EOS Med Chem, Medicinal Chemical is Big: EOS Med Chem Building block stock list 2349

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

Name: Euscaphic acid, CAS: 53155-25-2, stock 25.9g, assay 98.1%, MWt: 488.70, Formula: C30H48O5, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: PI3K/Akt/mTOR;Apoptosis;Cell Cycle/DNA Damage, Target: PI3K;Apoptosis;DNA/RNA Synthesis, Biological_Activity: Euscaphic acid, a DNA polymerase inhibitor, is a triterpene from the root of the R. alceaefolius Poir. Euscaphic inhibits calf DNA polymerase α (pol α) and rat DNA polymerase β (pol β) with IC50 values of 61 and 108 μM[1]. Euscaphic acid induces apoptosis[2].
IC50 & Target: IC50: 61 μM (calf DNA polymerase α); 108 μM (rat DNA polymerase β)[1]; apoptosis[2]
In Vitro: Euscaphic acid induces apoptosis and cell cycle arrest in NPC cells by suppression of the PI3K/AKT/mTOR signaling pathway[2].

Name: Britannin, CAS: 33627-28-0, stock 11g, assay 98.4%, MWt: 366.41, Formula: C19H26O7, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Apoptosis;Autophagy, Target: Apoptosis;Autophagy, Biological_Activity: Britannin, isolated from Inula aucheriana, is a sesquiterpene lactone. Britannin induces apoptosis and autophagy by activating AMPK regulated by ROS in liver cancer cells. Britannin has anti-proliferative and anti-inflammatory activities[1][2][3].

Name: Corytuberine, CAS: 517-56-6, stock 38.2g, assay 98.2%, MWt: 327.37, Formula: C19H21NO4, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Corytuberine is an aporphine alkaloid isolated from Dicranostigma leptopodum. Corytuberine displays cytotoxicity against SMMC-7721 tumor cells[1].

Name: Corydine, CAS: 476-69-7, stock 32.3g, assay 98.5%, MWt: 341.40, Formula: C20H23NO4, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Anti-infection;Anti-infection, Target: Reverse Transcriptase;HIV, Biological_Activity: Corydine is a naturally occurring alkaloid which can be extracted from plants such as Croton echinocarpus leaves. Corydine is efficient on inhibiting reverse transcriptase (RT) activity with an IC50 of 356.8 μg/mL. Corydine displays significant in vitro anti-HIV potential, inhibiting 40% of the HIV-1 reverse transcriptase enzyme activity at a concentration of 450 μg/mL of Corydine[1].

Name: Nepetin 6-Methoxyluteolin, CAS: 520-11-6, stock 26.8g, assay 98.5%, MWt: 316.26, Formula: C16H12O7, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Nepetin (6-Methoxyluteolin) is a natural flavonoid isolated from Eupatorium ballotaefolium HBK with potent anti-inflammatory activities. Nepetin inhibits IL-6, IL-8 and MCP-1 secretion with IC50 values of 4.43 μM, 3.42 μM and 4.17 μM, respectively in ARPE-19 cells[1][2].
In Vitro: Pretreatment with Nepetin dose-dependently inhibited IL-6, IL-8 and MCP-1 secretion with IC50 values of 4.43, 3.42 and 4.17 μM, respectively[1]. 
Nepetin (2.5-10 μM; 25 hours; ARPE-19 cells) treatment suppresses IL-1β-induced cytokine (IL-6, IL-8 and MCP-1) expression at mRNA level in ARPE-19 cells[1]. 
Nepetin (2.5-10 μM; 1.5 hours; ARPE-19 cells) treatment dose-dependently inhibits phosphorylation of IKKα/β and IκBα, and nuclear translocation of p65. Nepetin decreases the level of phosphorylated ERK1/2, JNK and p38 MAPK in activated ARPE-19 cells[1].

Name: Gitogenin, CAS: 511-96-6, stock 5.3g, assay 98.5%, MWt: 432.64, Formula: C27H44O4, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Glucosidase, Biological_Activity: Gitogenin is a natural steroid isolated from the whole plant of Tribulus longipetalus. Gitogenin is a selective inhibitor of UDP-glucuronosyltransferase 1A4 (UGT1A4) and enzyme α-glucosidase with IC50 values of 0.69 μM (use trifluoperazine as a substrate) and 37.2 μM, respectively, and does not inhibit the activities of major human cytochrome P450 isoforms[1][2].
IC50 & Target: IC50: 0.69 µM (UDP-glucuronosyltransferase 1A4)[1]; IC50: 37.2 μM (α-glucosidase)[2]
In Vitro: When tamoxifen is used as the substrate metabolized by UGT1A4 in HLMs, Gitogenin exhibits potent inhibition of tamoxifen, with an IC50 value of 6.13 µM. Similarly, for midazolam as the substrate of UGT1A4, the IC50 value is 5.7 µM. In addition, when olanzapine is used as a substrate of UGT1A4, the IC50 value is determined as 6.0 µM. Finally, we also evaluats Gitogenin for asenapine glucuronidation mediated by UGT1A4, and similar inhibition effect is observed, with an IC50 value of 22.0 µM[1].
In Vivo: Stimulation of growth hormone release is investigated on rat pituitary cells in vitro. Gitogenin (20 μg/mL) shows rat growth-hormone (rGH) release stimulating activities (26.1 ng/mL)[3].

Name: Hypocrellin A, CAS: 77029-83-5, stock 3.1g, assay 98.5%, MWt: 546.52, Formula: C30H26O10, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: TGF-beta/Smad;Epigenetics, Target: PKC;PKC, Biological_Activity: Hypocrellin A, a naturally occurring PKC inhibitor, has many biological and pharmacological properties, such as antitumour, antiviral, antibacterial, and antileishmanial activities. Hypocrellin A is a promising photosensitizer for anticancer photodynamic therapy (PDT)[1][2][3][4].
IC50 & Target: PKC[1]

Name: 1F-Fructofuranosylnystose, CAS: 59432-60-9, stock 34.9g, assay 98.9%, MWt: 828.72, Formula: C30H52O26, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: 1F-Fructofuranosylnystose can be used in the synthesis of Fructooligosaccharides (FOSs). Fructooligosaccharides exhibit lots of beneficial effects on our health and have been used as food ingredients.
In Vitro: Fructooligosaccharides (FOSs), as a mixture of 1-kestose, nystose, and 1F-fructofuranosylnystose oligosaccharides, exhibit lots of beneficial effects on our health and have been used as food ingredients[1].

Name: Sakuranetin, CAS: 2957-21-3, stock 13g, assay 98.8%, MWt: 286.28, Formula: C16H14O5, Solubility: DMSO : ≥ 125 mg/mL (436.64 mM), Clinical_Informat: No Development Reported, Pathway: Anti-infection, Target: Fungal, Biological_Activity: Sakuranetin is a rice flavonoid phytoalexin, shows strong antifungal activity[1]. Sakuranetin has anti-inflammatory and antioxidative activities. Sakuranetin ameliorates LPS-induced acute lung injury[2].

Name: 1-Kestose, CAS: 470-69-9, stock 19g, assay 98.8%, MWt: 504.44, Formula: C18H32O16, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: 1-Kestose, the smallest fructooligosaccharide component, which efficiently stimulates Faecalibacterium prausnitzii as well as Bifidobacteria.
In Vitro: Faecalibacterium prausnitzii is anti-inflammatory commensal bacterium identified by gut microbiota analysis of Crohn disease. Bifidobacteria exerts a beneficial effect on atopic dermatitis (AD)[1].

Name: Iridin, CAS: 491-74-7, stock 9.2g, assay 98.5%, MWt: 522.46, Formula: C24H26O13, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Iridin is an isoflavone isolated from Iris milesii[1].

Name: (2S)-Isoxanthohumol, CAS: 70872-29-6, stock 10.1g, assay 98.7%, MWt: 354.40, Formula: C21H22O5, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: (2S)-Isoxanthohumol is a microbial biotransformed metabolite of the hop prenylflavanone Isoxanthohumol[1].

Name: Tenuifoliside C, CAS: 139726-37-7, stock 39.3g, assay 98.1%, MWt: 768.71, Formula: C35H44O19, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Tenuifoliside C, isolated from polygala tenuifolia willd, significantly inhibits chlorzoxazone 6-hydroxylation catalyzed by CYP2E1[1].

Name: Irigenin, CAS: 548-76-5, stock 3.7g, assay 98.8%, MWt: 360.31, Formula: C18H16O8, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Cytoskeleton, Target: Integrin, Biological_Activity: Irigenin is a is a lead compound, and mediates its anti-metastatic effect by specifically and selectively blocking α9β1 and α4β1 integrins binding sites on C-C loop of Extra Domain A (EDA). Irigenin shows anti-cancer properties. It sensitizes TRAIL-induced apoptosis via enhancing pro-apoptotic molecules in gastric cancer cells[1].
In Vitro: Irigenin specifically targets α9β1 and α4β1 integrin binding sites on Extra Domain A (EDA) comprising LEU46, PHE47, PRO48, GLU58, LEU59 and GLN60 in its C-C loop. Irigenin binds to the C-C loop of EDA, thereby blocking its interaction with integrins on the cell surface and thus abrogating subsequent Epithelial-Mesenchymal transition[1].

Name: Lupenone, CAS: 1617-70-5, stock 5.1g, assay 98.2%, MWt: 424.70, Formula: C30H48O, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Lupenone, isolated from Rhizoma Musae, belongs to lupane type triterpenoids. Lupenone shows various pharmacological activities including anti-inflammatory, anti-virus, anti-diabetes, anti-cancer, improving Chagas disease without major toxicity[1][2].

Name: Isocorydine, CAS: 475-67-2, stock 18.7g, assay 99%, MWt: 341.40, Formula: C20H23NO4, Solubility: 10 mM in DMSO, Clinical_Informat: Launched, Pathway: Others, Target: Others, Biological_Activity: Isocorydine is isolated from Dicranostigma leptopodum (Maxim.) Fedde (DLF). Isocorydine combines with Doxorubicin (DOX) has a promising potential to eradicate hepatocellular carcinoma (HCC)[1].
In Vitro: Isocorydine (0-400 ug/ml; 48 hours) show a significant decrease in the IC50 for ICD and DOX, the CI values are 0.605, 0.644, 0.804, and 0.707 respectively for Huh-7, Hep-G2, SNU-449 and SNU-387[1].
Isocorydine (0-400 ug/ml; 48 hours) abrogates DOX-induced upregulation of mesenchymal markers and the downregulation of epithelial markers in human HCC cell lines[1].
In Vivo: Isocorydine (intraperitoneal injection; 0.4 mg/kg; every 2 days for 2 weeks) retards the tumor growth, but the combined treatment of Doxorubicin (DOX) or ICD significantly inhibits tumor growth[1].

Name: Isorhapontigenin, CAS: 32507-66-7, stock 30.3g, assay 98.2%, MWt: 258.27, Formula: C15H14O4, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Autophagy, Target: Autophagy, Biological_Activity: Isorhapontigenin, an orally bioavailable dietary polyphenol isolated from the Chinese herb Gnetum cleistostachyum, displays anti-inflammatory effects. Isorhapontigenin induces autophagy and inhibits invasive bladder cancer formation[1][2].

Name: NS13001, CAS: 1063331-94-1, stock 12.7g, assay 98.3%, MWt: 353.81, Formula: C17H16ClN7, Solubility: DMSO : 100 mg/mL (282.64 mM; Need ultrasonic); H2O : < 0.1 mg/mL (insoluble), Clinical_Informat: No Development Reported, Pathway: Membrane Transporter/Ion Channel, Target: Potassium Channel, Biological_Activity: NS13001 is a potent, selective, orally active allosteric positive modulator of SK channels (small conductance calcium-activated potassium channels). The EC50s are 1.8 and 0.14 μM for SK2 and SK3, respectively. NS13001 holds promise as a potential therapeutic agent for treatment of spinocerebellar ataxia type 2 (SCA2) and possibly other cerebellar ataxias[1].
IC50 & Target: EC50: 1.8 μM (SK2), 0.14 μM (SK3)[1]

Name: SAFit1, CAS: 1643125-32-9, stock 20.2g, assay 98.6%, MWt: 747.87, Formula: C42H53NO11, Solubility: DMSO : 62.5 mg/mL (83.57 mM; Need ultrasonic); Methanol : 125 mg/mL (167.14 mM; Need ultrasonic); H2O : < 0.1 mg/mL (insoluble), Clinical_Informat: No Development Reported, Pathway: Immunology/Inflammation;Apoptosis;Autophagy, Target: FKBP;FKBP;FKBP, Biological_Activity: SAFit1 is a FK506 binding protein 51 (FKBP51)-specific inhibitor with a Ki of 4±0.3 nM[1][2].
IC50 & Target: Ki: 4±0.3 nM (FKBP51), >50000 nM (FKBP52)[1]
In Vitro: SAFit1 (1-1000 nM) potently stimulates neurite outgrowth in two neuronal cell lines (N2a and SH-SY5Y) as well as in primary hippocampal neurons. SAFit1 is active over a wide concentration range[1].

Name: SAFit2, CAS: 1643125-33-0, stock 26.7g, assay 98.1%, MWt: 802.99, Formula: C46H62N2O10, Solubility: DMSO : 125 mg/mL (155.67 mM; Need ultrasonic); H2O : < 0.1 mg/mL (insoluble), Clinical_Informat: No Development Reported, Pathway: Immunology/Inflammation;Apoptosis;Autophagy, Target: FKBP;FKBP;FKBP, Biological_Activity: SAFit2 is a highly potent, highly selective FK506-binding protein 51 (FKBP51) inhibitor with a Ki of 6 nM and also enhances AKT2-AS160 binding.
IC50 & Target: Ki: 6 nM (FKBP51)[1]
In Vitro: SAFit2 treatment increases the expression of pAKT2 (soleus and EDL muscle) and pAS160 (EDL muscle) in WT cells, but there is no effect of FKBP51 antagonism in 51KO cells. Moreover, following SAFit2 treatment, GLUT4 expression increases in the membrane fraction of primary EDL myotubes from WT mice, but not from 51KO mice[2].
In Vivo: It is found that 30 days of SAFit2 administration leads to a reduction in body weight under both control and high-fat diet (HFD) conditions. SAFit2 significantly increases phosphorylated AKT2 and AS160 in EDL muscle and likewise increases expression of GLUT4 at the membrane in soleus muscle[2]. When SAFit2 is applied 1 h before testing, no alterations in anxiety-related behavior are observed. However, SAFit2 treatment induces an anxiolytic phenotype in mice injected 16 h prior testing, which is reflected in a significantly increased open arm time in the elevated plus maze (EPM) (z=-2.183, p<0.05). SAFit2 treatment leads to a significantly reduced latency to enter the lit compartment (z=-2 to 265, p<0.05), as well as a significantly increased distance traveled (t(20)=-2.371, p<0.05) in the lit compartment[3].

Name: Bruceine D, CAS: 21499-66-1, stock 30.1g, assay 98.5%, MWt: 410.42, Formula: C20H26O9, Solubility: DMSO : 100 mg/mL (243.65 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Apoptosis;Stem Cell/Wnt;Neuronal Signaling, Target: Apoptosis;Notch;Notch, Biological_Activity: Bruceine D is a Notch inhibitor with anti-cancer activity and induces apoptosis in several human cancer cells. Bruceine D is an effective botanical insect antifeedant with outstanding systemic properties, causing potent pest growth inhibitory activity[1][2].
IC50 & Target: Notch[1]
In Vitro: Bruceine D inhibits the cell viability of H460 and A549 cells in a dose-dependent manner with IC50 values of 0.5 and 0.6 μM, respectively, at 48 h of treatment[1]. 
Bruceine D (0.125-1.0 μM) dose-dependently promotes chromatin condensation, Annexin V-positive cell population and caspase-dependent apoptosis in H460 and A549 cells[1].

Name: Artemitin, CAS: 479-90-3, stock 10.9g, assay 98%, MWt: 388.37, Formula: C20H20O8, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Artemitin is a flavonol found in Laggera pterodonta (DC.) Benth., with antioxidative, anti-inflammatory, and antiviral activity[1].

Name: Isomaltose 6-O-α-D-Glucopyranosyl-D-glucose; D-Isomaltose, CAS: 499-40-1, stock 24.4g, assay 98.2%, MWt: 342.30, Formula: C12H22O11, Solubility: H2O : 150 mg/mL (438.21 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: Isomaltose is composed of two glucose units and suitable as a non-cariogenic sucrose replacement and is favorable in products for diabetics and prediabetic dispositions.

Name: AZD-5438, CAS: 602306-29-6, stock 26.1g, assay 98.9%, MWt: 371.46, Formula: C18H21N5O2S, Solubility: DMSO : 100 mg/mL (269.21 mM; Need ultrasonic), Clinical_Informat: Phase 1, Pathway: Cell Cycle/DNA Damage, Target: CDK, Biological_Activity: AZD-5438 is a potent inhibitor of CDK1/2/9 with IC50 of 16 nM/6 nM/20 nM in cell-free assays. It also inhibits GSK3β, but is less potent to CDK5/6.
IC50 & Target: IC50: 16 nM (CDK1), 6 nM (CDK2), 20 nM (CDK9)
[1]
In Vitro: AZD5438 potently inhibits the kinase activity of cyclin E-cdk2, cyclin A-cdk2, cyclin B1-cdk1, p25-cdk5, cyclin D3-cdk6, and cyclin T-cdk9 (IC50, 6, 45, 16, 21, and 20 nM, respectively). AZD5438 potently inhibits the kinase activity of cyclin E-cdk2, cyclin A-cdk2, cyclin B1-cdk1, p25-cdk5, cyclin D3-cdk6, and cyclin T-cdk9 (IC50, 6, 45, 16, 21, and 20 nM, respectively). In common with many other cdk inhibitors, AZD5438 also inhibits the kinase activity of p25-cdk5 and glycogen synthase kinase 3β in vitro (IC50, 14 and 17 nM, respectively)[1]. AZD5438 significantly augments cellular radiosensitivity in NSCLC cells. Combined treatment with AZD5438 and irradiation also enhances tumor growth delay, with an enhancement factor ranging from 1.2-1.7[2].
In Vivo: AZD5438 (50 mg/kg twice daily or 75 mg/kg, p.o.) inhibits human tumor xenograft growth. In vivo, AZD5438 reduces the proportion of actively cycling cells. Further pharmacodynamic analysis of AZD5438-treated SW620 xenografts shows that efficacious doses of AZD5438 (>40% tumor growth inhibition) maintains suppression of biomarkers, such as phospho-pRbSer249/Thr252, for up to 16 hours following a single oral dose[1].

Name: Kuwanon H, CAS: 76472-87-2, stock 39.7g, assay 98.2%, MWt: 760.82, Formula: C45H44O11, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein, Target: Bombesin Receptor, Biological_Activity: Kuwanon H is a flavonoid isolated from Morus bombycis, which acts as a potent non-peptide bombesin receptor antagonist. Kuwanon H selectively inhibits binding of gastrin releasing peptide CRP to GRP-preferring recepotr, with a Ki value of 290 nM in cells[1].
IC50 & Target: Ki: 290 nM (GRP-preferring recepotr)[1]

Name: Bayogenin 3-O-β-D-glucopyranoside, CAS: 104513-86-2, stock 21.6g, assay 98.1%, MWt: 650.84, Formula: C36H58O10, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Bayogenin 3-O-β-D-glucopyranoside, a triterpenoid saponin isolated from Polygala japonica, possesses anti-inflammatory activities[1].

Name: D-chiro-Inositol, CAS: 643-12-9, stock 5.3g, assay 98.4%, MWt: 180.16, Formula: C6H12O6, Solubility: 10 mM in DMSO; H2O : 75 mg/mL (416.30 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: D-chiro-Inositol is an epimer of myo-inositol found in certain mammalian glycosylphosphatidylinositol protein anchors and inositol phosphoglycans possessing insulin-like bioactivity. D-chiro-Inositol is used clinically for the treatment of polycystic ovary syndrome (PCOS) and diabetes mellitus, which can reduce hyperglycemia and ameliorate insulin resistance[1][2][3].

Name: Camelliaside B, CAS: 131573-90-5, stock 3.9g, assay 98.8%, MWt: 726.63, Formula: C32H38O19, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Camelliaside B is a flavonoid from the methanol extract of tea (Camellia oleifera) seed pomace[1].

Name: Deacylmetaplexigenin, CAS: 3513-04-0, stock 31.6g, assay 98.2%, MWt: 380.48, Formula: C21H32O6, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Deacylmetaplexigenin is a pregnane glycoside isolated from Asclepias incarnate[1].

Name: 3-O-Acetyloleanolic acid, CAS: 4339-72-4, stock 12.7g, assay 98.4%, MWt: 498.74, Formula: C32H50O4, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Apoptosis, Target: Apoptosis, Biological_Activity: 3-O-Acetyloleanolic acid (3AOA), an oleanolic acid derivative isolated from the seeds of Vigna sinensis K., induces in cancer and also exhibits anti-angiogenesis activity[1].
IC50 & Target: Apoptosis[1].

Name: Evodol, CAS: 22318-10-1, stock 39.9g, assay 98.4%, MWt: 484.50, Formula: C26H28O9, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Evodol is a natural product isolated from the dried and nearly ripe fruits of Euodia rutaecarpa. Evodol shows inhibitory activity against NO production[1]. Evodol possesses larvicidal activity against the Asian tiger mosquitoes with a LC50 value of 32.43 μg/ml[2].

Name: Soyasaponin Ab, CAS: 118194-13-1, stock 13g, assay 98.1%, MWt: 1437.52, Formula: C67H104O33, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Soyasaponin Ab is a soyasaponin that exerts an anti-obesity effect in 3T3-L1 adipocytes through downregulation of peroxisome proliferator-activated receptor γ (PPARγ)[1].

Name: Alloimperatorin Prangenidin, CAS: 642-05-7, stock 30g, assay 98.9%, MWt: 270.28, Formula: C16H14O4, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Alloimperatorin (Prangenidin), a coumarin compound, is extracted from Angelica dahurica. Alloimperatorin (Prangenidin) has antitumor activity[1][2].

Name: Soyasaponin Aa, CAS: 117230-33-8, stock 37.7g, assay 98.1%, MWt: 1365.46, Formula: C64H100O31, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Soyasaponin Aa is a soyasaponin that exerts an anti-obesity effect in 3T3-L1 adipocytes through downregulation of peroxisome proliferator-activated receptor γ (PPARγ)[1].

Name: Epimedoside A, CAS: 39012-04-9, stock 33.9g, assay 98.7%, MWt: 662.64, Formula: C32H38O15, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Epimedoside A is a flavonoid isolated from the roots of Epimedium wushanense. Epimedoside A exhibits significant antioxidant activity in vitro[1].

Name: Taccalonolide B, CAS: 108885-69-4, stock 38.8g, assay 98.4%, MWt: 660.71, Formula: C34H44O13, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Cell Cycle/DNA Damage;Cytoskeleton, Target: Microtubule/Tubulin;Microtubule/Tubulin, Biological_Activity: Taccalonolide B is microtubule stabilizer isolated from Tacca plantaginea, with antitumor activity. Taccalonolide B is effective in vitro against cell lines that overexpress P-glycoprotein (Pgp) and multidrug-resistance protein (MRP7). Taccalonolide B inhibits growth of SK-OV-3 cells with an IC50 of 208 nM[1][2].
IC50 & Target: microtubule[2]

Name: Erigeroside, CAS: 59219-76-0, stock 19g, assay 98.9%, MWt: 274.22, Formula: C11H14O8, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Erigeroside is as a derivatives of -glucose extracted from Satureja khuzistanica Jamzad. Erigeroside has good ability of anti-oxidation and scavenging oxidation free radical[1].

Name: Noreugenin, CAS: 1013-69-0, stock 15.2g, assay 98.1%, MWt: 192.17, Formula: C10H8O4, Solubility: H2O : < 0.1 mg/mL (insoluble); DMSO : 250 mg/mL (1300.93 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Noreugenin, 5,7-dihydroxy-2-methyl-4H-chromen-4-one, is a new chromone from Hymenocallis littoralis Salisb. (Amaryllidaceae)[1].

Name: Uvarigrin, CAS: 200563-11-7, stock 10.6g, assay 99%, MWt: 608.93, Formula: C37H68O6, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Apoptosis, Target: Apoptosis, Biological_Activity: Uvarigrin, isolated from the roots of Uvaria calamistrata, induces tumor multidrug resistance cell apoptosis and triggers Caspase-9 activation[1][2].

Name: Grosvenorine, CAS: 156980-60-8, stock 19.5g, assay 98.7%, MWt: 740.66, Formula: C33H40O19, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Anti-infection, Target: Bacterial, Biological_Activity: Grosvenorine is the major flavonoid compound of the fruits of Siraitia grosvenorii. Grosvenorine exhibits good antibacterial and antioxidant activities[1].

Name: Uvarigranol B, CAS: 164204-79-9, stock 4.4g, assay 98.5%, MWt: 426.42, Formula: C23H22O8, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Uvarigranol B, a polyoxygenated cyclohexene, is obtained from the roots of Uvaria grandiflora Roxb (Annonaceae)[1].

Name: Uvarigranol C, CAS: 172104-04-0, stock 17.1g, assay 99%, MWt: 412.43, Formula: C23H24O7, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Uvarigranol C, a polyoxygenated cyclohexene, is isolated from the stems of Uvaria boniana Finet. (Annonaceae)[1].

Name: Ilexsaponin A, CAS: 108524-93-2, stock 31.6g, assay 98.5%, MWt: 664.82, Formula: C36H56O11, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Apoptosis, Target: Apoptosis, Biological_Activity: Ilexsaponin A, isolated from the root of Ilex pubescens, attenuates ischemia-reperfusion-induced myocardial injury through anti-apoptotic pathway. Ilexsaponin A can reduce myocardial infarct size, lower the serum levels of LDH, AST and CK-MB, increase cellular viability and inhibit apoptosis in hypoxia/reoxygenation cardiomyocytes[1].
In Vitro: Ilexsaponin A significantly reduces proapoptotic proteins including caspase-3, cleaved caspase-3 and bax and increases anti-apoptotic protein bcl-2 in hypoxia/reoxygenation cardiomyocytes. Ilexsaponin A treatment increases the expression levels of p-Akt in hypoxia/reoxygenation cellular model and myocardial ischemia/reperfusion animal model[1].
In Vivo: Ilexsaponin A (10 or 40 mg/kg) reduce the myocardial infarct size in a dose dependent manner in male Sprague-Dawley rats weighing 280-320 g[1].

Name: N-Benzyllinolenamide, CAS: 883715-18-2, stock 4.5g, assay 98.3%, MWt: 367.57, Formula: C25H37NO, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Neuronal Signaling;Metabolic Enzyme/Protease;Autophagy, Target: FAAH;FAAH;Autophagy, Biological_Activity: N-Benzyllinolenamide is a natural macamide isolated from Lepidium meyenii, acts as an inhibitor of fatty acid amide hydrolase (FAAH) with an IC50 of 41.8 μM[1].
IC50 & Target: IC50: 41.8 μM (FAAH)[1]

Name: Piperlotine C, CAS: 886989-88-4, stock 4.5g, assay 98.3%, MWt: 291.34, Formula: C16H21NO4, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Piperlotine C is an alkaloid isolated from Piper lolot, with anti-platelet aggregation induced by arachidonic acid, and the IC50 is 26.6 µg/mL[1].

Name: Piperlotine A, CAS: 389572-70-7, stock 38.5g, assay 98.8%, MWt: 231.29, Formula: C14H17NO2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Piperlotine A is an alkaloid isolated from Piper lolot, with potent antiplatelet aggregation activity[1].

Name: Gusacitinib ASN-002, CAS: 1425381-60-7, stock 17.1g, assay 98.8%, MWt: 460.53, Formula: C24H28N8O2, Solubility: DMSO : 100 mg/mL (217.14 mM; Need ultrasonic), Clinical_Informat: Phase 2, Pathway: Epigenetics;Stem Cell/Wnt;JAK/STAT Signaling;Protein Tyrosine Kinase/RTK, Target: JAK;JAK;JAK;Syk, Biological_Activity: Gusacitinib (ASN-002) is a potent dual inhibitor of spleen tyrosine kinase (SYK) and janus kinase (JAK) with IC50 values of 5-46 nM.
IC50 & Target: IC50: 5-46 nM (SYK, JAK)[1].
In Vitro: In mechanistic cell-based studies involving IgE and cytokine stimulations, Gusacitinib (ASN-002) strongly suppresses the SYK and JAK family kinase signaling pathways measured as pLAT and pSTAT levels, respectively. Gusacitinib (ASN-002) shows anti-proliferative activity in a broad panel of human cancer cell lines including DHL6, DHL4, OCI-LY10, H929, Pfeiffer, HT-1376, and Lovo, suggesting activity in both solid and hematological tumor types[1].
In Vivo: In a multiple myeloma (H929) xenograft model, Gusacitinib (ASN-002) exhibits significant efficacy in inhibiting tumor growth (>95%). It also significantly delays the onset of hind limb paralysis in the human erythroleukemia (HEL) mouse model. Gusacitinib (ASN-002) has good oral bioavailability, metabolic stability, is not a Pgp substrate, and shows little to no inhibition of CYP450 isozymes. Gusacitinib (ASN-002) shows a favorable safety profile in rat and dog toxicology studies[1].

Name: Pinostilbene, CAS: 42438-89-1, stock 27g, assay 98.1%, MWt: 242.27, Formula: C15H14O3, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Pinostilbene is a major metabolite of Pterostilbene. Pinostilbene exhibits inhibitory effects on colon cancer cells[1].
In Vitro: Pinostilbene (0- 40 μM; 24 hours, 48 hours) does not cause significant inhibition on the growth of normal colon cells[1]. 
Pinostilbene (20 μM, 40 μM; 24 hours, 48 hours) causes a significant and dose-dependent increase in the percentage of cells in S phase in both HCT116 and HT29 cells compared to the control cells[1]. 
Pinostilbene at μM also induces a modest increase of cell population in G2/M phase in HT29 cells[1]. 
Pinostilbene(20 μM, 40 μM; 24 hours, 48 hours) modulates expression of key signaling proteins related to cell proliferation and apoptosis[1]. 
Pinostilbene also acts as a resveratrol methylated derivative and displays protective effects against 6-hydroxydopamine-induced neurotoxicity in SH-SY5Y cells[2].

Name: (+)-BAY-1251152, CAS: 1610358-56-9, stock 7.1g, assay 98.6%, MWt: 404.43, Formula: C19H18F2N4O2S, Solubility: DMSO : 113.3 mg/mL (280.15 mM; Need ultrasonic and warming), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: (-)-BAY-1251152 is an enanthiomer of BAY-1251152 with rotation (+). BAY-1251152 is a potent and highly selective PTEF/CDK9 inhibitor.

Name: BAY-1816032, CAS: 1891087-61-8, stock 18.8g, assay 98.7%, MWt: 534.51, Formula: C27H24F2N6O4, Solubility: H2O : < 0.1 mg/mL (insoluble); DMSO : 25 mg/mL (46.77 mM; Need ultrasonic and warming), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: BAY-1816032 is a potent and oral available BUB1 (budding uninhibited by benzimidazoles 1) kinase inhibitor with an IC50 of 7 nM.
IC50 & Target: IC50: 7 nM (BUB1)[1]
In Vitro: BAY-1816032 inhibits BUB1 enzymatic activity with an IC50 of 7 nM, shows slow dissociation kinetics resulting in a long target residence time of 87 min, and an excellent selectivity on a panel of 395 kinases. Mechanistically BAY-1816032 abrogates nocodazole-induced Thr-120 phosphorylation of the major BUB1 target protein histone H2A in HeLa cells with an IC50 of 29 nM, induced lagging chromosomes and mitotic delay. Persistent lagging chromosomes and missegregation are observed upon combination with low concentrations of paclitaxel. Single agent BAY-1816032 inhibits proliferation of various tumor cell lines with a median IC50 of 1.4 μM and demonstrates synergy or additivity with paclitaxel or docetaxel in almost all cell lines evaluated (minimal combination index 0.3)[1].
In Vivo: In tumor xenograft studies BAY 1816032 only marginally inhibits tumor growth as single agent upon oral administration, however, upon combination with paclitaxel or docetaxel a strong and statistically significant reduction of tumor size as compared to the respective monotherapy is observed[1].

Name: LY3200882, CAS: 1898283-02-7, stock 23.5g, assay 98.4%, MWt: 435.52, Formula: C24H29N5O3, Solubility: DMSO : 130 mg/mL (298.49 mM; Need ultrasonic and warming), Clinical_Informat: Phase 1, Pathway: TGF-beta/Smad, Target: TGF-β Receptor, Biological_Activity: LY3200882 is a novel and highly selective inhibitor of TGF-β receptor type 1 (TGFβRI).
IC50 & Target: TGFβRI[1]
In Vitro: LY3200882 is a novel, highly selective inhibitor of TGF-β receptor type 1 (TGFβRI). LY3200882 potently inhibits TGFβ mediated SMAD phosphorylation in vitro in tumor and immune cells. LY3200882 has shown anti-metastatic activity in vitro in migration assays. In in vitro immune suppression assays, LY3200882 has shown the ability to rescue TGFβ1 suppressed or T regulatory cell suppressed naïve T cell activity and restore proliferation[1].
In Vivo: LY3200882 potently inhibits TGFβ mediated SMAD phosphorylation in vivo in subcutaneous tumors in a dose dependent fashion. LY3200882 has shown anti-metastatic activity in vivo in an experimental metastasis tumor model (intravenous EMT6-LM2 model of triple negative breast cancer)[1].

Name: 7-O-Geranylscopoletin 7-Geranyloxy-6-methoxycoumarin, CAS: 28587-43-1, stock 32.3g, assay 98.2%, MWt: 328.40, Formula: C20H24O4, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: 7-O-Geranylscopoletin is a coumarin from the root of Atalantia monophylla. Various parts of this plant have been used for folk medicine for several purposes such as the treatment of chronic rheumatism, paralysis, antispasmodic, stimulant and hemiplegia[1].

Name: Palbinone, CAS: 139954-00-0, stock 19.8g, assay 98.9%, MWt: 358.47, Formula: C22H30O4, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Palbinone is a terpenoid isolated from the roots of Paeonia albiflora Pallas, potently inhibits 3α-hydroxysteroid dehydrogenase (3α-HSD), with an IC50 of 46 nM. Anti-inflammatory activity[1].
IC50 & Target: IC50: 46 nM (3α-HSD)[1]

Name: 8-Prenylnaringenin, CAS: 53846-50-7, stock 37.5g, assay 98.7%, MWt: 340.37, Formula: C20H20O5, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Apoptosis, Target: Apoptosis, Biological_Activity: 8-prenylnaringenin is a prenylflavonoid isolated from hop cones (Humulus lupulus), with cytotoxicity. 8-prenylnaringenin has anti-proliferative activity against HCT-116 colon cancer cells via induction of intrinsic and extrinsic pathway-mediated apoptosis. 8-Prenylnaringenin also promotes recovery from immobilization-induced disuse muscle atrophy through activation of the Akt phosphorylation pathway in mice[1] [2] [3].

Name: Osajin CID 95168; NSC 21565, CAS: 482-53-1, stock 15.9g, assay 98.9%, MWt: 404.46, Formula: C25H24O5, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Apoptosis, Target: Apoptosis, Biological_Activity: Osajin is the major bioactive isoﬂavone present in the fruit of Maclura pomifera with antitumor, antioxidant and anti-inflammatory activities.
IC50 & Target: Apoptosis[1]
In Vitro: Osajin significantly decreases the viability of human NPC cells (TW076, CG1 and TW04 cells) in a dose-dependent manner. Osajin induces apoptosis in human NPC cells through multiple apoptotic pathways, including the extrinsic death receptor pathway, and intrinsic pathways relying on mitochondria and endoplasmic reticulum stress[1]. Osajin exhibits growth inhibitory activity on six human cancer cell lines, including kidney, lung, prostate, breast, melanoma and colon cancer cells[2].
In Vivo: Osajin and pomiferin attenuates the myocardial dysfunction provoked by ischemia reperfusion. This is confirmed by an increase in both antioxidant enzyme values and total antioxidant activity. The cardioprotection provided by osajin and pomiferin treatment results from the suppression of oxidative stress and this correlates with improved ventricular function[3].

Name: GSK962, CAS: 2049872-86-6, stock 13.8g, assay 98.2%, MWt: 230.31, Formula: C14H18N2O, Solubility: DMSO : 75 mg/mL (325.65 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: GSK962 is an inactive enantiomer of GSK963 and can be used to confirm on-target effects[1].

Name: Digitonin, CAS: 11024-24-1, stock 28.3g, assay 98.2%, MWt: 1229.31, Formula: C56H92O29, Solubility: H2O : 50 mg/mL (40.67 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Digitonin, a glycoside obtained from Digitalis purpurea, could increase cell permeability by binding to cholesterol molecules and reduce tumor growth.
In Vitro: Digitonin, a detergent that increases cell permeability by binding to cholesterol molecules in the cell membrane, can increase cisplatin accumulation and reduce tumour growth in vitro[1].
In Vivo: In the liver parenchyma the concentrations are of the same magnitude. Measured with the 133Xe-clearance technique, Digitonin does not alter the tumor blood flow. Digitonin enhances the tumor-growth retarding effect of CBDCA given intra-aterially at 5 mg/kg but not at 25 mg/kg[1].

Name: Ursolic acid acetate Acetylursolic acid; 3-Acetylursolic acid, CAS: 7372-30-7, stock 8.7g, assay 98.7%, MWt: 498.74, Formula: C32H50O4, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Ursolic acid acetate (Acetylursolic acid), isolated from the aerial roots of Ficus microcarpa, exhibits cytotoxicity against KB cells with IC50 of 8.4 μM[1].

Name: ML327, CAS: 1883510-31-3, stock 39.6g, assay 98.7%, MWt: 366.37, Formula: C19H18N4O4, Solubility: DMSO : 32 mg/mL (87.34 mM; Need ultrasonic and warming), Clinical_Informat: No Development Reported, Pathway: Apoptosis;Autophagy, Target: c-Myc;Autophagy, Biological_Activity: ML327 is a blocker of MYC which can also de-repress E-cadherin transcription and reverse Epithelial-to-Mesenchymal Transition (EMT).
IC50 & Target: MYC[1]
In Vitro: Treatment with ML327 induces an elongated morphology in neuroblastoma cells. BE(2)-C cells treated with ML327 demonstrates G1 cell cycle arrest with a concordant decrease in S phase population, and a significant increase in the sub G0 population. ML327 induces the expression of CDH1 in all seven of the neuroblastoma cell lines with a 50 to 1,400-fold induction of CDH1 mRNA expression. ML327 blocks the expression of MYC family of oncogenic transcription factors in all tested neuroblastoma cell lines. Immunoblotting time course demonstrates early repression of N-MYC expression within 2 h of treatment with ML327 (10 µM). p53 levels are also suppressed by treatment with ML327. ML327-pretreated cells demonstrates reduced proliferative potential in both tetrazolium-based (p<0.0001) and adherent 2D colony formation (41 vs. 400; p<0.0001)[1]. ML327 reduces SW620inv cell invasion through Matrigel by ~60% and reduces H520 cell invasion by ~30% in these in vitro assays. ML327 partially restores E-cadherin expression at the plasma membrane in NMuMG cells induced to undergo Epithelial-to-Mesenchymal Transition (EMT) by TGF-β1 treatment[2].
In Vivo: ML327 treatment significantly reduces tumor volume by three-fold over the two-week treatment period (p=0.02). Tumor explant weights are approximately three-fold smaller in the ML327-treated mice (p=0.01). Mice treated with ML327 lost 12% more body weight than vehicle treated mice. ML327 treatment results in a two-fold decrease in MYCN expression, confirming that ML327 inhibits xenograft MYCN expression (p=0.0035)[1].

Name: Obtucarbamate A, CAS: 6935-99-5, stock 0.7g, assay 98.6%, MWt: 238.24, Formula: C11H14N2O4, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Obtucarbamate A isolated from Disporum cantoniense has antitussive activity[1].

Name: Andropanoside, CAS: 82209-72-1, stock 27.9g, assay 98.5%, MWt: 496.59, Formula: C26H40O9, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Andropanoside is a natural product isolated and purified from the herbs of Andrographis paniculata. Andrographis paniculata possesses a protective activity against various liver disorders[1].

Name: Dihydrokaempferol, CAS: 480-20-6, stock 0.4g, assay 98.4%, MWt: 288.25, Formula: C15H12O6, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Apoptosis;Apoptosis, Target: Apoptosis;Bcl-2 Family, Biological_Activity: Dihydrokaempferol is isolated from Bauhinia championii (Benth). Dihydrokaempferol induces apoptosis and inhibits Bcl-2 and Bcl-xL expression. Dihydrokaempferol is a good candidate for new antiarthritic drugs[1].
IC50 & Target: Apoptosis; Bcl-2; Bcl-xL[1]
In Vitro: Dihydrokaempferol (0.3-300 μM; 48 hours) has no significant effect on normal synoviocytes, but dependently decreases the viability of RA-FLSs[1].
Dihydrokaempferol (3-30 μM; 48 hours) increases the percentage of apoptotic cells (including early and late apoptotic cells; ~3.8% and ~9.6%, respectively)[1].
Dihydrokaempferol (3-30 μM; 48 hours) promotes Bax and Bad expression and inhibits Bcl-2 and Bcl-xL expression, increases the cleaved fragments of caspase-3, caspase-9 and cleaved PARP[1].

Name: TLR7 agonist 2, CAS: 1642857-69-9, stock 29.6g, assay 98.9%, MWt: 336.35, Formula: C17H16N6O2, Solubility: DMSO : 160 mg/mL (475.69 mM; Need ultrasonic and warming), Clinical_Informat: No Development Reported, Pathway: Immunology/Inflammation, Target: Toll-like Receptor (TLR), Biological_Activity: TLR7 agonist 2 is a potent and selective Toll-like Receptor 7 (TLR7) agonist with a LEC of 0.4 μM.
IC50 & Target: LEC: 0.4 μM (TLR7)[1]
In Vitro: TLR7 agonist 2 is a potent and selective Toll-like Receptor 7 (TLR7) agonist with a lowest effective concentration (LEC) of 0.4 μM in HEK293 cell. TLR7 agonist 2 is found to be selective for TLR7 over TLR8 with LEC of >100 μM for human TLR8. TLR7 agonist 2 demonstrates low inhibition across five CYP450 isozymes (IC50 >10 μM) and is also not a time dependent inhibitor of CYP450 3A4. TLR7 agonist 2 has limited inhibition of the hERG potassium ion channel 3H-dofetilide binding in vitro (IC50 >50 μM)[1].
In Vivo: TLR7 agonist 2 is found to be rapidly cleared in conjunction with our target profile. Both Cmax and AUC increase less than dose proportionally between 0.3 and 3 mg/kg and more than dose-proportionally between 3 and 10 mg/kg. TLR7 agonist 2 can induce an antiviral interferon stimulated gene (ISG) response without inducing an IFNα response at a low dose. TLR7 agonist 2 also induces a 2.7 log decrease in serum HBV viral load from 0.3 mg/kg, and a maximum 3.1 log decrease is observed for doses between 1 and 5 mg/kg[1].

Name: Zuranolone, CAS: 1632051-40-1, stock 28.6g, assay 98.5%, MWt: 409.56, Formula: C25H35N3O2, Solubility: DMSO : ≥ 100 mg/mL (244.16 mM), Clinical_Informat: Phase 3, Pathway: Neuronal Signaling;Membrane Transporter/Ion Channel, Target: GABA Receptor;GABA Receptor, Biological_Activity: Zuranolone is a potent GABAA receptor agonist with EC50s of 296 and 163 nM for α1β2γ2 and α4β3δ GABAA receptors, respectively.
IC50 & Target: EC50: 296 nM (α1β2γ2 GABAA receptor), 163 nM (α4β3δ GABAA receptor)[1]
In Vitro: Zuranolone is a potent GABAA receptor agonist with EC50s of 296 and 163 nM for α1β2γ2 and α4β3δ GABAA receptors, respectively. Zuranolone is currently being studied in parallel phase 2 clinical trials for the treatment of postpartum depression (PPD) and major depressive disorder (MDD). Zuranolone shows >30 μM inhibition in a cardiac panel of eight relevant cardiac ion channels. At 10 μM concentration of Zuranolone, only binding at the glycine (57%), sigma receptors (88%), and inhibition of the transient receptor potential vanilloid 1 (TRPV1, 95%) is noted[1].
In Vivo: Acute administration of Zuranolone (0.3 to 10 mg/kg, ip) effectively reduces pentylenetretazol (PTZ)-induced seizures in mice (MECplasma=85 nM) as well as produces a dose-dependent anticonvulsant effect in the mouse 6 Hz electrical stimulation model. In the rat model of status epilepticus (SE), Zuranolone (0.3 to 5 mg, iv) abolishes both behavioral and electrographic seizure activity, even when administered 60 min after induction of SE. Additional PK studies of Zuranolone in dog show low clearance (<10% of hepatic blood flow), resulting in excellent oral bioavailability (F=68%)[1].

Name: Neotuberostemonine, CAS: 143120-46-1, stock 0.3g, assay 98.9%, MWt: 375.50, Formula: C22H33NO4, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Neotuberostemonine, one of the main antitussive alkaloids in the root of Stemona tuberosa Lour, attenuates bleomycin-induced pulmonary fibrosis by suppressing the recruitment and activation of macrophages[1].

Name: Brevilin A, CAS: 16503-32-5, stock 4.9g, assay 98.5%, MWt: 346.42, Formula: C20H26O5, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Apoptosis;Epigenetics;Stem Cell/Wnt;JAK/STAT Signaling;Autophagy;JAK/STAT Signaling;Stem Cell/Wnt, Target: Apoptosis;JAK;JAK;JAK;Autophagy;STAT;STAT, Biological_Activity: Brevilin A is a sesquiterpene lactone isolated from Centipeda minima with anti-tumor activity. Brevilin A is a selective inhibitor of JAK-STAT signal pathway by attenuating the JAKs activity and blocking STAT3 signaling (IC50 = 10.6 µM) in Cancer Cells. Brevilin A induces apoptosis and autophagy via mitochondrial pathway and PI3K/AKT/mTOR inactivation in colon adenocarcinoma cell CT26[1][2].
IC50 & Target: IC50: 10.6 µM (STAT3 signaling)[1]

Name: Naringenin trimethyl ether, CAS: 38302-15-7, stock 37.9g, assay 98.7%, MWt: 314.33, Formula: C18H18O5, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Naringenin trimethyl ether is a constituent of twigs and leaves of Aglaia duperreana. Naringenin trimethyl exhibits significant molluscicidal activity, with a LC50 of 3.9 μg/ mL for P. canaliculata[1].
IC50 & Target: LC50: 3.9 μg/ mL (P. canaliculata)[1]

Name: Naringenin triacetate, CAS: 3682-04-0, stock 9.7g, assay 98.3%, MWt: 398.36, Formula: C21H18O8, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Naringenin triacetate is a flavonoid isolated from plant, exhibits a good binding affinity with multiple crystal structures of first bromodomain BRD4 (BRD4 BD1)[1].

Name: Nagilactone B, CAS: 19891-51-1, stock 5.9g, assay 98.6%, MWt: 364.39, Formula: C19H24O7, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: LXR, Biological_Activity: Nagilactone B, extracted from the root bark of Podocarpus nagi, is a liver X receptor (LXR) agonist.
IC50 & Target: LXR[1]
In Vitro: RAW264.7 cells are co-incubated with oxLDL (20 μg/mL) and Nagilactone B (0.02, 0.1, and 0.5 μM) for 24 h. Oil Red O (ORO) staining reveals significant lipid accumulation and foam cell formation in RAW264.7 cells following oxLDL treatment. Nagilactone B (NLB) significantly ameliorates intracellular lipid accumulation. ORO positive areas are reduced by 30.05±7.49 (P<0.01), 47.25±5.39 (P<0.001), and 48.65±7.44% (P<0.001) in Nagilactone B (0.02, 0.1, and 0.5 μM)-treated groups, respectively. The effects of Nagilactone B are evaluated ton cholesterol efflux. Nagilactone B (0.02, 0.1, and 0.5 μM) markedly promotes cholesterol efflux to extracellular apolipoprotein A-I (apoA-I) and high density lipoprotein (HDL) with maximal 5.72- (P<0.05) and 2.34-fold (P<0.01), respectively[1].
In Vivo: Nagilactone B (NLB) suppresses atherosclerosis in apoE-/- mice by inducing ATP-binding cassette transporter A1 (ABCA1) and G1 (ABCG1) mediated cholesterol efflux in macrophages. Male apoE-deficient mice on C57BL/6J background receive Nagilactone B (10 and 30 mg/kg) for 12 weeks. Compared with the model group, Nagilactone B treatment (10 and 30 mg/kg) significantly reduces en face lesions of total aorta areas. Six-week-old male apoE-/- mice on an HFD are randomized to receive Atorvastatin (10 mg/kg/day), Nagilactone B (10 and 30 mg/kg/day), or CMC-Na for 12 weeks. Mice on chow diet are administered CMC-Na as the normal diet control group. En face aortic lesion areas are evaluated with Sudan IV staining and lesion areas in the aortic sinus monitored via ORO staining. Atherosclerosis developes slowly in the normal diet group, whereas lesions in the HFD model group are significantly increased in en face aortas. Nagilactone B treatment (10 and 30 mg/kg/day) significantly reduces en face aortic lesions, compared with the HFD group by 54.96±10.06% (P<0.01), 71.50±15.37% (P<0.001) in both NLB (L) and NLB (H) groups. In particular, Nagilactone B markedly attenuates atherosclerotic plaque lesion areas in the aortic arch aorta, thoracic aorta, and abdominal aorta [P<0.01 in NLB (H) group][1].

Name: ACY-957, CAS: 1609389-52-7, stock 35.2g, assay 98.2%, MWt: 429.54, Formula: C24H23N5OS, Solubility: DMSO : 83.33 mg/mL (194.00 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Epigenetics;Cell Cycle/DNA Damage, Target: HDAC;HDAC, Biological_Activity: ACY-957 is an orally active and selective inhibitor of HDAC1 and HDAC2, with IC50s of 7 nM, 18 nM, and 1300 nM against HDAC1/2/3, respectively, and shows no inhibition on HDAC4/5/6/7/8/9.
IC50 & Target: IC50: 7 nM (HDAC1), 18 nM (HDAC2), 1300 nM (HDAC3)[1]
In Vitro: ACY-957 is a selective inhibitor of HDAC1 and HDAC2, with IC50s of 7 nM, 18 nM, and 1300 nM against HDAC1/2/3, respectively, and shows no inhibition on HDAC4/5/6/7/8/9. ACY-957 has an IC50 of 304 nM for HDAC2 in primary hematopoietic progenitors[1].

Name: 16α-Hydroxydehydrotrametenolic acid 3β,16α-Dihydroxylanosta-7,9(11),24-trien-21-oic acid, CAS: 176390-66-2, stock 31.7g, assay 98.5%, MWt: 470.68, Formula: C30H46O4, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: 16α-Hydroxydehydrotrametenolic acid is a triterpene Acid in fermented mycelia of edible fungus Poria cocos[1].

Name: Dehydropachymic acid, CAS: 77012-31-8, stock 17.2g, assay 98.8%, MWt: 526.75, Formula: C33H50O5, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Autophagy, Target: Autophagy, Biological_Activity: Dehydropachymic acid is one of the major triterpenes isolated from Poria cocos. Dehydropachymic acid is more effective in autophagy-lysosome pathway (ALP) impaired cells rather than normal cells[1].

Name: 3-O-Acetyl-16α-hydroxytrametenolic acid, CAS: 168293-13-8, stock 32.4g, assay 98.2%, MWt: 514.74, Formula: C32H50O5, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: 3-O-Acetyl-16α-hydroxytrametenolic acid (Compound 3) is a triterpene found in Poria cocos, with anti-oxidant and anti-cancer activity[1].

Name: Poricoic acid A Poricoic acid A(F), CAS: 137551-38-3, stock 0.5g, assay 98.2%, MWt: 498.69, Formula: C31H46O5, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Poricoic acid A, isolated from Poria cocos, possesses anti-tumor activity[1]. Poricoic acid A enhances melatonin inhibition of AKI-to-CKD transition by regulating Gas6/AxlNFκB/Nrf2 axis[2].

Name: Deacetyl Ganoderic Acid F, CAS: 100665-44-9, stock 15.4g, assay 98.3%, MWt: 528.63, Formula: C30H40O8, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Deacetyl Ganoderic Acid F is a 7-anostane triterpenoid from Ganoderma lucidum.

Name: Ophiopogonin D', CAS: 65604-80-0, stock 3.2g, assay 98.3%, MWt: 855.02, Formula: C44H70O16, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Epigenetics;Cell Cycle/DNA Damage, Target: Sirtuin;Sirtuin, Biological_Activity: Ophiopogonin D', isolated from the tubers of Ophiopogon japonicus, is a rare naturally occurring C29 steroidal glycoside. Ophiopogonin D' shows cytotoxic activity against two human tumor cell lines MG-63 and SNU387 with IC50s of 3.09 μM and 3.63 μM, respectively[1]. Ophiopogonin D' activates SIRT1 in a dose-dependent manner[2].
IC50 & Target: SIRT1[2]

Name: 14-Hydroxy sprengerinin C, CAS: 1111088-89-1, stock 33.2g, assay 98.5%, MWt: 871.02, Formula: C44H70O17, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: 14-Hydroxy sprengerinin C is a steroidal compound found in Ophiopogon japonicus.

Name: Islatravir MK-8591, CAS: 865363-93-5, stock 14.4g, assay 98%, MWt: 293.25, Formula: C12H12FN5O3, Solubility: DMSO : 250 mg/mL (ultrasonic), Clinical_Informat: Phase 2, Pathway: Anti-infection;Anti-infection, Target: Reverse Transcriptase;HIV, Biological_Activity: Islatravir (MK-8591) is a potent anti-HIV-1 agent, acting as a nucleoside reverse transcriptase inhibitor, with EC50s of 0.068 nM, 3.1 nM and 0.15 nM for HIV-1 (WT), HIV-1 (M184V), HIV-1 (MDR), respectively.
IC50 & Target: EC50: 0.068 nM (HIV-1 (WT)), 0.15 nM (HIV-1 (MDR)), 3.1 nM (HIV-1 (M184V))[1]
In Vitro: Islatravir (MK-8591) (4'Ed2FA) is a potent anti-HIV-1 agent, acting as a nucleoside reverse transcriptase inhibitor, with EC50s of 0.068 nM, 3.1 nM and 0.15 nM for HIV-1 (WT), HIV-1 (M184V), HIV-1 (MDR), respectively[1].

Name: Mulberrin Kuwanon C, CAS: 62949-79-5, stock 33.3g, assay 98.6%, MWt: 422.47, Formula: C25H26O6, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Mulberrin is a strong inhibitor of organic anion-transporting polypeptide 2B1 (OATP2B1)-mediated estrone-3-sulfate (E3S) uptake with an IC50 value being 1.8 ±1.5 μM.
In Vitro: Mulberrin is a flavone with two isopentenyl groups at positions 3 and 8. Mulberrin is a strong inhibitor of OATP2B1 with more than 80% inhibition.Mulberrin also inhibits organic anion-transporting polypeptide (OATP)-mediated uptake of Atorvastatin, Fluvastatin, and Rosuvastatin[1].

Name: Kuwanon E, CAS: 68401-05-8, stock 4.1g, assay 98.2%, MWt: 424.49, Formula: C25H28O6, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Kuwanon E is a flavonoid isolated from Morus alba, cytotoxic to human monocytic leukemic cell lines, and reduces the level of IL-1β[1].
IC50 & Target: Kuwanon E shows cytotoxic activity against THP-1 human monocytic leukemic cell line, with an IC50 of 4.0±0.08 μM[1].

Name: Platycodin D3, CAS: 67884-03-1, stock 20.6g, assay 98.8%, MWt: 1387.46, Formula: C63H102O33, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Anti-infection, Target: HCV, Biological_Activity: Platycodin D3 is a triterpenoid saponin isolated from Platycodon grandiflorum, with anti-HCV activity[1].
IC50 & Target: HCV[1]

Name: Deapi-platycodin D3, CAS: 67884-05-3, stock 30g, assay 98.1%, MWt: 1255.35, Formula: C58H94O29, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Deapi-platycodin D3 is a triterpenoid saponin from the roots of Platycodon grandiflorum[1].

Name: Platycoside G1 Deapi-platycoside E, CAS: 849758-42-5, stock 12.8g, assay 98.2%, MWt: 1417.49, Formula: C64H104O34, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Platycoside G1, a natural product found in Platycodon grandiflorum, is a triterpenoid saponin. Platycoside G1 has potent antioxidant activities[1].

Name: NecroX-5, CAS: 1383718-29-3, stock 1.3g, assay 98%, MWt: 645.81, Formula: C27H39N3O9S3, Solubility: DMSO : 170 mg/mL (263.24 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Membrane Transporter/Ion Channel;Neuronal Signaling, Target: Calcium Channel;Calcium Channel, Biological_Activity: NecroX-5 is a derivative of the NecroX, reduces intracellular calcium concentration, and possesses anti-inflammatory and anti-cancer activity.
IC50 & Target: Calcium channel[1]
In Vitro: NecroX-5 (10 or 40 μM) inhibits breast cancer cell migration, which is correlated with mitoROS reduction, and mediated by AKT inhibition. NecroX-5 (10 μM) decreases intracellular calcium concentration in 4T1 cells by blocking Ca2+ influx, which mediated the inhibition of cell migration, AKT downregulation and the reduction of mitochondrial ROS levels[1]. NecroX-5 (10 µM) treatment for 24 h, effectively decreases the increased TNFα, TGFβ1, pSmad2 and the expression of Dcn in LPS-stimulated H9C2 cells[2].
In Vivo: NecroX-5 (2.5 mg/kg, everyday other day) inhibits breast cancer cell metastasis in TUBO-P2J tumour-bearing mice[1].

Name: Calycanthoside, CAS: 483-91-0, stock 38.8g, assay 98.8%, MWt: 384.33, Formula: C17H20O10, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Calycanthoside is a natural compound isolated from Angelica tenuissima[1].

Name: GSK840 GSK'840, CAS: 2361146-30-5, stock 32.5g, assay 98.1%, MWt: 365.43, Formula: C21H23N3O3, Solubility: DMSO : 110 mg/mL (301.02 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Apoptosis, Target: RIP kinase, Biological_Activity: GSK840 (GSK'840) is a receptor-interacting protein kinase 3 (RIP3 or RIPK3) inhibitor, which binds RIP3 kinase domain with an IC50 of 0.9 nM, and inhibits kinase activity with an IC50 of 0.3 nM[1].
IC50 & Target: IC50: 0.3 nM (RIP3)[1]

Name: Methyl rosmarinate, CAS: 99353-00-1, stock 28.8g, assay 99%, MWt: 374.34, Formula: C19H18O8, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Tyrosinase, Biological_Activity: Methyl rosmarinate is a noncompetitive tyrosinase inhibitor which is isolated from Rabdosia serra, with an IC50 of 0.28 mM for mushroom tyrosinase, and also inhibits a-glucosidase[1].
IC50 & Target: IC50: 0.28 mM (mushroom tyrosinase), a -glucosidase[1]

Name: Diethyl-pythiDC, CAS: 1821370-70-0, stock 36.7g, assay 98.5%, MWt: 306.34, Formula: C14H14N2O4S, Solubility: H2O : < 0.1 mg/mL (insoluble); DMSO : 33.33 mg/mL (108.80 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Diethyl-pythiDC is an inhibitor of collagen prolyl 4-hydroxylases (CP4Hs).
IC50 & Target: CP4H[1]
In Vitro: Diethyl-pythiDC inhibits CP4H activity in cultured cells at concentrations that do not cause iron deficiency. MDA-MB-231 cells are treated with biheteroaryl dicarboxylates, and assayed for cytotoxicity and indicators of iron deficiency. None of the esterified biheteroaryl dicarboxylates exhibited cytotoxic activity at high micromolar concentrations. Cells treated with dihydroxybenzoate (EDHB demonstrate a strong iron-deficient phenotype. In contrast, cells treated with Diethyl-pythiDC (Diethyl pythiDC) appear to be normal at concentrations as high as 500 µM. Treatment with Diethyl-pythiDC and low levels of diethyl pyimDC does not affect the level of TfR, HIF-1α, or ferritin[1].

Name: Caryophyllene oxide (-)-Caryophyllene oxide, CAS: 1139-30-6, stock 5.8g, assay 98.8%, MWt: 220.35, Formula: C15H24O, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Caryophyllene oxide, isolated from from Annona squamosa L. bark., possesses analgesic and anti-inflammatory activity[1].

Name: CLK1-IN-1, CAS: 2123491-32-5, stock 30.7g, assay 98.9%, MWt: 409.42, Formula: C24H16FN5O, Solubility: DMSO : 25 mg/mL (61.06 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Cell Cycle/DNA Damage, Target: CDK, Biological_Activity: CLK1-IN-1 is a potent and selective of Cdc2-like kinase 1 (CLK1) inhibitor, with an IC50 of 2 nM.
IC50 & Target: IC50: 2 nM (CLK1)[1].
In Vitro: CLK1 is the most potently inhibited kinase (IC50: 2 nM). In addition to CLK1, only two kinases have an IC50 value less than 100 nM, namely CLK2 (IC50: 31 nM) and CLK4 (IC50: 8 nM), DYRK1A is the strongest off-target. The ability of CLK1-IN-1 to induce autophagy in BNL CL.2 and SKOV-3 (human ovarian cancer cell line) cells is also examined. The effects of CLK1-IN-1 on yellow LC3 puncta also displays obvious dose dependency, and a dose of 10 μM shows the best performance. In addition, in CLK1-IN-1-treated cells, the number of red LC3 puncta (mRFP signals only35) increases compared with that of DMSO-treated cells, indicating the formation of autolysosomes. Importantly, CLK1-IN-1 stimulats the degradation of SQSTM1/p62 and increases the ratio of red LC3 puncta to yellow LC3 puncta, both of which indicate an induction of autophagic flux by CLK1-IN-1[1].
In Vivo: APAP exposure results in severe liver injury, and treatment with CLK1-IN-1 (ip, 30 mg/kg) imparts a significant hepatoprotective effect. The results show that treatment with CLK1-IN-1 decreases serum ALT and AST levels significantly such that both marker enzymes return to normal levels[1].

Name: GPR40 agonist 4, CAS: 2102196-57-4, stock 18.4g, assay 98.6%, MWt: 416.87, Formula: C21H17ClO5S, Solubility: DMSO : 160 mg/mL (383.81 mM; Need ultrasonic and warming), Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein, Target: GPR40, Biological_Activity: GPR40 agonist 4 is a potent free fatty acid receptor 1 (FFA1/ GPR40) agonist with a pEC50 of 7.54.
IC50 & Target: pEC50: 7.54 (FFA1/GPR40)[1]
In Vitro: GPR40 agonist 4 tends to have a low risk of activating caspase-3/7[1].
In Vivo: Single oral administration of GPR40 agonist 4 (compound 20) robustly reduces the plasma glucose excursion and enhances insulin secretion during an oral glucose tolerance test (OGTT) in a dose-dependent manner from 1 to 10 mg/kg when GPR40 agonist 4 is dosed 60 min prior to the oral glucose challenge. The area under the curve of blood glucose (AUC0-120min) and blood insulin (AUC0-120min) reveal that the minimum effective dose of GPR40 agonist 4 is 3 mg/kg. The hyperglycemia state is also markedly improved in GPR40 agonist 4 (20 mg/kg) treated group[1].

Name: T-3775440 hydrochloride, CAS: 1422535-52-1, stock 2.5g, assay 98.7%, MWt: 346.85, Formula: C18H23ClN4O, Solubility: DMSO : ≥ 30.18 mg/mL (87.01 mM), Clinical_Informat: No Development Reported, Pathway: Epigenetics, Target: Histone Demethylase, Biological_Activity: T-3775440 (hydrochloride) is an irreversible lysine-specific histone demethylase (LSD1) inhibitor with an IC50 value of 2.1 nM.
IC50 & Target: IC50: 2.1 nM (LSD1)[1].
In Vitro: T-3775440 demonstrates irreversible inhibition of recombinant human LSD1, with a kinact/KI value of 1.7×105 (sec−1 M−1). T-3775440 is highly selective for LSD1 relative to other monoamine oxidases (e.g., MAO-A and MAO-B), with an IC50 value of 2.1 nM). T-3775440 blocks the proliferation of several cell lines as quickly as day 3 of treatment. Notably, the granulocyte/macrophage markers CD86 and CD11b are commonly upregulated on both TF-1a and HEL92.1.7 cells in response to T-3775440 treatment, whereas the erythroid markers CD235a and CD71 are downregulated by this treatment. In CMK11-5 cells, CD86 mRNA expression is also clearly upregulated by T-3775440 in a concentration-dependent manner, although only a modest increase in cell surface CD86 expression is observed. T-3775440 treatment disrupts the LSD1-GFI1B association in a concentration-dependent manner. T-3775440 decreases LSD1 binding but not GFI1B binding and increases the level of dimethylated H3K4 at the PI16 locus[1].
In Vivo: T-3775440 upregulates CD86 mRNA expression in tumor xenografts of HEL92.1.7 cells in a dose-dependent manner following the oral administration of single doses ranging from 3 to 30 mg/kg. To investigate target engagement of this compound in tumors, PI16 expression levels is tested as a direct biomarker. As expected, PI16 suppression is dramatically reversed by T-3775440 treatment. In a TF-1a (AEL) tumor xenograft model, T-3775440 exhibits significant antitumor effects, with 15-day T/C values of 15.6% and <0% at doses of 20 and 40 mg/kg, respectively. T-3775440 also exhibits potent antitumor effects in an additional AEL model of HEL 92.1.7 and an AMKL model of CMK11-5, leading to nearly complete tumor growth suppression during the dosing period. It is found that in mice, T-3775440 treatment results in a transient reduction in platelets, followed by a significant rebound; this is considered a mechanism-based adverse effect of LSD1 inhibition. On a dosing schedule comprising 5 days on/2 days off, a statistically significant difference in body weight is observed between vehicle- and T-3775440–treated tumor xenograft model mice at higher doses. However, efficacious T-3775440 doses are tolerated in all subcutaneous tumor xenograft models[1].

Name: Meranzin (hydrate), CAS: 5875-49-0, stock 35.9g, assay 98.8%, MWt: 278.30, Formula: C15H18O5, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Meranzin hydrate, an absorbed bioactive compound from the Traditional Chinese Medicine (TCM) Chaihu-Shugan-San (CSS), possess anti-depression and anti-atherosclerosis effects[1][2].

Name: Ceanothic acid Emmolic acid, CAS: 21302-79-4, stock 30.7g, assay 98.4%, MWt: 486.68, Formula: C30H46O5, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Ceanothic acid (Emmolic acid) is a ring-A homologue of betulinic acid. Ceanothic acid inhibits OVCAR-3, HeLa, and FS-5 cells with the cell survival of 68%, 65%, and 81%, respectively[1].

Name: Paris saponin VII Chonglou Saponin VII, CAS: 68124-04-9, stock 15.6g, assay 98.3%, MWt: 1031.18, Formula: C51H82O21, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Membrane Transporter/Ion Channel;MAPK/ERK Pathway;Epigenetics;Cell Cycle/DNA Damage;Apoptosis;PI3K/Akt/mTOR;Autophagy;Apoptosis, Target: P-glycoprotein;p38 MAPK;PARP;PARP;Caspase;Akt;Autophagy;Bcl-2 Family, Biological_Activity: Paris saponin VII (Chonglou Saponin VII) is a steroidal saponin isolated from the roots and rhizomes of Trillium tschonoskii Maxim. Paris saponin VII-induced apoptosis in K562/ADR cells is associated with Akt/MAPK and the inhibition of P-gp. Paris saponin VII attenuates mitochondrial membrane potential, increases the expression of apoptosis-related proteins, such as Bax and cytochrome c, and decreases the protein expression levels of Bcl-2, caspase-9, caspase-3, PARP-1, and p-Akt. Paris saponin VII induces a robust autophagy in K562/ADR cells and provides a biochemical basis in the treatment of leukemia[1].
In Vitro: Paris saponin VII (Chonglou Saponin VII) inhibits the growth of adriamycin-resistant human leukemia cells (K562/ADR) in a dose-dependent manner. Paris saponin VII significantly suppresses cell proliferation by cell cycle arrest in the G0/G1 phase[1].
In Vivo: Paris saponin VII (Chonglou Saponin VII) (intravenous administration) significantly enhances anticancer efficacy of adriamycin to MCF-7/ADR xenograft model in nude mice[2].

Name: Cimiside B, CAS: 152685-91-1, stock 34.9g, assay 98.9%, MWt: 752.93, Formula: C40H64O13, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Cimiside B, a glycoside alkaloid, isolated from the rhizome of Cimicifuga dahurica.

Name: Coniferin Laricin, CAS: 531-29-3, stock 14.4g, assay 98.6%, MWt: 342.34, Formula: C16H22O8, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Anti-infection, Target: Fungal, Biological_Activity: Coniferin (Laricin) is a glucoside of coniferyl alcohol. Coniferin inhibits fungal growth and melanization[1].
IC50 & Target: Fungal[1]

Name: Cotoin, CAS: 479-21-0, stock 25g, assay 98.6%, MWt: 244.24, Formula: C14H12O4, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Cotoin is a natural product isolated from the stem bark of Garcinia virgate[1].

Name: CGP60474, CAS: 164658-13-3, stock 39.6g, assay 98.3%, MWt: 355.82, Formula: C18H18ClN5O, Solubility: DMSO : ≥ 50 mg/mL (140.52 mM); H2O : < 0.1 mg/mL (insoluble), Clinical_Informat: No Development Reported, Pathway: Protein Tyrosine Kinase/RTK;TGF-beta/Smad;Epigenetics, Target: VEGFR;PKC;PKC, Biological_Activity: CGP60474 is a potent VEGFR-2 inhibitor, with an IC50 of 84 nM, and also an ATP-competitive PKC inhibitor.
IC50 & Target: IC50: 84 nM (VEGFR-2)[1] 
PKC[2]
In Vitro: CGP60474 (Compound A) is a potent VEGFR-2 inhibitor, with an IC50 of 84 nM[1]. CGP60474 is also a PKC inhibitor, with competitive kinetics relative to ATP[2].

Name: Loganetin, CAS: 29748-10-5, stock 25.9g, assay 98.9%, MWt: 228.24, Formula: C11H16O5, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Anti-infection, Target: Bacterial, Biological_Activity: Loganetin is a non-toxic natural product that may be applied in the antibacterial drug development for treating multidrug-resistant Gram negative infections.
In Vitro: Although Loganetin does not possess antibacterial activity of its own, but in combination, it appreciably reduces the minimum inhibitory concentration (MIC) of nalidixic acid (NA) against nalidixic acid resistant (NAREC) and nalidixic acid sensitive (NASEC) strains of Escherichia coli. Loganetin, a very common, inexpensive, and non-toxic natural product may finds its application in the antibacterial drug development for treating multidrug-resistant Gram negative infections[1].

Name: NPS ALX Compound 4a, CAS: 299433-10-6, stock 12.9g, assay 98.4%, MWt: 431.55, Formula: C25H25N3O2S, 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: NPS ALX Compound 4a is a potent and selective 5-hydroxytryptamine6 (5-HT6) receptor antagonist with an IC50 of 7.2 nM, which also has a great binding affinity with Ki of 0.2 nM[1].
IC50 & Target: IC50: 7.2 nM (5-HT6 receptor) 
Ki: 0.2 nM (5-HT6 receptor)

Name: D-Arabitol, CAS: 488-82-4, stock 30.5g, assay 98.9%, MWt: 152.15, Formula: C5H12O5, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: D-Arabitol is a polyol and its accumulation may cause a neurotoxic effect in human.

Name: Licoisoflavone A, CAS: 66056-19-7, stock 24.3g, assay 98.3%, MWt: 354.35, Formula: C20H18O6, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Licoisoflavone A, an isoflavone, mainly derived from Glycyrrhiza uralensis Fisch.[1]. Licoisoflavone A inhibits lipid peroxidation with an IC50 of 7.2 μM[1].

Name: Dihydroresveratrol, CAS: 58436-28-5, stock 0.5g, assay 98.1%, MWt: 230.26, Formula: C14H14O3, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Estrogen Receptor/ERR, Biological_Activity: Dihydroresveratrol, a potent phytoestrogen, is a hormone receptor modulator. Dihydroresveratrol exhibits proliferative effects in androgen-independent prostate and breast cancer cells at picomolar and nanomolar concentrations[1].
In Vitro: Treatment with 0.1 nM-0.1 μM of Dihydroresveratrol significantly increases the growth of PC-3 prostate cancer cells[1].

Name: Kaempferol 3-O-arabinoside, CAS: 99882-10-7, stock 20.6g, assay 99%, MWt: 418.35, Formula: C20H18O10, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Kaempferol 3-O-arabinoside is an antioxidant flavonoids isolated from ethyl acetate fraction (EAF) obtained from the leaves of Nectandra hihua. Kaempferol 3-O-arabinoside has good antioxidant capacity[1].

Name: Eleutheroside C Ethyl α-D-galactoside;Ethyl α-D-galactopyranoside, CAS: 15486-24-5, stock 28g, assay 98%, MWt: 208.21, Formula: C8H16O6, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Eleutheroside C (Ethyl α-D-galactoside) is a glycoside isolated from the bulbs of Polianthes tuberosa[1].

Name: Fananserin RP 62203, CAS: 127625-29-0, stock 17.6g, assay 98.3%, MWt: 425.52, Formula: C23H24FN3O2S, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein;Neuronal Signaling;Neuronal Signaling;GPCR/G Protein, Target: Dopamine Receptor;Dopamine Receptor;5-HT Receptor;5-HT Receptor, Biological_Activity: Fananserin (RP 62203) is an orally bioavailable, potent and selective 5-hydroxytryptamine2 (5-HT2) receptor antagonist, with a Ki of 0.37 nM for the rat 5-HT2A receptor. Fananserin also is a selective dopamine D4 receptor antagonist, with a Ki of 2.93 nM for the human dopamine D4 receptor[1].
IC50 & Target: Ki: 0.37 nM (5-HT2), 2.93 nM (human DA D4 receptor)[1]
In Vitro: Fananserin is relatively selective for 5-HT2 receptor, having lower affinity for the 5-HT1A receptor and very low affinity for the 5-HT3 receptor[1]. 
Fananserin displaces [3H]spiperone binding to recombinant human dopamine D 4 receptors with a Ki of 2.93 nM[1]. 
RP 62203 displays low to moderate affinity for α1-adrenoceptors, dopamine D2 receptors and histamine H 1 receptors[2]. 
In Vivo: Fananserin displaces [125I]AMIK from 5-HT2 receptors with an IC50 of 0.21 nM in rat frontal cortex[2]. 
Fananserin shows moderate affinity for alpha 1-adrenoceptors in the rat thalamus (IC50 = 14 nM) and for histamine H1 receptors in the guinea-pig cerebellum (IC50 = 13 nM)[2]. 
Fananserin (0.5-4 mg/kg; p.o.) increases the duration of deep nonrapid eye movement (NREM) sleep at the expense of wakefulness in a dose-dependent manner[3].

Name: Isomerazin, CAS: 1088-17-1, stock 22.6g, assay 98.5%, MWt: 260.29, Formula: C15H16O4, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Neuronal Signaling, Target: AChE, Biological_Activity: Isomerazin is a coumarin isolated from Poncirus trifoliate Raf., and shows cholinesterase inhibition[1][2].

Name: SB 243213 (hydrochloride), CAS: 200940-23-4, stock 34.1g, assay 98.7%, MWt: 464.87, Formula: C22H20ClF3N4O2, 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: SB 243213 hydrochloride is a selective and high-affinity 5-hydroxytryptamine (5-HT)2C receptor antagonist with a pKi of 9.37 and a pKb of 9.8 for human 5-HT2C receptor. SB 243213 hydrochloride has improved anxiolytic profile[1].
In Vivo: SB-243213 hydrochloride is a potent inhibitor of central 5-HT2C receptor-mediated function in rats. SB-243213 hydrochloride exhibits anxiolytic-like activity in both the social interaction and Geller-Seifter conflict tests[1].

Name: Heraclenol, CAS: 31575-93-6, stock 29.9g, assay 98.4%, MWt: 304.29, Formula: C16H16O6, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Anti-infection, Target: Bacterial, Biological_Activity: Heraclenol, a coumarin, is isolated from the fruits of Angelica lucida, and exhibits antibacterial activities[1].

Name: Heraclenin, CAS: 2880-49-1, stock 10.1g, assay 98%, MWt: 286.28, Formula: C16H14O5, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Heraclenin, a natural furanocoumarin, isolated from the root parts of the plant Prangos pabularia. Heraclenin significantly inhibits T cell receptor-mediated proliferation in human primary T cells in a concentration-dependent manner by targeting nuclear factor of activated T-cells (NFAT)[1].
IC50 & Target: NFAT[1]

Name: Guaiol Champacol; Guaiac alcohol, CAS: 489-86-1, stock 30.6g, assay 98.1%, MWt: 222.37, Formula: C15H26O, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Guaiol is a sesquiterpene alcohol that has been found in several traditional Chinese medicinal plants and has antiproliferative, pro-autophagic, insect repellent, and insecticidal biological activities[1][2][3].

Name: PNU-142633, CAS: 187665-65-2, stock 6.5g, assay 98.3%, MWt: 422.52, Formula: C24H30N4O3, 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: PNU-142633 is a high affinity, selective and orally active 5-HT1D receptor agonist with Kis of 6 nM and > 18 000 nM for human 5-HT1D receptor and human 5-HT1B receptor, respectively. PNU-142633 has anti-migraine efficacy[1][2].
In Vitro: The intrinsic activity of PNU-142633 at the human 5-HT1D receptor is determined to be 70% that of 5-HT in a cytosensor cell-based assay compared with 84% for that of Sumatriptan[1].
In Vivo: PNU-142633 (0.03-1 mg/kg; intravenous injection; male Hartley guinea pigs) treatment blocks neurogenic plasma protein extravasation. And PNU-142633 fails to alter resistance in these vascular beds[1].

Name: AS19, CAS: 1000578-26-6, stock 5.5g, assay 98.4%, MWt: 283.41, Formula: C18H25N3, 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: AS19 is a potent, selective 5-HT7 receptor agonist with an IC50 value of 0.83 nM and a Ki of 0.6 nM. AS19 is selective for 5-HT7 over 5-HT1A, 5-HT1B, 5-HT1D, and 5-HT5A receptors (Kis = 89.7 nM, 490 nM, 6.6 nM and 98.5 nM, respectively). AS19 enhances memory consolidation and reverses Scopolamine- or Dizocilpine-induced amnesia[1][2][3].
In Vitro: The proliferation of T-cell from parachlorophenylalanine-treated mice is significantly reduced, addition of AS19 (1 μM) completely restores T-cell proliferation after 48 hours[2].
In Vivo: AS19 (0.5-10 mg/kg; subcutaneous injection; for 24 hours; male Wistar rats) treatment improves memory consolidation in an autoshaping Pavlovian/instrumental learning task[1].

Name: Zamicastat BIA 5-1058, CAS: 1080028-80-3, stock 18.4g, assay 98.8%, MWt: 401.47, Formula: C21H21F2N3OS, Solubility: H2O : < 0.1 mg/mL (insoluble); DMSO : 150 mg/mL (373.63 mM; Need ultrasonic), Clinical_Informat: Phase 1, Pathway: Membrane Transporter/Ion Channel;Metabolic Enzyme/Protease;Membrane Transporter/Ion Channel, Target: P-glycoprotein;Dopamine β-hydroxylase;BCRP, Biological_Activity: Zamicastat (BIA 5-1058) is a dopamine β-hydroxylase (DBH) inhibitor that could cross the blood-brain barrier (BBB) and cause central as well as peripheral effects. Zamicastat is also a concentration-dependent dual P-gp and BCRP inhibitor with IC50 values of 73.8 μM and 17.0 μM, respectively[1]. Reduces high blood pressure[2].
IC50 & Target: Dopamine β-hydroxylase (DBH)[1] 
IC50: 73.8 μM (P-gp), 17.0 μM (BCRP)[1]
In Vitro: Following 4 hours of incubation (5, 10, 20, 50, 80, 100 μM), a significant loss of cell viability is verified with 100 μM Zamicastat (p=0.010) in MDCK-BCRP cells. No significant losses of cell viability are observed after 4 h of incubation for other concentrations in all cell lines. By decreasing the incubation period to 30 min, there is no significant loss of cell viability (p>0.05) at 100 μM in all cell lines[1].
In Vivo: Zamicastat (10, 30 and 100 mg/kg/day; oral bolus, 7 days) is tested acutely against salt-induced hypertension in the Dahl SS rat. Zamicastat produces a dose-dependent decrease in blood pressure. 24 h after Zamicastat administration mean systolic blood pressure (SBP) decrease is -12.6±4.1 mm Hg (P=0.0284), -15.2±2.7 mm Hg (P=0.0026) and -19.0±3.7 mm Hg (P=0.0036) for the 10, 30, and 100 mg/kg body weight dose, respectively. Zamicastat administration also produces a significant 24-h average decrease in diastolic blood pressure (DBP) of - 14.6±3.4 mm Hg (P=0.0073) with 10 mg/kg body weight dose, -13.0±4.5 mm Hg (P=0.0347) with 30 mg/kg body weight dose and -15.0±3.1 mm Hg (P=0.0046) with 100 mg/kg body weight dose. Zamicastat administration leads to a decrease in the 24h post-dose mean arterial pressure (MAP) of -13.4±3.8 mm Hg (P=0.0162), -14.0±3.5 mm Hg (P=0.0101) and -20.6±3.7 mm Hg (P=0.0026) for the 10, 30, and 100 mg/kg body weight dose, respectively. There is a small, but significant, effect of Zamicastat on the 24-h mean heart rate (HR) post-dose for all tested doses (10 mg/kg: -19.1±3.2 beats/min, P=0.0019; 30 mg/kg: -13.0±4.5 beats/min, P=0.0347; 100 mg/kg: -21.6±6.6 beats/min, P=0.0235)[2].

Name: Alagebrium chloride ALT711, CAS: 341028-37-3, stock 3.9g, assay 98.1%, MWt: 267.77, Formula: C13H14ClNOS, Solubility: H2O : 50 mg/mL (186.73 mM; Need ultrasonic); DMSO : ≥ 25 mg/mL (93.36 mM), Clinical_Informat: Phase 3, Pathway: Others, Target: Others, Biological_Activity: Alagebrium chloride is an advanced glycation end product (AGE) inhibitor.
IC50 & Target: AGE[1]
In Vitro: Alagebrium chloride is an advanced glycation end product (AGE) inhibitor. Endothelial cell (EC) proliferation is increased for all groups receiving Alagebrium (ALT-711), particularly when seeded on matrix from the AAo of obese (ZO) and diabetic (ZD) rats[2].
In Vivo: Blood pressure is not affected by treatment with Alagebrium. In diabetic RAGE apoE double-KO mice, treatment with Alagebrium is associated with a modest reduction in renal mass and reduces hyperfiltration compare with nontreated mice. Treatment with Alagebrium in diabetic RAGE apoE double-KO mice is associated with a further reduction in glomerular collagen IV levels, approaching levels observed in control mice[1]. Body weight, heart rate (HR), and mean blood pressure (BP) are similar in Zucker lean (ZL), obese (ZO), and diabetic (ZD) groups in the absence or presence of Alagebrium (ALT-711). Alagebrium increases blood flow (BF) in ZO rats but reduces distal vascular resistance in ZD rats. A decrease in neointimal hyperplasia (NH) intrastrut thickness as a function of local radius is found in all groups with Alagebrium treatment. A significant increase in TGF-β expression is also found in the AAo of ZL rats treated with Alagebrium[2].

Name: SB228357, CAS: 181629-93-6, stock 35.8g, assay 98.7%, MWt: 431.38, Formula: C22H17F4N3O2, 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: SB228357 is a selective, potent oral active 5-HT2C/2B receptor antagonist with pKi values of 6.9, 8.0 and 9.0 for 5-HT2A, 5-HT2B and 5-HT2C, respectively. SB228357 has antidepressant/anxiolytic effects[1][2].
In Vivo: SB228357 (0-10 mg/kg; oral administration; for 90 minutes; male Sprague Dawley rats) treatment significantly reverses Haloperidol-induced catalepsy[2].

Name: Selumetinib (sulfate) AZD6244 (sulfate);ARRY-142886 (sulfate), CAS: 943332-08-9, stock 38.8g, assay 98.3%, MWt: 555.76, Formula: C17H17BrClFN4O7S, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Apoptosis;MAPK/ERK Pathway, Target: Apoptosis;MEK, Biological_Activity: Selumetinib (AZD6244) is selective, non-ATP-competitive oral MEK1/2 inhibitor, with an IC50 of 14 nM for MEK1. Selumetinib (AZD6244) inhibits ERK1/2 phosphorylation.
In Vitro: Selumetinib (AZD6244) causes a time- and dose-dependent reduction in DNA synthesis and cell viability in primary, induces growth arrest and apoptosis associated with the inactivation of ERK in primary 2-1318 cells[1].
Selumetinib (AZD6244) (1µM) shows anti-proliferative effects through G0/G1 arrest on H-441, H-1437 cells[2].
Selumetinib (AZD6244) results in the growth inhibition of several cell lines containing B-Raf and Ras mutations but has no effect on a normal fibroblast cell line[3].
In Vivo: Selumetinib (AZD6244, 50 and 100 mg/kg, p.o.) decreases the growth rate of 4-1318 xenografts in a dose-dependent manner; AZD6244 when given at the dose of 50 mg/kg also significantly suppresses the growth of the 5-1318, 2-1318, 26-1004, and 29-1104 xenografts[1].
Selumetinib (ARRY-142886, 10, 25, 50, or 100 mg/kg, p.o.) is capable of inhibiting both ERK1/2 phosphorylation and growth of HT-29 xenograft tumors in nude mice. Tumor regressions are also seen in a BxPC3 xenograft model[3].

Name: ALX 40-4C, CAS: 143413-49-4, stock 14.8g, assay 98.4%, MWt: 1464.74, Formula: C56H113N37O10, Solubility: 10 mM in H2O, Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein;Immunology/Inflammation, Target: CXCR;CXCR, Biological_Activity: ALX 40-4C is a small peptide inhibitor of the chemokine receptor CXCR4, inhibits SDF-1 from binding CXCR4 with a Ki of 1 μM, and suppresses the replication of X4 strains of HIV-1; ALX 40-4C Trifluoroacetate also acts as an antagonist of the APJ receptor, with an IC50 of 2.9 μM.
IC50 & Target: CXCR4[1] 
IC50: 2.9 μM (APJ receptor)[3]
In Vitro: ALX 40-4C is a small peptide inhibitor of the chemokine receptor CXCR4, interacts with the second extracellular loop of CXCR4 and inhibits infection exclusively by blocking direct virus-CXCR4 interactions[1]. ALX 40-4C shows potent anti HIV-1 effect, with EC50s of 0.34 ± 0.04 μg/mL, 0.37 ± 0.01 μg/mL for HIV-1 NL4-3, NC10, and 0.18 ± 0.11 μg/mL, 0.06 ± 0.02 μg/mL for HIV-1 HXB2, HC43, respectively, and with a CC50 (50% cytotoxic concentration) of 21 μg/mL. ALX 40-4C also exhibits potent activity against env-recombinant HIV, with EC50s of 0.38 ± 0.01 μg/mL, 0.40 ± 0.0 μg/mL for HIV-1 NL4-3 env, NC10, and 1.34 ± 0.06 μg/mL, 1.02 ± 0.29 μg/mL for HIV-1 HXB2 env, HC43, and a CC50 of 21 μg/mL[2]. ALX 40-4C binds to APJ with an IC50 of 2.9 μM. ALX 40-4C inhibits HIV-1 gp120/APJ-mediated cell membrane fusion, with an IC50s of 3.41 μM and 3.1 μM for IIIB isolate and 89.6 isolate, respectively[3].

Name: Bredinin aglycone 5-Hydroxy-1H-imidazole-4-carboxamide;SM-108, CAS: 56973-26-3, stock 36.5g, assay 98.8%, MWt: 127.10, Formula: C4H5N3O2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Bredinin aglycone (5-Hydroxy-1H-imidazole-4-carboxamide) is a purine nucleotide analogue. Bredinin aglycone can be used to examine the efficiency of catalysts for the preparation of purine nucleotide analogues[1].

Name: Dazoxiben, CAS: 74226-22-5, stock 18.2g, assay 98.3%, MWt: 268.70, Formula: C12H13ClN2O3, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein, Target: Prostaglandin Receptor, Biological_Activity: Dazoxiben is a potent and orally active thromboxane (TX) synthase inhibitor[1].
IC50 & Target: Thromboxane (TX) synthase[1]
In Vitro: Dazoxiben inhibits TXB2 production in clotting human whole blood with an IC50 of 0.3 μM and causes parallel enhancement of PGE2 greater than PGF2 alpha greater than 6-keto-PGF1 alpha production[1].
Dazoxiben inhibits TXB2 production in rat kidney glomeruli with an IC50 of 1.60 μM) than in rat whole blood (IC50= 0.32μM), and is not associated with changes in PGE2, PGF2 alpha and 6-keto-PGF1 alpha production[1].
In Vivo: Dazoxiben (intraperitoneal administration; 100 μg/kg) produces a marked prolongation of the tail bleeding time with 96.8 ± 10.8 secs[2].

Name: Furegrelate (sodium) U-63557A, CAS: 85666-17-7, stock 35.8g, assay 98.7%, MWt: 275.23, Formula: C15H10NNaO3, Solubility: 10 mM in DMSO, Clinical_Informat: Phase 1, Pathway: Others, Target: Others, Biological_Activity: Furegrelate Sodium (U-63557A) is a potent, orally available, and selective thromboxane synthase inhibitor. Furegrelate Sodium inhibits human platelet microsomal thromboxane A2 (TxA2) synthase with an IC50 of 15 nM. Furegrelate Sodium is being developed as an antiplatelet agent[1][2].
In Vivo: Furegrelate Sodium (U-63557A) (1-5 mg/kg; Oral) prevents blockage of the coronary artery[1]. 
Furegrelate Sodium (0.1-5 mg/kg; i.v.) prevents the blockage of stenosed coronary arteries caused platelet aggregation[1]. 
Furegrelate Sodium blunts the development of hypoxia-induced pulmonary arterial hypertension (PAH) in an established neonatal piglet model primarily by preserving the structural integrity of the pulmonary vasculature[2]. 
Furegrelate also is orally available, has a long half-life of 4.2–5.8 hours in adult humans (compared to several other therapies for PAH including nitric oxide and prostacyclin analogs), and reportedly is highly specific for its target enzyme[2].

Name: CY 208-243, CAS: 100999-26-6, stock 17.9g, assay 98.8%, MWt: 274.36, Formula: C19H18N2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein;Neuronal Signaling, Target: Dopamine Receptor;Dopamine Receptor, Biological_Activity: CY 208-243 is a selective dopamine D1 receptor agonist which exhibits antiparkinsonian activity[1].
IC50 & Target: dopamine D1 receptor[1]
In Vivo: Pretreatment with CY 208-243 (2.5 mg/kg; s.c.) prevents the increase of DA release and metabolism induced by the D-1 antagonist, SCH 23390 (0.05 mg/kg; s.c.)[1].

Name: Rusalatide acetate TP508 amide acetate, CAS: 875455-82-6, stock 1.7g, assay 98.3%, MWt: 2371.50, Formula: C99H151N29O37S, Solubility: H2O, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Rusalatide acetate (TP508 amide acetate), a regenerative peptide, mitigates radiation-induced gastrointestinal damage by activating stem cells and preserving crypt integrity[1].
In Vitro: Rusalatide (TP508) is a 23 amino acid peptide representing amino acids 508-530 of human prothrombin that was identified as the high-affinity binding domain of thrombin responsible for interaction with a subset of thrombin receptors on the surface of fibroblasts thought to initiate tissue repair[1].

Name: Implitapide AEGR 427, CAS: 177469-96-4, stock 14.8g, assay 98.9%, MWt: 531.69, Formula: C35H37N3O2, Solubility: 10 mM in DMSO, Clinical_Informat: Phase 2, Pathway: Others, Target: Others, Biological_Activity: Implitapide (AEGR 427) is a microsomal triglyceride transfer protein (MTP) inhibitor.
IC50 & Target: MTP[1]
In Vitro: Implitapide suppresses MTP activity using a recombinant human form complexed with protein disulphide isomerase (IC50=10 nM) and inhibit secretion of apoB-containing very low-density lipoprotein (VLDL)-like lipoproteins from a human hepatoma cell (HepG2) with an IC50 value of 1.1 nM[1].
In Vivo: Implitapide (3.2 mg/kg/d) significantly reduces the plasma lipid levels to nearly or below the chow diet (CD) level at 4 and 8 weeks of treatment (p<0.01). Implitapide (3.2 mg/kg/d) markedly suppresses lipid-stained lesions in the mice fed the western-type diet (WD). Implitapide (3.2 mg/kg/d) significantly decreases lesion area by 83% compared with that of the WD group (p<0.01). ApoE KO mice fed a WD containing Implitapide (1, 5, and 15 mg/kg/d) for 14 weeks have been shown to reduce significantly both plaque area (by 66, 78, and 93%, respectively) and lipid moieties within plaque (4.3, 2.6, and 0%, respectively, versus 9.5% in controls). Implitapide at a dosage of approximately 3.2 mg/kg/d significantly reduces the lipid-stained aortic lesions by 83% in apoE KO mice[1].

Name: Bimosiamose TBC 1269, CAS: 187269-40-5, stock 13.1g, assay 98.4%, MWt: 862.91, Formula: C46H54O16, Solubility: 10 mM in DMSO, Clinical_Informat: Phase 2, Pathway: Others, Target: Others, Biological_Activity: Bimosiamose is a pan-selectin antagonist, inhibits E-, P-, and L-selectin with IC50s of 88 μM, 20 μM, and 86 μM, respectively, and can be used in the research of inflammatory disease.
IC50 & Target: IC50: 88 μM (E-selectin), 20 μM (P-selectin), 86 μM (L-selectin)[1]
In Vitro: Bimosiamose is a pan-selectin antagonist, inhibits E-, P-, and L-selectin with IC50s of 88 μM, 20 μM, and 86 μM, respectively, and can be used in the research of inflammatory disease[1].
In Vivo: Bimosiamose (25 mg/kg, i.v.) significantly improves the survival in rats subjected to severe hepatic ischemia and reperfusion. Bimosiamose also causes lower ALT enzyme levels and decreases neutrophil infiltration[1].

Name: PD146176 NSC168807, CAS: 4079-26-9, stock 23g, assay 98.4%, MWt: 237.32, Formula: C15H11NS, Solubility: DMSO : 100 mg/mL (421.37 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Autophagy;Apoptosis, Target: Autophagy;Ferroptosis, Biological_Activity: PD146176 (NSC168807) is a 15-Lipoxygenase (15-LO) inhibitor, which inhibits rabbit reticulocyte 15-LO with a Ki of 197 nM. PD146176 (NSC168807) has a dramatic effect in reducing atherogenesis[1].
IC50 & Target: Ki: 197 nM (Rabbit reticulocyte 15-LO)[1]

Name: AZD-7762, CAS: 860352-01-8, stock 11.5g, assay 98.6%, MWt: 362.42, Formula: C17H19FN4O2S, Solubility: DMSO : 100 mg/mL (275.92 mM; Need ultrasonic), Clinical_Informat: Phase 1, Pathway: Cell Cycle/DNA Damage, Target: Checkpoint Kinase (Chk), Biological_Activity: AZD-7762 is a potent ATP-competitive checkpoint kinase (Chk) inhibitor in with an IC50 of 5 nM for Chk1.
IC50 & Target: IC50: 5 nM (ChK1), 5 nM (ChK2)[1]
In Vitro: AZD-7762 (AZD7762) is an equally potent inhibitor of Chk1 and Chk2 in vitro. AZD-7762 potently inhibits Chk1 and Chk2, abrogates DNA damage-induced S and G2 checkpoints, enhances the efficacy of NSC 613327 and SKF 104864A, and modulates downstream checkpoint pathway proteins. AZD-7762 potently inhibits Chk1 phosphorylation of a cdc25C peptide with an IC50 of 5 nM as measured by a scintillation proximity assay. The Ki for AZD-7762 is determined to be 3.6 nM. Kinetic characterization suggests that AZD-7762 binds in the ATP-binding site of Chk1 and is thought to compete directly for ATP binding in a reversible manner. AZD-7762 is shown to abrogate the G2 arrest induced by Camptothecin with an average EC50 of 10 nM (n=12) and maximal abrogation in the range of 100 nM[1].
In Vivo: In the rat H460-DNp53 xenograft study, AZD-7762 (AZD7762) potentiates the antitumor activity of NSC 613327 in a dose-dependent manner by a decrease in %T/C with increasing dose (48% and 32%, 10 and 20 mg/kg AZD-7762, respectively). In the mouse xenograft study in combination with CPT-11, SW620 established tumors are treated with vehicle, CPT-11 alone, AZD-7762 alone, or AZD-7762 in combination with CPT-11. AZD-7762 dosed alone shows insignificant antitumor activity, whereas CPT-11 alone displays striking and significant activity (%T/C with increasing dose is 9 and 1, respectively ). In combination with AZD-7762, %T/C increases significantly to -66% and -67%, respectively[1]. AZD7762 combination with CX-5461 induces cancer cell death of Tp53-null (Tp53-/-) Eμ-Myc lymphoma cells in vitro and in vivo[2].

Name: ABT-702 dihydrochloride, CAS: 1188890-28-9, stock 0.4g, assay 98.5%, MWt: 536.25, Formula: C22H21BrCl2N6O, Solubility: DMSO : ≥ 33.33 mg/mL (62.15 mM), Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease;Neuronal Signaling, Target: Adenosine Kinase;Adenosine Kinase, Biological_Activity: ABT-702 dihydrochloride is a potent adenosine kinase (AK) inhibitor (IC50=1.7 nM).
IC50 & Target: IC50: 1.7 nM (Adenosine kinase, AK)[1]
In Vitro: ABT-702 is an orally effective adenosine kinase inhibitor that has several orders of magnitude selectivity over other sites of adenosine (ADO) interaction (A1, A2A, A3 receptors, ADO transporter, and ADO deaminase). ABT-702 is equipotent (IC50=1.5±0.3 nM) in inhibiting native human AK (placenta), two human recombinant isoforms (AKlong and AKshort), and AK from monkey, dog, rat, and mouse brain. ABT-702 potently inhibits the activity of rat brain cytosolic AK in a concentration-dependent manner with an IC50 value of 1.7 nM. ABT-702 also potently inhibits AK activity in intact cultured IMR-32 human neuroblastoma cells (IC50=51 nM), indicating that ABT-702 can penetrate the cell membrane and potently inhibit AK at its intracellular site[1].
In Vivo: ABT-702 significantly reduces acute thermal nociception in a dose-dependent manner after both intraperitoneal (ED50=8 μmol/kg i.p.) and oral (ED50=65 μmol/kg p.o.) administration in the mouse hot-plate test. Consistent with its antinociceptive effects in the hot-plate assay, ABT-702 also produces dose-dependent antinociceptive effects (ED50=2 μmol/kg i.p.) in the abdominal constriction assay. Like Morphine (21 μmol/kg i.p.), ABT-702 exhibits full efficacy in this model of persistent chemical pain[1]. Rats are given an intraperitoneal injection of the adenosine A1 receptor antagonist DPCPX (3 mg/kg), ABT-702 (3 mg/kg), or vehicle 10 minutes prior to an intravenous injection of 2-18F-fluorodeoxy-D-glucose (FDG) (FDG, 15.4±0.7 MBq per rat). Rats are then subjected to a 15 minute static positron emission tomography (PET) scan. Reconstructed images are normalized to FDG PET template for rats and standard uptake values (SUVs) are calculated. To examine the regional effect of active treatment compared to vehicle, statistical parametric mapping analysis is performed. Whole-brain FDG uptake is not affected by drug treatment. Significant regional hypometabolism is detected, particularly in cerebellum, of DPCPX and ABT-702 treated rats, relative to vehicle-treated rats. Thus, endogenous adenosine can affect FDG accumulation although this effect is modest in quiescent rats. Body weight (316.8±28.4 g; mean±SD) and blood glucose (5.5±1.7 mM) are not significantly different among three groups. Whole-brain PET SUV values are 1.6±0.4, 1.6±0.6, and 1.8±0.6 for vehicle, ABT-702, and DPCPX-treated rats, respectively (F(2,9)=0.298, P=0.75). statistical parametric mapping (SPM) analysis reveals significant regional hypometabolism in the cerebellum, mesencephalic region, and medulla in the ABT-702-treated rats compared to the vehicle-treated rats[2].

Name: LY334370, CAS: 182563-08-2, stock 3.3g, assay 99%, MWt: 351.42, Formula: C21H22FN3O, Solubility: DMSO : ≥ 55.5 mg/mL (157.93 mM), Clinical_Informat: No Development Reported, Pathway: Neuronal Signaling;GPCR/G Protein, Target: 5-HT Receptor;5-HT Receptor, Biological_Activity: LY334370 is a selective 5-HT1F receptor agonist with a Ki of 1.6 nM.
IC50 & Target: Ki: 1.6 nM (5-HT1F)
In Vitro: LY334370 has no vasoconstrictor effects on human cerebral arteries in vitro until a dose of 10-5 M, at which it produces a contraction of 8.5±5.7%; however, this is not significant[1].
In Vivo: Following intravenous administration of LY334370 at 3 mg/kg (n=3) or 10 mg/kg (n=6) electrical stimulation evokes an increase in dural blood vessel diameter of 135±6% and 106±11%, respectively, which is not significantly different from the respective control values. LY334370 has no effect on dural blood vessel diameter per se, since the actual
dural blood vessel diameter is 43±4 arbitrary units before drug and 43±4 arbitrary units 15 min after injection of LY334370 (10 mg/kg)[1].

Name: Fantofarone SR 33557, CAS: 114432-13-2, stock 24.7g, assay 98.1%, MWt: 550.71, Formula: C31H38N2O5S, Solubility: DMSO : 150 mg/mL (272.38 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Membrane Transporter/Ion Channel;Neuronal Signaling, Target: Calcium Channel;Calcium Channel, Biological_Activity: Fantofarone is a highly potent Calcium Channel antagonist.
IC50 & Target: Calcium Channel[1].
In Vitro: It can be seen that the calcium channel blockers VIZ and Fantofarone (SR) possess a weak intrinsic antimalarial property compared to CQ, and both appear slightly more potent on the CQ-resistant than on the CQ-sensitive parasites. Interestingly, Fantofarone is ca. 10 times more potent than verapamil. Fantofarone (SR) is 10 times more potent than the phenylalkylamine verapamil (VR) on the two P. fdciparum strains. As revealed by the isobolograms, the two calcium channel blockers potentiate the CQ sensitivity activity on the CQ-resistant P. fufcipurum strain, verapamil appearing 2 to 3 times more potent than Fantofarone. Furthermore, when used at similar subinhibitory fractions of their IC50, VR is 2 to 3 times more potent than Fantofarone in decreasing CQ resistance[1].
In Vivo: Treatment with isosorbide dinitrate (0.3 mg/kg, i.v.) or Fantofarone (50 mg/kg, i.v.), a reduction is observed in the occurrence and severity of vasospasm, whereas verapamil (0.2 mg/kg, i.v.) is much less effective. Although it totally inhibits distal AIV, isosorbide dinitrate does not significantly affect proximal diameter decrease. The most potent compound with regard to both the distal and proximal vasospasms is Fantofarone, which significantly reduces AIV throughout the experiment. Verapamil does not reduce AIV significantly[2].

Name: Zaldaride maleate CGS-9343B;KW 5617, CAS: 109826-27-9, stock 17.9g, assay 98.6%, MWt: 544.60, Formula: C30H32N4O6, Solubility: 10 mM in H2O, Clinical_Informat: No Development Reported, Pathway: Neuronal Signaling;Membrane Transporter/Ion Channel, Target: nAChR;nAChR, Biological_Activity: Zaldaride maleate (CGS-9343B) is a potent and selective inhibitor of calmodulin. Zaldaride maleate (CGS-9343B) inhibits CaM (calmodulin)-stimulated cAMP phosphodiesterase activity, with an IC50 of 3.3 nM[1][2]. Zaldaride maleate (CGS-9343B) prevents estrogen-induced transcription activation by ER, reversibly blocks voltage-activated Na+, Ca2+ and K+ currents in PC12 cells and inhibits nAChR[3].
IC50 & Target: IC50: 3.3 nM (calmodulin)[1][2].

Name: Pimonidazole (hydrochloride), CAS: 70132-51-3, stock 35.3g, assay 98.5%, MWt: 290.75, Formula: C11H19ClN4O3, Solubility: H2O : 5 mg/mL (17.20 mM; ultrasonic and warming and heat to 80°C), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Pimonidazole is a novel hypoxia marker for complementary study of tumor hypoxia and cell proliferation in tumor[1]. Pimonidazole accumulates in hypoxic cells via covalent binding with macromolecules or by forming reductive metabolites after reduction of its nitro group, it can be used for qualitative and quantitative assessment of tumor hypoxia [2].

Name: Pimonidazole, CAS: 70132-50-2, stock 16.2g, assay 98.8%, MWt: 254.29, Formula: C11H18N4O3, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Pimonidazole is a novel hypoxia marker for complementary study of tumor hypoxia and cell proliferation in tumor[1]. Pimonidazole accumulates in hypoxic cells via covalent binding with macromolecules or by forming reductive metabolites after reduction of its nitro group, it can be used for qualitative and quantitative assessment of tumor hypoxia [2].

Name: CP-547632 (hydrochloride), CAS: 252003-71-7, stock 26.5g, assay 98.4%, MWt: 568.86, Formula: C20H25BrClF2N5O3S, Solubility: DMSO : 38.33 mg/mL (67.38 mM; Need ultrasonic); H2O : < 0.1 mg/mL (insoluble), Clinical_Informat: No Development Reported, Pathway: Protein Tyrosine Kinase/RTK;Protein Tyrosine Kinase/RTK, Target: VEGFR;FGFR, Biological_Activity: CP-547632 hydrochloride 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 hydrochloride 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 hydrochloride has antitumor efficacy[1].
In Vitro: CP-547632 hydrochloride (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 hydrochloride (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 hydrochloride (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: MRE3008F20, CAS: 252979-43-4, stock 2.9g, assay 98.4%, MWt: 432.44, Formula: C21H20N8O3, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein, Target: Adenosine Receptor, Biological_Activity: MRE3008F20 is a highly potent and selective antagonist of adenosine A3 receptor (AA3R), inhibits agonist-induced cAMP elevation in resting T lymphocytes with an IC50 of 5 nM[1].
IC50 & Target: IC50 : 5 nM (AA3R, resting T lymphocytes)[1]

Name: N3-PEG3-CH2COOH PROTAC Linker 14, CAS: 172531-37-2, stock 24.2g, assay 98.2%, MWt: 233.22, Formula: C8H15N3O5, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: PROTAC, Target: PROTAC Linker, Biological_Activity: N3-PEG3-CH2COOH (PROTAC Linker 14) is a PROTAC linker, which refers to the PEG composition. N3-PEG3-CH2COOH can be used in the synthesis of a series of PROTACs. PROTACs contain two different ligands connected by a linker; one is a ligand for an E3 ubiquitin ligase and the other is for the target protein. PROTACs exploit the intracellular ubiquitin-proteasome system to selectively degrade target proteins[1].

Name: Lidorestat IDD-676, CAS: 245116-90-9, stock 8.4g, assay 98.2%, MWt: 376.35, Formula: C18H11F3N2O2S, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Aldose Reductase, Biological_Activity: Lidorestat (IDD-676) is a potent, selective and orally active aldose reductase inhibitor with an IC50 of 5 nM. Lidorestat can be used to treat chronic diabetes complications. Lidorestat also improves nerve conduction and reduces cataract formation[1][2][3].
IC50 & Target: IC50: 5 nM (Rldose reductase)[1]
In Vitro: From in vitro experiments, Lidorestat has a reported IC50 against recombinant human aldose reductase (/h/-ALR2) of 5 μM. Against recombinant human aldehyde reductase (/h/-ALR1), Lidorestat has a reported IC50 of 27,000 μM, yielding a selectivity of /h/-ALR1//h/-ALR2 of 5400:1[1][2].
In Vivo: Lidorestat (25 mg/kg/day; oral administration; twice daily; for 6 weeks; diabetic mice) treatment decreases fructose and reduces mortality in diabetic hAR-expressing mice. And Lidorestat does not affect weight[1].

Name: Adenosine A1 receptor activator T62, CAS: 40312-34-3, stock 34.8g, assay 98.9%, MWt: 291.80, Formula: C15H14ClNOS, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein, Target: Adenosine Receptor, Biological_Activity: Adenosine A1 receptor activator T62 is an allosteric enhancer of adenosine A1 receptor. Adenosine A1 receptor activator T62 produces antinociception in animal models of acute pain and also reduces hypersensitivity in models of inflammatory and nerve-injury pain[1][2][3].
IC50 & Target: Adenosine A1 receptor[1]
In Vivo: Adenosine A1 receptor activator T62 (0.3-3 μg; intrathecal administration; male SpragueDawley rats) treatment produces a dose-dependent antihypersensitivity effect, with no effect on ambulation or activity level[1].

Name: Fidarestat SNK 860, CAS: 136087-85-9, stock 37.2g, assay 98.6%, MWt: 279.22, Formula: C12H10FN3O4, Solubility: DMSO : 250 mg/mL (895.35 mM; Need ultrasonic), Clinical_Informat: Launched, Pathway: Metabolic Enzyme/Protease, Target: Aldose Reductase, Biological_Activity: Fidarestat (SNK 860) is an inhibitor of aldose reductase, with IC50s of 26 nM, 33 μM, and 1.8 μM for aldose reductase, AKR1B10 and V301L AKR1B10, respectively; Fidarestat (SNK 860) has the potential to treat diabetic disease.
IC50 & Target: IC50: 26 nM (Aldose reductase), 33 μM (AKR1B10), 1.8 μM (V301L AKR1B10)[1]
In Vitro: Fidarestat is an inhibitor of aldose reductase, with IC50s of 26 nM, 33 μM, and 1.8 μM for aldose reductase, AKR1B10 and V301L AKR1B10, respectively[1].
In Vivo: Fidarestat (SNK-860; 1 or 4 mg/kg. p.o., daily for 4 weeks) reduces the concentrations of sorbitol and fructose in diabetic rats[2].

Name: Meclinertant SR 48692, CAS: 146362-70-1, stock 29g, assay 98.7%, MWt: 587.07, Formula: C32H31ClN4O5, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein;Neuronal Signaling, Target: Neurotensin Receptor;Neurotensin Receptor, Biological_Activity: Meclinertant (SR 48692) is a potent, selective, nonpeptide and orally active neurotensin receptor 1 (NTS1) antagonist. In human colon carcinoma (HT-29) cells, Meclinertant competitively antagonizes neurotensin-induced intracellular Ca2+ mobilization with a pA2 values of 8.13. Meclinertant has anxiolytic, anti-addictive and memory-impairing effects[1][2][3].
IC50 & Target: Neurotensin receptor 1 (NTS1)[1]
In Vitro: In vitro, Meclinertant (SR 48692) competitively inhibits 125I-labeled neurotensin binding to the high-affinity binding site present in brain tissue from various species with IC50 values of 0.99 nM (guinea pig), 4.0 nM (rat mesencephalic cells), 7.6 nM (COS-7 cells transfected with the cloned high-affinity rat brain receptor), 13.7 nM (newborn mouse brain), 17.8 nM (newborn human brain), 8.7 nM (adult human brain), and 30.3 nM (HT-29 cells). Meclinertant also displaces 125I-labeled neurotensin from the low-affinity levocabastine-sensitive binding sites but at higher concentrations (34.8 nM for adult mouse brain and 82.0 nM for adult rat brain)[1]. 
In guinea pig striatal slices, Meclinertant blocks K+-evoked release of [3H]dopamine stimulated by neurotensin with a potency (IC50 = 0.46 nM) that correlates with its binding affinity[1].
In Vivo: Meclinertant (SR 48692) treatment reverses at 80 μg/kg the turning behavior induced by intrastriatal injection of neurotensin in mice and with a long duration of action (6 hours)[1].

Name: MRS-1706, CAS: 264622-53-9, stock 2g, assay 98.7%, MWt: 503.55, Formula: C27H29N5O5, Solubility: DMSO : 6.4 mg/mL (12.71 mM; Need ultrasonic and warming); H2O : < 0.1 mg/mL (insoluble), Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein, Target: Adenosine Receptor, Biological_Activity: MRS-1706 is a potent and selective adenosine A2B receptor inverse agonist. MRS-1706 has Ki values of 1.39, 112, 157, and 230 nM for human A2B, A2A, A1 and A3 receptors respectively[1][2].
IC50 & Target: Ki: 1.39 (human A2B receptor), 112 (human A2A receptor), 157 (human A1 receptor), 230 nM (human A3 receptor)[2]

Name: NKH477 Colforsin dapropate hydrochloride, CAS: 138605-00-2, stock 13.8g, assay 98.2%, MWt: 546.09, Formula: C27H44ClNO8, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein, Target: Adenylate Cyclase, Biological_Activity: NKH477 (Colforsin dapropate hydrochloride) is a novel water-soluble forskolin derivative that improves cardiac failure mainly through its beneficial effects on diastolic cardiac function. NKH477 directly activates the catalytic unit of adenylate cyclase and increases intracellular cAMP. NKH477 exerts an antiproliferative effect in vivo with an altered cytokine profile to inhibit the acute rejection of rat orthotopic lung allografts[1].
IC50 & Target: Adenylate Cyclase[1]
In Vivo: NKH477 (Colforsin dapropate hydrochloride) (orally; 1-3 mg/kg/day; days 3 and 5) prolonged lung allograft survival in a dose dependent manner[1].

Name: KH7, CAS: 330676-02-3, stock 33.9g, assay 98.7%, MWt: 419.30, Formula: C17H15BrN4O2S, Solubility: H2O : < 0.1 mg/mL (insoluble); DMSO : ≥ 100 mg/mL (238.49 mM), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: KH7 is a soluble adenylyl cyclase (sAC)-specific inhibitor, with IC50s of 3-10 μM toward both recombinant purified human sACt protein and heterologously expressed sACt in cellular assays[1].
IC50 & Target: IC50: 3-10 μM (recombinant sACt)[1].

Name: Amibegron hydrochloride SR 58611A, CAS: 121524-09-2, stock 15.4g, assay 98.7%, MWt: 440.36, Formula: C22H27Cl2NO4, Solubility: 10 mM in DMSO, Clinical_Informat: Phase 3, Pathway: GPCR/G Protein;Neuronal Signaling, Target: Adrenergic Receptor;Adrenergic Receptor, Biological_Activity: Amibegron hydrochloride is a selective β3-adrenoceptor agonist, with an EC50 of 3.5 nM for β-adrenoceptor in rat colon; Amibegron hydrochloride has anxiolytic and antidepressant activity.
IC50 & Target: EC50: 3.5 nM (β-adrenoceptor, from rat colon), 499 nM (β-adrenoceptor, from rat uterus)[1], 1.2 μM (β2-adrenoceptor, from cerebellum), 4.6 μM (β1-adrenoceptor1, from cortex)[2]
In Vitro: Amibegron hydrochloride (SR 58611A) is a selective β-adrenoceptor agonist, with an EC50 of 3.5 nM for β-adrenoceptor in rat colon, and 499 nM in rat uterus[1]. Amibegron hydrochloride (SR 58611A) shows little effect on β1- and β2-adrenoceptors, 5-HT uptake, noradrenaline (NA) uptake, and dopamine (DA) uptake from rat brain tissue, with IC50s of 4.6 and 1.2, 0.58, 2.5 and 3.2 μM, respectively; exhibits no effect on 5-HT1A, 5-HT2, MAO-A and MAO-B (IC50 > 10 μM)[2].
In Vivo: Amibegron hydrochloride (SR 58611A, 0.1 to 0.3 mg/kg, i.p.) potentiates the toxicity produced by yohimbine in mice. Amibegron hydrochloride (0.6 and 2 mg/kg, i.p.) is also active in the learned helplessness model of antidepressant-like activity in rats. However, Amibegron hydrochloride exhibits no effect on the spontaneous locomotor activity of mice at up to 10 mg/kg and of rats at up tp 30 mg/kg[2]. Amibegron hydrochloride (3 and 10 mg/kg, p.o.) increases the synthesis of 5-HT and tryptophan (Trp) levels in several rodent brain areas such as cortex, hippocampus, hypothalamus, striatum. In addition, Amibegron hydrochloride (10 mg/kg, p.o.) promotes the release of 5-HT in rat prefrontal cortex. Systemic (3 mg/kg, i.v.) or chronic administration of SR58611A (10 mg/kg, p.o.) does not affect the activity of serotonergic neurons in the rat dorsal raphe nucleus[3].

Name: DSP-4 (hydrochloride) Neurotoxin DSP 4 (hydrochloride), CAS: 40616-75-9, stock 0.1g, assay 98.9%, MWt: 313.06, Formula: C11H16BrCl2N, Solubility: DMSO : 125 mg/mL (399.28 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: DSP-4 hydrochloride (Neurotoxin DSP 4 hydrochloride) is a highly selective neurotoxin and readily passes the blood-brain barrier with neurotoxic effects on noradrenergic neurons of adult and developing rats, can be used for the temporary selective degradation of the central and peripheral noradrenergic neurons, mainly those from the locus coeruleus (LC)[1][2].

Name: Bucindolol, CAS: 71119-11-4, stock 31.4g, assay 98.3%, MWt: 363.45, Formula: C22H25N3O2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein;Neuronal Signaling, Target: Adrenergic Receptor;Adrenergic Receptor, Biological_Activity: Bucindolol is a β1-adrenergic receptor blocker, with intrinsic sympathomimetic activity, used in the research of heart failure[1].

Name: β-Amyloid (1-15) Amyloid β-Protein (1-15), CAS: 183745-81-5, stock 13.4g, assay 98.5%, MWt: 1826.84, Formula: C78H107N25O27, Solubility: 10 mM in H2O, Clinical_Informat: No Development Reported, Pathway: Neuronal Signaling, Target: Amyloid-β, Biological_Activity: β-Amyloid (1-15) is a fragment of β-Amyloid peptide. Beta-amyloid is a peptide that forms amyloid plaques in the brains of Alzheimer's disease (AD) patients.
IC50 & Target: Amyloid-β[1]
In Vitro: β-Amyloid (1-15) is produced by concerted β- and α-secretase cleavage of amyloid-β protein precursor (AβPP). β-Amyloid (1-15) seems to be a sensitive acute pharmacodynamic biomarker for γ-secretase inhibition and may have several advantages compared to measuring longer CSF Aβ species. [1].

Name: Myelin Basic Protein (MBP) (68-82), guinea pig, CAS: 98474-59-0, stock 18.2g, assay 98.6%, MWt: 1736.79, Formula: C71H113N23O28, Solubility: H2O, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Myelin Basic Protein (MBP) (68-82), guinea pig is a fragment of myelin basic protein (MBP).
In Vitro: Multiple sclerosis is the most common autoimmune disorder affecting the central nervous system. In this study, whole blood samples are analyzed for activation capacity and the activatability of CD4+ and CD8+ T-lymphocytes by human total myelin basic protein (MBP), human MBP 104-118 fragment, and guinea pig MBP (68-82) fragment. A significant increase in the number of activated T-lymphocytes was observed in the whole blood. For all three tested MBPs, this increase in activated CD4+ and CD8+ T-lymphocytes is statistically significant (p<0.01). However, this increase in activated T-cells is most prominent following incubation with human total MBP, followed by human 104-118 fragment; the smallest increase is observed following incubation with guinea pig MBP (68-82) fragment (human total MBP>huMBP-104-118>guinea pig MBP (68-82))[1].
In Vivo: Whether pretreatment with bee venom acupuncture (BVA) from the same day of MBP (68-82) immunization can affect the induction and progression of experimental autoimmune encephalomyelitis (EAE) and weight loss is examined. At 5-9 days after immunization, rats in the myelin basic protein (MBP) group start displaying partial loss of tail tonus (clinical signs, 0.5) in a freely moving environment. At 10-16 days after immunization, most of the rats in the MBP group display more severe symptoms of neurological deficit including paraparesis of the hindlimb, paraplegia, tetraparesis, and tetraplegia. In contrast, rats in the MBP + BVA group display relatively slight neurological deficits in a dose-dependent manner at 11-15 days after immunization, compared to the rats in the MBP group. The onset of symptoms is slightly delayed (BVA 0.8 mg/kg, 6.4±0.6 days) and the maximal clinical score is markedly decreased (BVA 0.25 mg/kg, 3.7±0.2; BVA 0.8 mg/kg, 2.8±0.3), compared to that in the MBP group. At this time, the mean body weight of rats in the MBP group is decreased as compared to that of rats in the normal group, but it is significantly increased in rats of the MBP + BVA group as compared to rats in the MBP group[2].

Name: Orexin A (human, rat, mouse), CAS: 205640-90-0, stock 7.9g, assay 98.8%, MWt: 3561.10, Formula: C152H243N47O44S4, Solubility: H2O, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Orexin A human, rat, mouse is a 33 amino acid excitatory neuropeptide. Orexin A human, rat, mouse works on 2 specific G protein-coupled receptors (GPCRs): orexin-1 (OX1) and orexin-2 (OX2)[1].

Name: β-amyloid (12-28) Amyloid β-Protein (12-28), CAS: 107015-83-8, stock 5.8g, assay 98.3%, MWt: 1955.18, Formula: C89H135N25O25, Solubility: 10 mM in H2O, Clinical_Informat: No Development Reported, Pathway: Neuronal Signaling, Target: Amyloid-β, Biological_Activity: β-amyloid (12-28) is a 17-aa peptide fragment, which can produce amyloid aggregates, used in the research of Alzheimer’s disease.
IC50 & Target: Amyloid-β[1]
In Vitro: β-amyloid (12-28) preared freshly in solution has no cytotoxicity, but aged β12-28 peptide (0.001-40 μM) reduces the viability of PC12 cells in a concentration dependent manner[1].

Name: Delcasertib KAI-9803;BMS-875944, CAS: 949100-39-4, stock 29.2g, assay 98.2%, MWt: 2880.28, Formula: C120H199N45O34S2, Solubility: DMSO : ≥ 100 mg/mL (34.72 mM), Clinical_Informat: Phase 2, Pathway: TGF-beta/Smad;Epigenetics, Target: PKC;PKC, Biological_Activity: Delcasertib (KAI-9803) is a potent and selective δ-protein kinase C (δPKC) inhibitor.
IC50 & Target: δPKC[1]
In Vitro: Delcasertib (KAI-9803) is composed of a selective δ-protein kinase C (δPKC) inhibitor peptide derived from the δV1-1 portion of δPKC (termed “cargo peptide”), conjugated reversibly to the cell-penetrating peptide 11-amino acid, arginine-rich sequence of the HIV type 1 transactivator protein (TAT47–57; termed “carrier peptide”) via a disulfide bond[1].
In Vivo: Delcasertib (KAI-9803) administration at the end of ischemia has been found to reduce cardiac damage caused by ischemia-reperfusion in a rat model of acute myocardial infarction. 14C-KAI-9803 is rapidly delivered to many tissues, including the heart (1.21 μg eq/g tissue), while being quickly cleared from the systemic circulation. The distribution of Delcasertib (KAI-9803) to tissues such as the liver, kidney, and heart is facilitated by the reversible conjugation to TAT47–57[1]. KAI-9803 ameliorates pathological conditions in acute myocardial infarction and reduce pain via specific modulation of membrane-translocation of PKC delta or epsilon. Delcasertib (KAI-9803) has an acceptable safety and tolerability profile when delivered via intracoronary injection during primary percutaneous coronary intervention for ST-segment elevation myocardial infarction[2].

Name: Amyloid β-Protein (10-20), CAS: 152286-31-2, stock 7.9g, assay 98.1%, MWt: 1446.65, Formula: C71H99N17O16, Solubility: 10 mM in H2O, Clinical_Informat: No Development Reported, Pathway: Neuronal Signaling, Target: Amyloid-β, Biological_Activity: Amyloid β-Protein (10-20) is a fragment of Amyloid-β peptide, maybe used in the research of neurological disease.
IC50 & Target: Amyloid-β[1]
In Vitro: Amyloid β-Protein (10-20) is a fragment of Amyloid-β peptide[1].

Name: Loreclezole R 72063, CAS: 117857-45-1, stock 3.4g, assay 98.2%, MWt: 274.53, Formula: C10H6Cl3N3, Solubility: DMSO : 110 mg/mL (400.68 mM; Need ultrasonic); H2O : < 0.1 mg/mL (insoluble), Clinical_Informat: No Development Reported, Pathway: Neuronal Signaling;Membrane Transporter/Ion Channel, Target: GABA Receptor;GABA Receptor, Biological_Activity: Loreclezole, an antiepileptic compound, is a selective GABAA receptor modulator and acts as a positive allosteric modulator of β2 or β3-subunit containing receptors[1][2].
IC50 & Target: GABAA receptor[1].

Name: PF 04531083, CAS: 1079400-07-9, stock 32.5g, assay 98.4%, MWt: 357.79, Formula: C17H16ClN5O2, Solubility: DMSO : 125 mg/mL (349.37 mM; Need ultrasonic), Clinical_Informat: Phase 2, Pathway: Membrane Transporter/Ion Channel, Target: Sodium Channel, Biological_Activity: PF 04531083 is a selective NaV1.8 blocker, and used for the research of neuropathic/inflammatory pain.
IC50 & Target: NaV1.8[1]

Name: GYKI53655 hydrochloride, CAS: 143692-48-2, stock 9.7g, assay 98.3%, MWt: 388.85, Formula: C19H21ClN4O3, Solubility: H2O : 8 mg/mL (20.57 mM; Need ultrasonic and warming); DMSO : ≥ 160 mg/mL (411.47 mM), Clinical_Informat: No Development Reported, Pathway: Membrane Transporter/Ion Channel;Neuronal Signaling, Target: iGluR;iGluR, Biological_Activity: GYKI53655 hydrochloride is an α-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA) antagonist.
IC50 & Target: AMPA[1]</up>
In Vitro: GYKI53655 hydrochloride (LY300168) inhibits α-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA) (10 μM)-induced responses with IC50 value of 5.9±0.1 μM. GYKI53655 hydrochloride inhibits AMPA (10 μM) responses in
recombinant G1uR4 expressing HEK293 cells with IC50 value of 4.6±0.4 μM. Using 3 μM cyclothiazide the inhibition produced by GYKI53655 hydrochloride is 79±2% (n=4 cells). GYKI53655 hydrochloride produces only small inhibitions of kainate-induced currents at 30 μM and inhibits kainate-induced currents at a concentration of 100 μM by 12±2 (n=4) and 18±4 (n=4), respectively. GYKI53655 hydrochloride inhibits AMPA receptor-mediated responses in cerebella Purkinje neurons with an IC50 value of 1.5±0.1 μM[1].
In Vivo: GYKI53655 hydrochloride (4 mg/kg) is found to have a short-lasting depressant effect on neuronal responses to iontophoretic
α-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA), with a half-recovery time of approximately 7 min. GYKI53655 hydrochloride (4 and 8 mg/kg) substantially depresses or completely abolishes AMPA responses. Results demonstrate the dose-dependence of GYKI53655 hydrochloride (2 to 8 mg/kg) in depressing responses to AMPA. At the highest doses tested, GYKI53655 hydrochloride reduces AMPA responses to a comparable degree[2]. Tonic fit and death are completely prevented by GYKI53655 hydrochloride at dose over 5.0 mg/kg. The ED50 value of
GYKI53655 hydrochloride is 2.2 mg/kg i.p. The maximal effects of GYKI53655 hydrochloride lasts 3 h then the exit inhibition effect of GYKI53655 hydrochloride falls to 20% 1 h later[3].

Name: Smilagenin, CAS: 126-18-1, stock 1.2g, assay 98.5%, MWt: 416.64, Formula: C27H44O3, Solubility: DMSO : < 1 mg/mL (insoluble or slightly soluble); Ethanol : ≥ 10 mg/mL (24.00 mM), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Smilagenin (SMI) is a lipid-soluble small-molecule steroidal sapogenin from Rhizoma anemarrhenae and Radix asparagi widely used in traditional Chinese medicine for treating chronic neurodegeneration diseases[1].
Smilagenin (SMI) improves memory of aged rats by increasing the muscarinic receptor subtype 1 (M1)-receptor density[2].
Smilagenin (SMI) attenuates Aβ(25-35)-induced neurodegenerationvia stimulating the gene expression of brain-derived neurotrophic factor, may represents a novel therapeutic strategy for AD[3].
In Vitro: Smilagenin (10 μM; 24 hours) increases SH-SY5Y cell survival compared with Aβ(25-35) intoxicated cells[3].
Smilagenin (10 μM; 24 hours) increases neurotrophic factor (GDNF) and neurotrophic factor (BDNF) mRNA level by promoting CREB phosphorylation in 1-methyl-4-phenylpyridimium (MPP+) treated SH-SY5Y cells[2].
In Vivo: Smilagenin (intragastric administration; 10 or 26 mg/kg, once daily; 60 days) prevents the impairment of dopaminergic neurons in chronic MPTP/probenecid-induced mouse model[2].

Name: BAY 73-6691 (R)-BAY 73-6691, CAS: 794568-92-6, stock 30.4g, assay 98.4%, MWt: 356.73, Formula: C15H12ClF3N4O, Solubility: DMSO : 160 mg/mL (448.52 mM; Need ultrasonic and warming); H2O : < 0.1 mg/mL (insoluble), Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Phosphodiesterase (PDE), Biological_Activity: BAY 73-6691 is a potent, selective brain penetrant PDE9A inhibitor.
IC50 & Target: PDE9A[1]
In Vitro: The BAY 73-6691 dose-dependently alleviates cell viability loss due to Aβ25-35 treatment. It is found that when SH-SY5Y cells are cultured by Aβ25-35, a high degree of cell apoptosis is observed, while additional stimulation with BAY 73-6691 causes attenuation of cell apoptosis. BAY 73-6691 dose-dependently attenuates oxidative stress induced by Aβ25-35, and BAY 73-6691 at 200 μg/mL almost neutralizes Aβ25-35-induced oxidative damage. The BAY 73-6691 attenuates Aβ25-35-induced increase of apoptosis cells[1].
In Vivo: BAY 73-6691 dose-dependently improves the acquisition performance in the Aβ25-35-injected mice on days 7 to 10 (day 7, F(5,54)=65.153; day 8, F(5,54)=62.340; day 9, F(5,54)=37.529; day 10, F(5,54)=38.624; P<0.001). BAY 73-6691 at 3 mg/kg can almost completely abolish the prolongation of escape-latency on days 9 to 10. BAY 73-6691 dose-dependently elevates the Aβ25-35-induced decrease of the dwell time on the 10th day post Aβ25-35 injection (day 10, F(5,54)=27.360, P<0.001). Results reveal that the Aβ25-35 injection and BAY 73-6691 treatment cause no influence on the swimming speed. Treatment with BAY 73-6691 does not cause detectable alteration of spatial memory in sham mice. BAY 73-6691 alleviates Aβ25-35-induced abnormalities of the above indices. The BAY 73-6691 causes no influence on the four indices mentioned above in sham mice. The BAY 73-6691 has no significant effect on the apoptosis of hippocampal neurons in sham mice[1].

Name: HMR 1556, CAS: 223749-46-0, stock 7.5g, assay 98.3%, MWt: 411.44, Formula: C17H24F3NO5S, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Membrane Transporter/Ion Channel, Target: Potassium Channel, Biological_Activity: HMR 1556, a chromanol derivative, is a IKs blocker with IC50s of 10.5 nM and 34 nM in canine and guinea pig left ventricular myocytes, respectively[1][2].
IC50 & Target: IC50: 10.5 nM (IKs in canine left ventricular myocytes), 34 nM (IKs in guinea pig left ventricular myocytes)[1]
In Vitro: HMR 1556 inhibits Ito, ICa,L and IKr with IC50s of 33.9 μM, 27.5 μM, 12.6 μM in canine left ventricular myocytes, respectively[1].

Name: Carcainium (chloride) QX 572;RSD 931, CAS: 1042-42-8, stock 19.1g, assay 98.7%, MWt: 347.84, Formula: C18H22ClN3O2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Carcainium chloride (QX 572) is a quaternary derivative of the local anesthetic Lidocaine. Antitussive effect[1][2].

Name: D,L-Buthionine-(S,R)-sulfoximine Butionine sulfoximine, CAS: 5072-26-4, stock 5.3g, assay 98.4%, MWt: 222.31, Formula: C8H18N2O3S, Solubility: H2O : 41.67 mg/mL (187.44 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Apoptosis, Target: Ferroptosis, Biological_Activity: D,L-Buthionine-(S,R)-sulfoximine is a potent inhibitor of glutamylcysteine synthetase biosynthesis.
IC50 & Target: glutamylcysteine synthetase[1]
In Vitro: Buthionine sulfoximine is an analogs of methionine sulfoximine and inhibits gamma-glutamylcysteine synthetase about 20 times more effectively than prothionine sulfoximine and at least 100 times more effectively than methionine sulfoximine[1].
In Vivo: Treatment of mice bearing HT1080 and HT1080/DR4 xenografts with a continuous i.v infusion of nontoxic doses of D,L-Buthionine-(S,R)-sulfoximine (300 and 600 mg/kg/day) produce a 60% reduction of GSH plasma levels and greater than 95 % reduction in GSH tumor levels in both parental and multidrug-resistant tumors[2].

Name: Dexanabinol HU-211, CAS: 112924-45-5, stock 31g, assay 98.2%, MWt: 386.57, Formula: C25H38O3, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Immunology/Inflammation;Apoptosis;NF-κB, Target: Interleukin Related;TNF Receptor;NF-κB, Biological_Activity: Dexanabinol (HU-211) is an artificially synthesized cannabinoid derivative and lacks cannabimimetic effects. Dexanabinol exhibits not only the antioxidant and neuroprotective activities in brain but also anti-inflammatory activity by inhibiting NF-κB and decreasing cytokines such as TNFα and interleukin-6, which could ensure the integrity of BBB and reduce cell apoptosis and death. Dexanabinol is widely used in head injury or stroke treatment and has been shown to be safe in animals and humans[1].

Name: GSK-626616, CAS: 1025821-33-3, stock 27.7g, assay 98.5%, MWt: 401.27, Formula: C18H10Cl2N4OS, Solubility: DMSO : 50 mg/mL (124.60 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Protein Tyrosine Kinase/RTK, Target: DYRK, Biological_Activity: GSK-626616 is a potent, orally bioavailable inhibitor of DYRK3 (IC50=0.7 nM). GSK-626616 inhibits other members of the DYRK family (e.g., DYRK1A and DYRK2) with similar potency, which is a potential therapy for the treatment of anemia[1].
IC50 & Target: IC50: 0.7 nM (DYRK3)[1]

Name: Neu2000, CAS: 640290-67-1, stock 36.7g, assay 98.5%, MWt: 383.22, Formula: C15H8F7NO3, Solubility: DMSO : ≥ 112.5 mg/mL (293.57 mM), Clinical_Informat: No Development Reported, Pathway: Membrane Transporter/Ion Channel;Neuronal Signaling, Target: iGluR;iGluR, Biological_Activity: Neu2000 is an uncompetitive N-methyl-D-aspartate (NMDA) receptor antagonist.
IC50 & Target: NMDA receptor[1]
In Vitro: Neu2000 shows apparent neuroprotection against 300 μM N-methyl-D-aspartate (NMDA) at doses as low as 30 μM. Neu2000 does not protect cortical neurons against α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid- or kainate-mediates excitotoxicity. Neu2000 inhibits the electrophysiologic response of cultured cortical neurons to 300 μM NMDA in a concentration-dependent manner, indicating that the effect is mediated by a specific action at NMDA receptors. The Neu2000 dose-response has an IC50 of 35.38±5.94 μM and Hill's coefficient of 0.91 (n=8). Neu2000 (100 μM) significantly reduces the maximal NMDA response by 58.31±2.72% (n=5) and the EC50 values of NMDA from 18.88±1.85 to 9.92±0.17 μM (n=5, P<0.05)[1].
In Vivo: Pharmacokinetic analysis reveals that the half-life of Neu2000 is 1.42, 2.14, and 1.79 h following intraperitoneal administration of 10, 25, and 50 mg/kg, respectively. In addition, the Cmax (maximum plasma concentration) is calculated as 3.86, 18.73, and 52.83 μg/mL and the AUC (area under the curve) is determined to be 7.37, 55.15, and 96.77 μg/h/mL at the same respective doses. The levels of basal mitochondrial ROS are significantly elevated at 24 h post-surgery in both the vehicle-treated (4.1-fold, p<0.01) and Neu2000-treated (2.9-fold, p<0.01) groups compare to sham controls. The results of blood-brain barrier (BBB) test also reveals significant changes in open field locomotion in spinal cord-injured animals treated with Neu2000 compare to vehicle-treated animals. Single (p<0.05) or repeated (p<0.01) Neu2000 treatment results in a decreased swing to stance ratio compare to vehicle-treated animals. Repeated treatment with Neu2000 results in a 45.6% decrease (p<0.01) in overall lesion volume compare to vehicle treatment, while a single administration of Neu2000 results in a 36.8% decrease (p<0.05) in overall lesion volume[2].

Name: Rentiapril SA-446, CAS: 80830-42-8, stock 1.5g, assay 98.1%, MWt: 313.39, Formula: C13H15NO4S2, Solubility: DMSO : 200 mg/mL (638.18 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Angiotensin-converting Enzyme (ACE), Biological_Activity: Rentiapril is an orally active angiotensin converting enzyme (ACE) inhibitor with antihypertensive activity[1][2].
IC50 & Target: Angiotensin converting enzyme[1]

Name: Dicentrine, CAS: 517-66-8, stock 7g, assay 98.6%, MWt: 339.39, Formula: C20H21NO4, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein;Neuronal Signaling, Target: Adrenergic Receptor;Adrenergic Receptor, Biological_Activity: Dicentrine is a natural product isolated from the plant Lindera megaphylla with antihypertensive effect. Dicentrine is an α1-adrenoceptor antagonist which has effective against human hyperplastic prostates[1].
IC50 & Target: α1-adrenoceptor[1]

Name: Colivelin, CAS: 867021-83-8, stock 9.8g, assay 98.6%, MWt: 2645.10, Formula: C119H206N32O35, Solubility: 10 mM in H2O, Clinical_Informat: No Development Reported, Pathway: Neuronal Signaling;JAK/STAT Signaling;Stem Cell/Wnt, Target: Amyloid-β;STAT;STAT, Biological_Activity: Colivelin is a neuroprotective peptide and activator of STAT3.
IC50 & Target: STAT3, Amyloid-β[1]
In Vitro: Colivelin is a hybrid peptide composed of ADNF and AGA-(C8R)HNG17, a potent Humanin (HN) derivative[2]. Humanin (HN) and its derivatives, such as Colivelin (CLN), suppress neuronal death induced by insults related to Alzheimer's disease (AD) by activating STAT3[1]. Colivelin completely suppresses death induced by overexpressed FAD-causative genes and A 1-43 at a concentration of 100 fM, whereas AGA-(C8R)HNG17 does so at a concentration of 10 pM[2].
In Vivo: Humanin (HN) and its derivatives, such as Colivelin (CLN) also ameliorate functional memory impairment of mice induced by anticholinergic drugs or soluble toxic amyloid-β (Aβ) [1]. Intracerebroventricular administration of Colivelin not only completely suppresses impairment in spatial working memory induced by repetitive intracerebroventricular injection of Aβ25-35 or Aβ1-42, but also it antagonizes neuronal loss in the CA1 region of hippocampus induced by hippocampal injection of Aβ1-42[2].

Name: CITCO, CAS: 338404-52-7, stock 2.9g, assay 99%, MWt: 436.74, Formula: C19H12Cl3N3OS, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Apoptosis, Target: Apoptosis, Biological_Activity: CITCO, an imidazothiazole derivative, is a selective Constitutive androstane receptor (CAR) agonist. CITCO inhibits growth and expansion of brain tumour stem cells (BTSCs) and has an EC50 of 49 nM over pregnane X receptor (PXR), and no activity on other nuclear receptors[1].
IC50 & Target: CAR, PXR[1]
In Vitro: CITCO (1-50 μM; 48 hours) results in a dose-dependent inhibition of viable cell count and proliferation in both T98G and U87MG glioma and BTSCs[1]. 
CITCO (2.5, 5 μM; 48 hours) induces cell cycle arrest differentially in different BTSCs in culture, but not in normal astrocytes[1]. 
CITCO (2.5-10 μM; 48 hours) induces apoptosis in BTSCs in culture in dose dependently, but not in normal astrocytes[1]. 
CITCO (0-25 μM; 48 hours) causes the T98G and U87MG glioma and BTSCs expressing very low levels of CAR protein that increased significantly[1].
In Vivo: CITCO (intraperitoneal; on days 22, 24, 26, 30 and 36) with 25 μg results a significant decrease in tumour growth, which further decreases to an undetectable level after treatment with 100 μg CITCO [1].

Name: Toyocamycin Vengicide, CAS: 606-58-6, stock 3.5g, assay 98.2%, MWt: 291.26, Formula: C12H13N5O4, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Cell Cycle/DNA Damage, Target: IRE1, Biological_Activity: Toyocamycin (Vengicide) is an adenosine analog produced by Actinomycete, acts as an XBP1 inhibitor, inhibits IRE1α-induced ATP-dependent XBP1 mRNA cleavage, with an IC50 of 80 nM. Toyocamycin (Vengicide) induces apoptosis. Toyocamycin (Vengicide) shows no effect on IRE1α auto-phosphorylation[1].
IC50 & Target: IC50: 80 nM (XBP1 activation)[1]

Name: Voclosporin ISAtx-247, CAS: 515814-01-4, stock 28.6g, assay 98.7%, MWt: 1214.62, Formula: C63H111N11O12, Solubility: DMSO : ≥ 50 mg/mL (41.17 mM); H2O : < 0.1 mg/mL (insoluble), Clinical_Informat: Phase 3, Pathway: Others, Target: Others, Biological_Activity: Voclosporin is a calcineurin (CN) inhibitor.
IC50 & Target: Calcineurin[1]
In Vitro: This novel semi-synthetic calcineurin (CN) inhibitor is designated Voclosporin (ISATX247). The efficacy of Voclosporin as an immunosuppressive agent is examined using an in vitro calcineurin assay[1]. Voclosporin (ISATX247) is a calcineurin inhibitor that has shown more potency than Cyclosporine in vitro[2].
In Vivo: All animals tolerate Voclosporin (ISATX247) and Cyclosporine A (CsA) very well. There are no severe adverse effects associated with either drug. In the Voclosporin group, all animals except 1 have diarrhea of different durations during the study (mean 2.3 days, range 2 to 7 days). This differs from the CsA and the control groups, where no animals have diarrhea. Mean weight loss at the end of the study is slightly higher in the Voclosporin group than in the CsA and control groups (3.4% vs 2.0% and 1.0%, respectively)[2].

Name: Dexetimide (+)-Benzetimide;(S)-(+)-Dexetimide;Dexbenzetimide, CAS: 21888-98-2, stock 1.7g, assay 98.8%, MWt: 362.46, Formula: C23H26N2O2, Solubility: DMSO : ≥ 100 mg/mL (275.89 mM), Clinical_Informat: No Development Reported, Pathway: Neuronal Signaling;GPCR/G Protein, Target: mAChR;mAChR, Biological_Activity: Dexetimide ((+)-Benzetimide) is a high-affinity muscarinic receptor antagonist and a potent and persistent anticholinergic agent used to treat neuroleptic-induced parkinsonism[1].

Name: Viquidil, CAS: 84-55-9, stock 32.9g, assay 98%, MWt: 324.42, Formula: C20H24N2O2, Solubility: DMSO : 125 mg/mL (385.30 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Viquidil (LM 192) is a cerebral vasodilator agent [1].

Name: Tolycaine, CAS: 3686-58-6, stock 3.2g, assay 98.7%, MWt: 278.35, Formula: C15H22N2O3, Solubility: DMSO : ≥ 100 mg/mL (359.26 mM), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Tolycaine is a local anaesthetic agent.

Name: Hydrocortisone buteprate Hydrocortisone probutate;HBP, CAS: 72590-77-3, stock 3.9g, assay 98.1%, MWt: 488.61, Formula: C28H40O7, Solubility: DMSO : 250 mg/mL (511.66 mM; Need ultrasonic), Clinical_Informat: Launched, Pathway: Others, Target: Others, Biological_Activity: Hydrocortisone buteprate (Hydrocortisone probutate) is a medium potent, non-halogenated double-ester of hydrocortisone with a favorable benefit/risk ratio for the treatment of inflammatory skin disorders. Hydrocortisone buteprate (Hydrocortisone probutate) is available as a 0.1% cream or ointment formulation[1].

Name: SRX246, CAS: 512784-93-9, stock 34.6g, assay 98.5%, MWt: 703.87, Formula: C42H49N5O5, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein, Target: Vasopressin Receptor, Biological_Activity: SRX246 is a potent, CNS-penetrant, highly selective, orally bioavailable vasopressin 1a (V1a) receptor antagonist (Ki=0.3 nM for human V1a). SRX246 has no interaction at V1b and V2 receptors. SRX246 also displays negligible binding at 64 others receptors classes, including 35 G-proteincoupled receptors. SRX246 is under development for the treatment of stress-related disorders[1].
IC50 & Target: Ki: 0.3 nM (human vasopressin 1a receptor)[1]
In Vivo: SRX246 (2 mg/kg; i.v.) treatment shows that the Cmax, AUC0-∞ and t1/2 values are 953 ng/mL, 1141 ng ▪h/mL, and 6.02 hours, respectively, in plasma pharmacokinetics. Following an oral administration (dose 20 mg/kg), The Cmax, AUC0-∞ and t1/2 values are 98.4 ng/mL, 624 ng ▪h/mL and 2.38 hours, respectively[1].

Name: Polymyxin B nonapeptide, CAS: 86408-36-8, stock 32.4g, assay 98.1%, MWt: 963.13, Formula: C43H74N14O11, Solubility: H2O : ≥ 100 mg/mL (103.83 mM); DMSO : 16.67 mg/mL (17.31 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Anti-infection, Target: Bacterial, Biological_Activity: Polymyxin B nonapeptide is a cyclic peptide obtained from Polymyxin B by proteolytic removal of its terminal amino acyl residue[1]. Polymyxin B nonapeptide is less toxic, lacks bactericidal activity, and retains its ability to render gram-negative bacteria susceptible to several antibiotics by permeabilizing their outer membranes[2].
In Vitro: Polymyxin B nonapeptide, a cationic cyclic peptide derived by enzymatic processing from the naturally occurring peptide polymyxin B, is able to increase the permeability of the outer membrane of Gram-negative bacteria toward hydrophobic antibiotics probably by binding to the bacterial lipopolysaccharide (LPS)[1].

Name: ML221, CAS: 877636-42-5, stock 9g, assay 98%, MWt: 385.35, Formula: C17H11N3O6S, Solubility: DMSO : ≥ 31 mg/mL (80.45 mM), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: ML221 is a potent apelin (APJ) functional antagonist, inhibiting apelin-13-mediated activation of APJ, with IC50s of 0.70 μM in the cAMP assay, and 1.75 μM in the β-arrestin assay, and EC80 of 10 nM in both assays.
IC50 & Target: IC50: 1.75 μM (APJ, cell-based)[1]
In Vitro: ML221 is a potent apelin/APJ functional antagonist, inhibiting apelin-13-mediated activation of APJ, with IC50s of 0.70 μM in the cAMP assay, and 1.75 μM in the β-arrestin assay, and EC80 of 10 nM in both assays. ML221 is >37-fold selective over the closely related angiotensin II type 1 (AT1) receptor (IC50, >79 μM) in cells. ML221 displays limited cross reactivity against a range of GPCRs except the κ-opioid and benzodiazepinone receptors (<50/<70%I at 10 μM)[1].

Name: TC ASK 10, CAS: 1005775-56-3, stock 6.3g, assay 98%, MWt: 432.35, Formula: C21H23Cl2N5O, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Apoptosis;MAPK/ERK Pathway, Target: Apoptosis;MAP3K, Biological_Activity: TC ASK 10 (Compound 10) is a potent, selective and orally active apoptosis signal-regulating kinase 1 (ASK1) inhibitor with an IC50 of 14 nM. The inhibitory activities of TC ASK 10 towards other representative panel of kinases are less than 50%, except for ASK2 (IC50 of 0.51 μM)[1].
In Vitro: TC ASK 10 (Compound 10; 0-10 μM; 1 hour; INS-1 cells) treatment inhibits streptozotocin (STZ)-induced JNK in INS-1 pancreatic β cells from 0.3 μM. Phosphorylation of p38 is also inhibited in a dosedependent manner[1].
In Vivo: Pharmacokinetic profiles in rats are tested. TC ASK 10 (Compound 10•HCl; rat cassette doing at 0.1 mg/kg, iv and 1 mg/kg, po.) has a good oral bioavailability. The Cmax, Tmax and AUCpo,0-8h are 285.1 ng/mL, 1.67 h and 275.4 ng.h/mL, respectively for TC ASK 10[1].

Name: Sodium metatungstate Sodium polyoxotungstate;POM-1, CAS: 12141-67-2, stock 38g, assay 98.3%, MWt: 2986.01, Formula: H2Na6O40W12, Solubility: H2O : 50 mg/mL (16.74 mM; Need ultrasonic); DMSO : 50 mg/mL (16.74 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Sodium metatungstate (POM-1) is a potent ecto-nucleoside triphosphate diphosphohydrolase (NTPDase) inhibitor, with Ki values of 2.58 μM, 3.26 μM, and 28.8 μM for NTPDase 1, NTPDase 3 and NTPDase 2 respectively[1]. Sodium metatungstate (POM-1) inhibits ATP breakdown but also blocks central synaptic transmission, an action independent of NTPDase inhibition[2].
IC50 & Target: Ki: 2.58 μM (NTPDase 1), 3.26 μM (NTPDase 3), 28.8 μM (NTPDase 2)[1].

Name: Enterostatin, human, mouse, rat, CAS: 117830-79-2, stock 1.8g, assay 98.1%, MWt: 496.56, Formula: C21H36N8O6, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: Enterostatin, human, mouse, rat is a pentapeptide that reduces fat intake.
In Vitro: In the perfused ratpancreas, Enterostatin, at 100 mM, inhibits the insulin response to 9 mM glucose (by 70%), 0.1 mM tolbutamide (by 40%), and 5 mM arginine (by 70%)[1].
In Vivo: Chronically, enterostatin reduces fat intake, bodyweight, and body fat. This response may involve multiple metabolic effects of enterostatin, which include a reduction of insulin secretion, an increase in sympathetic drive to brown adipose tissue, and the stimulation of adrenal corticosteroid secretion[2]. Enterostatin enhances memory consolidation after central or oral administration at a dose of 10 nmol/mouse or 300 mg/kg, respectively, in a step-through type passive avoidance test in mice[3]. A dose of 38 nmol of enterostatin gives a significant inhibition of high-fat food intake, while at a higher dose of 76 nmol the inhibiting effect is lost. During the first hour, after injection of enterostatin, there is even a slight increase in food intake[4].

Name: Cyclopiazonic acid, CAS: 18172-33-3, stock 23.8g, assay 98.9%, MWt: 336.38, Formula: C20H20N2O3, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Membrane Transporter/Ion Channel;Neuronal Signaling, Target: Calcium Channel;Calcium Channel, Biological_Activity: Cyclopiazonic acid (CPA), a neurotoxic secondary metabolite (SM) made by A. flavus, is a nanomolar inhibitor of endoplasmic reticulum calcium ATPase (Ca2+ATPase; SERCA) and a potent inducer of cell death in plants[1].

Name: SCH28080, CAS: 76081-98-6, stock 33.6g, assay 98%, MWt: 277.32, Formula: C17H15N3O, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Membrane Transporter/Ion Channel, Target: Proton Pump, Biological_Activity: SCH28080 inhibits gastric H+/K+-ATPase by K+-competitive binding, with an IC50 value of 20 nM in rabbit microsomal membranes[1]. Antisecretory and cytoprotective activities[2].
IC50 & Target: IC50: 20 nM (H+/K+-ATPase, rabbit microsomal membranes)[1]

Name: ARL67156 trisodium salt, CAS: 1021868-83-6, stock 10.7g, assay 98.9%, MWt: 788.08, Formula: C15H24Br2N5Na3O12P3, Solubility: DMSO : < 1 mg/mL (insoluble or slightly soluble); H2O : 25 mg/mL (31.72 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: ARL67156 trisodium salt is an inhibitor of ecto-ATPase. ARL 67156 is a weak competitive inhibitor of NTPDase1 (CD39), NTPDase3 and NPP1, with Kis of 11, 18 and 12 μM, respectively[1].
IC50 & Target: Ki: 11 μM (NTPDase1), 18 μM (NTPDase3), 12 μM (NPP1)[1]
In Vitro: ARL67156 trisodium salt is also an effective inhibitor of UTP breakdown by superior cervical ganglion cells and to potentiate contractions elicited by this nucleotide in isolated tail artery of rat. ARL67156 is not an effective inhibitor of NTPDase2, NTPDase8, NPP3 and ecto-5′-nucleotidase (CD73), although it also reduces the activity of these enzymes[1].

Name: LTI-291, CAS: 1919820-28-2, stock 13.6g, assay 98.9%, MWt: 358.48, Formula: C20H30N4O2, Solubility: DMSO : 50 mg/mL (139.48 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: LTI-291 is an activator of glucocerebrosidase (Gcase) extracted from patent WO 2017192841 A1.
IC50 & Target: Gcase[1]

Name: BAI1, CAS: 335165-68-9, stock 34.9g, assay 98.3%, MWt: 467.20, Formula: C19H21Br2N3O, Solubility: H2O : < 0.1 mg/mL (insoluble); DMSO : 18.67 mg/mL (39.96 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Apoptosis, Target: Bcl-2 Family, Biological_Activity: BAI1 is a direct allosteric inhibitor of BAX.
IC50 & Target: BAX[1]

Name: MKC8866, CAS: 1338934-59-0, stock 1.6g, assay 98.9%, MWt: 361.35, Formula: C18H19NO7, Solubility: DMSO : 16.67 mg/mL (46.13 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Cell Cycle/DNA Damage, Target: IRE1, Biological_Activity: MKC8866, a salicylaldehyde analog, is a potent, selective IRE1 RNase inhibitor with an IC50 of 0.29 μM in human vitro. MKC8866 strongly inhibits DTT-induced X-box-binding protein 1-spliced (XBP1s) expression with an EC50 of 0.52 μM and unstresses RPMI 8226 cells with an IC50 of 0.14 μM[1]. MKC8866 inhibits IRE1 RNase in breast cancer cells leading to the decreased production of pro-tumorigenic factors and it can inhibits prostate cancer (PCa) tumor growth[2].
IC50 & Target: IC50: 0.29 μM (IRE1 RNase)[1]
In Vitro: MKC8866 (20 μM; 6 days) decreases proliferation of all breast cancer cell lines[2]. 
MKC8866 (20 μM; 48 hours) reduces the number of cells entering S phase[2]. 
MKC8866 (0.2-10 μM; 3 days) suppresses the viability of all four cell lines in a dose-dependent manner under normal conditions, with the most robust effect in LNCaP cells[1]. 
MKC8866 (20 μM; 72 hours) is sufficient to completely block NSC 125973-induced expression of XBP1s [1]. 
In Vivo: MKC8866 (oral ; 300 mg/kg; for 28 days) reduces tumor regrowth post-NSC 125973 withdrawal[1].

Name: Furprofen, CAS: 66318-17-0, stock 9.6g, assay 98.8%, MWt: 244.24, Formula: C14H12O4, Solubility: DMSO : 62.5 mg/mL (255.90 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Immunology/Inflammation, Target: PGE synthase, Biological_Activity: Furprofen is an non-steroidal anti-inflammatory drug (NSAID) with analgesic properties[1]. Furprofen acts via the inhibition of prostaglandin (PGE) synthesis. Furprofen can be treated orally for the relief of pain[2][3].
IC50 & Target: PGE[1]

Name: Saredutant SR 48968; SR 48968C, CAS: 142001-63-6, stock 28.6g, assay 98.7%, MWt: 552.53, Formula: C31H35Cl2N3O2, Solubility: DMSO : 250 mg/mL (452.46 mM; Need ultrasonic), Clinical_Informat: Phase 3, Pathway: Neuronal Signaling;GPCR/G Protein, Target: Neurokinin Receptor;Neurokinin Receptor, Biological_Activity: Saredutant is a selective NK2 receptor antagonist.
IC50 & Target: NK2 receptor[1]
In Vivo: Saredutant, an NK2 receptor antagonist, has both antidepressant-like effects and synergizes with desipramine in an animal model of depression. Saredutant has dose-dependent effects on swim test immobility, with the low dose of 1 mg/kg having no effect and the doses of 3 and 10 mg/kg significantly reducing immobility[1].

Name: Endovion NS3728, CAS: 265646-85-3, stock 17.9g, assay 98%, MWt: 495.18, Formula: C16H9BrF6N6O, Solubility: H2O : < 0.1 mg/mL (insoluble); DMSO : 125 mg/mL (252.43 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Membrane Transporter/Ion Channel, Target: Chloride Channel, Biological_Activity: Endovion (NS3728) is a pharmacological anion channel inhibitor (like chloride channel) and the specific VRAC/VSOAC blocker. Endovion (NS3728) is also an Anoctamin-1 (ANO 1) channel inhibitor[1][2].
IC50 & Target: Chloride channel, VRAC/VSOAC[1]. 
ANO1[2].

Name: Lexithromycin Erythromycin A 9-methoxime; Wy 48314, CAS: 53066-26-5, stock 24.2g, assay 98.5%, MWt: 762.97, Formula: C38H70N2O13, Solubility: H2O : < 0.1 mg/mL (insoluble); DMSO : ≥ 50 mg/mL (65.53 mM), Clinical_Informat: No Development Reported, Pathway: Anti-infection, Target: Bacterial, Biological_Activity: Lexithromycin is an erythromycin A derivative, with antibacterial activity.
IC50 & Target: Bacterial[1]
In Vitro: Lexithromycin is an erythromycin A derivative, with antibacterial activity. Lexithromycin shows minimal inhibitory concentration (MIC) of 0.06 μg/mL against S. pyogenes CN10A and Streptococcus sp. 64/848C, 0.25 μg/mL against Staphylococcus aureus Oxford, 0.5 μg/mL against S. aureus Russell and S. aureus T2, 4 μg/mL against S. pyogenes CN10A and Haemophilus influenzae Wy 21[1].

Name: Fosfructose Diphosphofructose;Esafosfan;FDP, CAS: 488-69-7, stock 18.8g, assay 98.1%, MWt: 340.12, Formula: C6H14O12P2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: Fosfructose (Diphosphofructose;Esafosfan;FDP) is a cytoprotective natural sugar phosphate for the potential treatment of cardiovascular ischemia, sickle cell anemia and asthma. It acts by stimulating anaerobic glycolysis which generates adenosine triphosphate under ischemic conditions.
IC50 & Target: Endogenous Metabolite[1]

Name: Fosfructose (trisodium) Diphosphofructose (trisodium);Esafosfan (trisodium);FDP (trisodium), CAS: 38099-82-0, stock 33.3g, assay 98.3%, MWt: 406.06, Formula: C6H11Na3O12P2, Solubility: H2O : 150 mg/mL (369.40 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: Fosfructose trisodium (Diphosphofructose trisodium;Esafosfan trisodium;FDP trisodium) is a cytoprotective natural sugar phosphate for the potential treatment of cardiovascular ischemia, sickle cell anemia and asthma. It acts by stimulating anaerobic glycolysis which generates adenosine triphosphate under ischemic conditions.
IC50 & Target: Endogenous Metabolite[1]

Name: Imatinib (Mesylate) STI571 (Mesylate);CGP-57148B (Mesylate), CAS: 220127-57-1, stock 2.6g, assay 99%, MWt: 589.71, Formula: C30H35N7O4S, Solubility: DMSO : ≥ 49 mg/mL (83.09 mM); H2O : ≥ 50 mg/mL (84.79 mM), Clinical_Informat: Launched, Pathway: Protein Tyrosine Kinase/RTK;Protein Tyrosine Kinase/RTK;Autophagy;Protein Tyrosine Kinase/RTK, Target: Bcr-Abl;PDGFR;Autophagy;c-Kit, Biological_Activity: Imatinib Mesylate (STI571 Mesylate) is a tyrosine kinases inhibitor that inhibits c-Kit, Bcr-Abl, and PDGFR (IC50=100 nM) tyrosine kinases.
IC50 & Target: IC50: ~100 nM (c-Kit, Bcr-Abl, and PDGFR)[1]
In Vitro: Imatinib (STI571) Mesylate inhibits c-Kit autophosphorylation, activation of MAPK, and activation of Akt without altering total protein levels of c-kit, MAPK, or Akt. The concentration that produces 50% inhibition for these effects is approximately 100 nM[1]. Imatinib (STI571) mesylate is very effective (in vitro IC50 of 25 nM) against the chronic myeloid leukemia-causing kinase Bcr-Abl. Imatinib also efficiently inhibits Kit (in vitro IC50, 410 nM) and PDGFR (in vitro IC50, 380 nM)[2]. Imatinib (STI571) mesylate is a multi-target inhibitor of v-Abl, c-Kit and inhibits Bcr/Abl, v-Abl, Tel/Abl, the native PDGFβ receptor, and c-Kit, but it does not inhibit Src family kinases, c-Fms, Flt3, the EGFR or multiple other tyrosine kinases. Imatinib inhibits tyrosine phosphorylation and cell growth of Ba/F3 cells expressing Bcr/Abl, Tel/Abl, Tel/PDGFβR, and Tel/Arg with an IC50 of approximately 0.5 μM in each case, but it has no effect on untransformed Ba/F3 cells growing in IL-3 or on Ba/F3 cells transformed by Tel/JAK2[3]. Imatinib mesylate selectively inhibits the activity of Bcr/Abl, c-Kit and PDGFR kinases. Imatinib mesylate reveals distinct and rapid antileukemic activity in chronic myelogenous leukemia (CML) and Philadelphia-positive (Ph+) acute lymphoblastic leukemia (ALL)[4].
In Vivo: Animals treated with Imatinib Mesylate show a decrease of mean body weight throughout the whole study. Body weight loss is noticeable in mice from groups that receive chemotherapy and the vitamin D analog combined treatment. The body weight decrease of mice treat with both combined Imatinib mesylate and PRI-2191 is the highest (15%) on Day 22 of the experiment, but after that day, mice start to recover[4]. In a rat Ischemia/reperfusion injury (IRI) model, Imatinib mesylate attenuates lung injury by an antipermeability and antiinflammatory effect. The delivery and function of Imatinib mesylate in the lung is also confirmed in this model[5].

Name: S 3304, CAS: 203640-27-1, stock 6.9g, assay 98.6%, MWt: 464.56, Formula: C24H20N2O4S2, Solubility: H2O : < 0.1 mg/mL (insoluble); DMSO : ≥ 83.3 mg/mL (179.31 mM), Clinical_Informat: Phase 2, Pathway: Metabolic Enzyme/Protease, Target: MMP, Biological_Activity: S 3304 is a novel matrix metalloproteinases (MMP) inhibitor specific for MMP-2 and MMP-9.
IC50 & Target: MMP-2, MMP-9[1]
In Vitro: S 3304 is a novel D-tryptophan derivative and a potent, orally active, noncytotoxic Matrix metalloproteinases inhibitor (MMPI). Biochemical studies show that S 3304 most potently inhibits the activities of MMP-2 and MMP-9 but does not inhibit MMP-1, MMP-3, or MMP-7 and may, therefore, lack the musculoskeletal side effects seen with nonspecific inhibitors[1].
In Vivo: In vivo pharmacologic studies have shown that the oral administration of S 3304, at a dose range of 20 to 200 mg/kg, inhibits angiogenesis, artificially induced in mice by the dorsal air-sac method. Similar oral doses of S 3304 result in potent inhibition of metastatic lung colonization of Lewis murine lung carcinoma injected via tail vein and liver metastasis of C-1H human colon cancer implanted into the spleen[1].

Name: MM 07, CAS: 1876450-21-3, stock 23.3g, assay 98.6%, MWt: 1539.89, Formula: C67H106N22O14S3, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: MM 07 is a biased apelin receptor agonist, with a KD of 300 nM in CHO-K1 cells and a KD of 172 nM in human heart.
IC50 & Target: KD: 300 nM (apelin receptor in CHO-K1 cells), 172 nM (apelin receptor in human heart)[1].
In Vitro: MM 07 competes with nanomolar affinities for binding of [Glp65,Nle75,Tyr77] [125I]apelin-13 to human apelin receptors in CHO-K1 cells (KD, 300 nM) and human heart (KD, 172 nM, n=3)[1].
In Vivo: MM 07 causes a dose-dependent increase in cardiac output, and although there is a decrease in vascular resistance, this is without corresponding effects on BP. Administration of SNAP produces a profound fall in BP in both [Pyr1]apelin-13 and MM 07-treated groups; however, although cardiac output is significantly increased in response to SNAP in the MM 07 group, it is significantly reduced in the [Pyr1]apelin-13 group. Neither peptide causes a significant change in heart rate, respiratory rate, or temperature. Both [Pyr1]apelin 13 and MM 07 increases peak velocity above basal levels[1].

Name: Mirogabalin besylate DS 5565 besylate, CAS: 1138245-21-2, stock 25g, assay 98.7%, MWt: 367.46, Formula: C18H25NO5S, Solubility: DMSO : 125 mg/mL (340.17 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Membrane Transporter/Ion Channel;Neuronal Signaling, Target: Calcium Channel;Calcium Channel, Biological_Activity: Mirogabalin besylate is a selective and orally available ligand for the α2δ subunit of voltage-gated calcium channels, with Kds of 13.5 nM, 22.7 nM, 27 nM, and 47.6 nM for human α2δ-1, human α2δ-2, rat α2δ-1, and rat α2δ-2, respectively.
IC50 & Target: Kd: 13.5 nM (Human α2δ-1), 22.7 nM (Human α2δ-2), 27 nM (Rat α2δ-1), 47.6 nM (Rat α2δ-2)[1]
In Vitro: Mirogabalin besylate is a ligand for the α2δ subunit of voltage-gated calcium channels, with Kds of 13.5 nM, 22.7 nM, 27 nM, and 47.6 nM for human α2δ-1, human α2δ-2, rat α2δ-1, and rat α2δ-2, respectively. Mirogabalin shows binding affinity for the gabapentin binding site in rat cortical brain homogenates with the IC50 value of 16.0 nM. Mirogabalin has no effect on any other receptors, channels, transporters, or enzymes at 50 μM[1].
In Vivo: Mirogabalin besylate (3 and 10 mg/kg) markedly increases AUC0-8 hours values in a dose-dependent manner in partial sciatic nerve ligation model rats. Mirogabalin (2.5, 5, and 10 mg/kg) causes significant and dose-dependent increase in AUC0-12 hours values and enhances analgesic effects, with estimated ED50 of 4.4, 3.1, and <2.5 mg/kg on day 1, day 3, and day 5, respectively. Moreover, Mirogabalin besylate shows no obvious effect on rota-rod performance and locomotor activity at 3 and 10 mg/kg via oral administration, exhibits significant inhibition on rota-rod performance at 10, 30, and 100 mg/kg, and decreases locomotor activity at 30 and 100 mg/kg in rats[1].

Name: PD176252, CAS: 204067-01-6, stock 2.4g, assay 98.2%, MWt: 584.67, Formula: C32H36N6O5, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein, Target: Bombesin Receptor, Biological_Activity: PD176252 is a potent antagonist of neuromedin-B preferring (BB1) and gastrin-releasing peptide-preferring (BB2) receptor with Kis of 0.17 nM and 1 nM for human BB1 and BB2 receptors, and 0.66 nM, 16 nM for Rat BB1 and BB2 receptors, respectively; PD176252 is also an agonist of N-Formyl peptide receptor1/2 (FPR1/FPR2), with EC50s of 0.31 and 0.66 μM in HL-60 cells.
IC50 & Target: Ki: 0.17 nM (Human BB1 receptor), 0.66 nM (Rat BB1 receptor), 1 nM (Human BB2 receptor), 16 nM (Rat BB2 receptor)[1] 
EC50: 0.31 μM (FPR1), 0.66 μM (FPR2)[2]
In Vitro: PD176252 is a potent antagonist of neuromedin-B preferring (BB1) and gastrin-releasing peptide-preferring (BB2) receptor with Kis of 0.17 nM and 1 nM for human BB1 and BB2 receptors, and 0.66 nM, 16 nM for Rat BB1 and BB2 receptors, respectively. PD176252 inhibits acidification responses to neuromedin-B or neuromedin-C at the human BB1 or BB2 receptors expressed in CHO cells, with the appKBs of 4.0 nM or 13 nM, and blocks bombesin-evoked increases in intracellular calcium levels in CHO cells stably expressing human BB1 or BB2 receptors, with appKBs of 2.3 nM and 36 nM, respectively. PD176252 is also an agonist of N-Formyl peptide receptor1/2 (FPR1/FPR2), with EC50s of 0.31 and 0.66 μM in HL-60 cells. PD176252 activates Ca2+ mobilization in HL-60 cells transfected with human FPRs (EC50, 0.72 ± 0.21 μM)[2]. PD176252 inhibits little specific 125I-gastrin releasing peptide binding to NCI-H345 cells at 1 nM and suppresses almost all specific bindings at 1000 nM, with an IC50 of 30 nM. PD176252 (10, 30 μM) significantly inhibits the growth of NCI-H345 or H1299 cells, with IC50s of 7 and 5 μM[3].
In Vivo: PD176252 (1, 10 μg, p.o.) potently inhibits the growth of the proliferation of NCI-H1299 xenografts in nude mice[3].

Name: Secretin (28-54), human Human secretin, CAS: 108153-74-8, stock 26.8g, assay 98.8%, MWt: 3039.46, Formula: C130H220N44O40, Solubility: H2O, Clinical_Informat: Launched, Pathway: Others, Target: Others, Biological_Activity: Secretin (28-54), human is a 27-amino acid residue C-terminally amidated peptide, which acts on human secretin receptors[1].
IC50 & Target: Human secretin receptor[1]
In Vitro: Secretin is a hormone produced and secreted from the endocrine S cells in response to the gastric acid and lipid components. Secretin potentiates enzyme secretion from the acinar cell. Secretin is also a putative mitogen to promote pancreatic growth. In the stomach and gall bladder, Secretin inhibits gastric emptying and acid release and stimulates biliary output of water and bicarbonate. Secretin elicits its biological effects by interacting with specific cell surface receptors[1].

Name: MSDC-0602, CAS: 1133819-87-0, stock 6.6g, assay 98.7%, MWt: 371.41, Formula: C19H17NO5S, Solubility: DMSO : 125 mg/mL (336.56 mM; Need ultrasonic); H2O : < 0.1 mg/mL (insoluble), Clinical_Informat: Phase 2, Pathway: Metabolic Enzyme/Protease, Target: Mitochondrial Metabolism, Biological_Activity: MSDC-0602, a PPARγ-sparing thiazolidinedione (TZD), interacts with the mitochondrial pyruvate carrier (MPC) and inhibits its activity and are effective for treatment of type 2 diabetes with reducing risk of PPARγ-mediated side effects[1][2].

Name: Pro-xylane Hydroxypropyl tetrahydropyrantriol, CAS: 439685-79-7, stock 9.3g, assay 98.8%, MWt: 192.21, Formula: C8H16O5, Solubility: DMSO : ≥ 83.33 mg/mL (433.54 mM), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Pro-xylane (Hydroxypropyl tetrahydropyrantriol) is a biologically active C-glycoside in aqueous media, acts as an activator of glycosaminoglycans (GAGs) biosynthesis. Pro-xylane is the first example of 'Green' chemical used in cosmetic[1].

Name: GW 766994 GW 994, CAS: 408303-43-5, stock 30.2g, assay 98.1%, MWt: 451.35, Formula: C21H24Cl2N4O3, Solubility: DMSO : 56 mg/mL (124.07 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Immunology/Inflammation;GPCR/G Protein, Target: CCR;CCR, Biological_Activity: GW 766994 is a specific and oral chemokine receptor-3 (CCR3) antagonist, which has entered clinical trial for asthma and eosinophilic bronchitis.
IC50 & Target: CCR3[1]
In Vitro: GW 766994 is a specific chemokine receptor-3 (CCR3) antagonist, which has entered clinical trial for asthma and eosinophilic bronchitis[1]. GW 766994 (10 μM) reverses CCL11-induced activation of CDK5, phosphorylations of CDK5, GSK3β, and increased phosphorylation of tau in hippocampal neurons[2].

Name: Lodenafil carbonate, CAS: 398507-55-6, stock 16.7g, assay 98.7%, MWt: 1035.20, Formula: C47H62N12O11S2, Solubility: 10 mM in DMSO, Clinical_Informat: Phase 4, Pathway: Metabolic Enzyme/Protease, Target: Phosphodiesterase (PDE), Biological_Activity: Lodenafil carbonate, a dimer that acts as a prodrug delivering Lodenafil in vivo, is an orally active phosphodiesterase type 5 (PDE5) inhibitor for the treatment of erectile dysfunction (ED)[1][2].
IC50 & Target: PDE5[1][2].

Name: Aspartyl-alanyl-diketopiperazine DA-DKP, CAS: 110954-19-3, stock 12g, assay 98.2%, MWt: 186.17, Formula: C7H10N2O4, Solubility: DMSO : 125 mg/mL (671.43 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Aspartyl-alanyl-diketopiperazine (DA-DKP) is an immunomodulatory molecule generated by cleavage and cyclization from the N-terminus of human albumin and can modulate the inflammatory immune response through a molecular pathway implicated in T- lymphocyte anergy[1][2].

Name: KG-501 Naphthol AS-E phosphate, CAS: 18228-17-6, stock 19.7g, assay 99%, MWt: 377.72, Formula: C17H13ClNO5P, Solubility: DMSO : 6 mg/mL (15.88 mM; Need ultrasonic and warming); H2O : < 0.1 mg/mL (insoluble), Clinical_Informat: No Development Reported, Pathway: Epigenetics, Target: Epigenetic Reader Domain, Biological_Activity: KG-501 is a CREB inhibitor, with an IC50 of 6.89 μM.
IC50 & Target: IC50: 6.89 μM (CREB)[1].
In Vitro: KG-501, which directly targets the KIX domain of CBP, results in a disrupted CREB-CBP complex, inhibits CREB-target gene induction, and inhibits IL-1β-mediated angiogenic activity in NSCLC[1]. KG-501 disrupts phospho (Ser-133) CREB binding to KIX with a Ki of ~90 μM, using concentrations of CREB that are within the linear range of the binding assay. Treatment of HEK293T cells with KG-501 also blocks induction of endogenous CREB target genes (NR4A2, αCG, c-fos, and RGS2) by forskolin, indicating that KG-501 likely exerts a general effect on CREB activity[2]. KG-501 can also inhibit NF-κB transcription activity because NF-κB also uses CBP as a cofactor to regulate gene expression. The migration of HUVECs induced by CM from A549 cells treated with IL-1β plus 10 μM of KG-501 is significantly lower than that induced by CM from A549 cells treated with IL-1β alone. At 10 μM, KG-501 suppresses the expression of all of the IL-1β–induced CXC chemokine genes except CXCL8. For the protein level, KG-501 significantly suppresses IL-1β–induced CXCL5 protein secretion. Similar effects of KG-501 are also observed in the H1734 cell line[3].

Name: Pamiparib BGB-290, CAS: 1446261-44-4, stock 36.3g, assay 98.6%, MWt: 298.31, Formula: C16H15FN4O, Solubility: DMSO : 62.5 mg/mL (209.51 mM; Need ultrasonic), Clinical_Informat: Phase 3, Pathway: Epigenetics;Cell Cycle/DNA Damage, Target: PARP;PARP, Biological_Activity: Pamiparib (BGB-290) is an orally active, potent, highly selective PARP inhibitor, with IC50 values of 0.9 nM and 0.5 nM for PARP1 and PARP2, respectively. Pamiparib has oral bioavailability, potent PARP trapping, and capability to penetrate the brain, and can be used for the treatment of various cancers including the solid tumor[1][2].
IC50 & Target: PARP[1]
In Vitro: Pamiparib shows potent DNA-trapping activity with an IC50 of 13 nM. In the cellular assays, Pamiparib inhibits intracellular PAR formation with an IC50 of 0.24 nM. Tumor cell lines with homologous recombination defects are profoundly sensitive to Pamiparib. Pamiparib is highly active both in vitro and in vivo in BRCA mutant tumors[3].
In Vivo: Pamiparib suppresses PARP activity in patient-derived glioblastoma multiforme and small-cell-lung cancer xenografts, and potentiates the effects of Temozolamide. In vivo activities of Pamiparib, and its combination activity with chemotherapies in patient biopsy derived small cell lung cancer (SCLC) xenograft models[4].

Name: JNJ-10229570, CAS: 524923-88-4, stock 21.6g, assay 98.9%, MWt: 389.47, Formula: C22H19N3O2S, Solubility: DMSO : 62.5 mg/mL (160.47 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein;Neuronal Signaling, Target: Melanocortin Receptor;Melanocortin Receptor, Biological_Activity: JNJ-10229570 is an antagonist of melanocortin receptor 1 (MC1R) and melanocortin receptor 5 (MC5R), which inhibits sebaceous gland differentiation and the production of sebum-specific lipids. JNJ-10229570 inhibits the binding of 125I-NDP-α-MSH to cells expressing human MC1R and MC5R, with IC50 values of 270 nM and 200 nM, respectively.
IC50 & Target: IC50: 270 nM (human MC1R), 200 nM (human MC5R)[1].
In Vitro: JNJ-10229570 dose dependently inhibits the production of sebaceous lipids in cultured primary human sebocytes. JNJ-7818369 inhibits the binding of 125I-NDP-α-MSH to cells expressing human MC1R and MC5R, with IC50s of 270±120 and 200±50 nM, respectively. Nearly-identical results are obtained with the free base form of the compound. Binding to MC4R of both forms of the compound is equipotent, with IC50s of 240±170 nM. JNJ-10229570-treated cells show strong inhibition of lipid granules at 0.01 μM, and complete inhibition at 0.05 μM[1].
In Vivo: Topical treatment with JNJ-10229570 of human skins transplanted onto SCID mice result in a marked decrease in sebum-specific lipid production, sebaceous gland's size and the expression of the sebaceous differentiation marker epithelial-membrane antigen (EMA). Topical treatment with 0.05% JNJ-10229570 leads to a distinct reduction in both the steady-state and the newly-synthesized sebum-specific lipids, with lesser effects on triglycerides and cholesterol[1].

Name: Ningetinib Tosylate, CAS: 1394820-77-9, stock 0.4g, assay 98.3%, MWt: 728.79, Formula: C38H37FN4O8S, Solubility: DMSO : 33.33 mg/mL (45.73 mM; Need ultrasonic); H2O : < 0.1 mg/mL (insoluble), Clinical_Informat: Phase 2, Pathway: Protein Tyrosine Kinase/RTK;Protein Tyrosine Kinase/RTK;Protein Tyrosine Kinase/RTK, Target: c-Met/HGFR;VEGFR;TAM Receptor, Biological_Activity: Ningetinib Tosylate is a potent, orally bioavailable small molecule tyrosine kinase inhibitor (TKI) with IC50s of 6.7, 1.9 and <1.0 nM for c-Met, VEGFR2 and Axl, respectively.
In Vitro: Ningetinib Tosylate is a potent, orally bioavailable small molecule tyrosine kinase inhibitor (TKI) with IC50s of 6.7, 1.9 and <1.0 nM for c-Met, VEGFR2 and Axl, respectively. In cell-based functional assays, Ningetinib Tosylate (CT053PTSA) inhibits HGF and VEGF-stimulated HUVEC proliferation and microvascular angiogenesis in rat aortic rings with IC50 values of 8.6 and 6.3 nM, respectively[1].
In Vivo: When single dosed orally (3 mg/kg) to U87MG tumor-bearing nude mice, Ningetinib Tosylate (CT053PTSA) potently inhibits the phosphorylation of c-Met and its downstream signaling kinases AKT and ERK1/2 for up to 6 hours in tumor tissues. In orthotopic U87MG human glioblastoma xenograft model, Ningetinib Tosylate prolongs the median survival time (MST) and yields significant increase in life-span value (ILS=32%, p=0.003) at an oral dose of 20 mg/kg/day (dosed 21 days) versus the vehicle-treated group[1].

Name: Amylin, amide, human DAP amide, human, CAS: 122384-88-7, stock 5.3g, assay 98.6%, MWt: 3903.28, Formula: C165H261N51O55S2, Solubility: H2O, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Amylin, amide, human, a 37-amino acid polypeptide, is a pancreatic hormone cosecreted with insulin that exerts unique roles in metabolism and glucose homeostasis. Amylin, amide, human inhibits glucagon secretion, delays gastric emptying, and acts as a satiety agent[1].
In Vitro: MCF-7 cells endogenously express human amylin receptor CTR1 and CTR2. Stimulation of the receptor with Amylin, amide, human results in the production of cAMP. Amylin, amide, human (0.001 nM-1000 μM) results in an EC50 of 35.2±7.5 nM[1].
In Vivo: Amylin, amide, human (400 μg peptide /kg body weight) is injected by subcutaneous route in separated groups of swiss male mice. A typical PK curve for the free amylin is observed, with a half-time of 23 min[1].

Name: Ningetinib, CAS: 1394820-69-9, stock 28.9g, assay 98.7%, MWt: 556.58, Formula: C31H29FN4O5, Solubility: H2O : < 0.1 mg/mL (insoluble); DMSO : 16.67 mg/mL (29.95 mM; Need ultrasonic), Clinical_Informat: Phase 2, Pathway: Protein Tyrosine Kinase/RTK;Protein Tyrosine Kinase/RTK;Protein Tyrosine Kinase/RTK, Target: c-Met/HGFR;VEGFR;TAM Receptor, Biological_Activity: Ningetinib is a potent, orally bioavailable small molecule tyrosine kinase inhibitor (TKI) with IC50s of 6.7, 1.9 and <1.0 nM for c-Met, VEGFR2 and Axl, respectively.
IC50 & Target: VEGFR, c-Met, and Axl[1]
In Vitro: Ningetinib is a potent, orally bioavailable small molecule tyrosine kinase inhibitor (TKI) with IC50s of 6.7, 1.9 and <1.0 nM for c-Met, VEGFR2 and Axl, respectively. In cell-based functional assays, Ningetinib (CT053PTSA) inhibits HGF and VEGF-stimulated HUVEC proliferation and microvascular angiogenesis in rat aortic rings with IC50 values of 8.6 and 6.3 nM, respectively[1].
In Vivo: When single dosed orally (3 mg/kg) to U87MG tumor-bearing nude mice, Ningetinib (CT053PTSA) potently inhibits the phosphorylation of c-Met and its downstream signaling kinases AKT and ERK1/2 for up to 6 hours in tumor tissues. In orthotopic U87MG human glioblastoma xenograft model, Ningetinib prolongs the median survival time (MST) and yields significant increase in life-span value (ILS=32%, p=0.003) at an oral dose of 20 mg/kg/day (dosed 21 days) versus the vehicle-treated group[1].

Name: MRS1845, CAS: 544478-19-5, stock 16.4g, assay 98.7%, MWt: 398.41, Formula: C21H22N2O6, Solubility: H2O : < 0.1 mg/mL (insoluble); DMSO : ≥ 83.33 mg/mL (209.16 mM), Clinical_Informat: No Development Reported, Pathway: Membrane Transporter/Ion Channel;Membrane Transporter/Ion Channel;Neuronal Signaling, Target: Calcium Channel;CRAC Channel;Calcium Channel, Biological_Activity: MRS1845 is a Ca2+ channel blocker with relative specificity for store-operated calcium entry (SOCE) channels[1].
IC50 & Target: Ca2+ channel[1]

Name: Bacitracin, CAS: 1405-87-4, stock 30.7g, assay 98%, MWt: 1422.69, Formula: C66H103N17O16S, Solubility: H2O : 50 mg/mL (35.14 mM; Need ultrasonic), Clinical_Informat: Launched, Pathway: Anti-infection, Target: Bacterial, Biological_Activity: Bacitracin is a polypeptide antibiotic used for staphylococcal infections. Bacitracin functions as an inhibitor of cell wall biosynthesis through its binding to the undecaprenyl pyrophosphate. The combination of bacitracin with other antibiotics has been efficient to be used as a topical agent[1].

Name: Lanifibranor IVA337, CAS: 927961-18-0, stock 2.7g, assay 98.8%, MWt: 434.92, Formula: C19H15ClN2O4S2, Solubility: DMSO : 100 mg/mL (229.93 mM; Need ultrasonic and warming), Clinical_Informat: Phase 2, Pathway: Cell Cycle/DNA Damage, Target: PPAR, Biological_Activity: Lanifibranor is a pan peroxisome proliferator-activated receptor (PPAR) agonist with EC50s of 1.5, 0.87 and 0.21 μM for human PPARα, PPARσ and PPARγ, respectively.
IC50 & Target: EC50: 1.5 μM (hPPARα), 0.87 μM (PPARσ), 0.21 μM (PPARγ)[1]
In Vivo: Lanifibranor is a pan peroxisome proliferator-activated receptor (PPAR) agonist with EC50s of 1.5, 0.87 and 0.21 μM for human PPARα, PPARσand PPARγ[1]. Skin fibrosis is attenuated by Lanifibranor (IVA337) (p<0.05, vehicle vs Lanifibranor at 30 mg/kg and p<0.001, vehicle vs Lanifibranor at 100 mg/kg). Both low and high doses of Lanifibranor cause a significant decrease of collagenous matrix deposition. Administration of high (100 mg/kg) doses of Lanifibranor results in reduced body weight compare with vehicle controls (p<0.05; Lanifibranor at 100 mg/kg vs vehicle). Results demonstrate that activation of Peroxisome proliferator-activated receptors (PPARs) with Lanifibranor induces a significant reduction in the infiltration of macrophages, CD45+ leucocytes and lymphocytes in Lanifibranor-treated mice compare with rosiglitazone-treated counterparts[2].

Name: Bepridil hydrochloride CERM 1978, CAS: 68099-86-5, stock 11.7g, assay 98.3%, MWt: 403.00, Formula: C24H35ClN2O, Solubility: DMSO : ≥ 150 mg/mL (372.21 mM), Clinical_Informat: Launched, Pathway: Membrane Transporter/Ion Channel;Neuronal Signaling, Target: Calcium Channel;Calcium Channel, Biological_Activity: Bepridil hydrochloride (CERM 1978) is a calcium channel blocker, with antianginal activity.
IC50 & Target: Calcium channel[1]
In Vitro: Bepridil hydrochloride is a calcium channel blocker, with antianginal activity[1].
In Vivo: Bepridil hydrochloride (21 mg/kg) reduces heart rate and mean arterial pressure, decreases the mean coronary vascular resistance and increases stroke volume in rats[1].

Name: Calmidazolium chloride R 24571, CAS: 57265-65-3, stock 21g, assay 98.1%, MWt: 687.70, Formula: C31H23Cl7N2O, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Neuronal Signaling;Autophagy, Target: CaMK;Autophagy, Biological_Activity: Calmidazolium chloride (R 24571) is a calmodulin (CaMK) antagonist, antagonizing CaM-dependent phosphodiesterase and calmodulin-induced activation of erythrocyte Ca2+-transporting ATPase with IC50s of 0.15 and 0.35 μM, respectively[1]. Also in anti-cancer research[2]. Calmidazolium binds to CaMK with a Kd of 3 nM.
IC50 & Target: Kd: 3 nM (Calmodulin)[3]
In Vitro: Calmidazolium chloride is widely used as a calmodulin (CaM) antagonist, but is also known to induce apoptosis in certain cancer cell lines. Calmidazolium chloride (3, 5, 7, 10 μM, 30 minutes-24 hours) inhibits growth of mouse F9 ECCs[2].

Name: β-Cyclodextrin, CAS: 7585-39-9, stock 27.3g, assay 98.2%, MWt: 1134.98, Formula: C42H70O35, Solubility: H2O : 38.75 mg/mL (34.14 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: β-Cyclodextrin is a cyclic polysaccharide composed of seven units of glucose (α-D-glucopyranose) linked by α-(1,4) type bonds. β-Cyclodextrin has often been used to enhance the solubility of drugs.
In Vitro: β-Cyclodextrin (Beta-cyclodextrin; β-CD) is a cyclic polysaccharide composed of seven units of glucose (α-D-glucopyranose) linked by α-(1,4) type bonds, which presents a hydrophilic external surface and a hydrophobic internal cavity[1]. In the pharmaceutical industry, β-Cyclodextrin (β-CD) has often been used to enhance the solubility of drugs, such as indomethacin, naringin, celecoxib, and citric acid[2].

Name: Lanicemine AZD6765, CAS: 153322-05-5, stock 4.3g, assay 98.8%, MWt: 198.26, Formula: C13H14N2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Membrane Transporter/Ion Channel;Neuronal Signaling, Target: iGluR;iGluR, Biological_Activity: Lanicemine (AZD6765) is a low-trapping NMDA channel blocker with a binding (Ki) of 0.56-2.1 μM[1].
IC50 & Target: NMDA Channel Blocker[1]

Name: Gap 26, CAS: 197250-15-0, stock 24.8g, assay 98.2%, MWt: 1550.78, Formula: C70H106N19O19S, Solubility: H2O : 50 mg/mL (32.24 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Cytoskeleton, Target: Gap Junction Protein, Biological_Activity: Gap 26 is a connexin mimetic peptide corresponding to the residues 63-75 of connexin 43, which is a gap junction blocker.
IC50 & Target: Gap Junction Protein[1]
In Vitro: Gap 26 is corresponding to the residues 63-75 of connexin 43, which is a gap junction blocker. Gap 26 (100-300 μM) dose-dependently reduces the rhythmic responses of rabbit superior mesenteric arteries, with IC50 of 28.4 ± 3.4 μM[1]. Gap 26 abolishes the inositol-1,4,5-trisphosphate (InsP3)-triggered ATP response and reduces the ATP release, but has no effect on gap junctional coupling[2].

Name: Furafylline, CAS: 80288-49-9, stock 23.3g, assay 98.7%, MWt: 260.25, Formula: C12H12N4O3, Solubility: DMSO : 12.5 mg/mL (48.03 mM; Need ultrasonic); H2O : < 0.1 mg/mL (insoluble), Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Cytochrome P450, Biological_Activity: Furafylline is a potent and selective inhibitor of human cytochrome P450IA2 with an IC50 of 0.07 μM.
IC50 & Target: IC50: 0.07 μM (human cytochrome P450IA2)[1]
In Vivo: Furafylline is a potent and selective inhibitor of human cytochrome P450IA2 with an IC50 of 0.07 μM in kinase experiment. Furafylline is a methylxanthine derivative that is introduced as a long-acting replacement for theophylline in the treatment of asthma. Administration of Furafylline is associated with an elevation in plasma levels of caffeine, due to inhibition of caffeine oxidation, a reaction catalysed by one or more hydrocarbon-inducible isoenzymes of P450. Furafylline has either very little or no effect on human monooxygenase activities catalysed by other isoenzymes of P450, including P4501ID1, P4501IC, P450IIIA[1].

Name: Adrenorphin Metorphamide, CAS: 88377-68-8, stock 38.1g, assay 98.8%, MWt: 984.18, Formula: C44H69N15O9S, Solubility: DMSO : 50 mg/mL (50.80 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein;Neuronal Signaling, Target: Opioid Receptor;Opioid Receptor, Biological_Activity: Adrenorphin is a opioid octapeptide, acting as a potent agonist of μ-opioid receptor, with Ki of 12 nM.
IC50 & Target: Ki: 12 nM (μ-opioid receptor)[1]
In Vitro: Adrenorphin (Metorphamide) is a opioid octapeptide from bovine brain, acts as a potent agonist of μ-opioid receptor, with Ki of 12 nM. The binding ratios of Ki for μ-opioid receptor/Ki for δ-opioid receptor of 0.04 and of Ki for μ-opioid receptor/Ki for κ-opioid receptor of 0.46[1]. Adrenorphin potently inhibits catecholamine secretion evoked by 10 μM nicotine in cultured human pheochromocytoma 6 cells, with an IC50 of 1.1 μM[2].

Name: G-1, CAS: 881639-98-1, stock 37.5g, assay 98.1%, MWt: 412.28, Formula: C21H18BrNO3, Solubility: H2O : < 0.1 mg/mL (insoluble); DMSO : 50 mg/mL (121.28 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Others, Target: Estrogen Receptor/ERR, Biological_Activity: G-1 is a nonsteroidal, high-affinity and selective agonist of GPR30 with a Ki of 11 nM.
IC50 & Target: Ki: 11 nM (GPR30)[1]
In Vitro: G-1 is a nonsteroidal, high-affinity and selective agonist of GPR30 with a Ki of 11 nM[1]. Treatment with G-1 (10 μM and 100 μM) for 48 and 72 h significantly decreases cell proliferation (P<0.001). At 72 h, the IC50 value for G-1 is calculated to be 20 μM. Treatment of A549 cells with G-1 at a concentration of 20 μM reveals a significant increase in apoptosis, consistent with its antiproliferative effect (P<0.001)[2]. Cell cycle analysis of H295R cells after 24 h of G-1 treatment demonstrates a cell cycle arrest in the G2 phase. The presence of G-1 increases Bax expression while decreases Bcl-2[3].
In Vivo: The results at 14 days post-injury show that the Basso mouse scale (BMS) scores are significantly higher in the G-1 group compared with the other groups (P<0.05). The number of caspase-3-positive cells in the cross sections is counted, and G-1 group has fewer positive cells compare with the other groups (P<0.05), and there is no difference between the two groups (P>0.05)[1]. G-1 administration produces a statistically significant decrease in tumor volume from day 14 post treatment. Grafted tumors harvested after three-week treatment with G-1 show a significant decrease in tumor weight compare to vehicle treated animals[3].

Name: AZD5423, CAS: 1034148-04-3, stock 1.9g, assay 98.6%, MWt: 487.45, Formula: C25H21F4N3O3, Solubility: 10 mM in DMSO, Clinical_Informat: Phase 2, Pathway: GPCR/G Protein, Target: Glucocorticoid Receptor, Biological_Activity: AZD5423 is an inhaled, potent, selective, and non-steroidal glucocorticoid receptor (GR) modulator (SGRM)[1]. AZD5423 effectively reduces allergen-induced responses in subjects with mild allergic asthma[2].
IC50 & Target: Glucocorticoid receptor[1]
In Vitro: The affinity of AZD5423 to the glucocorticoid receptor is high with an IC50 of 0.9 nM in a radioligand human glucocorticoid receptor assay, and selectivity towards other steroid hormone receptors is >900-fold[1].

Name: Berberine sulfate, CAS: 633-66-9, stock 9.2g, assay 98.9%, MWt: 434.44, Formula: C20H20NO8S+, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Cell Cycle/DNA Damage;Anti-infection;Autophagy;Metabolic Enzyme/Protease;NF-κB;Immunology/Inflammation, Target: Topoisomerase;Bacterial;Autophagy;Reactive Oxygen Species;Reactive Oxygen Species;Reactive Oxygen Species, Biological_Activity: Berberine sulfate is an alkaloid isolated from the Chinese herbal medicine Huanglian, as an antibiotic. Berberine sulfate induces reactive oxygen species (ROS) generation and inhibits DNA topoisomerase. Berberine sulfate has antineoplastic properties[1].
IC50 & Target: ROS[1] 
DNA topoisomerase[1]
In Vitro: Berberine sulfate (1.25-160 μM; 72 hours) has potential inhibitory effects on the proliferation of four colorectal carcinoma cell lines LoVo, HCT116, SW480, and HT-29[1]. 
Berberine sulfate (1.25-160 μM; 24-72 hours) induces a time- and dose-dependent inhibition of LoVo cell growth[1]. 
LoVo cells are exposure to Berberine sulfate (10-80 μM) for 24 h. Cell cycle analysis of 40 μM Berberine-treated LoVo cells by flow cytometry shows accumulation of cells in the G2/M phase[1]. 
Berberine sulfate (10-80 μM) suppresses cyclin B1, cdc2 and cdc25c protein expression after 24 h, especially at the dose of 80.0 μM[1].
In Vivo: Berberine sulfate (10, 30, or 50 mg/kg/day; gastrointestinal gavage; for 10 consecutive days) inhibits the growth of human colorectal adenocarcinoma in vivo. Berberine at doses of 30 and 50 mg/kg/day taken by gastrointestinal gavage shows inhibitory rates of 33.1% and 45.3% on the human colorectal adenocarcinoma xenograft growth in nude mice[1].

Name: Araloside V Congmunoside V, CAS: 340963-86-2, stock 31.6g, assay 98.7%, MWt: 1105.26, Formula: C54H88O23, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Araloside V (Congmunoside V) is a triterpenoid saponin isolated from Aralia elata[1].

Name: PETCM, CAS: 10129-56-3, stock 11.5g, assay 98.7%, MWt: 240.51, Formula: C8H8Cl3NO, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Apoptosis;Apoptosis, Target: Apoptosis;Caspase, Biological_Activity: PETCM is an activator of caspase-3. PETCM can induces cell apoptosis and stimulate apoptosome formation in HeLa cell cytosols[1].
IC50 & Target: IC50: caspase-3[1]

Name: SID 26681509, CAS: 958772-66-2, stock 0.2g, assay 98.8%, MWt: 539.65, Formula: C27H33N5O5S, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease;Anti-infection, Target: Cathepsin;Parasite, Biological_Activity: SID 26681509 is a potent, reversible, competitive, and selective inhibitor of human cathepsin L with an IC50 of 56 nM. SID 26681509 inhibits in vitro propagation of malaria parasite Plasmodium falciparum and inhibits Leishmania major with IC50s of 15.4 μM and 12.5 μM, respectively. SID 26681509 shows no inhibitory activity against cathepsin G[1].
IC50 & Target: IC50: 56 nM (Human cathepsin L), 15.4 μM (Plasmodium falciparum), 12.5 μM (Leishmania major)[1]
In Vitro: After a 4 hr preincubation with cathepsin L, SID 26681509 becomes more potent, demonstrating an IC50 of 1.0 nM. SID 26681509 is determined to be a slow-binding and slowly reversible competitive inhibitor. Through a transient kinetic analysis for single-step reversibility, inhibition rate constants are kon = 24,000 M-1s-1 and koff = 2.2 × 10-5 s-1 (Ki = 0.89 nM). Molecular docking studies are undertaken using the experimentally-derived X-ray crystal structure of papain/CLIK-148[1]. 
SID 26681509 inhibits papain and cathepsins B, K, S, and V with IC50 values determined after one hour ranging from 618 nM to 8.442 μM. SID 26681509 shows no inhibitory activity against the serine protease cathepsin G[1].
In Vivo: SID 26681509 treatment significantly improves survival in murine models of sepsis and reduces liver damage following warm liver ischemia/reperfusion (I/R) models[2].

Name: Pseudolaric acid B β-D-glucoside, CAS: 98891-41-9, stock 13.2g, assay 98%, MWt: 594.60, Formula: C29H38O13, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Pseudolaric acid B β-D-glucoside is a diterpenoid isolated from Pseudolarix kaempferi[1].

Name: Proglumide (sodium), CAS: 99247-33-3, stock 23g, assay 98.5%, MWt: 356.39, Formula: C18H25N2NaO4, Solubility: 10 mM in DMSO, Clinical_Informat: Launched, Pathway: GPCR/G Protein;Neuronal Signaling, Target: Cholecystokinin Receptor;Cholecystokinin Receptor, Biological_Activity: Proglumide sodium is a nonpeptide and orally active cholecystokinin (CCK)-A/B receptors antagonist. Proglumide sodium selective blocks CCK’s effects in the central nervous system (CNS). Proglumide sodium has ability to inhibit gastric secretion and to protect the gastroduodenal mucosa. Proglumide sodium also has antiepileptic and antioxidant activities[1][2][3][4][5].
IC50 & Target: Cholecystokinin (CCK)-A/B receptors[1][2]
In Vitro: In an in vitro study, Proglumide at concentrations between 0.3-10 mM inhibits CCK-stimulated amylase release dose-dependently, while Proglumide does not influence the basal amylase release at concentrations between 0-3 mM. Dose-response curves to CCK for amylase release shifted to the right with increase in Proglumide concentration. This inhibition by Proglumide is reversible. In addition, the effect of Proglumide is selective for CCK and its related peptide[2]. 
The incubation of HT29 cells with Proglumide significantly reduces the [3H]-thymidine incorporation to HT29 cells in a dose-dependent manner, with an IC50 of 6.5 mM. Proglumide reduces in a dose-dependent manner the percentage of necrosis with a parallel increase of apoptosis up to 70%[3].
In Vivo: Proglumide (250-750 mg/kg; intraperitoneal injection; adult male Sprague Dawley rats) treatment is significantly effective in ameliorating the seizure activities, cognitive dysfunctions, and cerebral oxidative stress[1].

Name: 1,3,5-Tricaffeoylquinic acid, CAS: 1073897-80-9, stock 21.8g, assay 98.9%, MWt: 678.59, Formula: C34H30O15, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Anti-infection, Target: HIV, Biological_Activity: 1,3,5-Tricaffeoylquinic acid is a tricaffeoylquinic acid derivative isolated from H. populifolium with anti-HIV effect[1].

Name: Gastrin-1, human, CAS: 10047-33-3, stock 15.9g, assay 98.8%, MWt: 2098.20, Formula: C97H124N20O31S, Solubility: DMSO : ≥ 50 mg/mL (23.83 mM), Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein;Neuronal Signaling, Target: Cholecystokinin Receptor;Cholecystokinin Receptor, Biological_Activity: Gastrin-1, human is the endogenous peptide produced in the stomach, and increases gastric acid secretion via cholecystokinin 2 (CCK2) receptor.
IC50 & Target: CCK2 receptor[1]
In Vitro: Gastrin-1, human is the endogenous peptide produced in the stomach, and acts via cholecystokinin 2 (CCK2) receptor[1].
In Vivo: Gastrin-1 (1.5, 5, 15 and 45 nmol/kg, i.v.) increases pepsinogen and acid secretion in rats[1].

Name: YM022, CAS: 145084-28-2, stock 12g, assay 98.3%, MWt: 516.59, Formula: C32H28N4O3, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Immunology/Inflammation;GPCR/G Protein, Target: CCR;CCR, Biological_Activity: YM022 is a highly potent, selective and orally active gastrin/cholecystokinin (CCK)-B receptor (CCK-BR) antagonist. YM022 shows the Ki values of 68 pM and 63 nM for CCK-B and CCK-A receptor, respectively[1]. YM022 can inhibit gastrin-induced gastric acid secretion and histidine decarboxylase activation in vivo[3].
IC50 & Target: Ki:68 pM (CCK-BR); 63 nM (CCK-AR)[1]
In Vitro: YM022 inhibits binding to canine pancreas CCK-A receptor in a dose-dependent manner, with an IC50 value for [3H]devazepide binding of 136 nM[1]. 
YM022 inhibits the binding of [125I]CCK-8 to canine cloned gastrin/CCK-B receptor in a dose-dependent manner, with an IC50 value for [125I]CCK-8 binding of 0.73 nM[1]. 
Selectivity [ratio of (IC50 for gastrin/CCK-B receptor)/(IC50for CCK-A receptor)] of YM022 is 186[1]. 
In Vivo: YM022 (intravenous injection; 0.01-1 μM/kg) dose-dependently inhibits pentagastrin- and peptone meal-induced acid secretion with ED50 values of 0.0261 and 0.0654 μmol/kg, respectively, without affecting histamine- or methacholine-induced acid secretion[3]. 
YM022 (subcutaneous injection; 300 μmol/kg; single dose) lowers the oxyntic mucosal HDC activity and raises the serum gastrin concentration in a dose-dependent manner (measured 24 h after dosage). Maximum enzyme inhibition is achieved at a dose of 300 μmol/kg for YM022 and the inhibition of HDC lasts for 4 weeks. At sacrifice, drug residues can be seen at the injection site for as long as 4 (YM022) weeks after injection in rat[3]. 
YM022 is suspended in 2% Methocel for oral ingestion and in PEG300 for subcutaneous injection[3].

Name: Garcinone D, CAS: 107390-08-9, stock 39.7g, assay 98.5%, MWt: 428.47, Formula: C24H28O7, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: JAK/STAT Signaling;Stem Cell/Wnt;NF-κB;Metabolic Enzyme/Protease;NF-κB;Immunology/Inflammation, Target: STAT;STAT;Keap1-Nrf2;Reactive Oxygen Species;Reactive Oxygen Species;Reactive Oxygen Species, Biological_Activity: Garcinone D, a natural xanthone from mangosteen, promotes the proliferation of C17.2 neural stem cell. Garcinone D increases the protein levels of phosphorylated signal transducer and activator of transcription 3 (p-STAT3), Cyclin D1 and nuclear factor erythroid 2-related factor (Nrf2), heme oxygenase-1 (HO-1) in concentration- and time- dependent manners[1].

Name: Garcinone C, CAS: 76996-27-5, stock 7.7g, assay 98.9%, MWt: 414.45, Formula: C23H26O7, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Cell Cycle/DNA Damage;Cell Cycle/DNA Damage;PI3K/Akt/mTOR;JAK/STAT Signaling;Stem Cell/Wnt, Target: CDK;ATM/ATR;ATM/ATR;STAT;STAT, Biological_Activity: Garcinone C, a xanthone derivative, is a natural compound extracted from Garcinia oblongifolia Champ that is used as an anti-inflammatory, analgesia, astringency and granulation-promoting medicine, and has potential cytotoxic effects on certain cancers. Garcinone C stimulates the expression levels of ATR and 4E-BP1, while efficiently inhibiting the expression levels of cyclin B1, cyclin D1, cyclin E2, cdc2, Stat3 and CDK7. Garcinone C significantly inhibits cell viability of the human Nasopharyngeal carcinoma (NPC) cell lines CNE1, CNE2, HK1 and HONE1 in a time‑ and dose‑dependent manner[1].

Name: SB297006, CAS: 58816-69-6, stock 18.2g, assay 98.2%, MWt: 342.35, Formula: C18H18N2O5, Solubility: H2O : < 0.1 mg/mL (insoluble); DMSO : 150 mg/mL (438.15 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Immunology/Inflammation;GPCR/G Protein, Target: CCR;CCR, Biological_Activity: SB297006 is a CCR3 antagonist, which significantly inhibits proliferation and neurosphere formation in CCL11-treated neural progenitor cells.
IC50 & Target: CCR3[1]
In Vitro: SB297006 is a CCR3 antagonist, significantly inhibits proliferation and neurosphere formation in CCL11-treated neural progenitor cells (NPCs) at 100 μM[1].

Name: Cimiracemoside C Cimicifugoside M, CAS: 256925-92-5, stock 13.7g, assay 98.2%, MWt: 620.81, Formula: C35H56O9, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Epigenetics;PI3K/Akt/mTOR, Target: AMPK;AMPK, Biological_Activity: Cimiracemoside C is an active component of Cimicifuga racemosa, activates AMPK, has the potential activity against diabetes[1].

Name: PG01, CAS: 853138-65-5, stock 32.3g, assay 98.2%, MWt: 439.55, Formula: C28H29N3O2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Membrane Transporter/Ion Channel, Target: CFTR, Biological_Activity: PG01 is a potent CFTR Cl- channel potentiator. PG01 can correct gating defects of CFTR mutants, is effective on b>E193K, G970R and G551D (CFTR mutants) with Kd values of 0.22 μM, 0.45 μM and 1.94 μM, respectively. PG01 is also effective on ΔF508 (Ka of 0.3 μM). PG01 increases ΔF508-CFTR Cl- current after adding Forskolin[1][2].
IC50 & Target: CFTR[1]
In Vitro: PG01 itself does not activate ∆F508-CFTR, produces substantial ∆F508-CFTR Cl- current after the addition of 0.5 and 2 μM Forskolin. PG01 at 100 nM strongly stimulates channel activity with multiple channel openings observed. The apparent Kd for PG01 for G551D-CFTR activation is 1 μM, approximately 100-fold better than that of genistein. The potency for activation G1349D-CFTR by PG01 is even better at 40 nM. PG01 produces large currents in both G551D- and G1349D-CFTR expressing cells. The currents are sensitive to CFTRinh-172 and are not seen in nontransfected cells[1].
In Vivo: Pharmacokinetic analysis of PG01 in rats is done by serial measurements of plasma concentrations after single bolus infusions (5 mg/kg). PG01 pharmacokinetics fitted a two-compartment model with half-times of ＜5 min and 130 min with volume of distribution 4 L. Microsome metabolism studies and rat pharmacokinetic analysis suggests significantly more rapid metabolism of PG01 than SF-03[1].

Name: DCPIB, CAS: 82749-70-0, stock 19.2g, assay 98.6%, MWt: 427.36, Formula: C22H28Cl2O4, Solubility: DMSO : ≥ 125 mg/mL (292.49 mM), Clinical_Informat: No Development Reported, Pathway: Membrane Transporter/Ion Channel;Membrane Transporter/Ion Channel, Target: Chloride Channel;Potassium Channel, Biological_Activity: DCPIB is a selective, reversible and potent inhibitor of volume-regulated anion channels (VRAC), voltage-dependently activates potassium channels TREK1 and TRAAK, inhibits TRESK, TASK1 and TASK3 (IC50s, 0.14, 0.95, 50.72 μM, respectively)[1]. DCPIB is also a selective blocker of swelling-induced chloride current (ICl,swell), with an IC50 of 4.1 μM in CPAE cells[2].
IC50 & Target: IC50：0.14 μM (TRESK), 0.95 μM (TASK1), 50.72 μM (TASK3)[1], 4.1 μM (ICl,swell, CPAE cells)[2]

Name: Phenserine (-)-Eseroline phenylcarbamate; (-)-Phenserine, CAS: 101246-66-6, stock 3.5g, assay 98.5%, MWt: 337.42, Formula: C20H23N3O2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Neuronal Signaling;Neuronal Signaling, Target: Amyloid-β;AChE, Biological_Activity: Phenserine ((-)-Eseroline phenylcarbamate) is a derivative of Physostigmine and is a potent, noncompetitive, long-acting and selective AChE inhibitor. Phenserine reduces β-amyloid precursor protein (APP) and β-amyloid peptide (Aβ) formation. Phenserine improves cognitive performance and attenuates the progression of Alzheimer's disease[1][2][3].
IC50 & Target: AChE; β-amyloid precursor protein; β-amyloid peptide[1]
In Vitro: Phenserine (1-25 μM; 48 hours; CHO APP751SW cells) treatment CHO APP751SW cell shows 18.6% reduction in cells treated with 10 μM of Phenserine, while 25 μM concentration of Phenserine reduces APP level by 51.4%[2].
In Vivo: Phenserine (1-4 mg/kg; intraperitoneal injection; for 4 days; male Fischer-344 rats) treatment improves learning when cholinergic function has been impaired in a spatial memory task[3].

Name: Groenlandicine, CAS: 38691-95-1, stock 32.8g, assay 98.8%, MWt: 322.33, Formula: C19H16NO4+, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Cell Cycle/DNA Damage, Target: Topoisomerase, Biological_Activity: Groenlandicine is a protoberberine alkaloid isolated from Coptidis Rhizoma. Groenlandicine exhibits moderate inhibitory effect with IC50 value of 154.2 μM for human recombinant aldose reductase (HRAR)[1]. Groenlandicine selectively induces topoisomerase I-mediated DNA cleavage[2].
IC50 & Target: IC50: 154.2 μM (HRAR)[1]

Name: Scutellarin methyl ester, CAS: 119262-68-9, stock 22.7g, assay 98.4%, MWt: 476.39, Formula: C22H20O12, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Scutellarin methyl ester is a constituent of Breviscapine which is a crude extract of several flavonoids of Erigeron breviscapus[1][2].

Name: 3-Isomangostin, CAS: 19275-46-8, stock 24.7g, assay 98.6%, MWt: 410.46, Formula: C24H26O6, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: 3-Isomangostin, extracted from Garciniamangostana.L. shell, is a potent MutT homologue 1 (MTH1) inhibitor with an IC50 value of 52 nM. 3-Isomangostin would be an attractive chemical tool for the development of anticancer agents[1].

Name: 1-Aminobenzotriazole ABT;3-Aminobenzotriazole, CAS: 1614-12-6, stock 16.2g, assay 98.6%, MWt: 134.14, Formula: C6H6N4, Solubility: DMSO : 125 mg/mL (931.86 mM; Need ultrasonic); H2O : 50 mg/mL (372.74 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Cytochrome P450, Biological_Activity: 1-Aminobenzotriazole is a nonspecific and irreversible inhibitor of cytochrome P450 (P450).
IC50 & Target: P450[1]
In Vitro: 1-Aminobenzotriazole (ABT) alone significantly increases the expression levels of CYP2B6 in two different hepatocytes (7.3- and 10.8-fold, respectively). Upon co-treatment with 1-Aminobenzotriazole, the induction of CYP2B6 expression by CITCO or rifampin is potentiated: 12.6- and 4.0-fold for CITCO as well as 3.9- and 2.5-fold for rifampin. 1-Aminobenzotriazole has a greater potentiation effect on CITCO than on rifampin. 1-Aminobenzotriazole alone increases the expression levels of CYP3A4 in tow different hepatocytes (by 2.0- and 3.8-fold). Upon co-treatment with 1-Aminobenzotriazole, the effects of CITCO on CYP3A4 expression levels are potentiated by 3.8- and 6.0- fold as compare to cells treated with CITCO alone[1]. 1-Aminobenzotriazole (ABT) (1 mM) shows pronounced (~95%) inhibition of the formation of N-acetylprocainamide compare with the control without 1-Aminobenzotriazole[2].
In Vivo: Oral 1-Aminobenzotriazole (ABT) (100 mg/kg, 2 h predose) decreases the clearance of intravenous procainamide (45%) in rats, accompanied by a decreased N-acetylprocainamide-to-procainamide ratio in urine (0.74 versus 0.21) and plasma (area under the curve ratio 0.59 versus 0.11). The urinary recovery of procainamide increases from 18 to 30%, whereas the recovery of N-acetylprocainamide in urine decreases from 13.3 to 6.5% with 1-Aminobenzotriazole[2]. Pretreatment of rats with 100 mg/kg oral 1-Aminobenzotriazole (ABT) administered 2 hours before a semisolid caloric test meal markedly delays gastric emptying. 1-Aminobenzotriazole also increases stomach weights by 2-fold[3].

Name: Eupalinilide B, CAS: 757202-08-7, stock 38.8g, assay 98.3%, MWt: 360.40, Formula: C20H24O6, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Eupalinilide B is a sesquiterpenoid isolated from Genus Eupatorium.

Name: Ganoderenic acid E, CAS: 110241-23-1, stock 26.4g, assay 98.6%, MWt: 528.63, Formula: C30H40O8, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Ganoderenic acid E is a lanostane-type triterpene isolated from Ganoderma lucidum.

Name: Lucidenic acid B, CAS: 95311-95-8, stock 9.1g, assay 98.7%, MWt: 474.59, Formula: C27H38O7, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Apoptosis, Target: Apoptosis, Biological_Activity: Lucidenic acid B is a natural compound isolated from Ganoderma lucidum, induces apoptosis of cancer cells, and causes the activation of caspase-9 and caspase-3, and cleavage of PARP. Lucidenic acid B does not affect the cell cycle profile, or the number of necrotic cells[1].
IC50 & Target: Apoptosis[1]

Name: Lucideric acid A, CAS: 95311-94-7, stock 15.9g, assay 98.8%, MWt: 458.59, Formula: C27H38O6, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: MMP, Biological_Activity: Lucideric acid A is a natural compound isolated from Ganoderma lucidum, inhibits PMA-induced MMP-9 activity, with anti-invasive effect on hepatoma cells[1].
IC50 & Target: MMP-9[1]

Name: TC HSD 21, CAS: 330203-01-5, stock 27.6g, assay 98.2%, MWt: 422.32, Formula: C17H12BrNO3S2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: TC HSD 21 is a potent 17β-hydroxysteroid dehydrogenase type 3 (17β-HSD3) inhibitor with an IC50 of 14 nM. TC HSD 21 shows excellent selectivity over 17β-HSD isoenzymes and nuclear receptors[1].
IC50 & Target: IC50: 14 nM (17β-HSD3)[1]

Name: Methylmalonic acid Methylpropanedioic acid;Methylmalonate, CAS: 516-05-2, stock 11g, assay 98.6%, MWt: 118.09, Formula: C4H6O4, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: Methylmalonic acid (Methylmalonate) is an indicator of Vitamin B-12 deficiency in cancer.
In Vitro: Vitamin B-12 is required for Methylmalonate (Methylmalonic acid; MMA) to be converted to succinyl-CoA, and in combination with folic acid, for homocysteine (HC) to be converted to methionine. Therefore, Methylmalonate is clearly more specific to vitamin B-12 deficiency compared to HC[1].

Name: Lucidenic acid C, CAS: 95311-96-9, stock 33.7g, assay 98%, MWt: 476.60, Formula: C27H40O7, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: MMP, Biological_Activity: Lucidenic acid C is a natural compound isolated from Ganoderma lucidum, inhibits PMA-induced MMP-9 activity, with anti-invasive effect on hepatoma cells[1].
IC50 & Target: MMP-9[1]

Name: Lucidenic acid LM1, CAS: 364622-33-3, stock 30.9g, assay 98.8%, MWt: 460.60, Formula: C27H40O6, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Lucidenic acid LM1 is a natural triterpenoid isolated from Ganoderma lucidum.

Name: Blasticidin S hydrochloride, CAS: 3513-03-9, stock 7.9g, assay 98.3%, MWt: 458.90, Formula: C17H27ClN8O5, Solubility: H2O : 20 mg/mL (43.58 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Anti-infection, Target: Bacterial, Biological_Activity: Blasticidin S hydrochloride is a nucleoside antibiotic isolated from Streptomyces griseochromogenes. Blasticidin S is a potent inhibitor of protein synthesis in both prokaryotic and eukaryotic cells[1].
IC50 & Target: Antibiotic[1]
In Vitro: Blasticidin S (BlaS) is a broad spectrum antibiotic and inhibits cell growth in prokaryotes, fungi, plants, and mammalian cells[1].

Name: HQL-79, CAS: 162641-16-9, stock 1g, assay 98.6%, MWt: 377.48, Formula: C22H27N5O, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Immunology/Inflammation, Target: PGE synthase, Biological_Activity: HQL-79 is a potent, selective and orally active human hematopoietic prostaglandin D synthase (H-PGDS) inhibitor, highly selectively inhibits the synthesis of PGD2, and acts as an anti-allergic agent, with a Kd of 0.8 μM and an IC50 of 6 μM. Shows no obvious effect on COX-1, COX-2, m-PGES, or L-PGDS[1].
IC50 & Target: IC50: 6 μM (H-PGDS)[1] 
Kd: 0.8 μM (H-PGDS)[1]
In Vitro: HQL-79 is a competitive inhibitor against substrate PGH2 and a non-competitive one against GSH[1].

Name: ABT-724 (trihydrochloride), CAS: 587870-77-7, stock 14.5g, assay 98.8%, MWt: 402.75, Formula: C17H22Cl3N5, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein;Neuronal Signaling, Target: Dopamine Receptor;Dopamine Receptor, Biological_Activity: ABT-724 trihydrochloride is a potent and highly selective dopamine D4 receptor agonist with an EC50 of 12.4 nM for human dopamine D4 receptor. ABT-724 trihydrochloride is a potent partial agonist at the rat D4 (EC50 of 14.3 nM) and the ferret D4 receptor (EC50 of 23.2 nM), and has no effect on dopamine D1, D2, D3, or D5 receptors. ABT-724 trihydrochloride could be useful for the treatment of erectile dysfunction and has favorable side-effect profile[1].
IC50 & Target: EC50: 12.4 nM (Human dopamine D4 receptor), 14.3 nM (Rat dopamine D4 receptor) and 23.2 nM (Ferret dopamine D4 receptor)[1]
In Vitro: ABT-724 exhibits a selective biochemical profile, as indicates by a lack of binding affinity for >70 neurotransmitter/uptake/ion channels including D2, D3, or D5 receptors up to a 10 μM concentration. A weak affinity to 5-HT1A receptors (Ki = 2780 nM) is observed. ABT-724 does not inhibit the PDE activity of PDE1, PDE5, or PDE6 at 10 μM concentrations[1].
In Vivo: ABT-724 (8.8 μg/kg; subcutaneous injection; daily; for 5 days; male adult Wistar rats) treatment dose-dependently facilitates penile erection when given s.c. to conscious rats[1].

Name: Carmoxirole (hydrochloride) EMD 45609 (hydrochloride), CAS: 115092-85-8, stock 21.3g, assay 98%, MWt: 410.94, Formula: C24H27ClN2O2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein;Neuronal Signaling, Target: Dopamine Receptor;Dopamine Receptor, Biological_Activity: Carmoxirole hydrochloride (EMD 45609 hydrochloride) is a selective, peripherally acting dopamine D2 receptor agonist and exhibits antihypertensive activities in vivo[1].
IC50 & Target: Dopamine D2 receptor[1]

Name: Raclopride, CAS: 84225-95-6, stock 30.1g, assay 98.1%, MWt: 347.24, Formula: C15H20Cl2N2O3, Solubility: DMSO : 100 mg/mL (287.99 mM; Need ultrasonic), Clinical_Informat: Phase 2, Pathway: GPCR/G Protein;Neuronal Signaling, Target: Dopamine Receptor;Dopamine Receptor, Biological_Activity: Raclopride is a dopamine D2/D3 receptor antagonist, which binds to D2 and D3 receptors with dissociation constants (Kis) of 1.8 nM and 3.5 nM, respectively, but has a very low affinity for D1 and D4 receptors with Kis of 18000 nM and 2400 nM, respectively[1].
IC50 & Target: Ki: 1.8 nM (D2 receptor), 3.5 nM (D3 receptor), 2400 nM (D4 receptor), 18000 nM (D1 receptor)[1]

Name: Tomeglovir BAY 38-4766, CAS: 233254-24-5, stock 31g, assay 98.1%, MWt: 441.54, Formula: C23H27N3O4S, Solubility: DMSO : ≥ 108 mg/mL (244.60 mM), Clinical_Informat: No Development Reported, Pathway: Anti-infection, Target: CMV, Biological_Activity: Tomeglovir is a potent anti-CMV agent, inhibiting processing of viral DNA-concatemers, with IC50s of 0.34 μM and 0.039 μM for HCMV and MCMV.
IC50 & Target: IC50: 0.34 μM (HCMV), 0.039 μM (MCMV)[1]
In Vitro: Tomeglovir (BAY 38-4766) is a potent anti-CMV agent, with IC50s of 0.34 μM and 0.039 μM for HCMV and MCMV. Tomeglovir also suppresses HELF and NIH 3T3 cells, with CC50s of 85 μM and 62.5 μM, respectively[1]. Tomeglovir (BAY 38-4766) inhibits HCMV Davis and various monkey CMV strains with EC50s of 1.03 ± 0.57 μM and < 1 μM[2].
In Vivo: Tomeglovir (BAY 38-4766; 3, 10, 30, 100 mg/kg, p.o.) dose-dependently reduces MCMV-DNA in salivary glands, livers and kidneys of MCMV-infected NOD-SCID mice, and prolongs the survival of the mice. Tomeglovir (10, 25 and 50 mg/kg) shows antiviral activity in the hollow fiber mouse model[1]. Tomeglovir (BAY 38-4766) shows antiviral activity in SCID mice with MCMV, and the LD50 is >2000 mg/kg in mice and rats[2].

Name: Gomisin N, CAS: 69176-52-9, stock 34.2g, assay 98.3%, MWt: 400.46, Formula: C23H28O6, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Apoptosis, Target: Apoptosis, Biological_Activity: Gomisin N, isolated from Schisandra chinensis, produces beneficial sedative and hypnotic bioactivity. Gomisin N has the potential for use in the treatment of allergy. Gomisin N is an anti-cancer drug candidate capable of inhibiting the proliferation and inducing the apoptosis in cancer[1][2][3].

Name: Flupentixol dihydrochloride Flupenthixol dihydrochloride, CAS: 2413-38-9, stock 9.9g, assay 98.7%, MWt: 507.44, Formula: C23H27Cl2F3N2OS, Solubility: DMSO : ≥ 83.3 mg/mL (164.16 mM), Clinical_Informat: Launched, Pathway: Others, Target: Others, Biological_Activity: Flupentixol dihydrochloride, a thioxanthene drug, is used in therapy of schizophrenia as well as in anxiolytic and depressive disorders.

Name: Armepavine, CAS: 524-20-9, stock 37.4g, assay 98.6%, MWt: 313.39, Formula: C19H23NO3, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: NF-κB, Target: NF-κB, Biological_Activity: Armepavine, an active compound from Nelumbo nucifera, exerts not only anti-inflammatory effects on human peripheral blood mononuclear cells, but also immunosuppressive effects on T lymphocytes and on lupus nephritic mice. Armepavine inhibits TNF-α-induced MAPK and NF-κB signaling cascades[1].

Name: Officinalisinin I, CAS: 57944-18-0, stock 34.5g, assay 98.2%, MWt: 921.07, Formula: C45H76O19, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Officinalisinin I is a steroidal saponin, isolated from Anemarrhena asphodeloides.

Name: Timosaponin B III, CAS: 142759-74-8, stock 31g, assay 98.5%, MWt: 903.06, Formula: C45H74O18, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Timosaponin B III is a major bioactive steroidal saponin isolated from Anemarrhena asphodeloides Bge, and exhibits anti-inflammatory, anti-platelet aggregative and anti-depressive effects[1][2][3].

Name: CGP52411 DAPH, CAS: 145915-58-8, stock 33.3g, assay 98.8%, MWt: 329.35, Formula: C20H15N3O2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Neuronal Signaling;JAK/STAT Signaling;Protein Tyrosine Kinase/RTK, Target: Amyloid-β;EGFR;EGFR, Biological_Activity: CGP52411 (DAPH) is a high selective, potent, orally active and ATP-competitive EGFR inhibitor with an IC50 of 0.3 μM. CGP52411 blocks the toxic influx of Ca2+ ions into neuronal cells, and dramatic inhibits and reverses the formation of β-amyloid (Aβ42) fibril aggregates associated with Alzheimer's disease[1][2].
In Vitro: CGP52411 (DAPH; 0-100 μM; 90 minutes; A431 cells) treatment inhibits autophosphorylation and c-src autophosphorylation in vitro in a dose-dependent manner with IC50s of 1 μM and 16 μM, respectively. CGP52411 treatment also shows a concentration-dependent reduction in tyrosine phosphorylation of p185c-erbB2 with an IC50 value of 10 μM[1]. 
CGP52411 (DAPH) inhibits c-src kinase with an IC50 value of 16 μM. CGP52411 inhibits PKC isozymes isolated from porcine brain with an IC50 of 80 μM. CGP52411 inhibits conventional PKC isozymes (cPKCs α, β-1, β-2, and γ) but not nonconventional PKC isozymes (nPKCs δ, ε, and ζ) or atypical PKC isozymes (aPKC η)[1].
In Vivo: CGP52411 (3.2 mg/kg, 6.3 mg/kg, 12.5 mg/kg, 25 mg/kg, and 50 mg/kg; oral administration; daily; for 15 days; female BALB/c nude mice) treatment in vivo against xenografts of the A431 and SK-OV-3 tumors, and has antitumor activity[1].

Name: TCS 21311 NIBR3049, CAS: 1260181-14-3, stock 16g, assay 98.3%, MWt: 526.51, Formula: C27H25F3N4O4, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Stem Cell/Wnt;PI3K/Akt/mTOR;TGF-beta/Smad;Epigenetics;Epigenetics;Stem Cell/Wnt;JAK/STAT Signaling, Target: GSK-3;GSK-3;PKC;PKC;JAK;JAK;JAK, Biological_Activity: TCS 21311 (NIBR3049) is a potent, highly selective JAK3 inhibitor with an IC50 of 8 nM, it displays >100-fold selectivity over JAK1, JAK2 and TYK2. TCS 21311 (NIBR3049) inhibits PKCα, PKCθ, and GSK3β with IC50s of 13, 68, and 3 nM, respectively[1].
In Vitro: TCS 21311 (NIBR3049) exhibits IC50 values of 1.017, 2.550 and 8.055 μM for JAK1, JAK2 and TYK2, respectively in a enzymatic Jak assay[1].
TCS 21311 (NIBR3049) shows moderate activity in this cellular assay (IC50=689 nM, Jurkat cells), which is in good agreement with its enzymatic Pkc activity[1].

Name: Zearalenone Mycotoxin F2;Toxin F2, CAS: 17924-92-4, stock 38.9g, assay 98.8%, MWt: 318.36, Formula: C18H22O5, Solubility: DMSO : 125 mg/mL (392.64 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Zearalenone is a mycotoxin produced mainly by fungi belonging to the genus Fusarium in foods and feeds. Possess oestrogenic activity in pigs, cattle and sheep, with low acute toxicity. Causes precocious development of mammae and other estrogenic effects in young gilts[1][2].
IC50 & Target: Zearalenone is frequently implicated in reproductive disorders of farm animals and occasionally in hyperoestrogenic syndromes in humans. There is evidence that ZEA and its metabolites possess oestrogenic activity in pigs, cattle and sheep. However, ZEA is of a relatively low acute toxicity after oral or interperitoneal administration in mice, rat and pig[1].

Name: G15, CAS: 1161002-05-6, stock 4.8g, assay 98.7%, MWt: 370.24, Formula: C19H16BrNO2, Solubility: DMSO : 41.67 mg/mL (112.55 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Others, Target: Estrogen Receptor/ERR, Biological_Activity: G15 is a high affinity and selective G-protein-coupled estrogen receptor (GPER/GPR30) antagonist with a Ki of 20 nM[1][2].
IC50 & Target: Ki: 20 nM (GPER/GPR30)[2]
In Vitro: G15 (0.1-10 μM; 2 days) inhibits GPER-mediated proliferation stimulated by 17β-estradiol (E2) in A549 and H1793 cell lines[1]. 
G15 (1 μM; 48 hours) inhibits the response of GPER stimulated by E2 and G1 in A549 and H1793 cell lines[1].
In Vivo: G15 (1.46 mg/kg; i.h.; twice a week for 14 weeks) decreases the number of tumor nodules and tumor index increased by the E2 or G1 group in urethane-induced adenocarcinoma mice[1].

Name: Dimethyl lithospermate B dmLSB, CAS: 875313-64-7, stock 24.8g, assay 98.1%, MWt: 746.67, Formula: C38H34O16, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Membrane Transporter/Ion Channel, Target: Sodium Channel, Biological_Activity: Dimethyl lithospermate B (dmLSB) is a selective Na+ channel agonist. Dimethyl lithospermate B slows inactivation of sodium current (INa), leading to increased inward current during the early phases of the action potential (AP)[1][2].
IC50 & Target: Na+ channel[1]

Name: Karacoline, CAS: 39089-30-0, stock 16.3g, assay 98.3%, MWt: 377.52, Formula: C22H35NO4, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Karacoline, a diterpene alkaloid found in the plant Aconitum kusnezoffii, reduces degradation of the extracellular matrix (ECM) in intervertebral disc degeneration (IDD) via the NF-κB signaling pathway[1].

Name: PHTPP, CAS: 805239-56-9, stock 21.7g, assay 98.6%, MWt: 423.31, Formula: C20H11F6N3O, Solubility: H2O : < 0.1 mg/mL (insoluble); DMSO : 25 mg/mL (59.06 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Others, Target: Estrogen Receptor/ERR, Biological_Activity: PHTPP is a selective ERβ antagonist.
IC50 & Target: ERβ[1]
In Vitro: PHTPP is a selective ERβ antagonist. PHTPP reduces FSH-mediated cAMP production by 80% (p<0.01) while it has no effect on basal cAMP[1]. PHTPP (10-6 M) inhibits E2-stimulated ERβ activity, but does not suppress E2-stimulated ERα activity. A high dose of PHTPP (10-6 M) slightly increases class 1 Igf1 mRNA expression, and facilitates the DPN-induced increase in class 1 Igf1 mRNA expression[2].

Name: Mogroside IV-A, CAS: 88901-41-1, stock 13.2g, assay 98%, MWt: 1125.29, Formula: C54H92O24, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Mogroside IV-A, 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: Isomogroside V, CAS: 1126032-65-2, stock 0.3g, assay 98%, MWt: 1287.43, Formula: C60H102O29, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Isomogroside V is a sweetener, which extracted from Siraitia grosvenorii (Swingle).

Name: IRL 2500, CAS: 169545-27-1, stock 20.2g, assay 98.9%, MWt: 573.68, Formula: C36H35N3O4, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein, Target: Endothelin Receptor, Biological_Activity: IRL 2500 is a potent Endothelin receptor antagonist. IRL 2500 shows IC50 values of 1.3 and 94 nM for ETB and ETA receptors, respectively. IRL 2500 inhibits ETB receptor-mediated blood pressure increase and renal vascular resistance in rats in vivo[1].
In Vivo: IRL 2500 (intravenous injection;10 mg/kg) inhibits the initial transient decrease in mean arterial pressure (MAP) induced by the ETB-selective agonist IRL 1620 in rats, IRL 2500 also attenuates the IRL 1620-mediated increase in renal vascular resistance (RVR) in the anesthetized rat[1].
IRL 2500 (intravenous injection;10 mg/kg) pre-reatment significantly reduces the initial vasodepressor response to endothelin-1 (ET-1) and IRL 1620, however, it is not alters the secondary and sustained pressor response to these agonists[2].

Name: Mogroside III-A1, CAS: 88901-42-2, stock 16.3g, assay 98.7%, MWt: 963.15, Formula: C48H82O19, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: , Target: , Biological_Activity: Mogroside III-A1, 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: Mogroside II-A2, CAS: 88901-45-5, stock 39.8g, assay 98.3%, MWt: 801.01, Formula: C42H72O14, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: , Target: , Biological_Activity: Mogroside II-A2, 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: Mogroside III-E, CAS: 88901-37-5, stock 9.7g, assay 98.4%, MWt: 963.15, Formula: C48H82O19, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Mogroside III-E is a cucurbitane-type compound isolated from Siraitia grosvenorii, inhibits NO release, with anti-fibrotic activity[1].

Name: K114, CAS: 872201-12-2, stock 28.8g, assay 98.5%, MWt: 393.27, Formula: C22H17BrO2, Solubility: DMSO : 100 mg/mL (254.28 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: K114, a fluorescent Congo Red analogue, binds tightly to amyloid fibrils with an EC50 of 20-30 nM[1]. K114 is an efficient detector of semen-derived enhancer of virus infection (SEVI)[2].
In Vitro: K114's unusually low buffer fluorescence is due to self-quenching in sedimentable aggregates or micelles which upon interacting with amyloid fibrils undergo an enhancement in fluorescence intensity and shifts in the excitation and emission spectra[1].

Name: Hederacolchiside A1, CAS: 106577-39-3, stock 31.3g, assay 98.7%, MWt: 897.10, Formula: C47H76O16, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: PI3K/Akt/mTOR;Apoptosis;PI3K/Akt/mTOR;PI3K/Akt/mTOR;Anti-infection, Target: PI3K;Apoptosis;mTOR;Akt;Parasite, Biological_Activity: Hederacolchiside A1, isolated from Pulsatilla chinensis, suppresses proliferation of tumor cells by inducing apoptosis through modulating PI3K/Akt/mTOR signaling pathway[1]. Hederacolchiside A1 has antischistosomal activity, affecting parasite viability both in vivo and in vitro[2].
In Vitro: Hederacolchiside A1 reduces the mitochondrial membrane potential and Bcl-2 protein levels, whereas cleaved caspase-3 was higher[1]. 
Hederacolchiside A1 effectively inhibits the phosphorylations of phosphatidylinositol 3 kinase (PI3K), protein kinase B (Akt), and mammalian target of rapamycin (mTOR) [1]. 
In Vivo: hederacolchiside A1 (3.0, 4.5, and 6.0 mg/kg, ip) can significantly inhibit the weight of tumor in an H22 xenograft model[1]. 
Hederacolchiside A1 (3.25, 7.5, and 15.0 mg/kg, ig) can significantly inhibit the weight of tumor in nude mice xenograft tumor models using human breast carcinoma MCF-7 cells[1].

Name: Mogroside IV, CAS: 89590-95-4, stock 11.7g, assay 98.3%, MWt: 1125.29, Formula: C54H92O24, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Mogroside IV, 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: WKYMVM, CAS: 187986-17-0, stock 39.1g, assay 98.5%, MWt: 856.11, Formula: C41H61N9O7S2, Solubility: H2O, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: WKYMVM is a potent N-formyl peptide receptor (FPR1) and FPRL1/2 agonist, also activates several leukocyte effector functions such as chemotaxis, mobilization of complement receptor-3, and activation of the NADPH oxidase[1][2].
IC50 & Target: FPR1, FPRL1[1], FPRL2[2]

Name: Pseudoginsenoside Rh2, CAS: 1370264-16-6, stock 27.7g, assay 98.5%, MWt: 622.87, Formula: C36H62O8, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Pseudoginsenoside Rh2, synthesized from Ginsenoside Rh2, possesses anti-cancer activitied[1].

Name: 25-O-Methylalisol A, CAS: 155801-00-6, stock 36.6g, assay 98.8%, MWt: 504.74, Formula: C31H52O5, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: 25-O-Methylalisol A is a protostane triterpenoids isolated from Alisma orientale. The dried rhizomes of the aquatic plant Alisma orientale known as Rhizoma Alismatis is a common traditional Chinese medicine used for diuretic, anti-inflammatory, and hypolipidemic purposes, as well as the treatment of diabetes[1].

Name: Ro15-4513, CAS: 91917-65-6, stock 2.7g, assay 98.9%, MWt: 326.31, Formula: C15H14N6O3, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Neuronal Signaling;Membrane Transporter/Ion Channel, Target: GABA Receptor;GABA Receptor, Biological_Activity: Ro15-4513, imidazobenzodiazepinone derivative, is a partial inverse agonist of benzodiazepine receptor (BZR)[1]. Ro15-4513 is a potent ethanol antagonist[2]. Ro15-4513 has anti-anxiety effect[3].
IC50 & Target: BZR[1]; ethanol[2];
In Vitro: Ro15-4513 usually acts as a partial inverse agonist at GABAA receptors, except an agonist for α4 and α6 subunit-containing ones[3].
In Vivo: Ro 15-4513 (i.p.; 3 mg/kg; 10 min before being tested) completely inhibits the ethanol-induced (1.8 g/kg) reduction in total locomotor activity and partly the reduction in rearing[2]. 
Ro 15-4513 (i.p.; 3 mg/kg; 15 min before administration of 1.5 g/kg ethanol) reverses ethanol-induced sedation in GABAA receptor δ subunit-deficient mice[2].

Name: KHK-IN-2, CAS: 2135304-43-5, stock 9.6g, assay 98.7%, MWt: 372.34, Formula: C16H19F3N4O3, Solubility: DMSO : 250 mg/mL (671.43 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Hexokinase, Biological_Activity: KHK-IN-2 is a potent and selective ketohexokinase (KHK) inhibitor with an IC50 of 0.45 μM.
IC50 & Target: IC50: 0.45 μM (KHK)[1]

Name: Theliatinib HMPL-309, CAS: 1353644-70-8, stock 17.5g, assay 98.1%, MWt: 442.51, Formula: C25H26N6O2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: JAK/STAT Signaling;Protein Tyrosine Kinase/RTK, Target: EGFR;EGFR, Biological_Activity: Theliatinib (HMPL-309) is a potent, ATP-competitive and highly selective EGFR inhibitor, significantly inhibits phosphorylation of EGFR (p-EGFR) and its downstream targets, AKT and ERK (p-AKT and p-ERK), with anti-tumor activity. Theliatinib (HMPL-309) shows a Ki of 0.05 nM for wild type EGFR, and IC50s of 3 and 22 nM for EGFR and EGFR T790M/L858R mutant, respectively[1].
IC50 & Target: IC50: 3 nM (EGFR), 22 nM (EGFR T790M/L858R)[1] 
Ki: 0.05 nM (EGFR)[1]

Name: JNJ0966, CAS: 315705-75-0, stock 5.9g, assay 98.1%, MWt: 360.45, Formula: C16H16N4O2S2, Solubility: DMSO : 100 mg/mL (277.43 mM; Need ultrasonic); H2O : < 0.1 mg/mL (insoluble), Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: MMP, Biological_Activity: JNJ0966 is a highly selective MMP-9 zymogen inhibitor with an IC50 of 440 nM.
IC50 & Target: IC50: 440 nM (MMP-9 zymogen)[1]
In Vitro: JNJ0966 is a highly selective MMP-9 zymogen inhibitor with an IC50 of 440 nM. The activations of proMMP-1, proMMP-2, and proMMP-3 are not significantly different in the presence or absence of 10 μM JNJ0966, whereas proMMP-9 activation by trypsin is significantly attenuated by JNJ0966. The addition of JNJ0966 to the reaction results in a significant reduction in fully processed MMP-9 and an apparent accumulation of the intermediate species[1].
In Vivo: The exposures of JNJ0966 are dose-dependent, with plasma and brain concentrations for the 10-mg/kg dose of 77.5±31.1 ng/mL (215 nM) and 481.6±162.5 ng/g (~1336 nM), respectively, whereas the 30-mg/kg dose achieves 293.6±118.4 ng/mL (815 nM) in plasma and 1394.0±649.1 ng/g (~3867 nM) in brain. JNJ0966 is preferentially partitioned in brain, with brain/plasma ratios of 6.2 for the 10-mg/kg dose and 4.7 for the 30-mg/kg dose[1].

Name: CDK8-IN-1, CAS: 1629633-48-2, stock 26.4g, assay 98.9%, MWt: 255.20, Formula: C11H8F3N3O, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Cell Cycle/DNA Damage, Target: CDK, Biological_Activity: CDK8-IN-1 is a potent and selective CDK8 inhibitor with an IC50 of 3 nM.
IC50 & Target: IC50: 3 nM (CDK8)[1].
In Vivo: CDK8-IN-1 displays low systemic clearance, very good exposure and oral bioavailability. The tmax is 0.25 h by PO. The mean values of Cmax are 9940 μg/L, 12740 μg/L by IV and PO respectively. The values of AUC are 9378, 25952 by IV and PO respectively[1].

Name: Motesanib AMG 706;, CAS: 453562-69-1, stock 36.3g, assay 98.7%, MWt: 373.45, Formula: C22H23N5O, Solubility: DMSO : ≥ 30 mg/mL (80.33 mM), Clinical_Informat: Phase 3, Pathway: Protein Tyrosine Kinase/RTK;Protein Tyrosine Kinase/RTK, Target: VEGFR;c-Kit, Biological_Activity: Motesanib is a potent ATP-competitive inhibitor of VEGFR1/2/3 with IC50s of 2 nM/3 nM/6 nM, respectively, and has similar activity against Kit, and is appr 10-fold more selective for VEGFR than PDGFR and Ret.
IC50 & Target: IC50: 2 nM (VEGFR1), 3 nM (VEGFR2), 6 nM (VEGFR3)
In Vitro: Motesanib has broad activity against the human VEGFR family, and displays > 1000 selectivity against EGFR, Src, and p38 kinase. Motesanib significantly inhibits VEGF-induced cellular proliferation of HUVECs with an IC50 of 10 nM, while displaying little effect at bFGF-induced proliferation with an IC50 of >3,000 nM. Motesanib also potently inhibits PDGF-induced proliferation and SCF-induced c-kit phosphorylation with IC50 of 207 nM and 37 nM, respectively, but not effective against the EGF-induced EGFR phosphorylation and cell viability of A431 cells[1]. Althouth displaying little antiproliferative activity on cell growth of HUVECs alone, Motesanib treatment significantly sensitizes the cells to fractionated radiation[2].
In Vivo: Motesanib (100 mg/kg) significantly inhibits VEGF-induced vascular permeability in a time-dependent manner. Oral administration of Motesanib twice daily or once daily potently inhibits, in a dose-dependent manner, VEGF-induced angiogenesis using the rat corneal model with ED50 of 2.1 mg/kg and 4.9 mg/kg, respectively. Motesanib induces a dose-dependent tumor regression of established A431 xenografts by selectively targeting neovascularization in tumor cells[1]. Motesanib in combination with radiation displays significant anti-tumor activity in head and neck squamous cell carcinoma (HNSCC) xenograft models[2]. Motesanib treatment also induces significant dose-dependent reductions in tumor growth and blood vessel density of MCF-7, MDA-MB-231, or Cal-51 xenografts, which can be markedly enhanced when combined with docetaxel or tamoxifen[3].

Name: (S)-SNAP5114, CAS: 157604-55-2, stock 19g, assay 98%, MWt: 505.60, Formula: C30H35NO6, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Neuronal Signaling;Membrane Transporter/Ion Channel, Target: GABA Receptor;GABA Receptor, Biological_Activity: (S)-SNAP5114 is a selective GABA transport inhibitor, with IC50 values of 5 μM and 21 μM for hGAT-3 and rGAT-2, respectively. (S)-SNAP5114 is an anticonvulsant drug[1][2].
IC50 & Target: IC50: 5 μM (hGAT-3), 21 μM (rGAT-2)[1].

Name: CGP52432, CAS: 139667-74-6, stock 17.9g, assay 98.2%, MWt: 384.24, Formula: C15H24Cl2NO4P, Solubility: DMSO : 5 mg/mL (13.01 mM; Need ultrasonic and warming), Clinical_Informat: No Development Reported, Pathway: Neuronal Signaling;Membrane Transporter/Ion Channel, Target: GABA Receptor;GABA Receptor, Biological_Activity: CGP52432 is a GABAB receptor antagonist, with an IC50 of 85 nM.
IC50 & Target: IC50: 85 nM (GABAB receptor)[1]
In Vitro: CGP52432 is a GABAB receptor antagonist, with an IC50 of 85 nM, 35- and 100-fold lower than at the receptors regulating somatostatin and glutamate overflow, respectively[1].
In Vivo: CGP52432 (10, 30 mg/kg) shows no effect on the total arm entries and total head dips of mice on the elevated-plus maze[2]. CGP52432 (100 nmol/kg, i.v., or 1 nmol/kg, i.c.v.) abolishes the suppressive effects of GABA ( 50 μmol/kg, i.v.) on enhanced renal sympathetic nerve activity (RSNA) during ischaemia, causeing elimination of the renoprotective effects of GABA in rats[3].

Name: Gabazine SR95531, CAS: 104104-50-9, stock 35.5g, assay 98.1%, MWt: 368.23, Formula: C15H18BrN3O3, Solubility: DMSO : ≥ 75 mg/mL (203.68 mM), Clinical_Informat: No Development Reported, Pathway: Neuronal Signaling;Membrane Transporter/Ion Channel, Target: GABA Receptor;GABA Receptor, Biological_Activity: Gabazine is a selective and competitive antagonist of GABAA receptor, with an IC50 of ~0.2 μM for GABA receptor.
IC50 & Target: 0.2 μM (GABA receptor)[1].
In Vitro: Both bicuculline and Gabazine (SR 95531) have been characterized as competitive inhibitors of GABA binding to the GABAA receptor. Gabazine is more potent than bicuculline at blocking currents elicited by GABA, with an IC50 for currents elicited by 3 μM GABA of ~0.2 μM and a Hill coefficient of 1.0. Gabazine reduces the currents elicited by 10 μM alphaxalone by ~30%, for responses of receptors containing wildtype β2 subunits. The concentration of Gabazine requires producing half the maximal block is ~0.2 μM. Gabazine also could only produce a partial block of currents gated by 300 μM pentobarbital. The maximal reduction, again, is ~30%, and the concentration of Gabazine required to produce half the maximal block is ~0.15 μM[1].

Name: Galanin (1-30), human, CAS: 119418-04-1, stock 6.6g, assay 98.2%, MWt: 3157.46, Formula: C139H210N42O43, Solubility: 10 mM in H2O, Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein;Neuronal Signaling, Target: Neuropeptide Y Receptor;Neuropeptide Y Receptor, Biological_Activity: Galanin (1-30), human is a 30-amino acid neuropeptide, and acts as an agonist of GalR1 and GalR2 receptors, with Kis of both 1 nM.
IC50 & Target: Kd: 1 nM (GalR1 receptor), 1 nM (GalR2 receptor)[2]
In Vitro: Galanin (1-30), human (Gal1-30) is an agonist of GalR1 and GalR2 receptors, with Kis of both 1 nM[1]. Galanin (1-30), human displaces 125I-labeled rat galanin with a Kd of 0.5 nM. Galanin (1-30), human (hGal) causes contractions of isolated longitudinal rat fundus strips, with an ED50 of 13.8 ± 1.6 nM[2].

Name: BETP, CAS: 1371569-69-5, stock 37.7g, assay 98.6%, MWt: 406.42, Formula: C20H17F3N2O2S, Solubility: DMSO : 100 mg/mL (246.05 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein, Target: Glucagon Receptor, Biological_Activity: BETP is an agonist of glucagon-like peptide-1 (GLP-1) receptor, with EC50s of 0.66 and 0.755 μM for human and rat GLP-1 receptor, respectively.
IC50 & Target: EC50: 0.66 μM (Human GLP-1 receptor), 0.755 μM (Rat GLP-1 receptor)[1]
In Vitro: BETP is a GLP-1 receptor agonist, with EC50s of 0.66 and 0.755 μM for human and rat GLP-1 receptor, respectively. BETP (Compound B) is inactive in cells expressing the GLP-2, GIP, PTH, or glucagon receptors. BETP (1-10 μM) enhances insulin secretion in normal and diabetic human islets. In addition, BETP in combination with GLP-1 shows additive effects on increasing GLP-1 receptor signaling[1]. BETP increases the potency of oxyntomodulin by 10-fold (EC50 of 80 pM). GLP-1 does not change the potencies and efficacies of both oxyntomodulin and glucagon at the glucagon receptor. BETP (0-30 μM) increases the binding affinity of oxyntomodulin for the GLP-1 receptor[2].
In Vivo: BETP has insulinotropic effect in SD rats. BETP (10 mg/kg, jugular vein cannula) exhibits insulin secretagogue activity in the intravenous glucose tolerance test (IVGTT) model. BETP (10 mg/kg, i.v.)-treated rats need 20% higher glucose infusion rates and demonstrates higher plasma insulin levels in SD rat hyperglycemic clamp model[1]. BETP (5 mg/kg) enhances oxyntomodulin-stimulated insulin secretion[2].

Name: Glucagon-like peptide 1 (1-37), human HuGLP-1, CAS: 87805-34-3, stock 6.5g, assay 98.9%, MWt: 4169.48, Formula: C186H275N51O59, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein, Target: Glucagon Receptor, Biological_Activity: Glucagon-like peptide 1 (1-37), human is a highly potent agonist of the GLP-1 receptor.
IC50 & Target: GLP-1 receptor[1]
In Vitro: Glucagon-like peptide-1 (GLP-1) is produced by the posttranslational processing of proglucagon and acts as a regulator of various homeostatic events. GLP-1(1-37) is more stable than GLP-1(7-37), with 94.7% of the initial amount of peptide left after a 4h exposure to mouse serum. GLP-1(1-37) is confirmed to be a highly potent agonist of the GLP-1 receptor (GLP-1R) by measuring the expression of the luciferase reporter gene expression in transiently transfected human embryonic kidney (HEK293) cells[1].
In Vivo: GLP-1(1–37) decreased glycemic excursion in a dose-dependent. The administration of GLP-1(1–37) or GLP-1(7–37) markedly decrease blood glucose levels at 15 min and 30 min compared with the control group[1].

Name: KDU731, CAS: 1610610-48-4, stock 20.4g, assay 98%, MWt: 396.40, Formula: C22H16N6O2, Solubility: DMSO : 83.33 mg/mL (210.22 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: PI3K/Akt/mTOR;Anti-infection, Target: PI4K;Parasite, Biological_Activity: KDU731, an orally active C. parvum PI4K inhibitor with an IC50 value of 25 nM, blocks Cryptosporidium infection in vitro and in vivo[1][2]. KDU731 is a promising drug candidate for the treatment of diarrhea caused by Cryptosporidium and meets a broad range of safety[2].
IC50 & Target: IC50: 25 nM (C. parvum PI4K)[2]
In Vivo: KDU731 (orally administration; 7 or 10mg/kg; 16 days) has potent activity against Cryptosporidium in immunocompromised IFN-γ KO mice and dramatically reduces oocyst shedding[2].
KDU731 (orally administration; 5 mg/kg; every 12 hours for 7 days) is tolerated in all calves, and treated calves shed significantly fewer oocysts than vehicle treated calves in their stool[2].

Name: Almitrine mesylate Almitrine bismesylate; Almitrine bismethanesulfonate; Almitrine dimesylate, CAS: 29608-49-9, stock 8.1g, assay 98.2%, MWt: 669.76, Formula: C28H37F2N7O6S2, Solubility: DMSO : 125 mg/mL (186.63 mM; Need ultrasonic), Clinical_Informat: Launched, Pathway: Membrane Transporter/Ion Channel, Target: Potassium Channel, Biological_Activity: Almitrine mesylate, a peripheral chemoreceptor agonist, inhibits selectively the Ca2+-dependent K+ channel.
IC50 & Target: K+ channel[1]
In Vitro: Almitrine inhibits the activity of a high-conductance (152±13 pS), Ca2+-dependent K+ channel by decreasing its open probability. The IC50 value of the effect is 0.22 μM. The inhibitory effect of Almitrine on Ca2+-dependent K+ channels also is observed in GH3 cells. Almitrine at concentrations up to 10 μM does not affect whole-cell voltage-dependent K+, Ca2+, or Na+ currents in rat or rabbit cells. However, this concentration of Almitrine significantly inhibits the Ca2+-dependent component of K+ currents in rat chemoreceptor cells[1].
In Vivo: Almitrine acts via the peripheral arterial chemoreceptors raising carotid sinus nerve output and minute ventilation. Almitrine also has a pulmonary vascular action causing a dose-dependent constriction and dilatation. At low doses Almitrine enhances hypoxic pulmonary vasoconstriction and may improve the overall ventilation/perfusion ratio[2].

Name: Azosemide, CAS: 27589-33-9, stock 16.1g, assay 98.7%, MWt: 370.84, Formula: C12H11ClN6O2S2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Membrane Transporter/Ion Channel, Target: NKCC, Biological_Activity: Azosemide, a sulfonamide loop diuretic, is a potent NKCC1 inhibitor with IC50s of 0.246 µM and 0.197 µM for hNKCC1A and NKCC1B, respectively[1].
IC50 & Target: IC50: 0.246 µM (hNKCC1A) and 0.197 µM (NKCC1B)[1]
In Vitro: Azosemide inhibits the sodium-potassium-chloride-cotransporter human variants hNKCC1A and hNKCC1B[1].
In Vivo: Azosemide shows a smaller AUC (81.9% decrease), shorter terminal half-life (50.9% decrease) and MRT (64.1% decrease), faster CL (454% increase), CLR (853% increase) and CLNR (307% increase) for NARs[2].

Name: Barnidipine (hydrochloride) Mepirodipine (hydrochloride);YM-09730-5, CAS: 104757-53-1, stock 21.4g, assay 98.5%, MWt: 528.00, Formula: C27H30ClN3O6, Solubility: DMSO : 250 mg/mL (473.48 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Membrane Transporter/Ion Channel;Neuronal Signaling, Target: Calcium Channel;Calcium Channel, Biological_Activity: Barnidipine hydrochloride (Mepirodipine hydrochloride) is an L-type calcium antagonist (CaA) with high affinity for [3H] initrendipine binding sites (Ki=0.21 nmol/l), has selective action against CaA receptors[1].
Barnidipine hydrochloride (Mepirodipine hydrochloride) is an antihypertensive drug and acts by the reduction of peripheral vascular resistance secondary to its vasodilatory action[2].
IC50 & Target: Ki: 0.21 nmol/l ([3H] initrendipine)[1]

Name: (Rac)-Telmesteine, CAS: 127657-29-8, stock 15.7g, assay 98.8%, MWt: 205.23, Formula: C7H11NO4S, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: (Rac)-Telmesteine is a protease inhibitor and is thus a suitable enzyme stabilizer extracted from patent WO 2017220302 A1, compound II-1. (Rac)-Telmesteine can be used as an enzyme stabilizer in protease-containing detergents and cleaning agents[1].
IC50 & Target: Protease[1]

Name: β-Elemene (-)-β-Elemene;Levo-β-elemene, CAS: 515-13-9, stock 24.4g, assay 98.6%, MWt: 204.35, Formula: C15H24, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Apoptosis, Target: Apoptosis, Biological_Activity: β-Elemene ((-)-β-Elemene; Levo-β-elemene) is isolated from natural plant Curcuma wenyujin with an antitumor activity. β-Elemene can induce cell apoptosis.
In Vitro: β-Elemene (0-200 µg/ml; 24 hours) shows IC50 values of 72.8 µg/ml; 47.4 µg/ml; 61.5 µg/ml; 3.661 µg/ml; 68 µg/ml; 72.12 µg/ml; 37.894 µg/ml and 37.703 µg/ml for SV-HUC-1, T24, 5637, TCCSUP, J82,UMUC-3,RT4, and SW780 cells, respectively[1].
β-Elemene (0-75 µg/ml; 24 hours) decreases cell number from 50 µg/ml and is notably decreased at 75 µg/ml, induces dose-dependent G1-phase arrest in T24cells and significantly reduces the percentage of cells in the S-phase [1].
β-Elemene (50 µg/ml; 12 hours) downregulates the expression levels of p-STAT3 and the cell cycle-related proteins cyclin D1, CDK4 and CDK6, and upregulates p21 and p27expression in T24 cells [1].
β-Elemene (50 µg/ml; 24 hours) enhances cisplatin-induced apoptosis by activating the ROS-AMPK signaling pathway[1].

Name: Cefathiamidine, CAS: 33075-00-2, stock 20.4g, assay 98.5%, MWt: 472.58, Formula: C19H28N4O6S2, Solubility: 10 mM in DMSO, Clinical_Informat: Launched, Pathway: Anti-infection, Target: Bacterial, Biological_Activity: Cefathiamidine is a first-generation cephalosporin antibacterial agent and is used to treat infections caused by susceptible bacteria. Cefathiamidine exhibits a wide spectrum of antimicrobial activity against bacteria. Cefathiamidine is used for the treatment of respiratory, liver, five senses, urinary tract infections, endocarditis and sepsis[1][2].
IC50 & Target: Bacterial[1]
In Vitro: The in-vitro activity of Cefathiamidine against Streptococcus faecalis and Streptococcus faecium are studied in comparison with other β-lactams. All the 56 strains of Str. faecalis tested are inhibited by 2 mg/L of Cefathiamidine. The MBCs of Cefathiamidine and Ampicillin for ten strains of Str. faecalis show that the ratios of MBC/MIC are greater than 64. The rates of killing of Str. faecalis are reduced at concentrations of Cefathiamidine and Ampicillin greater than the MIC. The most rapid killing is obtained at 2 mg/L Cefathiamidine or 4 mg/L of Ampicillin. With the addition of 1 mg/L gentamicin this paradoxical bacteriocidal effect is eliminated. Time killing studies show99.9% of the cells are killed within 6 hours by a combination of aminoglycoside and β-lactam[2].
In Vivo: Cefathiamidine is not absorbed orally and is, thus, administered through the parenteral route (intravenously or intramuscularly). Cefathiamidine is widely distributed in most bodily fluids and tissues; however, Cefathiamidine cannot pass through the blood-brain barrier. The protein-binding capacity of Cefathiamidine is 23%, and more than 90% of Cefathiamidine is excreted unchanged by the kidney[1].

Name: Nonaethylene glycol monododecyl ether Nonaoxyethylene monododecyl ether, CAS: 3055-99-0, stock 39.6g, assay 98.3%, MWt: 582.81, Formula: C30H62O10, Solubility: DMSO : 250 mg/mL (428.96 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Nonaethylene glycol monododecyl ether (Nonaoxyethylene monododecyl ether) is a nonionic surfactant and polyethylene glycol (PEG) detergent that can be used to form initial coalesced O/W emulsion droplets, as well as for protein separation and purification[1][2][3].
In Vitro: Examination of a series of non-ionic PEG detergents with several long-chain E-PDSs from different organisms reveals that in vitro incubations with Nonaethylene glycol monododecyl ether typically gave chain lengths that corresponded to those of the isoprenoid moieties in respiratory quinones synthesized in vivo[2].

Name: Pivagabine CXB-722, CAS: 69542-93-4, stock 38.2g, assay 98.4%, MWt: 187.24, Formula: C9H17NO3, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Pivagabine (CXB 722), a psychoactive drug, is a hydrophobic 4-aminobutyric acid derivative with neuromodulatory activity. Pivagabine penetrates the blood-brain barrier in rats. Pivagabine antagonizes the effects of foot shock on both GABAA receptor function and corticotropin-releasing factor (CRF) concentrations in rat brain[1][2].
In Vivo: Pivagabine (CXB 722) (200 mg/kg; i.p.; twice a day for 4 days and 1 hour before killing on the 5th day) prevents the effects of foot-shock stress on CRF concentration in both brain regions[2].

Name: Perfluamine Perfluorotripropylamine;FTPA;Tris(perfluoropropyl)amine, CAS: 338-83-0, stock 1g, assay 98.1%, MWt: 521.07, Formula: C9F21N, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Perfluamine (Perfluorotripropylamine), a hydrophobic carrier fluid, is used in the surface modification of droplet polymeric microfluidic devices. Perfluamine has a role as a blood substitute[1][2].

Name: Delapril (hydrochloride), CAS: 83435-67-0, stock 10.4g, assay 98.7%, MWt: 489.00, Formula: C26H33ClN2O5, Solubility: 10 mM in DMSO, Clinical_Informat: Launched, Pathway: Metabolic Enzyme/Protease, Target: Angiotensin-converting Enzyme (ACE), Biological_Activity: Delapril is an angiotensin-converting enzyme (ACE) inhibitor for the treatment of cardiovascular diseases[1].
IC50 & Target: ACE[1]
In Vivo: Delapril (3 mg/kg; administered orally for 2 weeks) exerts potent ACE inhibitory activity in spontaneously hypertensive rat (SHR) [1]. 
Delapril (1-10 mg/kg; orally) exerts a marked and long-lasting antihypertensive action in various experimental models of hypertension[1].

Name: Deserpidine Harmonyl, CAS: 131-01-1, stock 33.5g, assay 98.6%, MWt: 578.65, Formula: C32H38N2O8, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Angiotensin-converting Enzyme (ACE), Biological_Activity: Deserpidine (Harmonyl) is an alkaloid isolated from the root of Rauwolfia canescens related to Reserpine. Deserpidine is used as an antihypertensive agent and a tranquilizer. Deserpidine is a competitive angiotensin converting enzyme (ACE) inhibitor. Deserpidine also decreases angiotensin II-induced aldosterone secretion by the adrenal cortex[1][2][3].
IC50 & Target: Angiotensin converting enzyme (ACE)[3]
In Vitro: Deserpidine is an effective ganglionic blocking agent, which differs from Reserpine only by the absence of a methoxy group at C-11. Deserpidine has been used in the treatment of hypertension and psychosis. In addition, Deserpidine appears to act as a controller of other cardiac disorders[1][2].

Name: Enbucrilate Butyl cyanoacrylate, CAS: 6606-65-1, stock 28g, assay 98.5%, MWt: 153.18, Formula: C8H11NO2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Enbucrilate (Butyl cyanoacrylate) is a cyanoacrylate ester that has been used as surgical tissue adhesive.
In Vivo: Enbucrilate offers an important intervention in gastric variceal bleeding which should be further studied in the US. A randomized trial is warranted to compare this intervention to radiological therapy[1]. The tissue adhesive Enbucrilate seems to be a safe, efficient agent to obtain good results in a simple, quick approach in the surgical treatment of symptomatic nephroptosis[2].

Name: DUPA(OtBu)-OH, CAS: 1026987-94-9, stock 23.5g, assay 98.6%, MWt: 488.57, Formula: C23H40N2O9, Solubility: DMSO : 125 mg/mL (255.85 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: DUPA(OtBu)-OH is a DUPA precursor. DUPA is used as the targeting moiety to actively deliver Docetaxel (DTX) for treatment of Prostate-Specific Membrane Antigen (PSMA) expressing prostate cancer.
In Vitro: DUPA(OtBu)-OH (DUPA precursor 17) is a 2-[3-(1,3-dicarboxypropyl)ureido]pentanedioic acid (DUPA) reagent[1]. The targeting ligand DUPA enhances the transport capability and selectivity of Paclitaxel (PTX) to tumor cells via prostate-specific membrane antigen (PSMA) mediated endocytosis. Besides, DUPA is conjugated with PTX via a disulfide bond, which facilitates the rapid and differential drug release in tumor cells[2].
In Vivo: DUPA-targeted Docetaxel (DTX) conjugate with longer spacer has no toxicity in major organs of treated mice[3].

Name: Gadopentetic acid Gd-DTPA;gadolinium complex, CAS: 80529-93-7, stock 33.6g, assay 98.7%, MWt: 547.57, Formula: C14H20GdN3O10, Solubility: DMSO : < 1 mg/mL (insoluble or slightly soluble); H2O : 100 mg/mL (182.63 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Gadopentetic acid (Gd-DTPA) is an paramagnetic contrast agent commonly implemented by a bolus intravenous injection (i.v.) in Dynamic contrast-enhanced MRI (DCE-MRI) studies. The initial concentration of Gadopentetic acid (Gd-DTPA) in the plasma ([Gd-DTPA0]) is an important parameter for DCE-MRI. [Gd-DTPA0] is related to the administered bolus dose and varies with subjects. A bolus of 0.025 mmol/kg Gd-DTPA offers shorter acquisition time and less exposure of subjects, with a half-life of 37.3 mins, a mean residence time of 53.8 mins, and an AUC of 3.37 ± 0.47 mmol/min/L[1].

Name: Medronic acid Methylenediphosphonic acid, CAS: 1984-15-2, stock 3.4g, assay 98.4%, MWt: 176.00, Formula: CH6O6P2, Solubility: DMSO : 250 mg/mL (1420.45 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Medronic acid (Methylenediphosphonic acid) is a methylene-substituted bisphosphonate. Medronic acid has affinity for and adheres to the surface of hydroxyapatite crystals in the bone matrix. Medronic acid accumulates at sites of osteoid mineralization and can be used, complexed with radioisotopes in bone imaging.

Name: JAK1-IN-3, CAS: 2091134-68-6, stock 8.3g, assay 98.3%, MWt: 489.57, Formula: C25H31N9O2, Solubility: DMSO : 250 mg/mL (510.65 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Epigenetics;Stem Cell/Wnt;JAK/STAT Signaling, Target: JAK;JAK;JAK, Biological_Activity: JAK1-IN-3 is a selective JAK1 inhibitor, with an IC50 of 73 nM, weakly inhibits JAK2, and shows little inhibition on JAK3 (IC50, >14.7, >30 μM, respectively).
IC50 & Target: IC50: 73 nM (JAK1), >14.7 μM (JAK2), >30 μM (JAK3)[1]
In Vitro: JAK1-IN-3 (Example 32) is a selective JAK1 inhibitor, with an IC50 of 73 nM, weakly inhibits JAK2, and shows little inhibition on JAK3 (IC50, >14.7, >30 μM, respectively). JAK1-IN-3 significantly inhibits STAT3 phosphorylation in NCI-H 1975 cells with an IC50 of 161 nM[1].
In Vivo: JAK1-IN-3 (12.5 mg/kg BID (twice daily), 25 m/kg BID or 50 mg/kg BID, p.o.) alone has increasing antitumor effects, and ehances the antitumor activity of osimertinib, compared to treatment with osimertinib alone in mice bearing NCI-H1975 cells[1].

Name: CH7057288, CAS: 2095616-82-1, stock 22.9g, assay 98.3%, MWt: 569.67, Formula: C32H31N3O5S, Solubility: H2O : < 0.1 mg/mL (insoluble); DMSO : ≥ 34 mg/mL (59.68 mM), Clinical_Informat: No Development Reported, Pathway: Protein Tyrosine Kinase/RTK;Neuronal Signaling, Target: Trk Receptor;Trk Receptor, Biological_Activity: CH7057288 is a potent and selective TRK inhibitor.
IC50 & Target: TRK [1]
In Vitro: CH7057288 induces regression of intracranial tumors and greatly improves event-free survival in an intracranial implantation model mimicking brain metastasis. CH7057288 can be a promising therapeutic agent for TRK fusion-positive cancer. TRK receptor tyrosine kinases are expressed as fusion proteins encoded by various fusion genes across a wide variety of cancer types, including lung and colorectal cancer[1].

Name: SGN-2FF, CAS: 2089647-47-0, stock 26.8g, assay 98.2%, MWt: 166.15, Formula: C6H11FO4, Solubility: H2O : 36.67 mg/mL (220.70 mM; Need ultrasonic), Clinical_Informat: Phase 1, Pathway: Others, Target: Others, Biological_Activity: SGN-2FF is an oral inhibitor of fucosylation, directly inhibits fucosyltransferase activity, and possesses antitumor activity.
IC50 & Target: Fucosyltransferase[1]
In Vitro: SGN-2FF (2-Fluorofucose) is an inhibitor of fucosylation, inhibits cellular fucosylation by depleting the fucosylation substrate GDP-fucose, and by direct inhibition of fucosyltransferases, and leads to the production of afucosylated glycoproteins including antibodies. SGN-2FF activates human T cells in an antigen-dependent manner[1].
In Vivo: SGN-2FF exhibits antitumor activity in multiple mouse tumor models, showing substantial tumor growth delay. SGN-2FF elevates the protective effect of a lymphoma vaccine in a syngeneic mouse model[1].

Name: Epertinib S-22611, CAS: 908305-13-5, stock 0.8g, assay 98.5%, MWt: 560.02, Formula: C30H27ClFN5O3, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: JAK/STAT Signaling;Protein Tyrosine Kinase/RTK, Target: EGFR;EGFR, Biological_Activity: Epertinib is a potent, oral, reversible, and selective tyrosine kinase inhibitor of EGFR, HER2 and HER4, with IC50s of 1.48 nM, 7.15 nM and 2.49 nM, respectively. Epertinib shows potent antitumor activity.
IC50 & Target: IC50: 1.48 nM (EGFR), 7.15 nM (HER2), 2.49 nM (HER4)[1]
In Vitro: Epertinib (S-222611) is a potent, oral, reversible, and selective tyrosine kinase inhibitor of EGFR, HER2 and HER4, with IC50s of 1.48 nM, 7.15 nM and 2.49 nM, respectively, and shows no effect on KDR, IGF1R, SRC, KIT, and PDGFRβ (IC50, >10000 nM). Epertinib inhibits relative phosphorylation of EGFR and HER2 in NCI-N87 cells, with IC50s of 4.5 and 1.6 nM, respectively. Furthermore, Epertinib exhibits inhibitory activity against the growth of cancer cell lines expressing EGFR and/or HER2, with IC50s of 8.3 nM (NCI-N87 (stomach)), 9.9 nM (BT-474 (breast)), and 14 nM (SK-BR-3 (breast))[1]. Epertinib also inhibits MDA-MB-361 cell growth, with an IC50 of 26.5 nM[2].
In Vivo: Epertinib shows antitumor activity in nude mice bearing NCI-N87 xenograft via oral administration for 21 days, with an ED50 of 10.2 mg/kg. Epertinib (50 mg/kg, p.o.) is four times more potent activity than GW572016 and completely inhibits the growth of cancer cells in mice[1]. Epertinib (50 mg/kg, p.o.) markedly reduces the brain tumor volume in the breast cancer intraventricular injection mouse brain metastasis model (IVM)[2].

Name: Sardomozide dihydrochloride CGP 48664A, CAS: 138794-73-7, stock 28.7g, assay 98.5%, MWt: 303.19, Formula: C11H16Cl2N6, Solubility: DMSO : 25 mg/mL (82.46 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Sardomozide dihydrochloride 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: Biotin-DADOO Biotinyl-3,6-dioxaoctanediamine;EZ-Link Amine-PEO2-Biotin, CAS: 138529-46-1, stock 13.3g, assay 98.8%, MWt: 374.50, Formula: C16H30N4O4S, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Biotin-DADOO is a biotinylation reagent, which can be used to synthesize a biotin-estradiol conjugate (i.e., biotin-DADOO-estradiol) to develop a direct, broad range enzyme immunoassay to measure plasma estradiol concentrations.

Name: LCL521, CAS: 1226851-11-1, stock 18.6g, assay 98.6%, MWt: 592.77, Formula: C31H52N4O7, Solubility: DMSO : 165 mg/mL (278.35 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: LCL521 is an acid ceramidase (ACDase) inhibitor. LCL521 also inhibits the lysosomal acid sphingomyelinase (ASMase).
IC50 & Target: ACDase, ASMase[1]
In Vitro: LCL521 (1 µM) acts as a potent inhibitor of cellular ACDase activity, whereas 10 µM LCL521 has an additional, decreased affect on the α-form of this enzyme. LCL521 (10 µM) causes a time-dependent (1 hours and 5 hours) decrease of the α-ACDase form in MCF7 cells[1].

Name: LCL521 dihydrochloride 1,3DMG-B13 dihydrochloride, CAS: 1226759-47-2, stock 36.9g, assay 98.8%, MWt: 665.69, Formula: C31H54Cl2N4O7, Solubility: DMSO : 20.83 mg/mL (31.29 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: LCL521 dihydrochloride (1,3DMG-B13 dihydrochloride) is an acid ceramidase (ACDase) inhibitor. LCL521 also inhibits the lysosomal acid sphingomyelinase (ASMase).
IC50 & Target: ACDase, ASMase[1]
In Vitro: LCL521 (1 µM) acts as a potent inhibitor of cellular ACDase activity, whereas 10 µM LCL521 has an additional, decreased affect on the α-form of this enzyme. LCL521 (10µM) causes a time-dependent (1 hours and 5 hours) decrease of the α-ACDase form in MCF7 cells[1].

Name: Epithalon, CAS: 307297-39-8, stock 12.9g, assay 98.1%, MWt: 390.35, Formula: C14H22N4O9, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Cell Cycle/DNA Damage, Target: Telomerase, Biological_Activity: Epitalon is an anti-aging agent and a telomerase activator. Epitalon has an inhibitory effect of the on the development of spontaneous tumors in mice, has geroprotective actions and intranasal administration increases neuronal activity. Epitalon can be used for cancer, old age and Retinitis Pigmentosa[1].
In Vitro: Addition of Epithalon peptide in telomerase-negative human fetal fibroblast culture induced expression of the catalytical subunit, enzymatic activity of telomerase, and telomere elongation, which can be due to reactivation of telomerase gene in somatic cells and indicates the possibility of prolonging life span of a cell population and of the whole organism[1].
In Vivo: Epitalon increases the lifespan of mice and fruit flies and restores the circadian rhythms of melatonin and cortisol production in old rhesus monkeys. At the same time, Epitalon prolongs the functional integrity of the eye retina in Campbell rats with hereditary Retinitis Pigmentosa and improves the visual functions in patients with pigmental retinal degeneration[1].

Name: PF-04937319, CAS: 1245603-92-2, stock 29g, assay 98.7%, MWt: 432.43, Formula: C22H20N6O4, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Glucokinase, Biological_Activity: PF-04937319 is a glucokinase activator (GKA) with EC50 value of 154.4 μM, one of the most promising strategies for the treatment of type 2 diabetes mellitus[1].
PF-04937319 is designed to maintain glucose-lowering efficacy while mitigating the risk of hypoglycaemia observed with many other GKAs[2].
IC50 & Target: EC50: 154.4 μM (GSA) (PF-04937319)[1]

Name: AM-0902, CAS: 1883711-97-4, stock 15.6g, assay 98.4%, MWt: 370.79, Formula: C17H15ClN6O2, Solubility: DMSO : 150 mg/mL (404.54 mM; Need ultrasonic and warming), Clinical_Informat: No Development Reported, Pathway: Membrane Transporter/Ion Channel;Neuronal Signaling, Target: TRP Channel;TRP Channel, Biological_Activity: AM-0902 is a potent, selective transient receptor potential A1 (TRPA1) antagonist with IC50s of 71 and 131 nM for rTRPA1 and hTRPA1, respectively.
IC50 & Target: IC50: 71 nM (rTRPA1), 131 nM (hTRPA1)[1]
In Vitro: AM-0902 is a potent, selective antagonist of TRPA1 with IC50s of 71 and 131 nM for rTRPA1 and hTRPA1, respectively. AM-0902 is highly permeable (average Papp=44.5 μcm/s in MDCK cells), an unlikely substrate for P-gp (efflux ratio=1.3 in P-gp overexpressing MDCK cells), and demonstrates good solubility (PBS pH 7.4: 226 μM, SIF: 248 μM). AM-0902 shows good selectivity over other TRP channels, as no activity is observed against human TRPV1 or TRPV4, or rat TRPV1, TRPV3, or TRPM8, at concentrations up to 10 μM. AM-0902 inhibits 45Ca2+ flux upon activation of rat TRPA1 with methylglyoxal with an IC50 of 0.019 μM[1].
In Vivo: AM-0902 is a potent, selective antagonist of TRPA1 in vivo. AM-0902 has moderate terminal elimination half-life (t1/2=0.6 h and 2.8 h for rat (0.5 mg/kg, iv), rat (30 mg/kg, oral)). A dose-dependent reduction of allyl isothiocyanate (AITC)-induced flinching is observed for AM-0902, with a significant reduction in flinching observed postdosing of 10 and 30 mg/kg. The unbound plasma concentrations (Cu) at 1 h for the 1, 3, 10, and 30 mg/kg doses are 0.051±0.024 (n=8), 0.19±0.11 (n=8), 0.58±0.35 (n=8), and 2.2±0.40 (n=8) μM, covering the in vitro rat TRPA1 45Ca2+ IC50 at 0.72, 2.7, 8.2, and 30.3 fold, respectively. A good exposure-response relationship is observed in this target coverage model. An unbound in vivo IC50 of 0.35 μM, which is in good agreement with the in vitro rat TRPA1 45Ca2+ IC50, and unbound in vivo IC90 of 1.7 μM are determined. It is noteworthy that at a dose of 30 mg/kg, AM-0902 engages TRPA1 at concentrations that exceed the in vivo IC90, making it a useful tool for exploration of in vivo models of acute pain[1].

Name: (±)-BAY-1251152, CAS: 1610358-53-6, stock 8.6g, assay 98.7%, MWt: 404.43, Formula: C19H18F2N4O2S, Solubility: H2O : < 0.1 mg/mL (insoluble); DMSO : 50 mg/mL (123.63 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Cell Cycle/DNA Damage, Target: CDK, Biological_Activity: (±)-BAY-1251152 is a racemic mixture of BAY-1251152. BAY-1251152 is a potent and highly selective PTEF/CDK9 inhibitor.

Name: (-)-BAY-1251152, CAS: 1610358-59-2, stock 25.6g, assay 98%, MWt: 404.43, Formula: C19H18F2N4O2S, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Cell Cycle/DNA Damage, Target: CDK, Biological_Activity: (-)-BAY-1251152 is an enanthiomer of BAY-1251152 with rotation (-). BAY-1251152 is a potent and highly selective PTEF/CDK9 inhibitor.

Name: PF-05241328, CAS: 1387633-03-5, stock 38.9g, assay 98.1%, MWt: 436.91, Formula: C19H21ClN4O4S, Solubility: 10 mM in DMSO, Clinical_Informat: Phase 1, Pathway: Membrane Transporter/Ion Channel, Target: Sodium Channel, Biological_Activity: PF-05241328 is a potent and selective inhibitor of human Nav1.7 voltage-dependent sodium channels (Nav1.7), with an IC50 of 31 nM.
IC50 & Target: IC50: 31 nM (Nav1.7)[1].

Name: Sipatrigine 619C89;BW 619C89, CAS: 130800-90-7, stock 39.7g, assay 98.1%, MWt: 372.68, Formula: C15H16Cl3N5, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Membrane Transporter/Ion Channel;Membrane Transporter/Ion Channel;Neuronal Signaling, Target: Calcium Channel;Sodium Channel;Calcium Channel, Biological_Activity: Sipatrigine, a neuroprotective agent, is a glutamate release inhibitor, voltage-dependent sodium channel and calcium channel inhibitor, penetrating the central nervous system. Has potential to treat focal cerebral ischemia and stroke[1][2].
IC50 & Target: Sodium channel, calcium channel[1][2].

Name: UK 356618, CAS: 230961-08-7, stock 0g, assay 98.6%, MWt: 557.72, Formula: C34H43N3O4, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: MMP, Biological_Activity: UK 356618 (Compound 4j) is a potent and selective inhibitor of matrix metalloprotease-3 (MMP-3) with an IC50 of 5.9 nM. UK 356618 is less potent against MMP-1, MMP-2, MMP-9, MMP-13 and MMP-14 compared with MMP-3[1].
In Vitro: Inhibition of MMP-3 and selectivity over MMP-2 was remarkably sensitive to the size of the substituent and is clearly optimal for a methyl group (UK 356618, compound 4j). UK 356618 is more widely profiled against other MMPs[1]. 
MMP-13 is closely involved in IL-6 or TNF-α increasing tumor metastasis. MMP-13 deficiency abrogate TNF-α effect on lung cancer cell migration. UK 356618 treatment efficiently abolished the effect of TNF-α on cell migration in NCI-H446 cells[2].
In Vivo: UK 356618 (15 mg/kg; intravenous injection; for 24 h or 7 days; male Wistar rats) treatment at reperfusion significantly reduces MMP3 activity in the brain[3].

Name: PF-06471553, CAS: 1808094-07-6, stock 16.6g, assay 98.2%, MWt: 467.54, Formula: C23H25N5O4S, Solubility: DMSO : ≥ 150 mg/mL (320.83 mM), Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Acyltransferase, Biological_Activity: PF-06471553 is a potent, selective and orally available monoacylglycerol acyltransferase 3 (MGAT3) inhibitor, with an IC50 of 92 nM.
IC50 & Target: IC50: 92 nM (MGAT3)[1]
In Vitro: PF-06471553 (6f) is a potent and selective monoacylglycerol acyltransferase 3 (MGAT3) inhibitor, with an IC50 of 92 nM, and shows >160 fold in vitro selectivity for MGAT3 over DGAT1 (IC50, >50 μM), DGAT2 (IC50, >100 μM), MGAT1 (IC50, 14.9 μM), and MGAT2 (IC50, 19.8 μM). PF-06471553 exhibits inhibitory activity against MGAT3 in HEK-293 cells with an IC50 of 205 nM (pIC50, 6.69)[1].
In Vivo: PF-06471553 (200 mg/kg, p.o.) in addition with (DGAT1 and DGAT2) inhibitors shows additional inhibition of glycerol-d5 incorporated triolein in hMGAT3 mice, and with no effect on WT mice[1].

Name: SB-218078, CAS: 135897-06-2, stock 31.6g, assay 98.6%, MWt: 393.39, Formula: C24H15N3O3, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: TGF-beta/Smad;Epigenetics;Cell Cycle/DNA Damage;Cell Cycle/DNA Damage, Target: PKC;PKC;CDK;Checkpoint Kinase (Chk), Biological_Activity: SB-218078 is a potent, selective and cell-permeable checkpoint kinase 1 (Chk1) inhibitor that inhibits Chk1 phosphorylation of cdc25C with an IC50 of 15 nM. SB-218078 is less potently inhibits Cdc2 (IC50 of 250 nM) and PKC (IC50 of 1000 nM). SB-218078 causes apoptosis by DNA damage and cell cycle arrest[1][2][3].
In Vitro: SB-218078 (2.5-5 μM; 18 hours; HeLa cells) treatment abrogates G2 cell cycle arrest caused by either γ-irradiation or a topoisomerase I Topotecan inhibition[1]. 
SB-218078 (500-625 μM; 96 hours; HeLa and HT-29 cells) treatment significantly increases the cytotoxicity of DNA damage [1].
In Vivo: SB-218078 (5 mg/kg; intraperitoneal injection; for 16 hours; C57/Bl6 mice) treatment could promote a strong increase of γ-H2AX and apoptosis throughout the lymphoma, while having no effect on a healthy spleen in Myc-induced lymphomas mouse model[2].

Name: (3S,4S,5R)-1,3,4,5,6-Pentahydroxyhexan-2-one Tagatose, D- (8CI), CAS: 87-81-0, stock 28g, assay 98.7%, MWt: 180.16, Formula: C6H12O6, Solubility: , Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity:

Name: 6-Diazo-5-oxo-L-nor-Leucine L-6-Diazo-5-oxonorleucine;DON, CAS: 157-03-9, stock 6.4g, assay 98.8%, MWt: 171.15, Formula: C6H9N3O3, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Glutaminase, Biological_Activity: L-6-Diazo-5-oxonorleucine (L-6-Diazo-5-oxonorleucine) is a glutaminases antagonist with a Ki of 6 μM. L-6-Diazo-5-oxonorleucine exhibits analgesic, antibacterial, antiviral and anticancer properties. L-6-Diazo-5-oxonorleucine displays genetic toxicity in vitro. L-6-Diazo-5-oxonorleucine decreases the self-renewal potential and metastatic ability of tumor cell[1][2][3][4].
IC50 & Target: Ki: 6 μM (glutaminases)[4]

Name: NU6140, CAS: 444723-13-1, stock 4g, assay 98.4%, MWt: 422.52, Formula: C23H30N6O2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Cell Cycle/DNA Damage;Cell Cycle/DNA Damage;Epigenetics, Target: CDK;Aurora Kinase;Aurora Kinase, Biological_Activity: NU6140 is a selective CDK2-cyclin A inhibitor (IC50, 0.41 μM), exhibits 10- to 36-fold selectivity over other CDKs[1]. NU6140 also potently inhibits Aurora A and Aurora B, with IC50s of 67 and 35 nM, respectively[2]. Enhances the apoptotic effect, with anti-cancer activity[1][2].
In Vitro: NU6140 is less active on CDK1-cyclin B, CDK4-cyclin D, CDK5-p25 and CDK7-cyclin H, with IC50s of 6.6, 5.5, 15 and 3.9 μM, respectively[1]. 
NU6140 increases catalytic activity of capase-9 and capase-3, causes increase in the sub-G1 apoptotic cell population[1].

Name: PAT-1251, CAS: 2007885-39-2, stock 4.2g, assay 98.4%, MWt: 399.34, Formula: C18H17F4N3O3, Solubility: DMSO : ≥ 130 mg/mL (325.54 mM), Clinical_Informat: Phase 1, Pathway: Neuronal Signaling, Target: Monoamine Oxidase, Biological_Activity: PAT-1251 is a potent, selective and oral Lysyl Oxidase-Like 2 (LOXL2) inhibitor, with IC50s of 0.71 and 1.17 μM for hLOXL2 and hLOXL3, respectively, and also potently inhibits mouse, rat, and dog LOXL2 (IC50s, 0.10, 0.12, and 0.16 μM, respectively); PAT-1251 is used in the research of fibrotic diseases.
IC50 & Target: IC50: 0.10 μM (Mouse LOXL2), 0.12 μM (Rat LOXL2), 0.16 μM (Dog LOXL2), 0.71 μM (hLOXL2), 1.17 μM (hLOXL3)[1]
In Vitro: PAT-1251 is a Lysyl Oxidase-Like 2 (LOXL2) inhibitor, with IC50s of 0.71 and 1.17 μM for hLOXL2 and hLOXL3, respectively, and also potently inhibits mouse, rat, and dog LOXL2 (IC50s, 0.10, 0.12, and 0.16 μM, respectively). PAT-1251 shows highly selective for LOXL2 over other key members of the amine oxidase family, such as the copper-dependent amine oxidases semicarbazide-sensitive amine oxidase (SSAO) and diamine oxidase (DAO), in addition to the flavin-dependent monoamine oxidases A (MAO-A) and B (MAO-B), with <10% inhibition at 10 μM[1].

Name: BAY-299, CAS: 2080306-23-4, stock 37.3g, assay 98.9%, MWt: 429.47, Formula: C25H23N3O4, Solubility: DMSO : 25 mg/mL (58.21 mM; Need ultrasonic and warming), Clinical_Informat: No Development Reported, Pathway: Epigenetics, Target: Epigenetic Reader Domain, Biological_Activity: BAY-299 is a very potent, dual inhibitor with IC50s of 67 nM for BRPF2 bromodomains (BD), 8 nM for TAF1 BD2, and 106 nM for TAF1L BD2.
IC50 & Target: IC50: 8 nM (TAF1 BD2), 106 nM (TAF1L BD2), 67 nM (BRPF2 BD), 3150 nM (BRPF1 BD), 5550 nM (BRPF3 BD)[1]
In Vitro: BAY-299 is a dual inhibitor of the bromodomain and PHD finger (BRPF) family member BRPF2 and the TATA box binding protein-associated factors TAF1 and TAF1L. TR-FRET assays showed that BAY-299 is a potent inhibitor of BRPF2 BD with an IC50 of 67 nM, and a selectivity of 47- and 83-fold over BRPF1 and BRPF3 BDs. The profile of BAY-299 is further confirmed by AlphaScreen assay, where an IC50 of 97 nM and a selectivity of 23- and 25-fold over BRPF1 and BRPF3 BDs are measured. NanoBRET experiments show that the interaction of BRPF2 BD with histones H4 and H3.3 is blocked by BAY-299 with IC50 values of 575 and 825 nM, respectively. For TAF1 BD2, the IC50 values are 970 and 1400 nM, respectively. No inhibitory effect is observed for the interaction between BRPF1 or BRD4 and histone H4 up to 10 μM for BAY-299. BAY-299 inhibits MOLM-13, MV4-11, 769-P, Jurkat, NCI-H526, CHL-1, and 5637 cells proliferation with GI50s of 1060, 2630, 3210, 3900, 6860, 7400, and 7980 nM, respectively[1].
In Vivo: Studies of the in vivo pharmacokinetic properties of BAY-299 in rat reveal that blood clearance is low (ca. 17% of hepatic blood flow), volume of distribution in steady-state high, terminal half-life long to very long (t1/2=10 h), and bioavailability high (F=73%). In vivo blood clearance is as anticipated based on rat liver microsome values but lower than expected based on hepatocyte data[1].

Name: MZ 1, CAS: 1797406-69-9, stock 7.6g, assay 98.8%, MWt: 1002.64, Formula: C49H60ClN9O8S2, Solubility: H2O : < 0.1 mg/mL (insoluble); DMSO : 25 mg/mL (24.93 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Epigenetics;PROTAC, Target: Epigenetic Reader Domain;PROTAC, Biological_Activity: MZ 1 is a BRD4 protein degrader based on PROTAC technology.
IC50 & Target: BRD4[1]

Name: Alsterpaullone 9-Nitropaullone;NSC 705701, CAS: 237430-03-4, stock 25.2g, assay 98.7%, MWt: 293.28, Formula: C16H11N3O3, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Stem Cell/Wnt;PI3K/Akt/mTOR;Cell Cycle/DNA Damage, Target: GSK-3;GSK-3;CDK, Biological_Activity: Alsterpaullone (9-Nitropaullone;NSC 705701) is a potent CDK inhibitor, with IC50s of 35 nM, 15 nM, 200 nM and 40 nM for CDK1/cyclin B, CDK2/cyclin A, CDK2/cyclin E and CDK5/p35, respectively. Alsterpaullone also competes with ATP for binding to GSK-3alpha/GSK-3beta with IC50s of both 4 nM. Alsterpaullone has antitumor activity, and possesses potential for the treatment of neurodegenerative and proliferative disorders[1].
IC50 & Target: IC50: 35 nM (CDK1/cyclin B), 15 nM (CDK2/cyclin A), 200 nM (CDK2/cyclin E), 40 nM (CDK5/p35), 4 nM (GSK-3a/GSK-3beta)[1]

Name: PF-3644022, CAS: 1276121-88-0, stock 6.6g, assay 98.3%, MWt: 374.46, Formula: C21H18N4OS, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: MAPK/ERK Pathway;MAPK/ERK Pathway, Target: p38 MAPK;MAPKAPK2 (MK2), Biological_Activity: PF-3644022 is a potent, selective, orally active and ATP-competitive MAPKAPK2 (MK2) inhibitor with an IC50 of 5.2 nM and a Ki of 3 nM. PF-3644022 also inhibits MK3 and p38 regulated/activated kinase (PRAK) with IC50s of 53 nM and 5.0 nM, respectively. PF-3644022 potently inhibits TNFα production and has anti-inflammatory effect[1].
IC50 & Target: IC50: 5.2 nM (MK2), 5.0 nM (PRAK) and 53 nM (MK3)[1]. 
Ki: 3 nM (MK2)[1]
In Vitro: The inhibitory activity of PF-3644022 against other MAPKAP kinase family members is evaluated. Other than MNK2 with an IC50 of 148 nM, other family members are largely not inhibited, showing at least several hundred-fold selectivity versus MK2[1]. 
In the human U937 monocytic cell line or peripheral blood mononuclear cells, PF-3644022 potently inhibits TNFα production with similar activity (IC50 of 160 nM). PF-3644022 blocks TNFα and IL-6 production in LPS-stimulated human whole blood with IC50 values of 1.6 and 10.3 μM, respectively. Inhibition of TNFα in U937 cells and blood correlates closely with inhibition of phospho-heat shock protein 27, a target biomarker of MK2 activity[1].
In Vivo: PF-3644022 (3-100 mg/kg; oral gavage; twice a day; for 12 days; Lewis rats) treatment shows dose-dependent inhibition of chronic paw swelling measured on day 21 after 12 days of oral dosing, with ED50 value of 20 mg/kg[1].

Name: PDD 00017273, CAS: 1945950-21-9, stock 37.6g, assay 98.7%, MWt: 514.62, Formula: C23H26N6O4S2, Solubility: DMSO : 50 mg/mL (97.16 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: PDD 00017273 is a potent inhibitor of Poly(ADP-ribose) Glycohydrolase (PARG), with an IC50 of 26 nM, and a KD of 1.45 nM.
IC50 & Target: IC50: 26 nM (PARG)[1] 
KD: 1.45 nM (PARG)[1]
In Vitro: PDD 00017273 is a potent inhibitor of PARG, with an IC50 of 26 nM, and a KD of 1.45 nM. PDD 00017273 (10 μM) does not inhibit five common Cytochrome P450 enzymes. PDD 00017273 (30 μM) modestly increasess phosphorylated H2AX (γH2AX) intensity, PDD 00017273 also decreases in NAD/H through PARG inhibition after DNA damage. PDD 00017273 suppresses the ZR-75-1 cells carring BRCA1 and BRCA2 wild type, and exhibits less potent activities against MDA-MB-436 cells carry the 5396 + 1G>A mutation in BRCA1[1]. PDD 00017273 (0.3 μM) inhibits degradation of PAR polymers in MCF7 cells. PDD 00017273 (0.3 μM) also reduces the viability of BRCA1, BRCA2, PALB2, FAM175A, and BARD1 depleted cells. PDD 00017273 stalls replication forks and induces DNA damage that requires homologous recombination (HR) for repair[2].

Name: CCG-203971, CAS: 1443437-74-8, stock 18.4g, assay 98.8%, MWt: 408.88, Formula: C23H21ClN2O3, Solubility: DMSO : ≥ 155 mg/mL (379.08 mM); H2O : < 0.1 mg/mL (insoluble), Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein, Target: Ras, Biological_Activity: CCG-203971 is a second-generation RhoA/myocardin-related transcription factor A (MRTF-A) inhibitor. CCG-203971 potently targets RhoA/C-activated serum response element (SRE)-luciferase (IC50=6.2 μM).
IC50 & Target: RhoA/MRTF-A[1]
In Vitro: CCG-203971, a second-generation Ras homolog gene family, member A (RhoA)/myocardin-related transcription factor A (MRTF-A)/serum response factor (SRF) pathway inhibitor, represses both matrix-stiffness and transforming growth factor beta–mediated fibrogenesis as determined by protein and gene expression in a dose-dependent manner. CCG-203971 significantly represses TGF-β- induced MKL1 expression at 25 μM concentration[1]. Human dermal fibroblasts are plated onto 96-well plates and allowed to grow for 3 days in the presence of 30 μM CCG-203971 or DMSO vehicle. Viable cell density is assessed through enzymatic reduction of the water-soluble tetrazolium dye WST-1. Scleroderma dermal fibroblasts proliferate faster than normal cells, and this is inhibited by CCG-203971[2].
In Vivo: CCG-203971 is tested in a Bleomycin skin injury model. Bleomycin is administered in 50 μL of DMSO intraperitoneally. Preliminary studies show that Bleomycin administered in this manner is well tolerated at 100 mg/kg twice a day. Intradermal Bleomycin for 2 weeks along with the DMSO control (50 μL i.p.) results in marked dermal thickening (P<0.0001) compared with the PBS+DMSO group, which does not receive Bleomycin. CCG-203971 treatment strongly and significantly (P<0.001) suppresses the Bleomycin-induced skin thickening in this model. Skin collagen amounts, assessed by measurement of hydroxyproline content, show similar results. Bleomycin injections promote collagen deposition (P<0.01) and CCG-203971 is able to block this effect (P<0.05)[2].

Name: Abrocitinib PF-04965842, CAS: 1622902-68-4, stock 6g, assay 98.7%, MWt: 323.41, Formula: C14H21N5O2S, Solubility: DMSO : 125 mg/mL (386.51 mM; Need ultrasonic), Clinical_Informat: Phase 3, Pathway: Epigenetics;Stem Cell/Wnt;JAK/STAT Signaling, Target: JAK;JAK;JAK, Biological_Activity: Abrocitinib (PF-04965842) is a potent, orally active and selective JAK1 inhibitor, with IC50s of 29 and 803 nM for JAK1 and JAK2, respectively. Abrocitinib (PF-04965842) exhibits less active effect on TYK2 (IC50, 1.253 μM), and inhibits phosphorylation of STAT1, STAT3 and STAT5 after stimulation. Effective in autoimmune disease[1].
IC50 & Target: IC50: 29 (JAK1), 803 nM (JAK2)[1]
In Vitro: Abrocitinib (Compound 25) inhibits IFNα-stimulated phosphorylation of STAT3, IFN-stimulated phosphorylation of STAT1 in human whole blood (HWB), as well as pSTAT5 in CD34+ spiked into HWB (JAK2), with IC50s of 189, 163 nM, 7.178 μM, respectively[1].
In Vivo: Abrocitinib (Compound 25; 5, 15, 50 mg/kg, p.o., daily for 7 days) significantly reduces paw swelling in rat adjuvant-induced arthritis model[1].

Name: Oxythiamine Hydroxythiamin, CAS: 136-16-3, stock 21.2g, assay 98.5%, MWt: 266.34, Formula: C12H16N3O2S, Solubility: DMSO : 51.67 mg/mL (194.00 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Oxythiamine, an antimetabolite and a vitamin B1 antagonist, is a well-known thiamine antagonist and inhibitor of transketolase.
IC50 & Target: Vitamin B1, Thiamine, Transketolase[1].
In Vitro: Oxythiamine, an antimetabolite and a vitamin B1 antagonist, is a well-known thiamine antagonist and inhibitor of transketolase. Oxythiamine alters protein expression in a dose dependent manner. The level of alpha-enolase is increased by Oxythiamine treatment, while expression of 14-3-3 protein beta/alpha is suppressed by Oxythiamine at a stratified dose. Oxythiamine causes dynamic changes of total protein expression in time dependent fashion. Oxythiamine suppresses expression of cellular phosphor proteins significantly[2].

Name: U18666A, CAS: 3039-71-2, stock 29.1g, assay 98.7%, MWt: 424.06, Formula: C25H42ClNO2, Solubility: DMSO : 50 mg/mL (117.91 mM; Need ultrasonic); H2O : 10 mg/mL (23.58 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: U18666A, a cell permeable drug, is a cholesterol synthesis and transport inhibitor.
IC50 & Target: Cholesterol[1][2].
In Vitro: U18666A, the antiviral effect is found to result from two events: retarded viral trafficking in the cholesterol-loaded late endosomes/lysosomes and suppresse de novo sterol biosynthesis in treated infected cells. It is also observed an additive antiviral effect of U18666A with C75, a fatty acid synthase inhibitor, suggesting dengue virus relies on both the host cholesterol and fatty acid biosynthesis for successful replication[1][2].

Name: PROTAC CDK9 Degrader-1, CAS: 2118356-96-8, stock 39.5g, assay 98.3%, MWt: 613.66, Formula: C33H35N5O7, Solubility: DMSO : ≥ 104 mg/mL (169.47 mM), Clinical_Informat: No Development Reported, Pathway: Cell Cycle/DNA Damage;PROTAC, Target: CDK;PROTAC, Biological_Activity: PROTAC CDK9 Degrader-1 is a selective CDK9 degrader.
IC50 & Target: CDK9[1]

Name: PROTAC BRD9 Degrader-1, CAS: 2097971-01-0, stock 29.6g, assay 98%, MWt: 903.98, Formula: C42H45N7O12S2, Solubility: DMSO : 150 mg/mL (165.93 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Epigenetics;PROTAC, Target: Epigenetic Reader Domain;PROTAC, Biological_Activity: PROTAC BRD9 Degrader-1 is a lead PROTAC BRD9 chemical degrader (IC50=13.5 nM), which can be used as a selective probe useful for the study of BAF complex biology[1].
IC50 & Target: IC50: 13.5 nM (BRD9)[1] 
PROTAC[1]
In Vitro: PROTAC BRD9 Degrader-1 (Compound 1) inhibits BRD9, BRD4, and CRBN-DDB1 with IC50s of 13.5 nM, 3.78 μM, and 48.9 nM, respectively[1].

Name: PROTAC BET Degrader-1, CAS: 2093386-22-0, stock 34.3g, assay 98.7%, MWt: 871.90, Formula: C44H45N11O9, Solubility: DMSO : ≥ 50 mg/mL (57.35 mM), Clinical_Informat: No Development Reported, Pathway: Epigenetics;PROTAC, Target: Epigenetic Reader Domain;PROTAC, Biological_Activity: PROTAC BET Degrader-1 is a potent BET degrader based on PROTAC, decreasing BRD2, BRD3, and BRD4 protein levels at low concentration.
IC50 & Target: BET[1]
In Vitro: PROTAC BET Degrader-1 (Compound 9) is a potent BET degrader based on PROTAC, decreases the level of BRD2, BRD3, and BRD4 proteins in RS4;11 cells at 3-10 nM, and inhibits the growth of this cell line with an IC50 of 4.3 nM, and 45.5 nM for MOLM-13 cells[1].

Name: PROTAC Sirt2 Degrader-1, CAS: 2098487-75-1, stock 26.2g, assay 98.7%, MWt: 852.94, Formula: C40H40N10O8S2, Solubility: H2O : < 0.1 mg/mL (insoluble); DMSO : ≥ 100 mg/mL (117.24 mM), Clinical_Informat: No Development Reported, Pathway: Epigenetics;Cell Cycle/DNA Damage;PROTAC, Target: Sirtuin;Sirtuin;PROTAC, Biological_Activity: PROTAC Sirt2 Degrader-1 is a SirReal-based PROTAC, acts as a Sirt2 degrader, composed of a highly potent and isotype-selective Sirt2 inhibitor, a linker, and a bona fide cereblon ligand for E3 ubiquitin ligase. PROTAC Sirt2 Degrader-1 shows an IC50 of 0.25 μM for Sirt2, with no effect on Sirt1/Sirt3 (IC50s > 100 μM)[1].
IC50 & Target: IC50: 0.25 μM (Sirt2)[1]
In Vitro: PROTAC Sirt2 Degrader-1 (Compound 12; 10 µM, 1-6 hours) induces Sirt2 degradation in HeLa cells[1].

Name: N33-TEG-COOH N3-TEG-COOH;14-Azido-3,6,9,12-tetraoxatetradecanoic acid, CAS: 201467-81-4, stock 8.6g, assay 98.9%, MWt: 277.27, Formula: C10H19N3O6, Solubility: DMSO : ≥ 100 mg/mL (360.66 mM), Clinical_Informat: No Development Reported, Pathway: PROTAC, Target: PROTAC Linker, Biological_Activity: N33-TEG-COOH is a PROTAC linker containing four polyethylene glycol (PEG) units.
IC50 & Target: PROTAC linker[1]
In Vitro: N33-TEG-COOH is a long linker extracted from Reference PMID: 26035625, Compound 7. A PROTAC is a heterobifunctional compound that contains two ligands connected by a linker unit. One ligand binds an E3 ubiquitin ligase protein, while the other ligand binds to the target protein of interest, thereby bringing the ligase and the target in close proximity[1].

Name: Boc-C1-PEG2-C4-Cl PROTAC Linker 1, CAS: 1835705-53-7, stock 2.7g, assay 98.3%, MWt: 294.81, Formula: C14H27ClO4, Solubility: DMSO : ≥ 50 mg/mL (169.60 mM), Clinical_Informat: No Development Reported, Pathway: PROTAC, Target: PROTAC Linker, Biological_Activity: Boc-C1-PEG2-C4-Cl (PROTAC Linker 1) is a PROTAC linker utilized to connect the respective tyrosine kinase inhibitor (TKI) to the E3 recruiting ligand.
In Vitro: PROTAC technology employs small molecules that recruit target proteins for ubiquitination and removal by the proteasome. The synthesis of PROTAC compounds that mediate the degradation of c-ABL and BCR-ABL by recruiting either Cereblon or Von Hippel Lindau E3 ligases is reported. Boc-C1-PEG2-C4-Cl is designated as 6-2-2[1].

Name: Boc-C5-O-C5-O-C6-Cl PROTAC Linker 2, CAS: 1835705-52-6, stock 28.5g, assay 98%, MWt: 393.00, Formula: C21H41ClO4, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: PROTAC, Target: PROTAC Linker, Biological_Activity: Boc-C5-O-C5-O-C6-Cl (PROTAC Linker 2) is a PROTAC linker utilized to connect the respective tyrosine kinase inhibitor (TKI) to the E3 recruiting ligand.

Name: I-BET762 carboxylic acid Molibresib carboxylic acid;GSK525762A carboxylic acid;PROTAC BRD4-binding moiety 2, CAS: 1300019-38-8, stock 0.3g, assay 98.5%, MWt: 396.83, Formula: C20H17ClN4O3, Solubility: DMSO : 7.14 mg/mL (17.99 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Epigenetics;PROTAC, Target: Epigenetic Reader Domain;Ligand for Target Protein for PROTAC, Biological_Activity: I-BET762 carboxylic acid (Molibresib carboxylic acid) is an I-BET762-based warhead ligand for conjugation reactions of PROTAC targeting on BET. I-BET762 carboxylic acid (Molibresib carboxylic acid) is a BRD4 inhibitor with a pIC50 of 5.1[1].
IC50 & Target: pIC50: 5.1 (BRD4)[1]
In Vitro: I-BET762 carboxylic acid (Molibresib carboxylic acid) (Compound 27) inhibits peripheral blood mononuclear cells (PBMC) with a pIC50 of <4[1].

Name: PROTAC BET-binding moiety 1, CAS: 2093387-77-8, stock 9.9g, assay 98.9%, MWt: 487.51, Formula: C25H25N7O4, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: PROTAC, Target: Ligand for Target Protein for PROTAC, Biological_Activity: PROTAC BET-binding moiety 1 is a key intermediate for the synthesis of high-affinity BET inhibitors[1].

Name: SirReal1-O-propargyl PROTAC Sirt2-binding moiety 1, CAS: 1862237-99-7, stock 13.4g, assay 98.6%, MWt: 424.54, Formula: C21H20N4O2S2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: PROTAC, Target: Ligand for Target Protein for PROTAC, Biological_Activity: SirReal1-O-propargyl is a selective and highly potent Sirtuin 2 (Sirt2) inhibitor, with an IC50 of 2.4 μM. SirReal1-O-propargyl, the SirReal1-based moiety, binds to the cereblon ligand via a linker to form PROTAC to degrade Sirt2[1].
IC50 & Target: IC50: 2.4 μM (Sirt2)[1].

Name: OSS_128167, CAS: 887686-02-4, stock 9.6g, assay 98.8%, MWt: 366.32, Formula: C19H14N2O6, Solubility: DMSO : 103.3 mg/mL (281.99 mM; Need ultrasonic and warming), Clinical_Informat: No Development Reported, Pathway: Epigenetics;Cell Cycle/DNA Damage, Target: Sirtuin;Sirtuin, Biological_Activity: OSS_128167 is a selective SIRT6 inhibitor with IC50s of 89, 1578 and 751 μM for SIRT6, SIRT1 and SIRT2, respectively.
IC50 & Target: IC50: 89 μM (SIRT6), 1578 μM (SIRT1), 751 μM (SIRT2)[1]
In Vitro: OSS_128167 is a selective SIRT6 inhibitor with IC50s of 89, 1578 and 751 μM for SIRT6, SIRT1 and SIRT2, respectively. OSS_128167 inhibits SIRT6 in the micromolar range, but shows promising selectivity, since its IC50 value for SIRT6 is approximately 17 times lower compare to the IC50 for SIRT1 and 9 times lower compare to SIRT2[1]. OSS_128167 (200 μM) induces chemosensitization in primary multiple myeloma (MM) cells (NCI-H929), as well as in melphalan-resistant (LR-5) and doxorubicin-resistant (Dox40) MM cell lines[2].

Name: 3-Methoxytyramine 3-O-methyl Dopamine, CAS: 554-52-9, stock 27.9g, assay 98.8%, MWt: 167.21, Formula: C9H13NO2, Solubility: H2O : 2 mg/mL (11.96 mM; Need ultrasonic); DMSO : 12.5 mg/mL (74.76 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: 3-Methoxytyramine, a well known extracellular metabolite of 3-hydroxytyramine/dopamine, is a neuromodulator.
IC50 & Target: The major extracellular metabolite of dopamine, 3-Methoxytyramine (3-MT), can induce behavioral effects in a dopamine-independent manner and these effects are partially mediated by the trace amine associated receptor 1 (TAAR1). 3-Methoxytyramine causes a significant increase in the level of phosphorylated Erk2, thus indicating that certain receptor-mediated processes in striatal cells are affected by this treatment. 3-Methoxytyramine activates TAAR1-mediated signaling in vitro. 3-Methoxytyramine induces activation of human TAAR1 in cAMP assay and causes CREB and Erk2 phosphorylation in HEK-293 cells[1].
In Vivo: The extracellular dopamine (DA) metabolite 3-methoxytyramine (3-MT) induces significant behavioral activation in dopamine-deficient DAT-KO (DDD) mice. 3-Methoxytyramine induces behavioral activation and intracellular signaling in the striatum of DA deficient mice[1].

Name: E6130, CAS: 1427058-33-0, stock 28.6g, assay 98.4%, MWt: 556.06, Formula: C28H37ClF3N3O3, Solubility: DMSO : ≥ 250 mg/mL (449.59 mM), Clinical_Informat: Phase 1, Pathway: GPCR/G Protein;Immunology/Inflammation, Target: CXCR;CXCR, Biological_Activity: E6130 is an orally available and highly selective CX3CR1 modulator, that may be effective for treatment of inflammatory bowel disease.
IC50 & Target: CX3CR1[1]
In Vitro: E6130 is an orally available and highly selective CX3CR1 modulator, inhibits the fractalkine-induced chemotaxis of human peripheral blood natural killer cells (IC50, 4.9 nM), and down-regulates CX3CR1 on the cell surface of CD56+ NK cells with an EC50 value of 5.2 nM. E6130 also shows agonistic activity via CX3CR1 with respect to GTPγS binding (EC50 = 133 nM) and β-arrestin recruitment (EC50 = 2.4 μM) in CX3CR1-expressing CHO-K1 membrane but show no antagonistic activity[1].
In Vivo: E6130 (10 or 30 mg/kg, p.o.) reduces several inflammatory bowel disease-related parameters in a murine CD4+ CD45RBhigh T-cell-transfer colitis model and a murine oxazolone-induced colitis model[1].

Name: Talazoparib tosylate BMN 673ts, CAS: 1373431-65-2, stock 4g, assay 98.6%, MWt: 552.55, Formula: C26H22F2N6O4S, Solubility: DMSO : ≥ 108 mg/mL (195.46 mM), Clinical_Informat: Phase 3, Pathway: Epigenetics;Cell Cycle/DNA Damage, Target: PARP;PARP, Biological_Activity: Talazoparib tosylate (BMN 673ts) is a novel, potent and orally available PARP1/2 inhibitor with an IC50 of 0.57 nM for PARP1.
IC50 & Target: IC50: 0.57 nM (PARP1)[1]
In Vitro: Talazoparib is a potent PARP1/2 inhibitor (PARP1 IC50=0.57 nM), it has no effect on PARG activity at concentrations up to 1 μM. Talazoparib binds to PARP1 with a dissociation constant (KD) of 0.29 nM. Talazoparib inhibits PARP1 and -2 to a similar extent, with Kis of 1.20 and 0.85 nM, respectively. Talazoparib selectively targets tumor cells with BRCA1, BRCA2, or PTEN gene defects with 20- to more than 200-fold greater potency than existing PARP1/2 inhibitors. Talazoparib targets tumor cells with homologous recombination gene defects. Tumor models that are either BRCA1-deficient (MX-1 and SUM149) or BRCA2-deficient (Capan-1) are profoundly sensitive to Talazoparib. Talazoparib induces nuclear γ-H2AX foci at concentrations as low as 100 pM[1].
In Vivo: Talazoparib is readily orally bioavailable, with more than 40% absolute oral bioavailability in rats when dosed in carboxylmethyl cellulose. Oral administration of Talazoparib elicits remarkable antitumor activity; xenografted tumors that carry defects in DNA repair due to BRCA mutations or PTEN deficiency are profoundly sensitive to oral Talazoparib treatment at well-tolerated doses in mice. Synergistic or additive antitumor effects are also found when Talazoparib is combined with temozolomide, SN38, or platinum drugs[1].

Name: Endoxifen, CAS: 110025-28-0, stock 24.2g, assay 98.8%, MWt: 373.49, Formula: C25H27NO2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others;Others, Target: Estrogen Receptor/ERR;Aromatase, Biological_Activity: Endoxifen is a key active metabolite of tamoxifen (TAM) with higher affinity and specificity to estrogen receptor that also inhibits aromatase activity.
IC50 & Target: Estrogen Receptor[1][2].
In Vitro: Endoxifen, a hydroxylated tamoxifen metabolite, is approximately 100-fold more potent as an antagonist of the ER than tamoxifen. It also suggests that endoxifen but not 4-hydroxytamoxifen results in ER-alpha degradation in addition to its effects on the ER at the level of transcription[1]. Endoxifen, is a potent antiestrogen that targets estrogen receptor α for degradation in breast cancer cells. Additionally, it is showed that Endoxifen blocks ERA transcriptional activity and inhibits estrogen-induced breast cancer cell proliferation even in the presence of tamoxifen, N-desmethyl-tamoxifen, and 4-hydroxytamoxifen[2]. Endoxifen is strongly growth inhibitory at 10 μM for all the breast cancer cell lines except for moderate inhibition for MDAMB-468.Cytotoxic effects are quite significant at 10 μM concentration for MCF7, HS 578T, and BT-549 cells. At lower Endoxifen concentrations (0.01-1 μM), the inhibitory effects are not as significant as 10 μM, whereas 100 μM Endoxifen concentration found to be lethal for all tested cells[3].
In Vivo: Orally administered Endoxifen is rapidly absorbed and systemically available when tested in female rats. The Endoxifen-treated rats show 787% higher exposure (AUC0–∞) and 1,500% higher concentration (Cmax) levels of Endoxifen when compared with Tamoxifen. Oral Endoxifen administration once a day for 28 consecutive days at dosages 2, 4, and 8 mg/kg proves safe and results in progressive inhibition of the growth of the human mammary tumor xenografts in female mice[3].

Name: Glycochenodeoxycholic acid (sodium salt) Chenodeoxycholylglycine (sodium salt);Sodium glycochenodeoxycholate, CAS: 16564-43-5, stock 23.2g, assay 98.6%, MWt: 471.61, Formula: C26H42NNaO5, Solubility: DMSO : 250 mg/mL (530.10 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Apoptosis;Metabolic Enzyme/Protease, Target: Apoptosis;Endogenous Metabolite, Biological_Activity: Glycochenodeoxycholic acid sodium salt (Chenodeoxycholylglycine sodium salt) is a bile acid formed in the liver from chenodeoxycholate and glycine. It acts as a detergent to solubilize fats for absorption and is itself absorbed. Glycochenodeoxycholic acid sodium salt (Chenodeoxycholylglycine sodium salt) induces hepatocyte apoptosis[1][2].

Name: GSK8573, CAS: 1693766-04-9, stock 5.8g, assay 98.6%, MWt: 323.39, Formula: C20H21NO3, Solubility: DMSO : 25 mg/mL (77.31 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Epigenetics, Target: Epigenetic Reader Domain, Biological_Activity: GSK8573 (compound 23) is an inactive control compound for GSK2801. GSK8573 has binding activity to BRD9 with a Kd value of 1.04 μM and is inactive against BAZ2A/B and other bromodomain familiy[1].

Name: Cloprostenol sodium salt ICI 80996 sodium salt, CAS: 55028-72-3, stock 22.7g, assay 98.1%, MWt: 446.90, Formula: C22H28ClNaO6, Solubility: H2O : ≥ 150 mg/mL (335.65 mM), Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein, Target: Prostaglandin Receptor, Biological_Activity: Cloprostenol sodium salt (ICI 80996 sodium salt) is a potent synthetic prostaglandin analogue, acts as a luteolytic agent[1], and is a PGF2α receptor agonist[2].
IC50 & Target: PGF2α receptor[2]
In Vitro: Cloprostenol is a PGF2α receptor agonist[2]. 
Cloprostenol (0.1 μM) counteracts the adipogenic effects of statil, on both intracellular lipid accumulation and expression of transcripts for proadipogenic factors C/EBPα and PPARγ after treatment for 6 days[2].
In Vivo: Cloprostenol sodium salt (25 μg) decreases plasma progesterone in pregnant rats[1].

Name: LP-533401 hydrochloride, CAS: 1040526-12-2, stock 23.3g, assay 98.9%, MWt: 562.94, Formula: C27H23ClF4N4O3, Solubility: H2O : < 0.1 mg/mL (insoluble); DMSO : 25 mg/mL (44.41 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Tryptophan Hydroxylase, Biological_Activity: LP-533401 hydrochloride is a tryptophan hydroxylase 1 inhibitor that regulates serotonin production in the gut.
IC50 & Target: Tryptophan hydroxylase 1[1]
In Vitro: LP-533401 hydrochloride is a tryptophan hydroxylase 1 inhibitor. LP-533401 (1 μM) completely inhibits serotonin production in Tph1-expressing cells (RBL2H3 cells) after treatment for 3 days[1].
In Vivo: Oral administration once daily for up to 6 weeks of LP-533401 (25, 100 or 250 mg/kg) dose-dependently prevents the development of and fully rescues, osteoporosis in ovariectomized rodents because of an isolated increase in bone formation. Pharmacokinetic studies in rodents show that LP-533401 level in the brain is negligible following oral administration, indicating that it is virtually unable to cross the blood-brain barrier[1]. Mice treated repeatedly with LP-533401 (30-250 mg/kg per day) exhibit marked 5-HT content reductions in the gut, lungs, and blood, but not in the brain. After a single LP-533401 dose (250 mg/kg), lung and gut 5-HT contents decrease by 50%, whereas blood 5-HT levels remain unchanged, suggesting gut and lung 5-HT synthesis[2]. Adult, healthy mice treated with the Tph-1 inhibitor LP-533401 show 30% decrease in circulating serotonin levels, with a consequent 30% increase in osteoblast numbers. Administration of LP-533401 to mice injected with EL4 cells inhibits the decrement in osteoblast numbers and trabecular bone volume, prolongs survial, and decreases leukemic infiltration[3].

Name: YK11, CAS: 1370003-76-1, stock 34.5g, assay 98.4%, MWt: 430.53, Formula: C25H34O6, Solubility: DMSO : ≥ 64 mg/mL (148.65 mM), Clinical_Informat: No Development Reported, Pathway: Others, Target: Androgen Receptor, Biological_Activity: YK11 is a partial agonist of androgen receptor, with osteogenic activity.
IC50 & Target: Androgen receptor[1]
In Vitro: YK11 is a partial agonist of androgen receptor, and induces myogenic differentiation of C2C12 Cells at 500 nM via Fst mRNA upregulation by AR. YK11 enhances Myf5 and myogenin mRNA expression, but requires high concentrations (YK11, 100 nM or 500 nM)[1]. YK11 (0.5 µM) increases the cell growth of osteoblastic MC3T3-E1 cells, and enhances ALP activity via AR. YK11 also elevates osteoprotegerin mRNA expression (0.5 µM) and dose-dependently increases osteocalcin mRNA expression (0.1-1.0 µM). In addition, YK11 enhances phosphorylation of Akt protein via rapid non-genomic signaling[2].

Name: WHI-P258, CAS: 21561-09-1, stock 0.8g, assay 98.7%, MWt: 281.31, Formula: C16H15N3O2, Solubility: DMSO : 31.25 mg/mL (111.09 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: MAPK/ERK Pathway, Target: JNK, Biological_Activity: WHI-P258, a quinazoline compound, binds to the active site of JAK3 with an estimated Ki of 72 µM. WHI-P258 does not inhibit JAK3 and does not affect the thrombin-induced aggregation of platelets even at 100 μM[1][2].

Name: Nosiheptide Multhiomycin; RP 9671, CAS: 56377-79-8, stock 17.5g, assay 98.9%, MWt: 1222.36, Formula: C51H43N13O12S6, Solubility: DMSO : 125 mg/mL (102.26 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Anti-infection, Target: Bacterial, Biological_Activity: Nosiheptide (Multhiomycin), a thiopeptide antibiotic produced by Streptomyces actuosus, inhibits bacterial protein synthesis and bears a unique indole side ring system and regiospecific hydroxyl groups on the characteristic macrocyclic core. Nosiheptide has been widely used as a feed additive for animal growth[1][2].
In Vitro: Nosiheptide exhibits extremely potent activity against all contemporary Staphylococcus aureus strains tested including multiple drug-resistant clinical isolates, with MIC values ≤ 0.25 mg/L. Nosiheptide is also highly active against Enterococcus spp and the contemporary hypervirulent BI strain of Clostridium difficile but is inactive against most Gram-negative strains tested. Time-kill analysis reveals Nosiheptide to be rapidly bactericidal against Staphylococcus aureus in a concentration- and time-dependent manner, with a nearly 2-log kill noted at 6 hours at 10X MIC. Furthermore, Nosiheptide is found to be non-cytotoxic against mammalian cells at >> 100X MIC, and its anti-Staphylococcus aureus activity is not inhibited by 20% human serum. Notably, Nosiheptide exhibits a significantly prolonged post-antibiotic effect against both healthcare- and community-associated Staphylococcus aureus compared to vancomycin[1].
In Vivo: Nosiheptide (20 mg/kg; intraperitoneal injection; injected at 1 and 8 h post-infection; female CD1 mice) provids significant protection against mortality. Ten out of 10 of the Nosiheptide-treated mice remains alive on day 3, while 6/10 of the controls died on day 1[1].

Name: UVI 3003, CAS: 847239-17-2, stock 7.6g, assay 98.1%, MWt: 436.58, Formula: C28H36O4, Solubility: H2O : < 0.1 mg/mL (insoluble); DMSO : 100 mg/mL (229.05 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease;Autophagy, Target: RAR/RXR;Autophagy, Biological_Activity: UVI 3003 is a highly selective antagonist of retinoid X receptor (RXR), and inhibits xenopus and human RXRα in Cos7 cells, with IC50s of 0.22 and 0.24 μM, respectively.
IC50 & Target: IC50: 0.22 μM (Xenopus RXRα, in Cos7 cells), 0.24 μM (Human RXRα, in Cos7 cells)[1]
In Vitro: UVI3003 inhibits the activity of xenopus and human RXRα, with IC50s of 0.22 and 0.24 μM, respectively. UVI3003 fully activates xPPARγ with an EC50 of 12.6 μM, and is almost completely inactive on hPPARγ and mPPARγ[1]. UVI 3003 (10 μM) does not change the proliferation rate of extraocular muscles (EOM)-derived or LEG-derived EECD34 cells. UVI 3003 causes a 65.4% difference in EECD34 cell fusion and desmin expression[2].

Name: MN58b, CAS: 203192-01-2, stock 1.1g, assay 98.1%, MWt: 640.49, Formula: C32H40Br2N4, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Apoptosis, Target: Apoptosis, Biological_Activity: MN58b is a selective choline kinase α (CHKα) inhibitor, and results in inhibition of phosphocholine synthesis. MN58b reduces cell growth through the induction of apoptosis, and also has antitumoral activity[1][2].
IC50 & Target: Choline kinase α (CHKα)[1]
In Vitro: The IC50s of MN58b for parental and Gemcitabine-resistant Suit2 007 cells are 3.14 µM and 0.77 µM, respectively[1]. 
MN58b (1-5 µM; 72 hours; SK-PC-1, Suit2 008, IMIM-PC2, and RWP-1 cells) has a marked effect on colony formation at 1 µM, and growth is completely abolished at 5 µM in all the cell lines[1]. 
MN58b ((1-10 µM; 24-48 hours; SK-PC-1, Suit2 008, IMIM-PC2, and RWP-1 cells) induces apoptosis and this response correlates with CHKα expression[1].
In Vivo: MN58b (4 mg/kg; intraperitoneal injection; once a day; for 5 days; MF-1 nude mice) treatment significantly decreases phosphomonoesters in both HT29 and MDA-MB-231 xenografts. Phosphocholine levels are found to correlate with choline kinase activities[2].

Name: GNE-049, CAS: 1936421-41-8, stock 15.5g, assay 98.7%, MWt: 510.58, Formula: C27H32F2N6O2, Solubility: DMSO : 100 mg/mL (195.86 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Epigenetics;Epigenetics, Target: Epigenetic Reader Domain;Histone Acetyltransferase, Biological_Activity: GNE-049 is a highly potent and selective CBP inhibitor with an IC50 of 1.1 nM in TR-FRET assay. GNE-049 also inhibits BRET and BRD4(1) with IC50s of 12 nM and 4200 nM, respectively.
IC50 & Target: IC50: 1.1 nM (CBP), 12 nM (BRET), 4200 nM (BRD4(1))[1]
In Vitro: GNE-049 is selected for further profiling as it has the best balance of liver microsomes (LM) stability, selectivity, and cellular potency GNE-049 has excellent potency in the BRET cellular assay and, in an orthogonal measure of the target engagement, GNE-049 is shown to inhibit the expression of MYC (MV4-11 cell line) with an EC50 of 14 nM[1].
In Vivo: GNE-049 demonstrates acceptable PK in mouse, rat, dog, and monkey. Determination of potency versus a selection of bromodomains revealed that GNE-049 is selective for CBP/P300 and, importantly, quite selective (3820-fold) over BRD4(1). GNE-049 is further evaluated in a rat single dose (30-250 mg/kg QD) toxicokinetic study. Adverse central nervous system (CNS)-related signs (e.g., marked hyperactivity and vocalization) are observed in several of the rats at the 250 mg/kg dose level. Furthermore, at the 250 mg/kg dose level, the ratio of the unbound drug concentration in brain to unbound drug concentration in plasma (Kp,uu) 3 h post dose is determined to be 0.43, indicating that GNE-049 is penetrating into the CNS and potentially resulting in the observed toxicity[1].

Name: Neurodazine, CAS: 937807-66-4, stock 15.4g, assay 98.3%, MWt: 456.92, Formula: C27H21ClN2O3, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Stem Cell/Wnt;Stem Cell/Wnt, Target: Hedgehog;Wnt, Biological_Activity: Neurodazine is an imidazole-based small molecule, serve as a promoter of neurogenesisin pluripotent cells. Neurodazine promotes neurogenesis by activating Wnt and Shh signaling pathways. Neurodazine selectively suppresses astrocyte differentiation of P19 cells[1][2].

Name: Kynurenic acid (sodium), CAS: 2439-02-3, stock 35.3g, assay 98.5%, MWt: 212.16, Formula: C10H7NNaO3, Solubility: DMSO : 50 mg/mL (235.67 mM; Need ultrasonic); H2O : < 0.1 mg/mL (insoluble), Clinical_Informat: Phase 1, Pathway: GPCR/G Protein;Immunology/Inflammation;Membrane Transporter/Ion Channel;Neuronal Signaling, Target: CXCR;CXCR;iGluR;iGluR, Biological_Activity: Kynurenic acid sodium, an endogenous tryptophan metabolite, is a broad-spectrum antagonist targeting NMDA, glutamate, α7 nicotinic acetylcholine receptor. Kynurenic acid sodium is also an agonist of GPR35/CXCR8.
IC50 & Target: Target: GPR35[1], NMDA, glutamate, glutamate, α7 nicotinic acetylcholine[2]
In Vitro: GPR35 functions as a receptor for the kynurenine pathway intermediate kynurenic acid. Kynurenic acid elicits calcium mobilization and inositol phosphate production in a GPR35-dependent manner in the presence of G qi/o chimeric G proteins. Kynurenic acid stimulates [35S]guanosine 5′-O-(3-thiotriphosphate) binding in GPR35-expressing cells, an effect abolished by pertussis toxin treatment. Kynurenic acid also induces the internalization of GPR35[1]. KYNA’s neuroinhibitory qualities and its neuroprotective and anticonvulsant effects are discovered using concentrations of the compound in the millimolar range. This, as well as the low affinity of KYNA at each of the three ionotropic glutamate receptors responsible for these effects [NMDA, alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid (AMPA) and kainate], together with the realization that KYNA concentrations in the mammalian brain are in the sub-micromolar range, suggested that other receptors might serve as targets of endogenous Kynurenic acid. Kynurenic acid, with a shallower inhibition curve and non-competitively, antagonizes α7nAChRs on cultured hippocampal neurons with an IC50 in the low micromolar range[2].
In Vivo: Kynurenic acid affects the activity of leukocytes in the peripheral blood of mice, although the lowest one (2.5 mg/L) has the most profound influence in contrast to the highest one (250 mg/L), which produces the weakest effect. The lowest Kynurenic acid dose stimulates the proliferative response of T lymphocytes (p<0.05), after 7 and 28 days of administering the acid to the animals[3].

Name: LY367385, CAS: 198419-91-9, stock 37.5g, assay 98.2%, MWt: 209.20, Formula: C10H11NO4, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein;Neuronal Signaling, Target: mGluR;mGluR, Biological_Activity: LY367385 is a highly potent and selective mGluR1a antagonist. LY367385 has an IC50 of 8.8 μM for inhibits of quisqualate-induced phosphoinositide (PI) hydrolysis, compared with > 100 μM for mGlu5a. LY367385 has neuroprotective, anticonvulsant and antiepileptic effects[1][2].
In Vitro: LY367385 combined with N-methyl-D-aspartate (NMDA) during the toxic pulse attenuates neuronal degeneration in a concentration-dependent fashion, with a maximal reduction of NMDA toxicity ranging from 40 to 60%. LY367385 shows greater efficacy than LY367366 and neither of these compounds influenced neuronal viability per se. LY367385 shows potent neuroprotective effects, with causing a 50% reduction in (S)-3,5-Dihydroxyphenylglycine (DHPG) potentiation at a concentration of 10 nM. Under experimental conditions at higher concentrations of antagonist, LY367385 a completely antagonized the amplification of NMDA toxicity by DHPG[2].
In Vivo: LY367385 has been administered intracerebroventricularly (i.c.v.) to DBA/2 mice and lethargic mice (lh/lh), and focally into the inferior colliculus of genetically epilepsy prone rats (GEPR). In DBA/2 mice, LY367385 produces a rapid, transient suppression of sound-induced clonic seizures ED50 = 12 nM, i.c.v., 5 min). In lethargic mice, LY367385 significantly reduces the incidence of spontaneous spike and wave discharges on the electroencephalogram, from 30 to >150 min after the administration of LY367385, 250 nM, i.c.v[3]. 
In genetically epilepsy prone rats, LY367385 reduces sound-induced clonic seizures. LY367385, 160 nM bilaterally, fully suppresses clonic seizures after 2-4 h[3].

Name: Urotensin II (114-124), human, CAS: 251293-28-4, stock 37.3g, assay 98.3%, MWt: 1388.57, Formula: C64H85N13O18S2, Solubility: H2O, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Urotensin II (114-124), human, an 11-amino acid residue peptide, is a potent vasoconstrictor and agonist for the orphan receptor GPR14.
IC50 & Target: GPR14[1]
In Vitro: Human Urotensin II (U-II) binds to recombinant human GPR14 with high affinity, and the binding is functionally coupled to calcium mobilization. Human Urotensin II induces concentration-dependent increases in intracellular calcium in a HEK-293 cell line expressing human GPR14 (EC50=0:62±0.17 nM, n=6)[1].
In Vivo: Human Urotensin II (U-II) markedly increases total peripheral resistance in anaesthetized non-human primates, a response associated with profound cardiac contractile dysfunction[1].

Name: DL-TBOA, CAS: 205309-81-5, stock 4.7g, assay 99%, MWt: 239.22, Formula: C11H13NO5, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Membrane Transporter/Ion Channel, Target: EAAT2, Biological_Activity: DL-TBOA is a potent non-transportable inhibitor of excitatory amino acid transporters with IC50s of 70 μM, 6 μM and 6 μM for excitatory amino acid transporter-1 (EAAT1), EAAT2 and EAAT3, respectively. DL-TBOA inhibits the uptake of [14C]glutamate in COS-1 cells expressing the human EAAT1 and EAAT2 with Ki valuesof 42 μM and 5.7 μM, respectively. DL-TBOA blocks EAAT4 and EAAT5 in a competitive manner with Ki values of 4.4 μM and 3.2 μM, respectively[1][2][3].
IC50 & Target: IC50: 70 μM (EAAT1), 6 μM (EAAT2) and 6 μM (EAAT3); Ki: 42 μM (human EAAT1), 5.7 μM (human EAAT2), 4.4 μM (EAAT4) and 3.2 μM (EAAT5)[1][2][3]
In Vitro: DL-TBOA (70-350 μM; 48 hours; HCT116 and LoVo cell lines) treatment concentration-dependently enhances SN38-induced loss of viability. DL-TBOA reversed Oxaliplatin-induced loss of viability[4]. 
DL-TBOA (350 μM; 24 hours; HCT116 and LoVo cell lines) treatment decreases p53 induction by SN38 and oxaliplatin[4].

Name: 7-Chlorokynurenic acid sodium salt, CAS: 1263094-00-3, stock 27.2g, assay 98.4%, MWt: 245.59, Formula: C10H5ClNNaO3, Solubility: DMSO : ≥ 33.67 mg/mL (137.10 mM); H2O : 50 mg/mL (203.59 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Membrane Transporter/Ion Channel;Neuronal Signaling, Target: iGluR;iGluR, Biological_Activity: 7-Chlorokynurenic acid sodium salt is a potent and selective antagonist of the glycine B coagonist site of the N-methyl-D-aspartate (NMDA) receptor (IC50=0.56 μM). 7-Chlorokynurenic acid sodium salt is also a potent inhibitor of the reuptake of glutamate into synaptic vesicles with a Ki of 0.59 μM. 7-Chlorokynurenic acid sodium salt has potent antinociceptive actions after neuraxial delivery[1][2].
IC50 & Target: Ki: 0.59 μM (reuptake of glutamate)[1] 
IC50: 0.56 μM (Glycine B coagonist site of NMDA receptor)[2]
In Vivo: Male Sprague-Dawley rats pretreated with 7-Chlorokynurenic acid sodium salt (10 nM) shows a significant retardation of development of both the electroencephalographic and motor (17.7±2.9 daily stimulations) components of the seizure response[3].

Name: WAY-213613, CAS: 868359-05-1, stock 17.1g, assay 98.2%, MWt: 415.19, Formula: C16H13BrF2N2O4, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Membrane Transporter/Ion Channel, Target: EAAT2, Biological_Activity: WAY-213613 is a potent, selective nonsubstrate reuptake inhibitor of GLT-1/EAAT2 with IC50 of 85 nM EAAT2. It displays 59- and 44-fold selectivity over EAAT1 and EAAT3 (IC50s are 5 and 3.8 μM, respectively). WAY-213613 shows no activity at ionotropic and metabotropic glutamate receptors. It is a potential tool for the elucidation of EAAT2 function[1][2].
IC50 & Target: IC50: 85 nM (Human EAAT2), 3.8 μM (Human EAAT3), 5 μM (Human EAAT1)[1]

Name: WS-12, CAS: 68489-09-8, stock 27.6g, assay 98.2%, MWt: 289.41, Formula: C18H27NO2, Solubility: H2O : < 0.1 mg/mL (insoluble); DMSO : 20 mg/mL (69.11 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Membrane Transporter/Ion Channel;Neuronal Signaling, Target: TRP Channel;TRP Channel, Biological_Activity: WS-12 is an agonist of TRPM8 with an EC50 of 39 nM.
IC50 & Target: EC50: 39 nM (TRPM8)[1]

Name: A 1070722, CAS: 1384424-80-9, stock 4.7g, assay 98.7%, MWt: 362.31, Formula: C17H13F3N4O2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Stem Cell/Wnt;PI3K/Akt/mTOR, Target: GSK-3;GSK-3, Biological_Activity: A 1070722 is a potent and selective glycogen synthase kinase 3 (GSK-3) inhibitor, with a Ki of 0.6 nM for both GSK-3α and GSK-3β. A 1070722 can penetrate the blood-brain barrier (BBB) and accumulates in brain regions, thus potential for PET radiotracer for the quantification of GSK-3 in brain[1].
IC50 & Target: Ki: 0.6 nM (GSK-3)[1]

Name: N-Nonyldeoxynojirimycin NN-DNJ;Nonyl-DNJ, CAS: 81117-35-3, stock 15.6g, assay 99%, MWt: 289.41, Formula: C15H31NO4, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: N-Nonyldeoxynojirimycin (NN-DNJ) is a potent inhibitor of alpha-glucosidase and alpha-1,6-glucosidase (IC50s, 0.42, 8.4 μM, respectively), inhibits glycogen breakdown[1].
IC50 & Target: IC50: 0.42 μM (alpha-glucosidase), 8.4 μM (alpha-1,6-glucosidase)[1]

Name: A-967079, CAS: 1170613-55-4, stock 8g, assay 98.1%, MWt: 207.24, Formula: C12H14FNO, Solubility: DMS : 100 mg/mL (482.53 mM; Need ultrasonic); H2O : < 0.1 mg/mL (insoluble), Clinical_Informat: No Development Reported, Pathway: Membrane Transporter/Ion Channel;Neuronal Signaling, Target: TRP Channel;TRP Channel, Biological_Activity: A-967079 is a selective TRPA1 receptor antagonist with IC50s of 67 nM and 289 nM at human and rat TRPA1 receptors, respectively, and has good penetration into the CNS.
IC50 & Target: IC50: 67 nM (human TRPA1 receptor), 289 nM (rat TRPA1 receptor)[1]
In Vivo: Systemic injection of A-967079 (30 μmol/kg, i.v.) decreases the responses of wide dynamic range (WDR), and nociceptive specific (NS) neurons following noxious pinch stimulation of the ipsilateral hind paw in uninjured and CFA-inflamed rats. Similar to its actions in uninjured rats, administration of A-967079 (30 μmol/kg, i.v.) to complete Freund's adjuvant (CFA)-inflamed rats significantly reduces WDR neuronal responses to noxious pinch stimulation compared to baseline firing (p=0.0013, repeated-measures ANOVA) and the vehicle group (p=0.0001, two-way ANOVA). The maximum observed effect (61.1±10.97% decrease from baseline levels) on pinch-evoked activity in inflamed rats occur 35 min after injection. In contrast to uninjured rats, injection of A-967079 to CFA-inflamed rats also significantly (p=0.0004, and p=0.0001 for the repeated-measures and two-way ANOVA's, respectively) reduces responses of WDR neurons to 10-g von Frey hair stimulation. The maximal observed decrease in von Frey-evoked activity is 67.69±18.39% from baseline levels (35 min post-injection), and is thus comparable to the effects of A-967079 on pinch-evoked activity in inflamed rats[1].

Name: Timapiprant sodium OC000459 sodium, CAS: 950688-14-9, stock 24.9g, assay 98.5%, MWt: 371.36, Formula: C21H17FN2NaO2+, Solubility: DMSO : 100 mg/mL (269.28 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein, Target: Prostaglandin Receptor, Biological_Activity: Timapiprant sodium (OC000459 sodium) is a potent, selective, and orally active D prostanoid receptor 2 (DP2, also known as CRTH2) antagonist. Timapiprant sodium (OC000459 sodium) potently displaces [3H] PGD2 from human recombinant DP2 (Ki=13 nM), rat recombinant DP2 (Ki=3 nM), and human native DP2 (Ki=4 nM). Timapiprant sodium (OC000459 sodium) inhibits mast cell activation of Th2 lymphocytes and eosinophils[1].
IC50 & Target: Ki: 0.013 μM (human recombinant DP2); 0.003 μM (rat recombinant DP2) and 0.004 μM (human native DP2)[1]
In Vitro: Timapiprant sodium (OC000459 sodium) (0.0001 μM-10 μM; 5 hours) inhibits chemotaxis (IC50=0.028 μM) of human Th2 lymphocytes and cytokine production (IC50=0.019 μM) by human Th2 lymphocytes[1].
Timapiprant sodium (OC000459 sodium) (1 μM) inhibits the activation of Th2 cells and eosinophils in response to supernatants from IgE/anti-IgE-activated human mast cells[1].
Timapiprant sodium (OC000459 sodium) (1 nM-1000 nM; 16 hours) inhibits the anti-apoptotic effect of PGD2 on Th2 cells with an IC50 of 0.035 uM[1].
In Vivo: Timapiprant sodium (OC000459 sodium) (gavage; 2 mg/kg, 10 mg/kg) inhibits blood eosinophilia induced by 13,14-dihydro-15-keto-PGD2 (DK-PGD2) in Rat (ED50=0.04 mg/kg)[1].
Timapiprant sodium (OC000459 sodium) (gavage; 0.01 mg/kg, 0.1 mg/kg, 1.0 mg/kg) inhibits airway eosinophilia in response to an aerosol of DK-PGD2 in guinea pigs (ED50=0.01 mg/kg)[1].

Name: Pyr3, CAS: 1160514-60-2, stock 4g, assay 99%, MWt: 456.63, Formula: C16H11Cl3F3N3O3, Solubility: DMSO : ≥ 125 mg/mL (273.74 mM), Clinical_Informat: No Development Reported, Pathway: Membrane Transporter/Ion Channel;Neuronal Signaling, Target: TRP Channel;TRP Channel, Biological_Activity: Pyr3 is a selective inhibitor of transient receptor potential canonical channel 3 (TRPC3), with an IC50 of 700 nM for TRPC3-mediated Ca2+ influx.
IC50 & Target: IC50: 700 nM (TRPC3)[1].
In Vitro: Pyr3 selectively and directly inhibits TRPC3 channels among TRPC family members. Application of Pyr3 inhibits TRPC3-mediated Ca2+ influx in a dose-dependent manner with the IC50 value of 700 nM. Pyr3 becomes apparent at 0.3 μM, and is almost complete at 3 μM. Interestingly, Ca2+ influx is inhibited by Pyr3 in cells co-expressing TRPC3 plus TRPC6 but not in cells coexpressing TRPC1 plus TRPC5. The Ang II-induced NFAT translocation is suppressed by Pyr3, but weakly by Pyr2 in a concentration-dependent manner (IC50 value was 0.05 μM for Pyr3 and 2 μM for Pyr2)[1].

Name: Oleoylethanolamide N-Oleoylethanolamide;Oleamide MEA;Oleic acid monoethanolamide, CAS: 111-58-0, stock 7.9g, assay 98.9%, MWt: 325.53, Formula: C20H39NO2, Solubility: H2O : < 0.1 mg/mL (insoluble); DMSO : 20.83 mg/mL (63.99 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Cell Cycle/DNA Damage;Metabolic Enzyme/Protease, Target: PPAR;Endogenous Metabolite, Biological_Activity: Oleoylethanolamide is a high affinity endogenous PPAR-α agonist, which plays an important role in the treatment of obesity and arteriosclerosis.
IC50 & Target: PPAR-α[1]
In Vitro: Oleoylethanolamide (OEA), an endogenous PPAR-α ligand, attenuates liver fibrosis targeting hepatic stellate cells. Oleoylethanolamide suppresses TGF-β1 induced hepatic stellate cells (HSCs) activation in vitro via PPAR-α. To assess the impact of Oleoylethanolamide on HSCs activation, the expression levels of α-SMA and Col1a in TGF-β1-stimulated HSCs are examined by qPCR. The mRNA levels of α-SMA and Col1a are markedly induced in the group of CFSC cells with TGF-β1 (5 ng/mL) stimulation for 48h, while the mRNA levels are suppressed when treated with Oleoylethanolamide in a dose-dependent manner. Immunofluorescence and western blot results show that Oleoylethanolamide treatment dose-dependently inhibits the protein expression of α-SMA, the marker of HSC activation. The inhibitory effects of Oleoylethanolamide on HSCs activation are completely blocked by PPAR-α antagonist MK886 (10 μM). Moreover, the mRNA and protein expression levels of PPAR-α are down-regulated with TGF-β1 stimulation, while Oleoylethanolamide treatment restores these changes in dose-dependent manner. In addition, the phosphorylation of Smad 2/3 is upregulated in the presence of TGF-β1 stimulation, consistent with the observed effects on HSC activation, while Oleoylethanolamide (10 μM) reduces the phosphorylation of Smad2/3 in CFSC simulated with TGF-β1[1].
In Vivo: Oleoylethanolamide (OEA) can significantly suppress the pro-fibrotic cytokine TGF-β1 negatively regulate genes in the TGF-β1 signaling pathway (α-SMA, collagen 1a, and collagen 3a) in mice models of hepatic fibrosis. Treatment with Oleoylethanolamide (5 mg/kg/day, intraperitoneal injection, i.p.) significantly attenuates the progress of liver fibrosis in both two experimental animal models by blocking the activation of hepatic stellate cells (HSCs)[1].

Name: Ro 08-2750, CAS: 37854-59-4, stock 30.8g, assay 98.9%, MWt: 270.24, Formula: C13H10N4O3, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Ro 08-2750 is a non-peptide and reversible nerve growth factor (NGF) inhibitor which binds to NGF, and with an IC50 of ~ 1 µM. Ro 08-2750 inhibits NGF binding to p75NTR selectively over TRKA[1].
IC50 & Target: IC50: ~ 1 µM (NGF)[1]
In Vitro: Ro 08-2750 binds to the NGF dimer thereby probably inducing a change in its conformation such that NGF cannot bind to p75NTR anymore[2]. 
Ro 08-2750 (10 nM) completely rescues cells from undergoing NGF-induced SK-N-MC 103 cells death[2].

Name: CU-CPT22, CAS: 1416324-85-0, stock 7.7g, assay 98.9%, MWt: 362.37, Formula: C19H22O7, Solubility: DMSO : ≥ 125 mg/mL (344.95 mM); H2O : < 0.1 mg/mL (insoluble), Clinical_Informat: No Development Reported, Pathway: Immunology/Inflammation, Target: Toll-like Receptor (TLR), Biological_Activity: CU-CPT22 is a potent protein complex of toll-like receptor 1 and 2 (TLR1/2) inhibitor, and competes with the synthetic triacylated lipoprotein (Pam3CSK4) binding to TLR1/2 with a Ki of 0.41 µM. CU-CPT22 blocks Pam3CSK4-induced TLR1/2 activation with an IC50 of 0.58 µM[1].
IC50 & Target: Ki: 0.41 μM (TLR1/2)[1]
In Vitro: CU-CPT22 is a toll-like receptor 1 and 2 (TLR1/2) inhibitor with an IC50 of 0.58±0.09 µM. It is demonstrated that CU-CPT22 is able to compete with Pam3CSK4 for binding to TLR1/2 with an inhibition constant (Ki) of 0.41±0.07 µM, which is consistent with its potency observed in the whole cell assay. Increasing the concentration of CU-CPT22 to 6 µM decreases the anisotropy to background levels. It is found that CU-CPT22 inhibits TLR1/2 signaling without affecting other TLRs, showing it is highly selective in intact cells. CU-CPT22 is found to have no significant cytotoxicity at various concentrations up to 100 µM in RAW 264.7 cells. The result demonstrates that CU-CPT22 can inhibit about 60% of TNF-αand 95% of IL-1β at 8 µM[1].

Name: Garcinol, CAS: 78824-30-3, stock 15.6g, assay 98.8%, MWt: 602.80, Formula: C38H50O6, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Apoptosis;Neuronal Signaling;Epigenetics, Target: Apoptosis;AChE;Histone Acetyltransferase, Biological_Activity: Garcinol, a polyisoprenylated benzophenone harvested from Garcinia indica, exerts anti-cholinesterase properties towards acetyl cholinesterase (AChE) and butyrylcholinesterase (BChE) with IC50s of 0.66 µM and 7.39 µM, respectively[1]. Garcinol also inhibits histone acetyltransferases (HATs, IC50= 7 μM) and p300/CPB-associated factor (PCAF, IC50 = 5 μM). Garcinol has anti-inflammatory and anti-cancer activity[2].
IC50 & Target: IC50: 0.66 µM (AChE); 7.39 µM (BChE)[1]; 7 μM (HATs); 5 µM (PCAF) [2]
In Vitro: Garcinol (10-50 µM; 24-72 hours) can inhibit the proliferation of two HNSCC cell lines tested (CAL27 and UMSCC1) in a time- and dose-dependent manner[3]. 
Garcinol (10-50 µM; 24-72 hours) induces apoptosis in HNSCC cells[3]. 
Garcinol (50 µM; 1-6 hours) suppresses phosphorylation and degradation of the constitutive IκBα in a time-dependent manner[3]. 
In Vivo: Garcinol (i.p.; 1 and 2 mg/kg; five times/week for 4 consecutive weeks) induces significant inhibition of tumor growth[3].

Name: Loxoribine 7-Allyl-8-oxoguanosine; RWJ 21757, CAS: 121288-39-9, stock 36.1g, assay 98.7%, MWt: 339.30, Formula: C13H17N5O6, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Immunology/Inflammation, Target: Toll-like Receptor (TLR), Biological_Activity: Loxoribine (7-Allyl-8-oxoguanosine) is a guanosine analog with anti-viral and anti-tumor activities. Loxoribine is an orally bioavailable and selective Toll-like receptor (TLR) 7 agonist[1][2][3].
IC50 & Target: TLR7[1]
In Vitro: Loxoribine induces maturation of human monocyte-derived dendritic cells DCs and stimulates their Th-1- and Th-17-polarizing capability[2]. 
Loxoribine (250 μM; 48 hours) stimulates maturation of MoDCs as shown by up-regulation of CD80, CD83, CD40, CD54 and CCR7[2]. 
loxoribine activates cells of the innate immune system selectively via the Toll-like receptor (TLR) 7/MyD88-dependent signaling pathway[1]. 
In Vivo: Loxoribine (2 mg; s.c.or i.v.) activates murine natural killer (NK) cells in vivo[3].

Name: Nolatrexed dihydrochloride AG 337;Thymitaq, CAS: 152946-68-4, stock 15.2g, assay 98.1%, MWt: 357.26, Formula: C14H14Cl2N4OS, Solubility: DMSO : 41.67 mg/mL (116.64 mM; Need ultrasonic), Clinical_Informat: Phase 3, Pathway: Apoptosis, Target: Thymidylate Synthase, Biological_Activity: Nolatrexed dihydrochloride (AG 337) is a non-competitive lipophilic inhibitor of thymidylate synthase, interacts at the folate cofactor binding site of the enzyme, with a Ki of 11 nM for human thymidylate synthase[1]. Nolatrexed dihydrochloride (AG 337) has anti-cancer activity, induces cell cycle arrest in S phase of cancer cells[2].
IC50 & Target: Ki: 11 nM (Human Thymidylate Synthase)[1]

Name: TMPyP4 tosylate TMP 1363, CAS: 36951-72-1, stock 39.2g, assay 98%, MWt: 1363.60, Formula: C72H66N8O12S4, Solubility: H2O : 6.2 mg/mL (4.55 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Cell Cycle/DNA Damage;Cell Cycle/DNA Damage, Target: Telomerase;G-quadruplex, Biological_Activity: TMPyP4 tosylate (TMP 1363) is a quadruplex-specific ligand, which inhibits the interaction between G-quadruplexes and IGF-1[1]. TMPyP4 tosylate (TMP 1363) is a telomerase inhibitor with antitumor effects in osteosarcoma cell lines[2].
IC50 & Target: G-quadruplex[2] 
Telomerase[2]

Name: Eledoisin Related Peptide Eledoisin-Related Peptide;Eledoisin RP, CAS: 2990-43-4, stock 32.8g, assay 98.2%, MWt: 706.94, Formula: C34H58N8O6S, Solubility: H2O, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Eledoisin Related Peptide is a Substance P analog that excites neurons and triggers behavioral responses. Eledoisin Related Peptide is also a tachykinin receptor ligand.
IC50 & Target: Tachykinin receptor[1]
In Vivo: Eledoisin Related Peptide shares with Substance P (SP) a common N-terminal amino acid sequence and has been shown by to have SP-like activity in the periphery (gut and salivary glands) and the CNS. Eledoisin-related peptide seems to be roughly equipotent with Substance P at identical ejection currents on the single-cell activity of neurons in this nucleus[2]. Both glutamate and substance P (and its analogue, eledoisin-related peptide) have excitatory effects on the activity of respiratory neurons and reflex interneurons[3].

Name: JNK Inhibitor VIII TCS JNK 6o, CAS: 894804-07-0, stock 27.8g, assay 98.3%, MWt: 356.38, Formula: C18H20N4O4, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: MAPK/ERK Pathway, Target: JNK, Biological_Activity: JNK Inhibitor VIII (TCS JNK 6o) is a c-Jun N-terminal kinases (JNK-1, -2, and -3) inhibitor with Ki values of 2 nM, 4 nM, 52 nM, respectively, and has IC50 values of 45 nM and 160 nM for JNK-1 and -2, respectively[1].
IC50 & Target: Ki: 2 nM (JNK-1), 4 nM (JNK-2), 52 nM (JNK-3)[1] 
IC50: 45 nM (JNK-1), 160 nM (JNK-2)[1]
In Vitro: JNK Inhibitor VIII (TCS JNK 6o) shows over 1000- fold selective for JNK-1 and -2 over other MAP kinases including ERK2, p38α, and p38δ[1].

Name: UBP 302, CAS: 745055-91-8, stock 28.9g, assay 98.9%, MWt: 333.30, Formula: C15H15N3O6, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Membrane Transporter/Ion Channel;Neuronal Signaling, Target: iGluR;iGluR, Biological_Activity: UBP 302 is a potent and selective GLUK5-subunit containing kainate receptor antagonist (apparent Kd=402 nM), and displays very little affinity on GluK2 (GluR6) kainate receptors. Anxiolytic effects[1][2][3].
IC50 & Target: apparent Kd: 402 nM (GLUK5)[2] 
IC50: 106 μM (AMPA receptors)[2]

Name: Fatostatin (hydrobromide) 125B11 (hydrobromide), CAS: 298197-04-3, stock 39.7g, assay 98.7%, MWt: 375.33, Formula: C18H19BrN2S, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Fatty Acid Synthase (FAS), Biological_Activity: Fatostatin hydrobromide (125B11 hydrobromide), a specific inhibitor of SREBP activation, impairs the activation of SREBP-1 and SREBP-2. Fatostatin hydrobromide binds to SCAP (SREBP cleavage-activating protein), and inhibits the ER-Golgi translocation of SREBPs. Fatostatin hydrobromide decreases the transcription of lipogenic genes in cells. Fatostatin hydrobromide possesses antitumor properties, and lowers hyperglycemia in ob/ob mice[1][2].
In Vitro: Fatostatin hydrobromide (125B11 hydrobromide) (0.1-1 μM; 3 days) inhibits the androgen-independent prostate cancer cell proliferation (IC50=0.1 μM) in an independent of the known IGF1-signaling pathway. Fatostatin hydrobromide inhibits insulin-induced adipogenesis of 3T3-L1 cells[1].
In Vivo: Fatostatin hydrobromide (125B11 hydrobromide) (30 mg/kg; 150 mL; i.p.; daily for 28 days) reduces adiposity, ameliorates fatty liver by reducing triglyceride (TG) storage, and lowers hyperglycemia in ob/ob mice[2].

Name: R 59-022 DKGI-I; Diacylglycerol kinase inhibitor I, CAS: 93076-89-2, stock 13g, assay 98.8%, MWt: 459.58, Formula: C27H26FN3OS, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: TGF-beta/Smad;Epigenetics;Neuronal Signaling;GPCR/G Protein, Target: PKC;PKC;5-HT Receptor;5-HT Receptor, Biological_Activity: R 59-022 (DKGI-I) is a diacylglycerol kinase inhibitor (IC50=2.8 μM). R 59-022 is a 5-HTR antagonist, and activates protein kinase C (PKC). R 59-022 potentiates thrombin-induced diacylglycerol production in platelets and inhibits phosphatidic acid production in neutrophils[1][2][3][4].
In Vitro: In the intact platelet, R 59-022 is able to interrupts thrombin-induced inositol lipid cycling at the level of diacylglycerol and leads to an elevation of protein kinase C activity[1]. 
R 59-022 (10 μM) potentiates aggregation, but not shape change induced by sub-maximal concentrations of thrombin. R59022 (10 μM) had no significant effect on the dose-response curve for the mobilization of intracellular Ca2+ by thrombin in either the presence or the absence of extracellular Ca2+[2]. 
R 59-022, an inhibitor of filovirus entry, prevents the macropinocytic uptake of filoviral particles, inhibits entry mediated by multiple filovirus GPs, and blocks replicative EBOV growth. R 59-022 blocks entry of EBOV pseudotypes in a concentration-dependent manner (IC50: ~5 µM). R 59-022 dose-dependent decreases in entry by the VLPs harboring the EBOV GP (IC50: ~2 µM). R 59-022 (2-12 μM; 1 hour) can inhibit EBOV GP-mediated entry in multiple cell types. R 59-022 (5 µM; 30 minutes) blocks macropinocytosis in vero cells[5].

Name: Pyronaridine tetraphosphate, CAS: 76748-86-2, stock 21.5g, assay 98.3%, MWt: 910.03, Formula: C29H44ClN5O18P4, Solubility: DMSO : 25 mg/mL (27.47 mM; Need ultrasonic and warming), Clinical_Informat: Phase 4, Pathway: Anti-infection, Target: Parasite, Biological_Activity: Pyronaridine tetraphosphate is a Mannich base anti-malarial with demonstrated efficacy against drug resistant Plasmodium falciparum, P. vivax, P. ovale and P. malariae.

Name: CYM50260, CAS: 1355026-60-6, stock 29.2g, assay 98.8%, MWt: 350.60, Formula: C14H11Cl3FNO2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein, Target: LPL Receptor, Biological_Activity: CYM50260 is a potent and exquisitely selective sphingosine-1-phosphate 4 receptor (S1P4-R) agonist with an EC50 of 45 nM. CYM50260 displays no activity against S1P1-R, S1P2-R, S1P3-R and S1P5-R[1].
IC50 & Target: EC50: 45 nM (S1P4-R)[1]
In Vitro: CYM50260 (Compound 22aa) is a synthetic S1P4-R agonist. CYM50260 is found 3.5-fold more potent than the hit compound (HTS-hit)[1]. 
CYM50260 suppresses the collagen-stimulated platelet aggregation, PDGF-AB secretion and sCD40L release. CYM50260 reduces the release of phosphorylated-HSP27 by collagen as well as the phosphorylation of HSP27[2].

Name: CYM50308, CAS: 1345858-76-5, stock 24.3g, assay 98.9%, MWt: 405.46, Formula: C20H21F2N3O2S, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein, Target: LPL Receptor, Biological_Activity: CYM50308 is a potent, selective and high affinity sphingosine-1-phosphate receptor 4 (S1P4-R) agonist with an EC50 of 56 nM. CYM50308 displays 37-fold more selective for S1P4-R than S1P5-R. CYM50308 has no activity at S1P1-R, S1P2-R and S1P3-R subtypes at concentrations up to 25 μM[1].
IC50 & Target: EC50: 56 nM (S1P4-R), 2100 nM (S1P5-R)[1]
In Vitro: The disclosed lead molecule CYM50308 (Compound 24f) displays low nanomolar S1P4-R agonist activity and exquisite selectivity over the other S1P-Rs subtypes. Noteworthy, CYM50308 provides a valuable pharmacological tool to explore the effects of the S1P4-R signaling cascade and elucidate the molecular basis of the in vivo receptor function[1].

Name: L-803087, CAS: 217480-26-7, stock 30g, assay 98.5%, MWt: 485.53, Formula: C25H29F2N5O3, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein;Neuronal Signaling, Target: Somatostatin Receptor;Somatostatin Receptor, Biological_Activity: L-803087 is a potent and selective somatostatin sst4 receptor agonist with a Ki of 0.7 nM, which is > 280-fold higher than other somatostatin receptors. L-803087 facilitates AMPA-mediated hippocampal synaptic responses in vitro and increases kainate-induced seizures in mice[1][2].
IC50 & Target: Ki: 0.7 nM (sst4 receptor), 199 nM (sst1 receptor), 4720 nM (sst2 receptor), 1280 nM (sst3 receptor) and 3880 nM (sst5 receptor)[1]
In Vitro: L-803087 has Ki values for cloned human sst1, sst2, sst3 and sst5 receptors of 199, 4720, 1280 and 3880 nM, respectively[1]. 
L-803087 has a diamine moiety that maps to lysine on the phmacophore, but relation of this molecule to the aromatic and the Trp substituents of the phmacophore are not obvious. L-803087 does not inhibit secretion of growth hormone, insulin, or glucagon[1].
In Vivo: L-803087 (5 nmol) is doubled seizure activity in wild-type mice on average. Interestingly, this effect is blocked by 3 nmol Octreotide. In hippocampal slices from wild-type mice, Octreotide (2 μM) does not modify AMPA-mediated synaptic responses while facilitation occurred with L-803087 (2 μM)[2].

Name: TC-MCH 7c, CAS: 864756-35-4, stock 32.1g, assay 98.4%, MWt: 408.47, Formula: C24H25FN2O3, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein;Neuronal Signaling, Target: MCHR1 (GPR24);MCHR1 (GPR24), Biological_Activity: TC-MCH 7c, a phenylpyridone derivative, is an orally available, selective and brain-penetrable MCH1R antagonist with an IC50 of 5.6 nM for hMCH1R[1]. TC-MCH 7c has Kis of 3.4 nM and 3.0 nM of human and mouse MCH1R, respectively[2].
IC50 & Target: IC50: 5.6 nM (hMCH1R)[1] 
Ki: 3.4 nM (hMCH1R) and 3.0 nM (mouse MCH1R)[1]
In Vitro: TC-MCH 7c has an IC50 of 9.7 μM for MCH1R in [Ca2+]i mobilization[1]. 
TC-MCH 7c has IC50s of 23 nM and 9.0 μM for FLIPR and hERG, respectively[2]. 
In Vivo: TC-MCH 7c (oral; 3-30 mg/kg; once-daily for 1.5 months) exhibits excellent body weight reduction in a dose-dependent manner in DIO mice model[1]. 
TC-MCH 7c (oral; 3-30 mg/kg) with 30 mg/kg has plasma concentrations of 5.1, 1.8, and 0.7 μM at 2, 15, and 24 hours, respectively[2].

Name: Crizotinib PF-02341066, CAS: 877399-52-5, stock 9.9g, assay 98.6%, MWt: 450.34, Formula: C21H22Cl2FN5O, Solubility: DMSO : 55 mg/mL (122.13 mM; Need ultrasonic), Clinical_Informat: Launched, Pathway: Protein Tyrosine Kinase/RTK;Protein Tyrosine Kinase/RTK;Autophagy;Protein Tyrosine Kinase/RTK, Target: c-Met/HGFR;ROS;Autophagy;ALK, Biological_Activity: Crizotinib (PF-02341066) is an orally bioavailable, selective, and ATP-competitive dual ALK and c-Met inhibitor with IC50s of 20 and 8 nM, respectively. Crizotinib (PF-02341066) inhibits tyrosine phosphorylation of NPM-ALK and tyrosine phosphorylation of c-Met with IC50s of 24 and 11 nM in cell-based assays, respectively. Crizotinib (PF-02341066) is also a ROS proto-oncogene 1 (ROS1) inhibitor. Crizotinib (PF-02341066) has effective tumor growth inhibition[1][2][3].
IC50 & Target: IC50: 20 nM (ALK), 8 nM (c-Met)[3]
In Vitro: Crizotinib (PF-02341066) displays similar potency against c-Met phosphorylation in mIMCD3 mouse or MDCK canine epithelial cells with IC50 of 5 nM and 20 nM, respectivly. PF-2341066 shows improved or similar activity against NIH3T3 cells engineered to express c-Met ATP-binding site mutants V1092I or H1094R or the P-loop mutant M1250T with IC50 of 19 nM, 2 nM and 15 nM, respectively, compared with NIH3T3 cells expressing wild-type receptor with IC50 of 13 nM. In contrast, a marked shift in potency of PF-2341066 is observed against cells engineered to express c-Met activation loop mutants Y1230C and Y1235D with IC50 of 127 nM and 92 nM, respectively, compared with wild-type receptor. PF-2341066 also potently prevents the phosphorylation of c-Met in NCI-H69 and HOP92 cells, with IC50 of 13 nM and 16 nM, respectively, which express the endogenous c-Met variants R988C and T1010I, respectively[1]. 
Crizotinib (PF-02341066) also potently inhibits NPM-ALK phosphorylation in Karpas299 or SU-DHL-1 ALCL cells with an IC50 of 24 nM. PF-2341066 potently prevents cell proliferation, which is associated with G(1)-S-phase cell cycle arrest and induction of apoptosis in ALK-positive ALCL cells with IC50 of 30 nM, but not ALK-negative lymphoma cells[2].
In Vivo: Crizotinib (PF-02341066) reveals the ability to cause marked regression of large established tumors (> 600 mm3) in both the 50 mg/kg/day and 75 mg/kg/day treatment cohorts, with a 60% decrease in mean tumor volume over the 43-day administration schedule in the GTL-16 model. In an another study, PF-2341066 displays the ability to completely inhibits GTL-16 tumor growth for >3 months, with only 1 of 12 mice exhibiting a significant increase in tumor growth over the 3-month treatment schedule at 50 mg/kg/day. A significant dose-dependent reduction of CD31-positive endothelial cells is observed at 12.5 mg/kg/day, 25 mg/kg/day, and 50 mg/kg/day in GTL-16 tumors, indicating that inhibition of MVD shows a dose-dependent correlation to antitumor efficacy. PF-2341066 displays a significant dose-dependent reduction of human VEGFA and IL-8 plasma levels in both the GTL-16 and U87MG models. Marked inhibition of phosphorylated c-Met, Akt, Erk, PLCλ1, and STAT5 levels is observed in GTL-16 tumors following p.o. administration of PF-2341066[1]. 
Treatment of c-MET-amplified GTL-16 xenografts with 50 mg/kg PF-2341066 elicits tumor regression that is associated with a slow reduction in 18F-FDG uptake and decreases expression of the glucose transporter 1, GLUT-1[4].

Name: SNAP 94847, CAS: 487051-12-7, stock 37.3g, assay 98.6%, MWt: 478.57, Formula: C29H32F2N2O2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein;Neuronal Signaling, Target: MCHR1 (GPR24);MCHR1 (GPR24), Biological_Activity: SNAP 94847 is a novel, high affinity selective melanin-concentrating hormonereceptor1 (MCHR1) antagonist with (Ki= 2.2 nM, Kd=530 pM), it displays >80-fold and >500-fold selectivity over MCHα1A and MCHD2 receptors respectively. SNAP 94847 binds with high affinity to the mouse and rat MCHR1 with minimal cross-reactivity to other GPCR, ion channels, enzymes, and transporters[1][3].
IC50 & Target: Ki: 2.2 nM (MCHR1); Kd: 530 pM (MCHR1)[1]
In Vivo: SNAP 94847 (oral gavage; 20 mg/kg; 14 days) shows an exaggerated locomotor response to acute quinpirole [treatment: F(2,19)=11.31, treatment × time: F(34,323) = 4.061], the effect of SNAP 94847 on quinpirole-evoked ambulations over the entire observation period is significant compared to the untreated animals[2].
SNAP 94847 (oral administration; 20 mg/kg; 21 days) in drink water, produces a significant increase in ambulation relative to untreated animals [treatment: F(3,28) = 8.971; treatment × time: F(51,476)=11.50]. shows a marked increase in locomotion is apparent after 40 min in the SNAP 94847-treated group,this effect is significant over 180 min[2].
SNAP 94847 (oral administration; 10 mg/kg), has a good bioavailability (59%), low plasma and blood clearances of 4.2 L/hr/kg and 3.3 L/hr/kg, respectively, and the half-life was shown to be 5.2 h in rats in a PK study[3].

Name: Adrenocorticotropic Hormone (ACTH) (1-39), human 1-39-Corticotropin (human), CAS: 12279-41-3, stock 4.6g, assay 98.9%, MWt: 4541.14, Formula: C207H308N56O58S, Solubility: H2O, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Adrenocorticotropic Hormone (ACTH) (1-39), human is a melanocortin receptor agonist.
IC50 & Target: Melanocortin receptor[1]
In Vitro: Adrenocorticotropic Hormone (ACTH) (1-39), human (ACTH 1-39), a member of the melanocortin family, stimulates production of CS by the adrenals, but melanocortin receptors are also found in the central nervous system (CNS) and on immune cells. ACTH 1-39 protects neurons in vitro from several apoptotic, excitotoxic and inflammation-related insults[1]. The conditioned medium (CM) is prepared from untreated astroglia (AS) cultures and from AS cultures treated with 200 nM ACTH 1-39 for 24 h, washed to remove ACTH 1-39, then incubated for another 24 h in DMEM. In initial experiments, no difference is found in oligodendroglia (OL) viability in the presence of OL definedmediumwith 2% newborn calf serum (NCS) or AS CM (prepared in DMEM with no serum). After 24 h, OL death under each condition varies between 1 and 4%. Similar results for OL viability are obtained with microglia (MG) CM. In subsequent experiments, controls in each experiment consist of OL in defined medium with 2% NCS[2].

Name: Phosphocreatine (disodium) Disodium creatine phosphate, CAS: 922-32-7, stock 10.3g, assay 98.4%, MWt: 255.08, Formula: C4H8N3Na2O5P, Solubility: H2O : 125 mg/mL (490.04 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: Phosphocreatine disodium, one of organic compounds known as alpha amino acids and derivatives, is a substrate for the determination of creatine kinase and used to regenerate ATP during skeletal muscle contraction[1].

Name: QX-314 (chloride), CAS: 5369-03-9, stock 36.1g, assay 98.8%, MWt: 298.85, Formula: C16H27ClN2O, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Membrane Transporter/Ion Channel, Target: Sodium Channel, Biological_Activity: QX-314 chloride is a membrane-impermeable permanently charged sodium channel blocker[1].
IC50 & Target: sodium channel[1]
In Vitro: QX-314 chloride exerts biphasic effects on transient receptor potential vanilloid subtype 1 channels (TRPV1) in vitro[2]. 
QX-314 chloride (1–60 mM) directly activates TRPV1 in a concentration-dependent manner[2]. 
QX-314 chloride (10 mM) inhibits calcium currents in hippocampal CA1 pyramidal neurons intracellular, and the low-threshold (T-type) Ca2+ currents are on average < 45% of control amplitude[2].

Name: LL-37, Human, CAS: 154947-66-7, stock 11.3g, assay 98.3%, MWt: 4493.26, Formula: C205H340N60O53, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: LL-37, Human is a 37-residue, amphipathic, cathelicidin-derived antimicrobial peptide, which exhibits a broad spectrum of antimicrobial activity[1]. LL-37, Human could help protect the cornea from infection and modulates wound healing[2].

Name: A 1120, CAS: 1152782-19-8, stock 17.3g, assay 98.6%, MWt: 392.37, Formula: C20H19F3N2O3, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: A 1120, a nonretinoid retinol-binding protein 4 (RBP4) antagonist, has a high affinity with the Ki value of 8.3 nM, which disrupts the interaction between RBP4 and its binding partner transthyretin[1][2].
IC50 & Target: Ki: 8.3 nM (Retinol-binding protein 4)[1]
In Vitro: The IC50 of A 1120 is 90 nM on human RBP4 and 66 nM on mouse RBP4[1].

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2020年3月13日星期五

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