabetic db/db mice[2].

Name: Vitexin-2"-O-rhamnoside, CAS: 64820-99-1, stock 22.4g, assay 99%, MWt: 578.52, Formula: C27H30O14, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Vitexin-2-O-rhamnoside, a main flavonoid glycoside of the leaves of Cratagus pinnatifida Bge, contributes to the protection against H2O2-mediated oxidative stress damage and has potential to treat cardiovascular system diseases[1].

Name: Calceolarioside B, CAS: 105471-98-5, stock 3.2g, assay 98.4%, MWt: 478.45, Formula: C23H26O11, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Calceolarioside B is a natural product isolated from Stauntonia hexaphylla leaves. Calceolarioside B exhibits significant inhibitory activity against rat lens aldose reductase (RLAR) with an IC50 of 23.99 μM. Calceolarioside B displays inhibitory effect on DPPH radical scavenging activity with an IC50 of 94.60 μM [1].

Name: Limonene, CAS: 138-86-3, stock 31.5g, assay 98.6%, MWt: 136.23, Formula: C10H16, Solubility: 10 mM in DMSO, Clinical_Informat: Phase 1, Pathway: Anti-infection;Metabolic Enzyme/Protease;NF-κB;Immunology/Inflammation, Target: Bacterial;Reactive Oxygen Species;Reactive Oxygen Species;Reactive Oxygen Species, Biological_Activity: Limonene is a monoterpene in citrus peel oil. A popular disinfectant and food preservative. Antimicrobial activities[1]. Anti-proliferative activities[2]. Antioxidant and anti-inflammatory effect[3].
IC50 & Target: Bacterial[1]
In Vitro: Acute toxicity to limonene is largely due to the common oxidation product limonene-hydroperoxide. The mutant protein AhpCL177Q 35 is able to alleviate this toxicity by reducing the hydroperoxide to a more benign compound[1].
Limonene exerts anti-proliferative action on a lymphoma cell line without modifying normal lymphocyte viability[2].
In Vivo: Limonene (50-100 mg/kg) exerts gastroprotection through local mucosal defense mechanisms, such as increasing the mucus production, modulation of the oxidative stress and inflammatory response and inhibition of Nf-κb expression[3].

Name: Ligustroflavone Nuezhenoside, CAS: 260413-62-5, stock 10.1g, assay 98%, MWt: 724.66, Formula: C33H40O18, Solubility: DMSO : 250 mg/mL (344.99 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein, Target: CaSR, Biological_Activity: Ligustroflavone, extracted from Ligustrum lucidum, is a potential candidate as calcium-sensing receptor (CaSR) antagonist. Ligustroflavone exhibits protective effects against diabetic osteoporosis in mice[1].
IC50 & Target: CaSR[1].

Name: (-)-α-Pinene, CAS: 7785-26-4, stock 16.6g, assay 98.8%, MWt: 136.23, Formula: C10H16, Solubility: DMSO : 60 mg/mL (440.43 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Anti-infection;Neuronal Signaling;Membrane Transporter/Ion Channel;Anti-infection, Target: Bacterial;GABA Receptor;GABA Receptor;Virus Protease, Biological_Activity: (-)-α-Pinene is a monoterpene and shows sleep enhancing property through a direct binding to GABAA-benzodiazepine (BZD) receptors by acting as a partial modulator at the BZD binding site[1].
In Vitro: (-)-α-pinene enhances the quantity of non-rapid eye movement sleep (NREMS) without affecting the intensity of NREMS by prolonging GABAergic synaptic transmission, acting as a partial modulator of GABAA-BZD receptors and directly binding to the BZD binding site of GABAA receptor[1].

Name: Wedelolactone, CAS: 524-12-9, stock 35.8g, assay 98.7%, MWt: 314.25, Formula: C16H10O7, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Apoptosis;Apoptosis;Metabolic Enzyme/Protease, Target: Apoptosis;Caspase;Lipoxygenase, Biological_Activity: Wedelolactone, a natural product from Ecliptae herba, suppresses LPS-induced caspase-11 expression by directly inhibiting the IKK Complex[1]. Wedelolactone inhibits 5-lipoxygenase (5-Lox) (IC50~2.5 μM) activity by an oxygen radical scavenging mechanism. Wedelolactone induces caspase-dependent apoptosis in prostate cancer cells via downregulation of PKCε without inhibiting Akt[2]. Anti-cancer, anti-inflammatory, and antioxidant activities[3].

Name: Escin IA, CAS: 123748-68-5, stock 0.1g, assay 98.2%, MWt: 1131.26, Formula: C55H86O24, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: HIV Protease, Biological_Activity: Escin IA is a triterpene saponin isolated from horse chestnut, which inhibits HIV-1 protease with IC50 values of 35 μM. Escin IA has anti-TNBC metastasis activity, and its action mechanisms involved inhibition of epithelial-mesenchymal transition process by down-regulating LOXL2 expression[1][2].

Name: Escin IB, CAS: 26339-90-2, stock 9.5g, assay 98.8%, MWt: 1131.26, Formula: C55H86O24, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Escin IB is a saponin isolated from skin and the endosperm of seeds of horse chestnut (Aesculus hippocastanum). Escin IB shows inhibitory effect on pancreatic lipase activity[1][2].
IC50 & Target: Pancreatic lipase[2]

Name: Isoescin IA, CAS: 219944-39-5, stock 24.9g, assay 98.9%, MWt: 1131.26, Formula: C55H86O24, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: HIV Protease, Biological_Activity: Isoescin IA is a triterpenoid saponin isolated from the seeds of Aesculus chinensis. Isoescin IA has anti-HIV-1 protease activity[1].

Name: Alnustone, CAS: 33457-62-4, stock 37.7g, assay 98.9%, MWt: 262.35, Formula: C19H18O, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Alnustone, a non-phenolic diarylheptanoid found in herbs and spices, is a constituent of Curcuma xanthorrhiza. Alnustone displays anti-emetic and anti-inflammatory activities[1][2].

Name: PKR-IN-C16, CAS: 608512-97-6, stock 11.8g, assay 98.5%, MWt: 268.29, Formula: C13H8N4OS, Solubility: DMSO : 16.67 mg/mL (62.13 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: PKR-IN-C16 is a specific protein kinase (PKR) inhibitor. PKR-IN-C16 is able to inhibit the autophosphorylation of PKR and unlock the translation blockade induced by PKR in primary neuronal cultures[1].

Name: Alizarin, CAS: 72-48-0, stock 33.6g, assay 98.6%, MWt: 240.21, Formula: C14H8O4, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Alizarin is a natural dye extracted from the roots of madder plant and has been widely used as a pigment in textile fabrics and paintings[1].

Name: Hydroxytyrosol DOPET;3,4-Dihydroxyphenethyl alcohol;3-Hydroxytyrosol, CAS: 10597-60-1, stock 3.2g, assay 98.1%, MWt: 154.16, Formula: C8H10O3, Solubility: DMSO : 125 mg/mL (810.85 mM; Need ultrasonic), Clinical_Informat: Phase 4, Pathway: Others, Target: Others, Biological_Activity: Hydroxytyrosol (DOPET) is a phenolic compound drawn from the olive tree and its leaves with anti-oxidant, anti-atherogenic, anti-thrombotic, antimicrobial, anti-inflammatory and anti-tumour effects[1][2].
In Vitro: Hydroxytyrosol (DOPET) shows the inhibition of pro-inflammatory cytokines (TNF-α) and reduces the expression of cyclooxygenase-2 and inducible nitric oxide synthase (iNOS) more than 60%[1]. 
Hydroxytyrosol (DOPET) modulates the transcription factor NF-κB[1].
Hydroxytyrosol (DOPET) arrests the cell cycle, producing differentiation, apoptosis, or preventing DNA from oxidative stress[1].

Name: Pinocembrin (+)-Pinocoembrin; Dihydrochrysin; Galangin flavanone, CAS: 480-39-7, stock 15.2g, assay 98.7%, MWt: 256.25, Formula: C15H12O4, Solubility: DMSO : 125 mg/mL (487.80 mM; Need ultrasonic), Clinical_Informat: Phase 2, Pathway: Anti-infection;Autophagy;Metabolic Enzyme/Protease;NF-κB;Immunology/Inflammation, Target: Bacterial;Autophagy;Reactive Oxygen Species;Reactive Oxygen Species;Reactive Oxygen Species, Biological_Activity: Pinocembrin ((+)-Pinocoembrin) is a flavonoid found in propolis, acts as a competitive inhibitor of histidine decarboxylase, and is an effective anti-allergic agent, with antioxidant, antimicrobial and anti-inflammatory properties[1].
In Vitro: Pinocembrin (5, 10, 25, 50, 100 or 200 µM, 24 hours) significantly reduces cell viability of RBL-2H3 cells[1]. 
Pinocembrin (25 or 50 µM) suppresses iNOS, PGE-2 and COX-2 levels, increases p38-Mapk and IкB-α, and inhibits phosphorylation of IкB-α[1].

Name: Apiin, CAS: 26544-34-3, stock 11.5g, assay 98.4%, MWt: 564.49, Formula: C26H28O14, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Apiin, a major constituent of Apium graveolens leaves with anti-inflammatory properties. Apiin shows significant inhibitory activity on nitrite (NO) production (IC50 = 0.08 mg/mL) in-vitro and iNOS expression (IC50 = 0.049 mg/ mL) in LPS-activated J774.A1 cells[1].

Name: Fraxin Fraxoside, CAS: 524-30-1, stock 2g, assay 98.5%, MWt: 370.31, Formula: C16H18O10, Solubility: DMSO : 250 mg/mL (675.11 mM; Need ultrasonic), Clinical_Informat: Phase 1, Pathway: Metabolic Enzyme/Protease, Target: Phosphodiesterase (PDE), Biological_Activity: Fraxin isolated from Acer tegmentosum, F. ornus or A. hippocastanum, is a glucoside of fraxetin and reported to exert potent anti-oxidative stress action[1], anti-inflammatory and antimetastatic properties. Fraxin shows its antioxidative effect through inhibition of cyclo AMP phosphodiesterase enzyme[2].
IC50 & Target: Cyclo AMP phosphodiesterase enzyme[2].
In Vitro: Fraxin (100 μM) is non-cytotoxic on Hep G2 cells. Fraxin at non-cytotoxic concentrations significantly decreases the t-BHP-induced ROS generation in a dose-dependent manner[1]. 
Fraxin (0.5 mM) shows free radical scavenging effect at high concentration and cell protective effect against H2O2-mediated oxidative stress[2].
In Vivo: Fraxin (50 mg/kg, p.o.) significantly blocks the CCl4-induced elevation of ALT and AST. Fraxin (10 and 50 mg/kg, p.o.) significantly reduces the GSSG levels (1.7±0.3 and 1.5±0.2 nM/g liver, respectively) compared with the GSSG levels of the CCl4-treated group[1].

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