EOS Med Chem, Medicinal Chemical is Big: EOS Med Chem Building block stock list 2346

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

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Name: Fraxetin, CAS: 574-84-5, stock 30.4g, assay 98.8%, MWt: 208.17, Formula: C10H8O5, Solubility: DMSO : 250 mg/mL (1200.94 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Apoptosis, Target: Apoptosis, Biological_Activity: Fraxetin is isolated from Cortex Fraxini. Fraxetin has antitumor, anti-oxidation effects and anti-inflammory effects. Fraxetin induces apoptosis[1].

Name: Qingyangshengenin A, CAS: 106644-33-1, stock 29.4g, assay 98.6%, MWt: 933.09, Formula: C49H72O17, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Qingyangshengenin A, a C-21 steroidal glycoside isolated from the roots of Cynanchum otophyllum Schneid, has antiepileptic activity[1].

Name: Qingyangshengenin B, CAS: 106758-54-7, stock 0.5g, assay 98.5%, MWt: 923.13, Formula: C49H78O16, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Qingyangshengenin B, a C-21 steroidal glycoside isolated from Qingyangshen. Qingyangshengenin B protects against Aβ toxicity, which decreases Aβ deposition by decreasing the expression of Aβ at the mRNA level. Qingyangshengenin B has antiepileptic activity[1][2][3].

Name: Demethylzeylasteral, CAS: 107316-88-1, stock 26.3g, assay 98.1%, MWt: 480.59, Formula: C29H36O6, Solubility: DMSO : 250 mg/mL (520.19 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Apoptosis, Target: Apoptosis, Biological_Activity: Demethylzeylasteral is a triterpene compound isolated from Tripterygium wilfordii Hook F, with anti-inflammatory, immunosuppressive and anti-tumor activities[1][2][3][4][5]. Demethylzeylasteral can significantly alleviates atherosclerosis (AS)[5]. Demethylzeylasteral inhibits triple-negative breast cancer invasion by blocking the canonical and non-canonical TGF-β signaling pathways[2].

Name: TAS-116, CAS: 1260533-36-5, stock 0.2g, assay 98.9%, MWt: 454.53, Formula: C25H26N8O, Solubility: DMSO : 125 mg/mL (275.01 mM; Need ultrasonic), Clinical_Informat: Phase 1, Pathway: Metabolic Enzyme/Protease;Cell Cycle/DNA Damage, Target: HSP;HSP, Biological_Activity: TAS-116 is an oral bioavailable, ATP-competitive, highly specific HSP90α/HSP90β inhibitor (Kis of 34.7 nM and 21.3 nM, respectively) without inhibiting other HSP90 family proteins such as GRP94[1]. TAS-116 demonstrates less ocular toxicity[2].
In Vitro: TAS-116 binds not only to the conventional-binding pockets as existing Hsp-90 inhibitors, but also to a novel-binding pocket. Such a unique binding mode makes TAS-116 highly specific for Hsp-90α/β without inhibiting other Hsp-90 family proteins such as GRP94 in endoplasmic reticulum or TRAP-1 in mitochondria[3]. 
TAS-116 (0-5 μM, 48 hours) inhibits human retinal pigment epithelial ARPE-19 cell lines and NCI-H929 MM cells growth[2]. 
More significant degradation of p-C-Raf and p-MEK1/2, HSP90 client proteins and key RAS/RAF/MEK pathway regulators, is triggered by TAS-116 (0.125-1 μM, 24 hours) than 17-AAG in INA6 and NCI-H929 MM cells[2]. 
In Vivo: TAS-116 (12.0 mg/kg, p.o., 14 days) shows antitumor activity without inducing eye injury in rats. TAS-116 is distributed less in retina than in plasma in rats; consequently, TAS-116 does not produce any detectable photoreceptor injury[1]. TAS-116 triggers enhanced in vivo anti-MM activities, both alone and in combination with Bortezomib (BTZ), with a favorable safety profile. Mice treated with TAS-116 (10 mg/kg and 15 mg/kg, orally, 38 days), BTZ, or TAS-116 plus BTZ show significantly enhance growth inhibition versus the vehicle control group. Median overall survival of treated animals (TAS-116, orally, 10 mg/kg=33 days, 15 mg/kg=37 days, BTZ=36 days, and the combination=56.5 days) is significantly longer than vehicle control[2]. 
The favorable pharmacokinetic profile of TAS-116 is reflected in its dose-dependent antitumor activity; the T/C (tumor volume of TAS-116-treated mice vs. vehicle-treated mice) is 47%, 21%, and 9% for doses of 3.6 mg/kg, 7.1 mg/kg, and 14.0 mg/kg, respectively. TAS-116 is orally absorbed and has a bioavailability of almost 100% in mice, and 69.0% in rats. TAS-116 has moderate terminal elimination half-life (t1/2=8.2 h, 2.5 h, 4.4 h and 2.2 h for mouse (3.6 mg/kg, p.o.), mouse (7.1 mg/kg, p.o.), mouse (14.0 mg/kg, p.o.), rat (4 mg/kg, p.o.)). TAS-116 is more rapidly eliminated from retina (t1/2=3.4 hours) than the other HSP90 inhibitors (t1/2=7.1-19.1 hours)[1].

Name: Auglurant VU0424238, CAS: 1396337-04-4, stock 11.1g, assay 98.3%, MWt: 325.30, Formula: C16H12FN5O2, Solubility: H2O : < 0.1 mg/mL (insoluble); DMSO : 22.73 mg/mL (69.87 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein;Neuronal Signaling, Target: mGluR;mGluR, Biological_Activity: Auglurant (VU0424238) is a novel and selective mGlu5 antagonist with an IC50 value of 11 nM (rat) and an IC50 value of 14 nM (human). Auglurant (VU0424238) has an acceptable CNS penetration[1].
In Vitro: Auglurant (VU0424238) with an IC50 value of 14 nM in HEK293A cells. It also binding a known allosteric site with K i value of 4.4 nM in HEK293A cells.
In Vivo: Auglurant (VU0424238) had a clearance of 19.3 mL/min/kg in rats and demonstrates 50% mGlu5 PET ligand occupancy at an oral dose of 0.8 mg/kg in rats. Plus, it also had a clearance of 15.5 mL/min/kg in cynomolgus monkeys and demonstrates 50% mGlu5 PET ligand occupancy at an oral dose of 0.06 mg/kg in baboons[1].

Name: Nifenazone, CAS: 2139-47-1, stock 25.2g, assay 98.7%, MWt: 308.33, Formula: C17H16N4O2, Solubility: DMSO : 32 mg/mL (103.78 mM; Need ultrasonic), Clinical_Informat: Launched, Pathway: Others, Target: Others, Biological_Activity: Nifenazone is a pyrazole drug which can be used in the in the treatment of a variety of rheumatic disorders.

Name: Talc, CAS: 14807-96-6, stock 28.1g, assay 98.1%, MWt: 78.10, Formula: H2O3Si, Solubility: 10 mM in DMSO, Clinical_Informat: Launched, Pathway: Others, Target: Others, Biological_Activity: Talc, a naturally occurring mineral composed primarily of magnesium, silicon and oxygen, is used in many cosmetics, from baby powder to blush[1][2].

Name: SAR-260301, CAS: 1260612-13-2, stock 26.9g, assay 99%, MWt: 354.40, Formula: C19H22N4O3, Solubility: DMSO : 125 mg/mL (352.71 mM; Need ultrasonic), Clinical_Informat: Phase 1, Pathway: PI3K/Akt/mTOR, Target: PI3K, Biological_Activity: SAR-260301 is an orally available and selective PI3Kβ inhibitor with an IC50 of 23 nM.
In Vitro: In the UACC-62 tumor cell line assay, SAR-260301 inhibits pAktS473 with a measured IC50 at 0.06 μM and an estimated IC90 at 2 μM[1]. In MEF-3T3-myr-p110β mechanistic model, SAR260301 inhibits PI3Kβ-dependent proliferation/viability in low serum conditions with an IC50 of 196 nM. In PTEN-deficient human prostate tumor cells, SAR260301 inhibits LNCaP cell proliferation in low and high serum conditions with IC50 values of 2.9 and 5.0 μM, respectively, after 4-day treatment, whereas it is inactive in these conditions in PC3 cells at concentrations up to 10 μM, despite target engagement. After prolonged treatment, SAR260301 at 3 or 10 μM inhibits PC3 cell proliferation in low serum conditions, with a cytostatic effect achieved for 14 days, despite some cell death induction observed at 10 μM. SAR260301 also leads to antitumor activities in PTEN-deficient/BRAF-mutant human melanoma cells, inhibiting cell proliferation with IC40 values of 6.5 and 3.3 μM for UACC-62 and WM-266.4, respectively, after 4-day treatment[2].
In Vivo: SAR-260301 displays antitumor efficacy in human PTEN-deficient melanoma models in mice as a single agent. SAR-260301 treatment leads to a statistically significant tumor growth inhibition as measured by a ΔT/ΔC of 39% (p = 0.054 versus control mice) on day 15 post-tumor implantation. SAR-260301 is well tolerated at the active dose, with no sign of toxicity and no body weight loss. Oral administration of SAR-260301 reveals sustained target inhibition (≥50%) of pAkt-S473 for at least 7 h. SAR-260301 has moderate terminal elimination half-life (t1/2=0.87 h, 1.4 h, 2.5 h, 0.87h, 6.9 h and 4.5 h for female SCID mice (3 mg/kg, iv), mice (10 mg/kg, po), mice (100 mg/kg, po), female nude rats (3 mg/kg, iv), rat (10 mg/kg, po), male beagle dogs (10 mg/kg, po))[1].

Name: (2S,4S)-Sacubitril, CAS: 149709-63-7, stock 39.8g, assay 98.2%, MWt: 411.49, Formula: C24H29NO5, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: (2S,4S)-Sacubitril is the impurity of Sacubitril. Sacubitril is approved by the Food and Drug Administration for use in combination with valsartan for the treatment of patients with heart failure.

Name: 2R,4R-Sacubitril, CAS: 766480-48-2, stock 5.2g, assay 98.3%, MWt: 411.49, Formula: C24H29NO5, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: 2R,4R-Sacubitril is the impurity of Sacubitril. Sacubitril is approved by the Food and Drug Administration for use in combination with valsartan for the treatment of patients with heart failure.

Name: MK-7246, CAS: 1218918-62-7, stock 11.8g, assay 98.3%, MWt: 416.47, Formula: C21H21FN2O4S, Solubility: DMSO : ≥ 250 mg/mL (600.28 mM), Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein, Target: Prostaglandin Receptor, Biological_Activity: MK-7246 is a potent and selective CRTH2 antagonist with a Ki of 2.5±0.5 nM.
IC50 & Target: Ki: 2.5±0.5 nM (CRTH2), 373±96 nM (Prostaglandin D, DP), 7668±2169 nM (Prostaglandin E2, EP2), 3804±1290 nM (TXA2,TP)[1]
In Vitro: The affinity and selectivity of MK-7246 for human CRTH2 and recombinant human prostanoid receptors is determined by equilibrium competition analysis using the relevant radioligands and cell membranes expressing the various receptors. MK-7246 competes for [3H]PGD2 specific binding to cell membranes expressing recombinant human CRTH2 with high-affinity (Ki, 2.5 nM). MK-7246 displays a relatively high selectivity for CRTH2 with an affinity 149-fold lower for the DP receptor (Ki, 373±96 nM) and ≥1500-fold lower for the other prostanoid receptors (Ki, 7668±2169 nM for EP2, 3804±1290 nM for TP). MK-7246 is also tested in a panel of 157 enzyme and receptor assays at concentrations up to 100 μM and small but significant activity is detected only on phosphodiesterase 1 (PDE1, IC50=33.2 μM) and MAPK3 (ERK1, IC50=49.4 μM)[1].
In Vivo: Whether the inhibition of a clinically-relevant mechanism of allergic lung inflammation such as CRTH2 will lead to a suppression of inflammatory responses is investigated in A. alternata challenged Brown Norway rats (n=8 per group). Mast cell derived production of Prostaglandin D2 (PGD2) is believed to be a prime mediator of allergic inflammation. Since CRTH2 plays an important role in the early aspects of the allergic inflammation cascade, the effect of the CRTH2 antagonist is examined on A. alternate elicited pulmonary inflammatory responses. CRTH2 inhibitor MK-7246 is orally administered 1 h before and 23 h post-intratracheal instillation of the A. alternata. MK-7246 produces a dose dependent decrease in the number of eosinophils with a maximal inhibition of 74±5% in the 100 mg/kg group (P<0.05), IL-5 (80±12%) and IL-13 (76±14%) cytokines levels (P<0.05) [2].

Name: Targapremir-210, CAS: 1049722-30-6, stock 39.8g, assay 98.2%, MWt: 592.69, Formula: C32H36N10O2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Epigenetics, Target: MicroRNA, Biological_Activity: Targapremir-210 is a potent miR-210 inhibitor with an IC50 of 200 nM in MDA-MB-231 cells. Targapremir-210 binds to the Dicer site of the miR-210 hairpin precursor. This interaction inhibits production of the mature miRNA.
IC50 & Target: IC50: 200 nM (miR-210, in MDA-MB-231 cells)[1].

Name: FTI 276, CAS: 170006-72-1, stock 12.2g, assay 98.3%, MWt: 433.59, Formula: C21H27N3O3S2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Farnesyl Transferase, Biological_Activity: FTI-276 is a protein farnesyl transferase (PFT) inhibitor with IC50s of 0.9 and 0.5 nM for Plasmodium falciparum and human.
IC50 & Target: IC50: 0.9 and 0.5 nM for Plasmodium falciparum and human[1].

Name: LY2119620, CAS: 886047-22-9, stock 11.7g, assay 98.8%, MWt: 437.94, Formula: C19H24ClN5O3S, Solubility: DMSO : 67.5 mg/mL (154.13 mM; Need ultrasonic); H2O : < 0.1 mg/mL (insoluble), Clinical_Informat: No Development Reported, Pathway: Neuronal Signaling;GPCR/G Protein, Target: mAChR;mAChR, Biological_Activity: LY2119620 is a high-affinity muscarinic M2/M4 receptor agonist.
IC50 & Target: M2/M4 receptor[1]
In Vitro: LY2119620 shows a modest allosteric agonism of 23.2±2.18% and 16.8±5.01% at the M2 and M4 receptors, respectively. Minimal allosteric agonism (<20%) is observed for LY2119620 at the M1, M3, and M5 receptors. The variable KB of LY2119620 for the allosteric binding site on the unoccupied receptor is found to be consistently about 1.9 to 3.4 µM. Results show a Bmax increase at the M2 receptor from 793±1.95 fmol/mg to 2850±162 fmol/mg upon addition of 10 µM LY2119620, and about a 5-fold increase in Bmax at the M4 receptor, 284±18.3 fmol/mg to 1340±42.2 fmol/mg[1].

Name: Enrofloxacin (monohydrochloride) BAY Vp 2674 (monohydrochloride);PD160788 (monohydrochloride), CAS: 93106-59-3, stock 0.5g, assay 98%, MWt: 395.86, Formula: C19H23ClFN3O3, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Anti-infection, Target: Bacterial, Biological_Activity: Enrofloxacin monohydrochloride (BAY Vp 2674 monohydrochloride) is an effective antibiotic with an MIC90 of 0.312 μg/mL for Mycoplasma bovis.
IC50 & Target: MIC90: 0.312 μg/mL ( Mycoplasma bovis)[1]
In Vitro: Mycoplasma bovis is a worldwide pathogen, causative agent of pneumonia, mastitis, arthritis, and a variety of other symptoms in cattle. The antibiotic susceptibility profiles of the Hungarian strains are consistent within the tested group of fluoroquinolones. Three isolates (MYC44, MYC45 and MYC46) have high MIC values (≥10 μg/mL) to Enrofloxacin, while the rest of the strains are inhibited by Enrofloxacin with MICs ≤0.312 or 0.625 μg/mL[1].
In Vivo: Mice (n=80) undergo transient middle cerebral artery occlusion (MCAo) with reperfusion after 60 minutes. After MCAo, animals are randomly assigned to receive either a daily preventive medication (n=26, Enrofloxacin) starting at the day of MCAo or a therapeutic medication (n=25; Enrofloxacin) after diagnosis of lung infection. Standard treatment started immediately after the appearance of clinical signs (general health score>6) usually between day 4 and 6 after stroke. Both, preventive and standard antibiotic treatment using Enrofloxacin improve survival in a similar way compared with placebo treatment[2].

Name: Sucralfate Sucrose octasulfate–aluminum complex, CAS: 54182-58-0, stock 0.3g, assay 98.5%, MWt: 2046.42, Formula: C12H14Al16O75S8, Solubility: H2O : 0.4 mg/mL (0.20 mM; ultrasonic and adjust pH to 2 with HCl), Clinical_Informat: Launched, Pathway: Anti-infection, Target: Bacterial, Biological_Activity: Sucralfate is a cytoprotective agent which has been employed for prevention and treatment of several gastrointestinal diseases.
In Vivo: Sucralfate is a cytoprotective agent which has been employed for prevention and treatment of several gastrointestinal diseases. Enemas containing Sucralfate improves the inflammation and increases the tissue contents of neutral and acid mucins. The content of neutral mucins does not change with the time or concentration of Sucralfate used, while acid mucins increases with concentration and time of intervention. A significant increase in tissue content of neutral mucins in animals subjected to irrigation with Sucralfate (SCF) is found compare to animals irrigated with S.F. 0.9%, regardless of the concentration and duration of intervention[1].

Name: L-Asparaginase L-ASNase, CAS: 9015-68-3, stock 21.7g, assay 98.5%, MWt: 1000, Formula: N/A, Solubility: 10 mM in DMSO, Clinical_Informat: Phase 4, Pathway: Others, Target: Others, Biological_Activity: L-Asparaginase (L-ASNase), a hydrolase that catalyzes the conversion of L-asparagine, used in acute lymphoblastic leukemia treatment. L-Asparaginase depletes L-asparagine from plasma resulting in inhibition of RNA and DNA synthesis with the subsequent blastic cell apoptosis[1].

Name: Urapidil, CAS: 34661-75-1, stock 7.8g, assay 98.8%, MWt: 387.48, Formula: C20H29N5O3, Solubility: H2O : < 0.1 mg/mL (insoluble); DMSO : 25 mg/mL (64.52 mM; Need ultrasonic), Clinical_Informat: Launched, Pathway: GPCR/G Protein;Neuronal Signaling;GPCR/G Protein;Neuronal Signaling, Target: Adrenergic Receptor;5-HT Receptor;5-HT Receptor;Adrenergic Receptor, Biological_Activity: Urapidil is an α1 adrenoreceptor antagonist and a 5-HT1A receptor agonist.
IC50 & Target: α1 adrenoreceptor, 5-HT1A receptor[1]
In Vitro: Urapidil is an α1 adrenoreceptor antagonist and a 5-HT1A receptor agonist. Urapidil does not affect vascular tone at concentrations up to 10-5 M. Urapidil (10-5 M) markedly inhibits the alpha 1-adrenergic agonist (phenylephrine)-induced concentration-dependent contractions in aortic rings without endothelium and also to some extent in those with endothelium. Moreover, the inhibitory effect of Urapidil is more pronounced in rings without endothelium than in those with endothelium. Urapidil (10-5 M) affects neither the vascular tone nor the concentration-dependent contraction to serotonin[1].

Name: Deapioplatycodin D, CAS: 78763-58-3, stock 0.4g, assay 98.8%, MWt: 1093.21, Formula: C52H84O24, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Anti-infection, Target: HCV, Biological_Activity: Deapioplatycodin D is a triterpenoid saponin isolated from Platycodon grandiflorum, with anti-HCV activity[1].

Name: Dehydrodiisoeugenol, CAS: 2680-81-1, stock 38.2g, assay 98.7%, MWt: 326.39, Formula: C20H22O4, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Immunology/Inflammation;NF-κB, Target: COX;NF-κB, Biological_Activity: Dehydrodiisoeugenol is isolated from Myristica fragrans Houtt, shows anti-inflammatory and anti-bacterial actions[1]. Dehydrodiisoeugenol inhibits LPS- stimulated NF-κB activation and cyclooxygenase (COX)-2 gene expression in murine macrophages[2].
IC50 & Target: NF-κB; COX-2[2]

Name: Demethyleneberberine, CAS: 25459-91-0, stock 21.3g, assay 98.7%, MWt: 324.35, Formula: C19H18NO4+, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Epigenetics;PI3K/Akt/mTOR;NF-κB, Target: AMPK;AMPK;NF-κB, Biological_Activity: Demethyleneberberine is a natural mitochondria-targeted antioxidant. Demethyleneberberine alleviates mice colitis and inhibits the inflammatory responses by inhibiting NF-κB pathway and regulating the balance of Th cells. Demethyleneberberine could serve as a AMPK activator for treating non-alcoholic fatty liver disease (NAFLD)[1][2][3].

Name: Deacetylasperulosidic Acid, CAS: 14259-55-3, stock 12.6g, assay 98.8%, MWt: 390.34, Formula: C16H22O11, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Immunology/Inflammation, Target: Interleukin Related, Biological_Activity: Deacetylasperulosidic acid (DAA) is a major phytochemical constituent of Morinda citrifolia fruit. Deacetylasperulosidic acidhas antioxidant activity by increasing superoxide dismutase activity. Deacetylasperulosidic acid has anticlastogenic activity, suppressing the induction of chromosome aberrations in hamster ovary cells and mice[1]. Deacetylasperulosidic acid prevents 4-nitroquinoline 1-oxide (4NQO) induced DNA damage in vitro, suppresses IL-2 production along with the activation of natural killer cells[2].

Name: Ginsenoside F2, CAS: 62025-49-4, stock 26g, assay 98.4%, MWt: 785.01, Formula: C42H72O13, Solubility: , Clinical_Informat: No Development Reported, Pathway: Apoptosis;Autophagy, Target: Apoptosis;Autophagy, Biological_Activity: Ginsenoside F2, a metabolite from Ginsenoside Rb1, induces apoptosis accompanied by protective autophagy in breast cancer stem cells[1].

Name: Ginsenoside F3, CAS: 62025-50-7, stock 5.4g, assay 98.1%, MWt: 770.99, Formula: C41H70O13, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Immunology/Inflammation, Target: Interleukin Related, Biological_Activity: Ginsenoside F3, a component of PPTGs (an minor saponin in the leaves of Panax ginseng), has immunoenhancing activity by regulating production and gene expression of type 1 cytokines (IL-2, IFN-gamma) and type 2 cytokines (IL-4 and IL-10)[1].

Name: trans-Cinnamic acid trans-3-Phenylacrylic acid, CAS: 140-10-3, stock 20.5g, assay 98.8%, MWt: 148.16, Formula: C9H8O2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Anti-infection, Target: Bacterial, Biological_Activity: trans-Cinnamic acid is a natural antimicrobial, with minimal inhibitory concentration (MIC) of 250 μg/mL against fish pathogen A. sobria, SY-AS1[1].
IC50 & Target: Bacterial[1]
In Vitro: trans-Cinnamic acid is an antimicrobial activity, with minimal inhibitory concentration (MIC) of 250 μg/mL against fish pathogen A. sobria, SY-AS1. trans-cinnamic acid shows moderate inhibition on the rainbow trout intestinal isolates A. sobria SY-AS3 and S. baltica, SY-S145, gill isolate F. spartansii SY-FS1 and fish pathogens A. salmonicida ATCC 33658, Listonella anguillarum, SY-L24, V. crassostreae SY-VC10 and Y. ruckeri E42. trans-cinnamic acid is more effective on bacteria when the pH of the culture media is not neutralized[1].

Name: Trifolirhizin, CAS: 6807-83-6, stock 3.3g, assay 98.9%, MWt: 446.40, Formula: C22H22O10, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Tyrosinase, Biological_Activity: Trifolirhizin is a pterocarpan flavonoid isolated from the roots of Sophora flavescens. Trifolirhizin possesses potent tyrosinase inhibitory activity with an IC50 of 506 μM[1]. Trifolirhizin exhibits potential anti-inflammatory and anticancer activities[2].
IC50 & Target: IC50: 506 μM (tyrosinase)[1]

Name: Sanggenon D, CAS: 81422-93-7, stock 14.8g, assay 98%, MWt: 708.71, Formula: C40H36O12, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Sanggenon D is a Diels-Alder-type adduct from Chinese crude drug root bark of Morus cathayana. Sanggenon D possesses antioxidant and inhibits Pancreatic lipase (PL) with the an IC50 of 0.77 μM[1].

Name: Mulberroside C, CAS: 102841-43-0, stock 28.7g, assay 98.4%, MWt: 458.46, Formula: C24H26O9, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Anti-infection, Target: HCV, Biological_Activity: Mulberroside C is one of the main bioactive constituents in mulberry (Morus alba L.)[1]. Mulberroside C is a HCV replicon inhibitor. Antiviral activity[2].

Name: Kaempferitrin Lespedin;Lespenephryl, CAS: 482-38-2, stock 26.5g, assay 98.2%, MWt: 578.52, Formula: C27H30O14, Solubility: DMSO : 125 mg/mL (216.07 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Protein Tyrosine Kinase/RTK, Target: Insulin Receptor, Biological_Activity: Kaempferitrin is a natural flavonoid, possesses antinociceptive, anti-inflammatory, anti-diabetic, antitumoral and chemopreventive effects, and activates insulin signaling pathway.
IC50 & Target: Insulin Receptor[1]
In Vitro: Kaempferitrin activates insulin signaling pathway. Kaempferitrin causes survival rates higher than 90% at 1-20 μM in matured 3T3-L1 adipocyte, and the survival rates decline rapidly at 25 and 50 μM. Kaempferitrin (15 μM) increases insulin receptor beta tyrosine phosphorylation and tyrosine phosphorylation of the insulin receptor substrate 1, and such effects are similar to that of 10 nM insulin. Kaempferitrin (15 μM) also stimulates akt phosphorylation on ser473, and the stimulation can be blocked by a PI3-K inhibitor wortmannin. Kaempferitrin potently exerts the translocation of GLUT4 to the membrane of adipocytes at 15 μM, and this is suppressed by wortmannin. In addition, Kaempferitrin increases the total levels of Glu4 protein in differentiated cells and secreted adiponectin in mature 3T3-L1 adipocytes[1]. Kaempferitrin is cytotoxic to human cancer cells such as HeLa and MDA-MB231 cells, with IC50s of 45 ± 2.6 and 65 ± 2.6 μM, and shows low toxic effects on non-tumorigenic cells. Kaempferitrin (45 μM) induces apoptosis of HeLa cells after treatment for 24 and 48 h, and causes reactive oxygen species (ROS) generation in HeLa cells. Furthermore, Kaempferitrin (45 μM) exerts G1 arrest, causes the expression of proteins associated with intrinsic pathway of apoptosis and activates caspase 3 in HeLa cells[2].
In Vivo: Kaempferitrin (2.5, 10 and 25 mg/kg, i.p.) markedly suppresses the growth of tumor by 40%, 87% and 97%, and decreases tumor weight by 37%, 81% and 95%, respectively in nu/nu mice bearing HeLa tumor. Kaempferitrin also inhibits cell proliferation and extends life span in mice bearing tumor[2].

Name: Cornuside, CAS: 131189-57-6, stock 31.2g, assay 98%, MWt: 542.49, Formula: C24H30O14, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: MAPK/ERK Pathway;NF-κB, Target: p38 MAPK;NF-κB, Biological_Activity: Cornuside is a secoiridoid glucoside isolated from the fruit of Cornus officinalis Sieb. et Zucc., which is a traditional oriental medicine for treating inflammatory diseases and invigorating blood circulation. Cornuside inhibits mast cell-mediated allergic response by down-regulating MAPK and NF-κB signaling pathways. Cornuside has anti-allergic effects in vivo and in vitro which suggests a therapeutic application of this agent in inflammatory allergic diseases[1].

Name: Esculentoside A, CAS: 65497-07-6, stock 36.9g, assay 98.7%, MWt: 826.96, Formula: C42H66O16, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Immunology/Inflammation;NF-κB, Target: COX;NF-κB, Biological_Activity: Esculentoside A (EsA), a kind of triterpene saponin isolated from roots of Phytolacca esculenta[1].
Esculentoside A (EsA) possesses anti-inflammatory activity in acute and chronic experimental models[2], has selective inhibitory activity towards cyclooxygenase-2 (COX-2)[1].
Esculentoside A (EsA) suppresses inflammatory responses in LPS-induced acute lung injury (ALI) through inhibition of the nuclear factor kappa B (NF-ΚB) and mitogen activated protein kinase (MAPK) signaling pathways[3].
In Vitro: Esculentoside A (0-10 μM; 24 hours) reduced the release of TNF concentration in primed macrophages [4].
In Vivo: Esculentoside A (EsA) (intraperitoneal injection; 20 mg/kg; once a day; 4 weeks) plays significant roles in the treatment of BXSB mice through modulation of inflammatory cytokines, inhibition of renal cell proliferation and induction of apoptosis [2].
Esculentoside A (EsA) (injected intraperitoneally; 5, 10 and 20 mg/kg; once a day; 7 days) dose-dependently decreases the TNF, IL-1 and IL-6 levels in the sera of mice following LPS challenge[4].

Name: Methoxyflurane, CAS: 76-38-0, stock 15g, assay 98.5%, MWt: 164.97, Formula: C3H4Cl2F2O, Solubility: 10 mM in DMSO, Clinical_Informat: Launched, Pathway: Others, Target: Others, Biological_Activity: Methoxyflurane is a halogenated volatile anaesthetic agent with potent analgesic effects at sub-anaesthetic doses. Methoxyflurane widely used as an open-circuit anaesthetic in small laboratory animals for several decades. Methoxyflurane has the risk of nephrotoxicity[1][2].
In Vitro: Methoxyflurane is delivered via a hand-held inhaler[3].
In Vivo: The developmental toxicity of trace, subanesthetic, and anesthetic exposure to Methoxyflurane is examined in Swiss/ICR mice. No adverse effects on reproduction or fetal development were demonstrated following exposure to trace (2 ppm) and subanesthetic (60 ppm) concentrations of Methoxyflurane for 4 hours daily on days 6 through 15 of pregnancy. Exposure to an anesthetic concentration (2000 ppm; 0.2%) for the same period resulted in decreased fetal weight, decreased ossification, and delayed renal maturation. Additionally, the incidence of minor skeletal anomalies was increased. It is concluded that gestational exposure of mice to trace of subanesthetic concentrations of Methoxyflurane does not result in reproductive loss or morphologic abnormalities in their offspring[4].

Name: Revaprazan (hydrochloride), CAS: 178307-42-1, stock 7.4g, assay 98.9%, MWt: 398.90, Formula: C22H24ClFN4, Solubility: DMSO : 8.33 mg/mL (20.88 mM; Need ultrasonic), Clinical_Informat: Launched, Pathway: Immunology/Inflammation;Anti-infection, Target: COX;Bacterial, Biological_Activity: Revaprazan hydrochloride is a novel acid pump antagonist (APA). Revaprazan hydrochloride reduces COX-2 expression and has significant anti-inflammatory actions activities in H. pylori infection[1].
IC50 & Target: Acid pump; COX-2[1]

Name: Citicoline cytidine diphosphate-choline;CDP-Choline;cytidine 5'-diphosphocholine, CAS: 987-78-0, stock 33.8g, assay 98.3%, MWt: 488.32, Formula: C14H26N4O11P2, Solubility: H2O : ≥ 103.33 mg/mL (211.60 mM), Clinical_Informat: Launched, Pathway: Others, Target: Others, Biological_Activity: Citicoline is an intermediate in the synthesis of phosphatidylcholine, a component of cell membranes. Citicoline exerts neuroprotective effects.
In Vitro: To determine the potential neuroprotective activity of Citicoline and Homotaurine, treated retinal cells are treated with increasing concentrations of Citicoline or Homotaurine for 24 hours. 1 μM, 10 μM and 100 μM of Citicoline or Homotaurine are used to investigate whether may contribute to a reduced cell viability in retinal cells. Retinal cells are well preserved in Citicoline- or Homotaurine-treated cultures, with no evidence of toxicity or significant loss of viability after treatments. 100 μM of Citicoline is not harmful to retinal neuroglial cells in vitro and 100 μM of Homotaurine is an effective concentration to enhance neuroprotection in a model of experimental glaucoma. Therefore, this concentration of Citicoline and Homotaurine is used for all subsequent experiments. To evaluate whether cotreatment with Citicoline and Homotaurine is able to induce a synergistic neuroprotective effect against glutamate excitotoxicity, retinal cell cultures are exposed to Citicoline 100 μM, Homotaurine 100 μM, and Citicoline+Homotaurine 100 μM, 24 hours before glutamate treatment. In the presence of 100 μM Citicoline, a significant increase in cell viability is observed[1].
In Vivo: Administration of Citicoline in a dose of 1000 mg/kg produces more pronounced increase in the threshold of clonic seizures and tonic phase of seizures with lethal outcome (by 18.54 and 50.08% respectively, in comparison with the control). The anticonvulsant effect is most pronounced after injection of Citicoline in a dose of 1000 mg/kg[2].

Name: Pipecuronium (bromide), CAS: 52212-02-9, stock 39.4g, assay 98.7%, MWt: 762.70, Formula: C35H62Br2N4O4, Solubility: 10 mM in DMSO, Clinical_Informat: Launched, Pathway: Neuronal Signaling;Membrane Transporter/Ion Channel, Target: nAChR;nAChR, Biological_Activity: Pipecuronium bromide is a potent long-acting nondepolarizing steroidal neuromuscular blocking agent (NMBA), and a bisquaternary ammonium compound. Pipecuronium bromide is a powerful competitive nAChR antagonist with a Kd of 3.06 μM[1][2][3][4][5].
IC50 & Target: nAChR[4][5]
In Vitro: Sugammadex has a high affinity for Pipecuronium bromide. As Pipecuronium bromide is about 6 to 7 times more potent than Rocuronium, fewer molecules are required to achieve a comparative blockade than in the case of Rocuronium[1].
In Vivo: The average ED95 is 0.045mg/kg (0.035-0.059 mg/kg) of Pipecuronium bromide, the onset of action varies between 2 and 6.3 minutes, depending on the dose and the background anesthesia. Pipecuronium bromide does not liberate histamine, it has no cardiovascular side effects even in doses of 3× ED95, and anaphylaxis does not appear to be a problem[2]. 
Carboxymethylated γ-cyclodextrin shows efficient and complete reversal of the Pipecuronium bromide induced neuromuscular block in an ex vivo rat diaphragm experiment[3].

Name: Eriocitrin, CAS: 13463-28-0, stock 11.2g, assay 98.7%, MWt: 596.53, Formula: C27H32O15, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Apoptosis, Target: Apoptosis, Biological_Activity: Eriocitrin is a flavonoid isolated from lemon, which is a strong antioxidant agent. Eriocitrin could inhibit the proliferation of hepatocellular carcinoma cell lines by arresting cell cycle in S phase through up-regulation of p53, cyclin A, cyclin D3 and CDK6. Eriocitrin triggers apoptosis by activating mitochondria-involved intrinsic signaling pathway[1].

Name: Eriodictyol Huazhongilexone, CAS: 552-58-9, stock 2.8g, assay 98.1%, MWt: 288.25, Formula: C15H12O6, Solubility: H2O : < 0.1 mg/mL (insoluble); DMSO : 155 mg/mL (537.73 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: NF-κB;Metabolic Enzyme/Protease, Target: Keap1-Nrf2;Endogenous Metabolite, Biological_Activity: Eriodictyol is a flavonoid isolated from the Chinese herb, with antioxidant and anti-inflammatory activity. Eriodictyol induces Nrf2 signaling pathway.
IC50 & Target: Nrf2[1]
In Vitro: Eriodictyol is a flavonoid isolated from the Chinese herb, with antioxidant and anti-inflammatory activity[1]. Eriodictyol (20, 40, 80 μM) protects primary cultured cortical neurons against Aβ25-35-induced cytotoxicity and cell apoptosis via the Nrf2/ARE pathway. Eriodictyol (80 μM) induces nuclear expression of Nrf2 and the expression of ARE-regulated genes in primary cultured cortical neurons[2].
In Vivo: Eriodictyol shows protective effect against LPS-induced acute lung injury (ALI). Eriodictyol (30 mg/kg, p.o.) decreases the production of inflammatory cytokines, elevates survival rate, and decreases oxidative stress levels in LPS-induced ALI mice. Eriodictyol inhibits MPO activity and inflammatory neutrophil accumulation in the lung tissues. Eriodictyol treatment also enhances Trx1 expression by upregulating the Nrf2 expression in lung tissues[1].

Name: Dendrobine, CAS: 2115-91-5, stock 9.8g, assay 98.8%, MWt: 263.38, Formula: C16H25NO2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Anti-infection, Target: Influenza Virus, Biological_Activity: Dendrobine is an alkaloid isolated from Dendrobium nobile. Dendrobine possesses antiviral activity against influenza A viruses, with IC50s of 3.39 μM, 2.16 μM and 5.32 μM for A/FM-1/1/47 (H1N1), A/Puerto Rico/8/34 H274Y (H1N1) and A/Aichi/2/68 (H3N2), respectively[1].
IC50 & Target: IC50: 3.39 μM (A/FM-1/1/47), 2.16 μM (A/Puerto Rico/8/34 H274Y), 5.32 μM (A/Aichi/2/68)[1]

Name: Carnosol, CAS: 5957-80-2, stock 36.7g, assay 98.5%, MWt: 330.42, Formula: C20H26O4, Solubility: DMSO : ≥ 125 mg/mL (378.31 mM), Clinical_Informat: No Development Reported, Pathway: MAPK/ERK Pathway, Target: Ribosomal S6 Kinase (RSK), Biological_Activity: Carnosol is a potent Ribosomal S6 Kinase (RSK2) inhibitor that could be useful for treating gastric cancer, with an IC50 of ~5.5 μM.
IC50 & Target: IC50: 5.5 μM (RSK2)[1].
In Vitro: It is showed that carnosol has no cytotoxic effects on GES1 cells and 10 μM carnosol strongly suppresses RSK2 activity, but has little effect on any other kinase. Carnosol exerts strong dose-dependent inhibitory effects against RSK2 autophosphorylation and phosphorylation of its substrate ATF1[1].
In Vivo: Results indicate that Carnosol significantly decreaseS the volume and weight of gastric tumors relative to the vehicle-treated group. Additionally, mice tolerate treatment with carnosol without significant loss of body weight similar to the vehicle-treated group. The phosphorylation of CREB, a direct downstream protein of RSK2, Is strongly inhibited in the carnosol-treated group but the expression of total CREB is relatively unchanged[1].

Name: Carnosic acid, CAS: 3650-09-7, stock 12.3g, assay 98.9%, MWt: 332.43, Formula: C20H28O4, Solubility: DMSO : 130 mg/mL (391.06 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Apoptosis;Anti-infection, Target: Apoptosis;Bacterial, Biological_Activity: Carnosic acid has demonstrated inhibition of oxidative stress and inflammation, suppression of cell proliferation, and antibacterial activity.
In Vitro: Carnosic acid, a phenolic diterpene, is enriched in the leaves of Lamiaceae plants, and is particularly high in dried leaves of Rosmarinus officinalis L. and Salvia officinalis. Carnosic acid has demonstrated inhibition of oxidative stress and inflammation, suppression of cell proliferation, and antibacterial activity. It is widely reported that Carnosic acid has a therapeutic potential in different types of cancer, mostly based on in vitro experiments. Carnosic acid has also shown neuroprotective effects in experimental models of neurodegenerative diseases, mainly through activation of the antioxidant NRF2/ARE pathway[1].

Name: Silydianin, CAS: 29782-68-1, stock 9.5g, assay 98.3%, MWt: 482.44, Formula: C25H22O10, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Phosphatase, Biological_Activity: Silydianin is an active constituent of Silybium marianum, with exhibit anti-collagenase, antitumor and anti-elastase activities. Silydianin is a natural protein tyrosine phosphatase 1B (PTP1B) with an IC50 of 17.38 μM. Silydianin has inhibitory effect on the in vitro production and release of oxidative products[1][2][3].

Name: Silychristin, CAS: 33889-69-9, stock 12.4g, assay 98.9%, MWt: 482.44, Formula: C25H22O10, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Silychristin is an abundant flavonolignan present in the fruits of Silybum marianum, with antioxidant properties. Silychristin is a potent inhibitor of the thyroid hormone transporter MCT8, and elicits a strong inhibition of T3 uptake with an IC50 of 110 nM[1][2].
IC50 & Target: MCT8[2]
In Vitro: Silychristin exhibits a strong inhibition of MCT8-mediated T3 uptake with an IC50 of 110 nM in MCT8 overexpressing MDCK1-cells[2]. 
Silychristin causes no cytotoxic for fibroblasts[3]. 
Silychristin (6.5-75 μM; 24 hours) diminishes UVA toxicity and reduces ROS generation, and the protective effect is dose-dependent[3]. 
Silychristin (12.5μM, 25μM) reduces the metalloproteinase-1 (MMP-1) level in cells[3].

Name: Corypalmine, CAS: 27313-86-6, stock 0.6g, assay 98.3%, MWt: 341.40, Formula: C20H23NO4, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Anti-infection, Target: Fungal, Biological_Activity: Corypalmine is an alkaloid from Corydalis chaerophylla. Corypalmine is an antifungal.

Name: D-Pinitol 3-O-Methyl-D-chiro-inositol, CAS: 10284-63-6, stock 25.4g, assay 98.9%, MWt: 194.18, Formula: C7H14O6, Solubility: DMSO : 125 mg/mL (643.73 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: D-pinitol (3-O-Methyl-D-chiro-inositol) is a natural compound presented in several plants, like Pinaceae and Leguminosae plants. D-pinitol exerts hypoglycemic activity and protective effects in the cardiovascular system[1][2].
In Vitro: D-pinitol promotes apoptosis in MCF-7 cells via induction of p53 and Bax and inhibition of Bcl-2 and NF-κB[3].

Name: Alliin, CAS: 556-27-4, stock 3.7g, assay 98.3%, MWt: 177.22, Formula: C6H11NO3S, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Alliin, an orally active sulfoxide compound derived from garlic, exhibits hypoglycemic, antioxidant and anti-inflammatory activities[1][2].

Name: L-Aspartic acid, CAS: 56-84-8, stock 33g, assay 98.3%, MWt: 133.10, Formula: C4H7NO4, Solubility: H2O : 8.33 mg/mL (62.58 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: L-Aspartic acid is is an amino acid, shown to be a suitable prodrug for colon-specific drug deliverly.
In Vivo: L-Aspartic acid is shown to be a suitable prodrug for colon-specific drug deliverly[1]. L-[3H]Asp remaining in the brain at 5 min is increased by 206 and 178% by preadministration of 100 mM L-Aspartic acid and 100 mM L-Glu, respectively, whereas 100 mM D-Asp does not affect L-[3H]Asp efflux transport. That value for L-[3H]Glu at 20 min is increased by 145 and 156% by coadministration with 100 mM L-Aspartic acid and 100 mM L-Glu, respectively, but not by D-Asp. It is interesting that the apparent efflux rate of L-Aspartic acid across the BBB is sevenfold faster than that of L-Glu[2].

Name: L-Asparagine (-)-Asparagine; Asn; Asparamide, CAS: 70-47-3, stock 20.7g, assay 98.5%, MWt: 132.12, Formula: C4H8N2O3, Solubility: H2O : 6.67 mg/mL (50.48 mM; Need ultrasonic), Clinical_Informat: Launched, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: L-Asparagine is a non-essential amino acid that is involved in the metabolic control of cell functions in nerve and brain tissue.

Name: Pseudolaric Acid C, CAS: 82601-41-0, stock 37.8g, assay 98.6%, MWt: 390.43, Formula: C21H26O7, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Anti-infection, Target: Fungal, Biological_Activity: Pseudolaric C is a diterpenoid isolated from the root bark of Pseudolarix kaempferi Gorden, has antifungal activity[1].

Name: Pseudolaric Acid A, CAS: 82508-32-5, stock 31.4g, assay 98.5%, MWt: 388.45, Formula: C22H28O6, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Anti-infection, Target: Fungal, Biological_Activity: Pseudolaric Acid A is a diterpene acid isolated from Pseudolarix kaempferi, has antifungal, cytotoxic and antifertile activities[1][2][3].

Name: Pseudolaric Acid B, CAS: 82508-31-4, stock 37.2g, assay 99%, MWt: 432.46, Formula: C23H28O8, Solubility: DMSO : ≥ 125 mg/mL (289.04 mM), Clinical_Informat: No Development Reported, Pathway: Anti-infection;Anti-infection;Apoptosis;Autophagy;Apoptosis, Target: Fungal;HBV;Apoptosis;Autophagy;Ferroptosis, Biological_Activity: Pseudolaric Acid B is a diterpene isolated from the root of Pseudolarix kaempferi Gorden (pinaceae), has anti-cancer, antifungal, and antifertile activities, and shows immunosuppressive activity on T lymphocytes[1][2][3]. Pseudolaric Acid B inhibits hepatitis B virus (HBV) secretion through apoptosis and cell cycle arrest. Pseudolaric Acid B induces autophagy[4][5].

Name: Dehydroandrographolide succinate, CAS: 786593-06-4, stock 17.5g, assay 98.7%, MWt: 532.58, Formula: C28H36O10, Solubility: DMSO : 250 mg/mL (469.41 mM; Need ultrasonic), Clinical_Informat: Launched, Pathway: Others, Target: Others, Biological_Activity: Dehydroandrographolide succinate, extracted from herbal medicine Andrographis paniculata (Burm f) Nees, is widely used for the treatment of viral pneumonia and viral upper respiratory tract infections because of its immunostimulatory, anti-infective and anti-inflammatory effect[1].

Name: Pseudoprotodioscin, CAS: 102115-79-7, stock 34.4g, assay 98.8%, MWt: 1031.18, Formula: C51H82O21, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Epigenetics;Metabolic Enzyme/Protease, Target: MicroRNA;Fatty Acid Synthase (FAS), Biological_Activity: Pseudoprotodioscin, a furostanoside, inhibits SREBP1/2 and microRNA 33a/b levels and reduces the gene expression regarding the synthesis of cholesterol and triglycerides[1].
In Vitro: In Hep G2 cells, Pseudoprotodioscin increases ABCA1 protein and mRNA levels, and promotes the effluxion of ApoA-1-mediated cholesterol. Pseudoprotodioscin inhibits SREBP1c and SREBP2 transcription by decreasing microRNA 33a/b levels. This procedure reciprocally lead to the increase of ABCA1 levels. In THP-1 macrophages, Pseudoprotodioscin shows the similar effect, which reduces HMGCR, FAS and ACC mRNA levels and promotes low density lipoprotein receptor by decreasing the PCSK9 levels[1].

Name: Crocin, CAS: 42553-65-1, stock 19.6g, assay 98.3%, MWt: 976.96, Formula: C44H64O24, Solubility: 10 mM in DMSO, Clinical_Informat: Launched, Pathway: Others, Target: Others, Biological_Activity: Crocin is a nutraceutical and the main constituent isolated from the stigmas of Crocus sativus with immense pharmacological properties as anti-inflammatory, anticancer, antidepressant and anticonvulsant[1].

Name: Crocin II, CAS: 55750-84-0, stock 18.6g, assay 98.4%, MWt: 814.82, Formula: C38H54O19, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Immunology/Inflammation;Immunology/Inflammation, Target: COX;NO Synthase, Biological_Activity: Crocin II is isolated from the fruit of Gardenia jasminoides with antioxidant, anticancer, and antidepressant activity.
Crocin II inhibits NO production with an IC50 value of 31.1 μM.
Crocin II suppresses the expressions of protein and m-RNA of iNOS and COX-2[1].
IC50 & Target: IC50: 31.3 μM (NO production)[1]

Name: Daphnoretin Dephnoretin;Thymelol, CAS: 2034-69-7, stock 4.3g, assay 98.6%, MWt: 352.29, Formula: C19H12O7, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: TGF-beta/Smad;Epigenetics, Target: PKC;PKC, Biological_Activity: Daphnoretin (Dephnoretin), isolated from Wikstroemia indica, possesses antiviral activity[1]. Daphnoretin likes PMA, may direct activation of protein kinase C which in turn activated NADPH oxidase and elicited respiratory burst[2].

Name: (-)-Asarinin, CAS: 133-04-0, stock 12.1g, assay 98.8%, MWt: 354.35, Formula: C20H18O6, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: (-)-Asarinin is a extract lignan from Zanthoxylum armatum, mainly produced in roots of this herb[1].

Name: Schaftoside, CAS: 51938-32-0, stock 3.5g, assay 98%, MWt: 564.49, Formula: C26H28O14, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Cytoskeleton;Immunology/Inflammation;Autophagy;Immunology/Inflammation;Metabolic Enzyme/Protease, Target: Dynamin;MyD88;Autophagy;Toll-like Receptor (TLR);Mitochondrial Metabolism, Biological_Activity: Schaftoside is a flavonoid found in a variety of Chinese herbal medicines, such as Eleusine indica. Schaftoside inhibits the expression of TLR4 and Myd88. Schaftoside also decreases Drp1 expression and phosphorylation, and reduces mitochondrial fission[1].
In Vitro: Schaftoside inhibits three pro-inflammatory enzymatic activities: secretory phospholipase A2 (sPLA2), lipoxygenase (LOX), and cyclooxygenase 2 (COX-2). Schaftoside also inhibits mRNA and protein expressions of proinflammatory cytokines(IL-1β, TNF-α, and IL-6)[1].

Name: Agrimol B, CAS: 55576-66-4, stock 0.7g, assay 98.5%, MWt: 682.75, Formula: C37H46O12, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Cell Cycle/DNA Damage;Epigenetics;Cell Cycle/DNA Damage, Target: PPAR;Sirtuin;Sirtuin, Biological_Activity: Agrimol B is a polyphenol derived from Agrimonia pilosa Ledeb, suppresses adipogenesis via inducing SIRT1 translocation and expression, and reducing PPARγ expression[1].

Name: Curculigoside, CAS: 85643-19-2, stock 37.5g, assay 98.8%, MWt: 466.44, Formula: C22H26O11, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Epigenetics;Stem Cell/Wnt;JAK/STAT Signaling;JAK/STAT Signaling;Stem Cell/Wnt;NF-κB, Target: JAK;JAK;JAK;STAT;STAT;NF-κB, Biological_Activity: Curculigoside is the main saponin in C. orchioide, exerts significant antioxidant, anti-osteoporosis, antidepressant and neuroprotection effects. Curculigoside possesses significant anti-arthritic effects in vivo and in vitro via regulation of the JAK/STAT/NF-κB signaling pathway[1].
IC50 & Target: JAK; STAT; NF-κB[1]
In Vitro: Curculigoside (1-64 μg/ml; 72 hours) exerts significant inhibitory effects on MH7A cell viability between 1 and 64 µg/ml in MH7A cells[1].
Curculigoside (4-16 μg/ml; 24 hours) decreases the protein expression of JAK1, JAK3 and STAT3 compared to the TNF-α group[1].

Name: (R)-Apremilast (R)-CC-10004, CAS: 608141-44-2, stock 2.3g, assay 98.9%, MWt: 460.50, Formula: C22H24N2O7S, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: (R)-Apremilast ((R)-CC-10004) is a enantiomer of Apremilast[1].

Name: Vanillic acid, CAS: 121-34-6, stock 23.1g, assay 98.4%, MWt: 168.15, Formula: C8H8O4, Solubility: DMSO : ≥ 100 mg/mL (594.71 mM), Clinical_Informat: No Development Reported, Pathway: Anti-infection;NF-κB, Target: Bacterial;NF-κB, Biological_Activity: Vanillic acid is a flavoring agent found in edible plants and fruits. Vanillic acid inhibits NF-κB activation. Anti-inflammatory, antibacterial, and chemopreventive effects[1].
In Vitro: Vanillic acid is non-toxic to HT22 cells at all three concentrations (50, 100 and 200 μM); Vanillic acid co-treatment with Aβ1-42 significantly increases (1.5-, 1.9- and 2-fold respectively) cell viability[2]. 
In Vivo: Vanillic acid (3-30 mg/kg; i.p.; 5 hours) inhibits Carrageenan-induced mechanical hyperalgesia, paw edema, and neutrophil and macrophage recruitment[1].

Name: Carvacrol, CAS: 499-75-2, stock 34.3g, assay 98.5%, MWt: 150.22, Formula: C10H14O, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Anti-infection;Apoptosis;Stem Cell/Wnt;Neuronal Signaling, Target: Fungal;Apoptosis;Notch;Notch, Biological_Activity: Carvacrol is a monoterpenoid phenol isolated from Lamiaceae family plants, with antioxidant, anti-inflammatory and anticancer properties. Carvacrol causes cell cycle arrest in G0/G1, downregulates Notch-1, and Jagged-1, and induces apoptosis[1].

Name: Typhaneoside, CAS: 104472-68-6, stock 25g, assay 98.1%, MWt: 770.69, Formula: C34H42O20, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Autophagy, Target: Autophagy, Biological_Activity: Typhaneoside, extracted from Typha angustifolia L., Typhaneoside can inhibit the excessive autophagy of hypoxia/reoxygenation cells and increase the phosphorylation of Akt and mTOR. Typhaneoside has certain effects on the cardiovascular system, including lowering blood lipid levels, promoting antiatherosclerosis activities, as well as improving immune and coagulation function[1].

Name: Diosmetin-7-O-β-D-glucopyranoside, CAS: 20126-59-4, stock 6.7g, assay 98.8%, MWt: 462.40, Formula: C22H22O11, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Diosmetin-7-O-β-D-glucopyranoside is a natural product isolated from the flowers of Chrysanthemum morifolium, with antioxidant activity[1][2].

Name: Berbamine, CAS: 478-61-5, stock 36.5g, assay 98.9%, MWt: 608.72, Formula: C37H40N2O6, Solubility: 10 mM in DMSO, Clinical_Informat: Launched, Pathway: Autophagy;NF-κB, Target: Autophagy;NF-κB, Biological_Activity: Berbamine is a natural compound extracted from traditional Chinese medicine Barberry with anti-tumor, immunomodulatory and cardiovascular effects. Berbamine is a calcium channel blocker.

Name: Berberrubine (chloride), CAS: 15401-69-1, stock 23.3g, assay 98.6%, MWt: 357.79, Formula: C19H16ClNO4, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Berberrubine chloride is an active metabolite of berberine, attenuates ulcerative colitis in mice model[1].

Name: Berberine Natural Yellow 18, CAS: 2086-83-1, stock 0.9g, assay 98.5%, MWt: 336.36, Formula: C20H18NO4+, Solubility: 10 mM in DMSO, Clinical_Informat: Launched, 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 (Natural Yellow 18) is an alkaloid isolated from the Chinese herbal medicine Huanglian, as an antibiotic. Berberine (Natural Yellow 18) induces reactive oxygen species (ROS) generation and inhibits DNA topoisomerase. Berberine (Natural Yellow 18) has antineoplastic properties[1].
IC50 & Target: ROS[1] 
DNA topoisomerase[1]
In Vitro: Berberine (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 (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 (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 (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 (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: Fargesin, CAS: 31008-19-2, stock 24.5g, assay 98.4%, MWt: 370.40, Formula: C21H22O6, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Fargesin is a bioactive neolignan isolated from magnolia plants，with antihypertensive and anti-inflammatory effects[1][2][3].
In Vitro: Fargesin exhibits anti-inflammation effects on THP-1 cells via suppression of PKC pathway including downstream JNK, nuclear factors AP-1 and NF-ĸB[3]. 
Fargesin as a potential β₁ adrenergic receptor antagonist protects the hearts against ischemia/reperfusion injury in rats via attenuating oxidative stress and apoptosis[4]. 
In Vivo: Fargesin has antihypertensive effect in 2K1C hypertensive rats via inhibiting oxidative stress and promoting NO release[1].

Name: Dracorhodin perchlorate Dracohodin perochlorate, CAS: 125536-25-6, stock 18.9g, assay 98.8%, MWt: 366.75, Formula: C17H15ClO7, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Apoptosis, Target: Apoptosis, Biological_Activity: Dracorhodin perchlorate (Dracohodin perochlorate) is a natural product extracted from a natural medicine Dragon's blood. Dracorhodin perchlorate (Dracohodin perochlorate) inhibits cell proliferation, induces cell cycle arrest and apoptosis [1][2].

Name: Linoleic acid, CAS: 60-33-3, stock 26.8g, assay 98.7%, MWt: 280.45, Formula: C18H32O2, Solubility: DMSO : ≥ 43.33 mg/mL (154.50 mM), Clinical_Informat: Phase 3, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: Linoleic acid is a critical component of polyunsaturated fatty acids.
In Vitro: Linoleic acid contains unsaturated double bonds that are highly vulnerable to free radical attack and oxidation. If ROS are produced in great quantities, the body can no longer efficiently remove them. In such instances, ROS may be released into the extracellular space, causing damage to surrounding cells and tissues. Linoleic acid is a decomposition product of a free fatty acid and has been linked to erythrocyte damage[1].

Name: Diosgenin glucoside, CAS: 14144-06-0, stock 14.3g, assay 98.3%, MWt: 576.76, Formula: C33H52O8, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Apoptosis;Autophagy, Target: Apoptosis;Autophagy, Biological_Activity: Diosgenin glucoside, a saponin compound extracted from Tritulus terrestris L., provides neuroprotection by regulating microglial M1 polarization. Diosgenin glucoside protects against spinal cord injury by regulating autophagy and alleviating apoptosis [1][2].

Name: Genkwanin Puddumetin, CAS: 437-64-9, stock 27.9g, assay 98.9%, MWt: 284.26, Formula: C16H12O5, Solubility: DMSO : 5 mg/mL (17.59 mM; Need ultrasonic); H2O : < 0.1 mg/mL (insoluble), Clinical_Informat: No Development Reported, Pathway: Anti-infection, Target: Virus Protease, Biological_Activity: Genkwanin is a major non-glycosylated flavonoid with anti-flammatory activities.
In Vitro: Cell viability analysis shows that Genkwanin does not affect the cell viability up to a concentration of 50 μM. Genkwanin inhibits the LPS-induced production of NO in a concentration-dependent manner. iNOS only expresses in the present of external stimulus. Genkwanin could not significantly affect the activity of iNOS. The effect of Genkwanin on the production of proinflammatory cytokines is examined. Genkwanin suppresses the productions of TNF-a, IL-1b and IL-6 in LPS stimulated RAW264.7 macrophages in a concentration-dependent manner. Genkwanin significantly suppresses the AP-1 signaling pathway but has little effect on the NF-kB signaling pathway. It is indicated that Genkwanin suppresses the phosphorylation of p38 and JNK in a concentration-dependent manner, but little affects ERK1/2 phosphorylation. Originally identified as an immediate early gene, MKP-1 is then found to be a dual specificity phosphatase acting as a negative regulator of ERK1/2, JNK and p38 MAPK activities, with predominant effects on the latter two. Pretreatment with Genkwanin markedly up-regulates the expression of MKP-1 without affecting MKP-1 mRNA[1].

Name: Harmine (hydrochloride) Telepathine (hydrochloride), CAS: 343-27-1, stock 3.3g, assay 98.9%, MWt: 248.71, Formula: C13H13ClN2O, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Protein Tyrosine Kinase/RTK;Neuronal Signaling;GPCR/G Protein, Target: DYRK;5-HT Receptor;5-HT Receptor, Biological_Activity: Harmine Hydrochloride (Telepathine Hydrochloride) is a natural dual-specificity tyrosine phosphorylation-regulated kinase (DYRK) inhibitor with anticancer and anti-inflammatory activities. Harmine has a high affinity of 5-HT2A serotonin receptor, with an Ki of 397 nM[1].
IC50 & Target: Ki: 397 nM (5-HT2A serotonin receptor)[1], DYRK1A[2]
In Vitro: Harmine inhibits tau phosphorylation by DYRK1A by selected DANDYs, with an IC50 of 190 nM[2]. Harmine negatively regulates homologous recombination (HR) by interfering Rad51 recruitment, resulting in severe cytotoxicity in hepatoma cells. Furthermore, NHEJ inhibitor Nu7441 markedly sensitizes Hep3B cells to the anti-proliferative effects of Harmine[3].
In Vivo: It is shown that brain water content is significantly increased in the TBI group. Treatment with Harmine significantly reduces the tissue water content at 1, 3 and 5 days, compared with the TBI group. Harmine treatment significantly reduces the escape latency at 3 and 5 days, compared with the TBI group. Post-TBI administration of Harmine significantly improves the motor function recovery of the rats at 1, 3 and 5 days following TBI, compared with the TBI group without Harmine treatment. The neuronal survival rate in the Harmine-treated group is significantly increased, compared with the TBI group. Administration of Harmine results in marked elevation in the expression of GLT-1, compared with the TBI group. The administration of Harmine significantly reduces the expression of caspase 3, compared with the TBI group[4].

Name: Jatrorrhizine (chloride), CAS: 6681-15-8, stock 36.2g, assay 98.9%, MWt: 373.83, Formula: C20H20ClNO4, Solubility: DMSO : 5 mg/mL (13.38 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Jatrorrhizine chloride is a potent and orally active uptake-2 transporter inhibitor, it can be isolated from various Chinese medicinal plants[1]. Jatrorrhizine chloride exhibits a critical neuroprotective role in H2O2-induced apoptosis via inhibition of MAPK pathway in HT22 hippocampal neurons[2].
IC50 & Target: Uptake-2 transporter[1]
In Vitro: Organic cation transporters (OCTs) and the plasma membrane monoamine transporter (PMAT) are major uptake-2 transporters[1].
Jatrorrhizine chloride significantly inhibits the plasma membrane monoamine transporter (PMAT) -mediated MPP+ uptake in a concentration-dependent manner with an IC50 value of 1.05 μM[1].
Jatrorrhizine chloride demonstrates a more powerful inhibition on serotonin (5-HT) and norepinephrine (NE) uptake mediated by hOCT2 and hOCT3 than that mediated by PMAT[1].
Jatrorrhizine chloride attenuates the H2O2-induced Bcl-2/Bax ratio reduction and caspase-3 activation in these neurons[2].

Name: Senkyunolide A, CAS: 63038-10-8, stock 17.4g, assay 98.2%, MWt: 192.25, Formula: C12H16O2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Senkyunolide A, isolated from Ligusticum chuanxiong Hort, has cytoprotective and antiproliferative activities. Anti-tumor activity[1][2].

Name: Senkyunolide H, CAS: 94596-27-7, stock 7.4g, assay 98.5%, MWt: 224.25, Formula: C12H16O4, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Senkyunolide H is a natural compound isolated from Ligusticum chuanxiong Hort[1].

Name: Senkyunolide I, CAS: 94596-28-8, stock 26.2g, assay 98.8%, MWt: 224.25, Formula: C12H16O4, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Apoptosis, Target: Caspase, Biological_Activity: Senkyunolide I, isolated from Ligusticum chuanxiong Hort, is an anti-migraine compound. Senkyunolide I protects rat brain against focal cerebral ischemia-reperfusion injury by up-regulating p-Erk1/2, Nrf2/HO-1 and inhibiting caspase 3[1][2].

Name: Jatrorrhizine, CAS: 3621-38-3, stock 23.9g, assay 98.8%, MWt: 338.38, Formula: C20H20NO4+, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Jatrorrhizine is a potent and orally active uptake-2 transporter inhibitor, it can be isolated from various Chinese medicinal plants[1]. Jatrorrhizine exhibits a critical neuroprotective role in H2O2-induced apoptosis via inhibition of MAPK pathway in HT22 hippocampal neurons[2].
IC50 & Target: Uptake-2 transporter[1]
In Vitro: Organic cation transporters (OCTs) and the plasma membrane monoamine transporter (PMAT) are major uptake-2 transporters[1].Jatrorrhizine significantly inhibits the plasma membrane monoamine transporter (PMAT) -mediated MPP+ uptake in a concentration-dependent manner with an IC50 value of 1.05 μM[1].
Jatrorrhizine demonstrates a more powerful inhibition on serotonin (5-HT) and norepinephrine (NE) uptake mediated by hOCT2 and hOCT3 than that mediated by PMAT[1].
Jatrorrhizine attenuates the H2O2-induced Bcl-2/Bax ratio reduction and caspase-3 activation in these neurons[2].

Name: Eupalinolide B, CAS: 877822-41-8, stock 20.5g, assay 98.8%, MWt: 462.49, Formula: C24H30O9, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Eupalinolide B is a germacrane sesquiterpene isolated from Eupatorium lindleyanum. Eupalinolide B demonstrates potent cytotoxicity against A-549, BGC-823 and HL-60 tumour cell lines[1].

Name: Rhoifolin, CAS: 17306-46-6, stock 24.9g, assay 98.2%, MWt: 578.52, Formula: C27H30O14, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: MAPK/ERK Pathway;Protein Tyrosine Kinase/RTK;Autophagy;NF-κB, Target: p38 MAPK;Insulin Receptor;Autophagy;NF-κB, Biological_Activity: Rhoifolin is a flavone glycoside isolated from Citrus grandis (L.) Osbeck leaves. Rhoifolin is beneficial for diabetic complications through enhanced adiponectin secretion, tyrosine phosphorylation of insulin receptor-β and glucose transporter 4 (GLUT 4) translocation[1]. Rhoifolin ameliorates titanium particle-stimulated osteolysis and attenuates osteoclastogenesis via RANKL-induced NF-κB and MAPK pathways[2].

Name: Bornyl acetate, CAS: 76-49-3, stock 38g, assay 98.4%, MWt: 196.29, Formula: C12H20O2, Solubility: DMSO : ≥ 83.33 mg/mL (424.52 mM), Clinical_Informat: No Development Reported, Pathway: Apoptosis, Target: Apoptosis, Biological_Activity: Bornyl acetate is a potent odorant, exhibiting one of the highest flavor dilution factor (FD factor).
In Vitro: Bornyl acetate is characterized as one of the most important odorants of fresh ginger juice, as it exhibits one of the highest FD factors. Bornyl acetate is also identified as playing very important sensory roles in the aroma of fresh Japanese ginger.

Name: 8-O-Acetylharpagide, CAS: 6926-14-3, stock 30.3g, assay 98.6%, MWt: 406.38, Formula: C17H26O11, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: 8-O-Acetylharpagide is an iridoid isolated from Ajuga reptans with antitumoral, antiviral, antibacterial, and anti-inflammatory activities. 8-O-Acetylharpagide also has a biological activity on isolated smooth muscle preparations from guinea pig[1][2].

Name: Acetylcorynoline, CAS: 18797-80-3, stock 8.1g, assay 98.1%, MWt: 409.43, Formula: C23H23NO6, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Acetylcorynoline is the major alkaloid component derived from Corydalis bungeana, and has anti-inflammatory properties[1].
In Vitro: Acetylcorynoline significantly inhibits the secretion of tumor necrosis factor-α, interleukin-6, and interleukin-12p70 by LPS-stimulated Dendritic cells (DCs)[1]. 
Acetylcorynoline significantly inhibits LPS-induced activation of IκB kinase and mitogen-activated protein kinase[1].

Name: Isoliquiritin, CAS: 5041-81-6, stock 1g, assay 98.4%, MWt: 418.39, Formula: C21H22O9, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Anti-infection, Target: Fungal, Biological_Activity: Isoliquiritin, isolated from Licorice Root, inhibits angiogenesis and tube formation. Isoliquiritin also exhibits antidepressant-like effects and antifungal activity[1][2][3].

Name: Isoquercitrin Isoquercitroside, CAS: 21637-25-2, stock 17.4g, assay 98.2%, MWt: 464.38, Formula: C21H20O12, Solubility: DMSO : 125 mg/mL (269.18 mM; Need ultrasonic), Clinical_Informat: Phase 3, Pathway: Metabolic Enzyme/Protease;NF-κB;Immunology/Inflammation, Target: Reactive Oxygen Species;Reactive Oxygen Species;Reactive Oxygen Species, Biological_Activity: Isoquercitrin (Isoquercitroside) is an effective antioxidant and an eosinophilic inflammation suppressor.
In Vitro: Isoquercitrin occurs widely in plants.10 μM of Isoquercitrin of the seven compounds partially but significantly blunt the negative effect of H2O2 on RGC-5 cells, as the viability of cells in the presence of H2O2 is increased from approximately 63% to 83% and 90% at 10 and 50 μM, respectively. Indeed, 50 μM Isoquercitrin is more effective as a neuroprotectant than the same concentration of EGCG[1].
In Vivo: In animals receiving Isoquercitrin, eosinophil counts are lower in the BALF, blood and lung parenchyma. Neutrophil counts in blood and IL-5 levels in lung homogenate are lower only in Isoquercitrin-treated mice. No alterations in mononuclear cell numbers were observed[2].

Name: Isoliensinine, CAS: 6817-41-0, stock 32.2g, assay 98.8%, MWt: 610.74, Formula: C37H42N2O6, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Apoptosis, Target: Apoptosis, Biological_Activity: Isoliensinine is a bisbenzylisoquinoline alkaloid extracted from the seed embryo of Nelumbo nucifera, with anti-oxidant and anti-inflammatory and anti-cancer activities. Isoliensinine induces apoptosis in triple-negative human breast cancer cells[1][2].
In Vitro: Isoliensinine induces apoptosis in triple-negative human breast cancer cells through ROS generation and p38 MAPK/JNK activation[1]. 
Isoliensinine exerts antiproliferative effect on CASMCs induced by phenylephrine, and its mechanisms are related to decrease the overexpression of growth factors (PDGF-beta, bFGF), protooncogene (c-fos, c-myc) and hsp70[3].

Name: Isovitexin Saponaretin;Homovitexin, CAS: 38953-85-4, stock 8.7g, assay 98.2%, MWt: 432.38, Formula: C21H20O10, Solubility: DMSO : ≥ 86.6 mg/mL (200.29 mM), Clinical_Informat: No Development Reported, Pathway: MAPK/ERK Pathway;NF-κB, Target: JNK;NF-κB, Biological_Activity: Isovitexin is a flavonoid isolated from rice hulls of Oryza sativa, possesses anti-inflammatory and anti-oxidant activities; Isovitexin acts like a JNK1/2 inhibitor and inhibits the activation of NF-κB.
IC50 & Target: JNK1/2, NF-κB[1]
In Vitro: Isovitexin protects against LPS-induced oxidative damage by suppressing intracellular ROS generation, and also attenuates the effect of H2O2 on cell viability. Isovitexin (0-100 μg/mL) with LPS (2 μg/mL) is not cytotoxic to RAW 264.7 cells, but 200 μg/mL Isovitexin shows significant cytotoxicity. Isovitexin (25, 50 μg/mL) inhibits LPS-induced increases in TNF-α, IL-6, iNOS, and COX-2 levels. Isovitexin (25, 50 μg/mL) also suppresses the IκBα phosphorylation and degradation in RAW 264.7 cells, and such an effect is consistent with that of JNK1/2 inhibitor[1].
In Vivo: Isovitexin (50 and 100 mg/kg, i.p.) causes less severe histopathological changes in the lung sections, and reduces inflammatory cell count in LPS-induced mice. Isovitexin (50 and 100 mg/kg, i.p.) protects against LPS-induced inflammation and oxidative stress in LPS-induced ALI mice by decreasing TNF-α and IL-6 production, ROS generation, and MPO and MDA content, increasing SOD and GSH levels and effectively inhibiting the protein expression of iNOS and COX-2[1]. Isovitexin (25, 50, 100 mg/kg) dose-dependently reduces the survival rate of LPS/D-gal induced hepatic injury in mice. Isovitexin also inhibits NF-κB activation and up-regulates Nrf2 and HO-1 induced by LPS/D-gal in mice[2].

Name: Isorhamnetin-3-O-neohespeidoside, CAS: 55033-90-4, stock 19.5g, assay 98.5%, MWt: 624.54, Formula: C28H32O16, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Isorhamnetin-3-O-neohespeidoside is a flavonoid isolated from Pollen typhae[1].

Name: Linderalactone, CAS: 728-61-0, stock 13.7g, assay 98.6%, MWt: 244.29, Formula: C15H16O3, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Apoptosis, Target: Apoptosis, Biological_Activity: Linderalactone is an important sesquiterpene lactone isolated from Radix linderae. Linderalactone inhibits cancer growth by modulating the expression of apoptosis-related proteins and inhibition of JAK/STAT signalling pathway. Linderalactone also inhibits the proliferation of the lung cancer A-549 cells with an IC50 of 15 µM[1][2].
In Vitro: Linderalactone (0-100 μM; 24 hours; A549 cells) treatment inhibits the growth of A549 cells concentration-dependently. The IC50 of linderalactone is 15 µM[1]. 
Linderalactone (7.5-30 μM; A549 cells) treatment induces apoptosis in A549 cells in a dose-dependent manner[1]. 
Linderalactone (7.5-30 μM; 24 hours; A549 cells) treatment induces G2/M cell cycle arrest of A549 cells dose-dependently[1]. 
Linderalactone (7.5-30 μM; A549 cells) inhibits the expression of STAT1, JAK1 and JAK2. Linderalactone could also inhibit the phosphorylation of pSTAT1, pSTAT-2, pJAK1 and pJAk2[1].

Name: Ginkgolide J, CAS: 107438-79-9, stock 35.9g, assay 98.5%, MWt: 424.40, Formula: C20H24O10, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Apoptosis, Target: Apoptosis, Biological_Activity: Ginkgolide J is a main constituent of the non-flavone fraction of Ginkgo biloba with an IC50 range of 12-54 µM, has neuroprotective and anti neuronal apoptotic ability[1][2].
In Vivo: Ginkgolide J (100 μM) treatment reduces the apoptotic damage induced by serum deprivation (24h) or treatment with Staurosporine (200 nM, 24h) in cultured chick embryonic neurons[1].

Name: Delsoline, CAS: 509-18-2, stock 18.1g, assay 98.5%, MWt: 467.60, Formula: C25H41NO7, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Delsoline, a major alkaloid of Delphinium anthriscifolium Hance, has both a curare-like effect and a ganglion-blocking effect and is used to relieve muscle tension or hyperkinesia. D. anthriscifolium Hance has effects of dispelling wind and dampness, activating collaterals, and relieving pains and is used to treat rheumatism, hemiplegia, indigestion, and cough[1].

Name: Tectorigenin, CAS: 548-77-6, stock 17g, assay 98.4%, MWt: 300.26, Formula: C16H12O6, Solubility: DMSO : 150 mg/mL (499.57 mM; Need ultrasonic and warming), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Tectorigenin is a plant isoflavonoid originally isolated from the dried flower of Pueraria thomsonii Benth.
In Vitro: Tectorigenin is a plant isoflavonoid originally isolated from the dried flower of Pueraria thomsonii Benth. Palmitic acid (PA)-stimulated ROS production is abolished by treatment with Tectorigenin for HUVECs in a dose-dependent manner (0.1, 1, 10 μM). Treatment with Tectorigenin attenuates enhanced IKKβ phosphorylation and effectively blocks NF-κB activation by inhibition of p65 phosphorylation at concentrations ranging from 0.1 to 10 μM. Tectorigenin treatment also effectively inhibits PA-augmented TNF-α and IL-6 production in a concentration dependent manner[1]. The number of viable HepG2 cells treated by Tectorigenin decreases in a concentration- and time-dependent manner. When HepG2 cells are treated with Tectorigenin at 5, 10 and 20 mg/L for 24 h, the viability rate is 91%, 79% and 62%, respectively[2].

Name: Proanthocyanidins, CAS: 20347-71-1, stock 11.3g, assay 98.1%, MWt: 594.52, Formula: C30H26O13, Solubility: H2O : 5 mg/mL (8.41 mM; ultrasonic and adjust pH to 11 with Na2CO3), Clinical_Informat: No Development Reported, Pathway: Anti-infection;Anti-infection, Target: Fungal;Bacterial, Biological_Activity: Proanthocyanidins are a class of polyphenolic that are widely distributed in higher plants, consisted of an electrophilic flavanyl unit. Proanthocyanidins can be used as antioxidant and anti-cancers agent. Proanthocyanidins also exhibit anti-inflammatory, cardioprotective, antibacterial and antifungal properties, which can be used in the treatment of chronic venous insufficiency, capillary fragility, sunburn and retinopathy.[1].
In Vitro: Proanthocyanidins are present in plants as complex mixtures of polymers. Predominant food sources are red wine, tea, chocolate and fruits like grapes, apples, pears, and cranberries[1]. 
The most interesting antibacterial activity of Proanthocyanidins is related to their presence in cranberries (Vaccinium macrocarpon Ait.). A number of clinical trials have demonstrated the effectiveness of cranberry consumption in preventing urinary tract infections (UTIs). Although UTIs can be caused by many microorganisms, more than 85% are caused by Escherichia coli. The presence of P-fimbriae on E. coli, which are proteinaceous fibers on the bacterial cell wall, has been clearly established as a virulence factor, since they are responsible by producing adhesions for adherence to uroepithelial cells. Recently, it is demonstrated that cranberry Proanthocyanidins might inhibit P-fimbriated E. coli from adhering to uroepithelial cells. The antiadhesion activity of cranberry juice appears to be related to the presence of Proanthocyanidins with at least one A-type linkage[1].
In Vivo: The effects of cacao liquor Proanthocyanidins on 2- amino-1-methyl-6-phenylimidazo [4,5-b] pyridine-induced mutagenesis in vivo carcinogenesis in female Sprague-Dawley rats are investigated. In the Ames assay, Proanthocyanidins shows strong antimutagenic effects when assayed in the presence of S-9 mixture. They also inhibit significantly rat pancreatic carcinogenesis in the initiation stage, but not mammary carcinogenesis[1].

Name: Protosappanin B (-)-Protosappanin B, CAS: 102036-29-3, stock 0.5g, assay 98.9%, MWt: 304.29, Formula: C16H16O6, Solubility: DMSO : 250 mg/mL (821.58 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Apoptosis, Target: Apoptosis, Biological_Activity: Protosappanin B is a phenolic compound extracted from Lignum Sappan. Anti-cancer activity[1]. Protosappanin B induces apoptosis and causes G1 cell cycle arrest in human bladder cancer cells[2].
IC50 & Target: Apoptosis[2]
In Vitro: Protosappanin B (12.5, 25, 50, 100, 200 µg/mL, 48 hours) dose-dependently inhibits tumor cells, with IC50s of 21.32 µg/mL, 26.73 µg/mL, and 76.53 µg/mL for SW-480, HCT-116, and BTT cells, respectively[1].

Name: Swertiamarin, CAS: 17388-39-5, stock 32.7g, assay 98.8%, MWt: 374.34, Formula: C16H22O10, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: , Target: , Biological_Activity: Swertiamarin, a secoiridoid glycoside found in genera of Enicostemma Species, confers anti-hyperglycemic and anti-hyperlipidemic effects[1].

Name: Camphor (±)-Camphor, CAS: 76-22-2, stock 25.9g, assay 98.5%, MWt: 152.23, Formula: C10H16O, Solubility: 10 mM in DMSO, Clinical_Informat: Launched, Pathway: Membrane Transporter/Ion Channel;Anti-infection;Neuronal Signaling, Target: TRP Channel;Influenza Virus;TRP Channel, Biological_Activity: Camphor ((±)-Camphor) is a topical anti-infective and anti-pruritic and internally as a stimulant and carminative. However, Camphor is poisonous when ingested. Antiviral, antitussive, and anticancer activities[1]. Camphor is a TRPV3 agonist[2].
IC50 & Target: TRPV3[2]
In Vitro: Camphor induces fibroblast proliferation through the PI3K/AKT and ERK signaling pathways[3]. 
The MTT assay results show that 32.5, 65, 130, and 260 μM Camphor increase fibroblast viability to 108.9±6.6%, 118.6±2.8%, 127.7±4.2%, and 131.6±7.2%, respectively, compared to 0 μM Camphor treatment[3]. 
Camphor (0-260 μM) treatment for 24 hours increases the generation of ROS by up to 17.97% compared to 5.04% in the no-treatment control[3].
Camphor (0-260 μM, 24 hours) induces the phosphorylation of PI3K, AKT, ERK, and 4EBP1 in a dose- and time-dependent manner[3].

Name: Timosaponin AIII, CAS: 41059-79-4, stock 12.7g, assay 99%, MWt: 740.92, Formula: C39H64O13, Solubility: DMSO : 50 mg/mL (67.48 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Neuronal Signaling, Target: AChE, Biological_Activity: Timosaponin AIII could inhibit acetylcholinesterase (AChE) activity, with an IC50 of 35.4 μM.
IC50 & Target: IC50: 35.4 μM (AChE)[1].
In Vitro: Timosaponin AIII could inhibit acetylcholinesterase (AChE) activity, with an IC50 of 35.4 μM[1]. Timosaponin AIII is identified as a major selective cytotoxic activity in BN108, and its selective cytotoxic activity involves inhibition of mTOR, induction of ER stress and protective autophagy[2].
In Vivo: Of the tested steroidal saponins, Timosaponin AIII (TA3) most potently improves memory deficits. Timosaponin AIII increases the scopolamine-induced reduction in step-through latency by 17% (10 mg/kg), 28% (20 mg/kg), and 43% (40 mg/kg). During the acquisition trial, no differences in latent time are observed. Timosaponin AIII (20, 40 mg/kg, p.o.) potently inhibits this reduction of acetylcholine in scopolamine-treated mouse brain. The inhibitory effect of Timosaponin AIII is comparable to that of tacrine, which is used as a positive control[1].

Name: Anemarsaponin B, CAS: 139051-27-7, stock 26.8g, assay 98.6%, MWt: 903.06, Formula: C45H74O18, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Immunology/Inflammation;Immunology/Inflammation;NF-κB, Target: COX;NO Synthase;NF-κB, Biological_Activity: Anemarsaponin B is a steroidal saponin isolated from the rhizomes of A. asphodeloides (Liliaceae). Anemarsaponin B decreases the protein and mRNA levels of iNOS and COX-2. Anemarsaponin B reduces the expressions and productions of pro-inflammatory cytokines, including TNF-a and IL-6. Anemarsaponin B inhibits the nuclear translocation of the p65 subunit of NF-κB by blocking the phosphorylation of IκBα. Anemarsaponin B also inhibits the phosphorylation of MAP kinase kinases 3/6 (MKK3/6) and mixed lineage kinase 3 (MLK3). Anti-inflammatory effect [1].

Name: Timosaponin BII Prototimosaponin A III, CAS: 136656-07-0, stock 0.9g, assay 98.7%, MWt: 921.07, Formula: C45H76O19, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Timosaponin BII is an antioxidant and an anti-inflammatory agent.
In Vitro: Timosaponin BII is a steroidal glycoside separated from Zhi Mu, is found to have the inhibitory activity against the proliferation of HL-60 (leukemic), Hela (cervix), HepG2 and Bel-7402 (liver), HT-29 (colon), and MDA-MB-468 (breast) human carcinoma cell lines with an IC50 value of 15.5 μg/mL in the HL-60 cells[1].
In Vivo: Rat retinas in model group and vehicle control group manifest an apparent up-regulation of BACE1 expression. Meanwhile, the level of malonaldehyde (MDA), Aβ1-40 and β-CTF are increased. However, when comparing with the vehicle control group, the retinas in Timosaponin-BII treated group showed significantly less BACE1 and accumulated less Aβ1-40 or β-CTF. It also showed significantly decreased level of MDA and prolonged partial thromboplastin time[2].

Name: Anemarsaponin E, CAS: 136565-73-6, stock 38.8g, assay 98.7%, MWt: 935.10, Formula: C46H78O19, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Anemarsaponin E is extracted from Anemarrhena asphodeloides Bunge and has anti-inflammatory activity.

Name: Polyphyllin VI, CAS: 55916-51-3, stock 2.5g, assay 98.5%, MWt: 738.90, Formula: C39H62O13, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Apoptosis, Target: Apoptosis, Biological_Activity: Polyphyllin VI, an active saponin mainly isolated from traditional medicinal plant Paris polyphylla, possess anti-cancer activities. Polyphyllin VI induces G2/M cell cycle arrest and triggers apoptosis[1][2].

Name: Lithospermic acid (+)-Lithospermic acid, CAS: 28831-65-4, stock 39g, assay 98.6%, MWt: 538.46, Formula: C27H22O12, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Lithospermic acid ((+)-Lithospermic acid) is a plant-derived polycyclic phenolic carboxylic acid isolated from Salvia miltiorrhiza, and has the anti-oxidative and hepatoprotective activity on carbon tetrachloride (CCl4)-induced acute liver damage in vitro and in vivo[1].

Name: Corynoline, CAS: 18797-79-0, stock 32.1g, assay 98.4%, MWt: 367.40, Formula: C21H21NO5, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Neuronal Signaling;NF-κB, Target: AChE;Keap1-Nrf2, Biological_Activity: Corynoline, isolated from Corydalis incise (Papaveraceae), is a reversible and noncompetitive acetylcholinesterase (AChE) inhibitor with an IC50 of 30.6 μM[1]. Corynoline exhibits anti-inflammatory activity by activating Nrf2[2].

Name: Shionone, CAS: 10376-48-4, stock 14.7g, assay 98.4%, MWt: 426.72, Formula: C30H50O, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Shionone is the major triterpenoid isolated from Aster tataricus, has anti-tussive, anti-inflammatory activities[1][2]. Shionone possesses a unique six-membered tetracyclic skeleton and 3-oxo-4-monomethyl structure[1].
In Vivo: Shionone (orally administration; 80 mg/kg; 3 days; once daily) shows the trend of enhancing sputum secreting, but has no effect on ammonia-induced cough and reduces xylene-induced ear edema[1].

Name: Palmitic acid, CAS: 57-10-3, stock 31.8g, assay 98.2%, MWt: 256.42, Formula: C16H32O2, Solubility: DMSO : ≥ 50 mg/mL (194.99 mM); H2O : < 0.1 mg/mL (insoluble), Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: Palmitic acid is a long-chain saturated fatty acid commonly found in both animals and plants.

Name: Jaceosidin, CAS: 18085-97-7, stock 30.6g, assay 98.1%, MWt: 330.29, Formula: C17H14O7, Solubility: DMSO : 125 mg/mL (378.46 mM; Need ultrasonic); Ethanol : 7.14 mg/mL (21.62 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Apoptosis;Immunology/Inflammation;Apoptosis, Target: Apoptosis;COX;Bcl-2 Family, Biological_Activity: Jaceosidin is a flavonoid isolated from Artemisia vestita, induces apoptosis in cancer cells, activates Bax and down-regulates Mcl-1 and c-FLIP expression[1]. Jaceosidin exhibits anti-cancer[2], anti-inflammatory activities, decreases leves of inflammatory markers, and suppresses COX-2 expression and NF-κB activation[3].
In Vitro: Jaceosidin (30, 50, 75 μM) induces apoptosis in human renal carcinoma Caki cells after treatment for 24 h, shows no obvious effect on normal cells[1]. 
Jaceosidin (75 μM) reduces MMP levels and causes cytochrome c release into the cytoplasm through Bax activation[1]. 
Jaceosidin-mediated apoptosis is involved in downregulation of Mcl-1, c-FLIP expression, which is via inhibition of NF-κB and/or Sp1 transcriptional activity[1]. 
Jaceosidin shows cytostatic activity to HES and HESC cells with IC50s of 52.68 and 55.10 μM, and is less cytotocxic on Hec1 A and KLE (IC50, 70.54, 147.14 μM, respectively), after treatment for 48 h[2].
In Vivo: Jaceosidin (10 and 20 mg/kg, p.o., once a day for 3 days) blocks carrageenan-induced increase in leukocyte number and protein levels in air pouch exudates in mice[3]. 
Jaceosidin (10, 20 mg/kg, p.o.) suppresses COX-2 expression and NF-κB activation in mice[3]. 
Jaceosidin (20 mg/kg, p.o. for 2 hours) reduces hind paw edema volume in rats[3].

Name: DIDS sodium salt MDL101114ZA, CAS: 67483-13-0, stock 27.7g, assay 98.6%, MWt: 498.48, Formula: C16H8N2Na2O6S4, Solubility: DMSO : 50 mg/mL (100.30 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: DIDS sodium salt is a dual ABCA1 and VDAC1 inhibitor.
IC50 & Target: ABCA1[1], VDAC1[2].
In Vitro: Concentration less than 400 μM DIDS has no evident cytotoxic effect on cell viability Pre-treatment with DIDS at the concentration of 100 and 200 μM result in a prevented effect on ALA-SDT-induced cell death, while dose at 50 μM has no inhibition effect. At the concentration of 400 μM DIDS itself slightly decreases the cell viability, although there is no significant statistic difference as compared with the untreated control. Pre-treatment with DIDS (100 μM) clearly inhibit caspase-3 and caspase-9 activation[2].

Name: MLN8054, CAS: 869363-13-3, stock 17.8g, assay 98.4%, MWt: 476.86, Formula: C25H15ClF2N4O2, Solubility: DMSO : 30 mg/mL (62.91 mM; Need ultrasonic and warming), Clinical_Informat: Phase 1, Pathway: Cell Cycle/DNA Damage;Epigenetics, Target: Aurora Kinase;Aurora Kinase, Biological_Activity: MLN8054 is a potent, selective and orally available aurora A kinase inhibitor with an IC50 of 4 nM.
IC50 & Target: IC50: 4 nM (Aurora A), 172 nM (Aurora B)[1]
In Vitro: MLN8054 is an ATP-competitive, reversible inhibitor of recombinant Aurora A kinase. MLN8054 is >40-fold more selective for Aurora A compared with the family member Aurora B. MLN8054 selectively inhibits Aurora A over Aurora B in cultured human tumor cells. MLN8054 treatment results in G2/M accumulation and spindle defects and inhibits proliferation in multiple cultured human tumor cells lines. MLN8054 effectively inhibits the growth of cells from diverse tissue origins with IC50 values ranging from 0.11 to 1.43 μM[1]. Treatment of human tumor cells grown in culture with MLN8054 shows a number of morphologic and biochemical changes associated with senescence[2].
In Vivo: In the HCT-116 tumor-bearing mice, MLN8054 treatment inhibits tumor growth dose dependently. MLN8054 is generally well tolerated. MLN8054 also inhibits the growth of the PC-3 tumor xenograft in nude mice. MLN8054 Treatment Results in Inhibition of Aurora A, Accumulation of Mitotic Cells, and Apoptosis in vivo[1]. MLN8054 selectively inhibits Aurora A kinase activity when dosed at 30 mg/kg. At this dose in HCT116 tumor tissue, MLN8054 has been shown to inhibit Aurora A autophosphorylation, and induce an increase in the Aurora B substrate, pHisH3[2].

Name: 4-Methylherniarin 7-Methoxy-4-methylcoumarin, CAS: 2555-28-4, stock 13.6g, assay 98.9%, MWt: 190.20, Formula: C11H10O3, Solubility: H2O : < 0.1 mg/mL (insoluble); DMSO : 25 mg/mL (131.44 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Anti-infection, Target: Bacterial, Biological_Activity: 4-Methylherniarin (7-Methoxy-4-methylcoumarin) is a coumarin derivative and fluorescent label, has an antimicrobial activitiy against both gram positive and gram negative bacterial stains. 4-Methylherniarin displays good activity against B. subtilis and S.sonnei with IC50 values of 11.76 μg/ml and 13.47 μg/ml[1].
IC50 & Target: IC50: 11.76 μg/ml (B. subtilis); 13.47 μg/ml (S.sonnei)[1]

Name: 2'-Deoxycytidine Deoxycytidine;Cytosine deoxyriboside;Deoxyribose cytidine, CAS: 951-77-9, stock 21.5g, assay 98.2%, MWt: 227.22, Formula: C9H13N3O4, Solubility: DMSO : 50 mg/mL (220.05 mM; Need ultrasonic); H2O : 50 mg/mL (220.05 mM; Need ultrasonic), Clinical_Informat: Phase 1, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: 2'-Deoxycytidine, a deoxyribonucleoside, could inhibit biological effects of Bromodeoxyuridine (Brdu).

Name: Gallein Pyrogallol phthalein, CAS: 2103-64-2, stock 9.9g, assay 98.3%, MWt: 364.31, Formula: C20H12O7, Solubility: DMSO : 33.33 mg/mL (91.49 mM; ultrasonic and warming and heat to 80°C), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Gallein is a G protein βγ (Gβγ) subunit signalling inhibitor. Gallein disrupts the interaction of Gβγ subunits with the PI3Kγ. Anticancer agent[1]. Gallein used as a red dye, an acid-base indicator and as a detection reagent for phosphates[2].

Name: Direct Black 38 Chlorazol Black E; C.I. 30235, CAS: 1937-37-7, stock 28.3g, assay 98.2%, MWt: 781.73, Formula: C34H25N9Na2O7S2, Solubility: H2O : 5 mg/mL (6.40 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Direct Black 38 is an azo dye. Direct Black 38 induces unscheduled DNA synthesis in liver and micronucleus in bone marrow of rats in vivo[1].

Name: AZ82, CAS: 1449578-65-7, stock 3.1g, assay 98.7%, MWt: 560.63, Formula: C28H31F3N4O3S, Solubility: DMSO : 125 mg/mL (222.96 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Cytoskeleton;Cell Cycle/DNA Damage, Target: Kinesin;Kinesin, Biological_Activity: AZ82 is a selective kinesin-like protein KIFC1 (HSET/KIFC1) inhibitor, with a Ki of 43 nM and an IC50 of 300 nM for KIFC1.
IC50 & Target: IC50: 300nM(KIFC1) [1][2]. 
Ki: 43 nM (KIFC1)[1][2].
In Vitro: AZ82 is shown to specifically induce multipolar spindles in BT-549 cells, but not in cancer cells with normal centrosome number, such as HeLa[1]. AZ82 binds specifically to KIFC1/MT complex but not to KIFC1 or MT alone. Treatment with AZ82 caused centrosome declustering in BT-549 breast cancer cells with amplified centrosomes. AZ82 inhibits both processes with an IC50 of 0.90 ± 0.09 μM for mant-ATP binding and 1.26 ± 0.51 μM for mant-ADP releasing[2].

Name: TCS7010, CAS: 1158838-45-9, stock 29.9g, assay 98.6%, MWt: 588.08, Formula: C31H31ClFN7O2, Solubility: H2O : < 0.1 mg/mL (insoluble); DMSO : ≥ 100 mg/mL (170.04 mM), Clinical_Informat: No Development Reported, Pathway: Apoptosis;Cell Cycle/DNA Damage;Epigenetics, Target: Apoptosis;Aurora Kinase;Aurora Kinase, Biological_Activity: TCS7010 is a potent and highly selective Aurora A inhibitor with with an IC50 of 3.4 nM.
IC50 & Target: IC50: 3.4 nM (Aurora A), 3.4 μM (Aurora B)[1]
In Vitro: TCS7010 is exceptionally selective Aurora A inhibitors. TCS7010 is an useful tool compounds for investigating the cellular role of Aurora A kinases without the complication of also inhibiting Aurora B[1].

Name: 8-Bromo-cAMP sodium salt 8-Br-Camp sodium salt, CAS: 76939-46-3, stock 27.2g, assay 98.4%, MWt: 430.08, Formula: C10H10BrN5NaO6P, Solubility: H2O : ≥ 33.33 mg/mL (77.50 mM); DMSO : 125 mg/mL (290.64 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Stem Cell/Wnt;Protein Tyrosine Kinase/RTK, Target: PKA;PKA, Biological_Activity: 8-Bromo-cAMP sodium salt (8-Br-Camp sodium salt), a cyclic AMP analog, is an activator of cyclic AMP-dependent protein kinase (PKA)[1].
IC50 & Target: PKA[1]
In Vitro: 8-Bromo-cAMP sodium salt is a brominated derivative of cyclic AMP. 8-Bromo-cAMP sodium salt enhances the efficiency of cellular reprogramming. 8-Bromo-cAMP sodium salt improves the reprogramming efficiency of human neonatal foreskin fibroblast (HFF1) cells. 8-Bromo-cAMP sodium salt inhibits proliferation, induce differentiation and apoptosis in a malignant glioma cell line (A-172) and an esophageal cancer cell line (Eca-109)[1].

Name: TCS 2314, CAS: 317353-73-4, stock 16.5g, assay 98.8%, MWt: 522.59, Formula: C28H34N4O6, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Cytoskeleton, Target: Integrin, Biological_Activity: TCS 2314 (compound 3) is orally active and selective very late antigen-4 (VLA-4, α4β1, CD49d/CD29) antagonist with an IC50 of 4.4 nM[1].
IC50 & Target: IC50: 4.4 nM (Very late antigen-4)[1]

Name: EC23 AGN 190205;BASF-46928, CAS: 104561-41-3, stock 6.5g, assay 98.2%, MWt: 332.44, Formula: C23H24O2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: EC23 (AGN 190205) is a stable synthetic retinoid analogue and induces neuronal differentiation[1].
In Vitro: EC23 (AGN 190205) induces neural differentiation accompanying by elevated levels of stathmin and profilin-1. EC23 induces the expression of known cellular retinoid binding proteins in the TERA2.cl.SP12 cell line[1].

Name: 20(S)-Hydroxycholesterol 20α-Hydroxycholesterol, CAS: 516-72-3, stock 12.7g, assay 98.1%, MWt: 402.65, Formula: C27H46O2, Solubility: DMSO : 30 mg/mL (74.51 mM; ultrasonic and warming and heat to 60°C), Clinical_Informat: No Development Reported, Pathway: Stem Cell/Wnt, Target: Smo, Biological_Activity: 20(S)-hydroxyCholesterol (20α-Hydroxycholesterol) is an allosteric activator of the oncoprotein smoothened (Smo) that activates the hedgehog (Hh) signaling pathway with an EC50 of 3 μM in a gene transcription reporter assay using NIH3T3 cells[1][2].
IC50 & Target: EC50: 3 μM (hedgehog signaling pathway)[1]

Name: Tpl2 Kinase Inhibitor 1, CAS: 871307-18-5, stock 29.1g, assay 98.3%, MWt: 404.83, Formula: C21H14ClFN6, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: MAPK/ERK Pathway, Target: MAP3K, Biological_Activity: Tpl2 Kinase Inhibitor 1 (Compound 1) is a potent and selective Tpl2 (COT kinase, MAP3K8) inhibitor, plays an important role in the regulation of the inflammatory response and the progression of some cancers[1].
IC50 & Target: Tpl2/COT kinase/MAP3K8[1]
In Vitro: Cancer Osaka thyroid (COT) kinase (Tpl2) is an important regulator of pro-inflammatory cytokines in macrophages[1].

Name: L-Alloisoleucine (3R)-LS-Isoleucine; L-Allo-isoleucine, CAS: 1509-34-8, stock 17.1g, assay 98.8%, MWt: 131.17, Formula: C6H13NO2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: L-Alloisoleucine is a branched chain amino acid and is a stereo-isomer of L-isoleucine. L-Alloisoleucine is a common constituent of human plasma (albeit at low levels).

Name: NS-2028, CAS: 204326-43-2, stock 28.4g, assay 98.6%, MWt: 269.05, Formula: C9H5BrN2O3, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein, Target: Guanylate Cyclase, Biological_Activity: NS-2028 is a highly selective soluble Guanylyl Cyclase (sGC) inhibitor with IC50 values of 30 nM and 200 nM for basal and NO-stimulated enzyme activity[1]. NS-2028 inhibits soluble Guanylyl Cyclase activity in homogenates of mouse cerebellum and neuronal NO synthase with IC50 values of 17 nM and 20 nM[1]. NS-2028 inhibits 3-morpholino-sydnonimine (SIN-1)-elicited formation of cyclic GMP in human cultured umbilical vein endothelial cells with an IC50 of 30 nM[1]. NS-2028 is commonly used in the research of nitric oxide signaling pathways, it inhibits NO-dependent relaxant responses in non-vascular smooth muscle completely (1 μM)[1]. NS-2028 reduces vascular endothelial growth factor-induced angiogenesis and permeability[2].
IC50 & Target: IC50: 30 nM (soluble Guanylyl Cyclase sGC)[1]
In Vitro: NS-2028 (10 μM; 24 hours) inhibits 25% cell number in comparation with those grown in the presence of vehicle[2].
NS-2028 (10 μM; 30 mins) attenuates VEGF-induced EC migration by inhibiting p38 MAPK activation[2].
In Vivo: NS-2028 (Deliver orally; 1 g/L; 8 days) exhibits a significant reduction of new vessel formation in the avascular rabbit cornea in response to VEGF pellet implants[2].

Name: FMK-MEA, CAS: 1414811-15-6, stock 19.9g, assay 98.7%, MWt: 399.46, Formula: C21H26FN5O2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: MAPK/ERK Pathway, Target: Ribosomal S6 Kinase (RSK), Biological_Activity: FMK-MEA is a potent and selective p90 Ribosomal S6 Kinase (RSK) inhibitor.
IC50 & Target: p90 RSK[1]
In Vitro: FMK-MEA is a water-soluble derivative of fmk. FMK-MEA treatment inhibits RSK2 kinase activity in diverse, highly invasive human cancer cell lines including 212LN, M4e, A549, and SKBR3 cells. Treatment with the RSK-specific inhibitor FMK-MEA significantly attenuates RSK2 activity, as assessed by the phosphorylation levels of Ser-386 and the consequent invasive ability of A549 cells[1].
In Vivo: FMK-MEA treatment (80 mg/kg/day for 16 days by intraperitoneal injection) in highly metastatic M4e cell xenograft nude mice results in a significant attenuation of LN metastasis. FMK-MEA treatment has no effect on the tumor size, and the proliferation rate of the primary tumor[1].

Name: Tenosal, CAS: 95232-68-1, stock 18.8g, assay 98.1%, MWt: 248.25, Formula: C12H8O4S, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Tenosal is a new compound obtained by esterifying salicylic acid with 2-thiophene-carboxylic acid and displays anti-inflammatory, analgesic and antipyretic properties.
In Vivo: Tenosal is a new compound obtained by esterifying salicylic acid with 2-thiophene-carboxylic acid and displays anti-inflammatory, analgesic and antipyretic properties. Extraction recovery measured is on average 95.75% for Tenosal, 98.71% for salicylic acid (SA) and 91.11% for TA. In the whole analysis of Tenosal extracted from plasma, the inter-assay coefficient of variation (C.V.) ranges from 1.00 to 5.86% and the intra assay C.V. is 5.01%. The administration of Tenosal allows a higher bioavailability of SA to be achieved than after dosing with ASA[1].

Name: Lofepramine Lopramine, CAS: 23047-25-8, stock 18.4g, assay 98.6%, MWt: 418.96, Formula: C26H27ClN2O, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Lofepramine (Lopramine) is a potent tricyclic antidepressant and is extensively metabolised to Desipramine. The antidepressant activity of Lofepramine stems from the facilitation of noradrenergic neurotransmission by uptake inhibition. Lofepramine may also potentiate serotoninergic neurotransmission by inhibition of the neuronal uptake of serotonin and the enzyme tryptophan pyrrolase. Lofepramine has significant anxiolytic efficacy in addition to its antidepressant properties[1].

Name: Diminazene (aceturate) Diminazene (diaceturate), CAS: 908-54-3, stock 29.8g, assay 98.5%, MWt: 515.52, Formula: C22H29N9O6, Solubility: DMSO : 25 mg/mL (48.49 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease;Anti-infection, Target: Angiotensin-converting Enzyme (ACE);Parasite, Biological_Activity: Diminazene aceturate (Diminazene diaceturate) is an anti-trypanosome agent for livestock. The main biochemical mechanism of the trypanocidal actions of Diminazene aceturate is by binding to trypanosomal kinetoplast DNA (kDNA) in a non-intercalative manner through specific interaction with sites rich in adenine-thymine base pairs. Diminazene aceturate is also an angiotensin-converting enzyme 2 (ACE2) activator and has strong and potent anti-inflammatory properties[1][2][3].
IC50 & Target: Parasite[1][2]; Angiotensin-converting enzyme 2 (ACE2)[3]
In Vitro: Pre-treatment of bone marrow-derived macrophages (BMDM) and dendritic cells (BMDC) with Diminazene aceturate (Berenil) downregulats LPS-, CpG- and Poly I:C-induced proinflammatory cytokine production, suggesting that it may be affecting common pathways through which these molecules stimulate proinflammatory cytokine production. Indeed, Diminazene aceturate does not alter the expression of different TLRs (including TLR2, TLR4 and TLR9), on macrophages and DCs when assessed by flow cytometry. Instead, Diminazene aceturate dramatically downregulats the phosphorylation of MAPKs (ERK, p38 and JNK), STATs (STAT1 and STAT3) and NFκB p65 subunit, which are key signaling molecules and transcription factors involved in the production of proinflammatory cytokines[2].
In Vivo: Diminazene aceturate (14 mg/kg; intraperitoneal injection; female BALB/c mice and C57BL/6 mice) treatment significantly reduces the percentages of CD25+ cells, a concomitant reduction in the percentage of regulatory (CD4+Foxp3+) T cells and a striking reduction in serum levels of disease exacerbating pro-inflammatory cytokines including IL-6, IL-12, TNF and IFN-γ[1].

Name: JNJ-47117096 hydrochloride MELK-T1 hydrochloride, CAS: 1610536-69-0, stock 23g, assay 98.3%, MWt: 398.89, Formula: C21H23ClN4O2, Solubility: DMSO : ≥ 250 mg/mL (626.74 mM), Clinical_Informat: No Development Reported, Pathway: Protein Tyrosine Kinase/RTK;PI3K/Akt/mTOR, Target: FLT3;MELK, Biological_Activity: JNJ-47117096 hydrochloride is potent and selective MELK inhibitor, with an IC50 of 23 nM, also effectively inhibits Flt3, with an IC50 of 18 nM.
IC50 & Target: IC50: 23 nM (MELK), 18 nM (Flt3)[1]
In Vitro: JNJ-47117096 hydrochloride is potent and selective MELK inhibitor, with an IC50 of 23 nM, also effectively inhibits Flt3, with an IC50 of 18 nM, and slighitly blocks CAMKIIδ, Mnk2, CAMKIIγ, and MLCK (IC50, 810 nM, 760 nM, 1000 nM, 1000 nM). JNJ-47117096 (MELK-T1) suppresses the proliferation of Flt3-driven Ba/F3 cell lines, with an IC50 of 1.5 μM in the absence of IL-3, while no inhibitory activity is observed in the presence of IL-3. JNJ-47117096 does not inhibit the proliferation of Ba/F3 cell lines transfected with either FGFR1, FGFR3, or KDR, either in the presence or absence of IL-3[1]. JNJ-47117096 (MELK-T1, 10 μM) delays the progression of MCF-7 cells through S-phase. JNJ-47117096 inhibits MELK, and then exerts stalled replication forks and DNA double-strand breaks (DSBs). JNJ-47117096 activates the ATM-mediated DNA-damage response (DDR). JNJ-47117096 (3, 10 μM) results in a growth arrest and a senescent phenotype. Moreover, JNJ-47117096 induces a strong phosphorylation of p53, a prolonged up-regulation of p21 and a down-regulation of FOXM1 target genes[2].

Name: Voruciclib, CAS: 1000023-04-0, stock 7.7g, assay 98.5%, MWt: 469.84, Formula: C22H19ClF3NO5, Solubility: DMSO : 125 mg/mL (266.05 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Cell Cycle/DNA Damage, Target: CDK, Biological_Activity: Voruciclib is a clinical stage orally active and selective CDK inhibitor with Ki values of 0.626 nM-9.1 nM. Voruciclib potently blocks CDK9, the transcriptional regulator of MCL-1. Voruciclib represses expression of MCL-1 in multiple models of diffuse large B-cell lymphoma (DLBCL)[1].
In Vitro: Voruciclib (0.5-5 µM; 6 hours) shows targeted downregulation of MCL-1 in both ABC and GCB subtypes[1]. 
In Vivo: Combination of Voruciclib hydrochloride (200 mpk; Oral gavage) and Venetoclax (10 mpk, 1 mpk, 50 mpk, 25 mpk in U2932, RIVA, SU-DHL-4 and NU-DHL-1, respectively) leads to enhance tumor growth inhibition compared to either drug alone in U2932, RIVA, SU-DHL-4 (six days per week for 4 weeks), and NU-DHL-1 models (five days per week for 3 weeks) of DLBCL[1].

Name: Gilteritinib hemifumarate ASP2215 hemifumarate, CAS: 1254053-84-3, stock 30.8g, assay 98.8%, MWt: 610.75, Formula: C29H44N8O3 0.5C4H4O4, Solubility: H2O : 2 mg/mL (3.27 mM; Need ultrasonic); DMSO : 1.74 mg/mL (2.85 mM; Need ultrasonic and warming), Clinical_Informat: Launched, Pathway: Protein Tyrosine Kinase/RTK;Protein Tyrosine Kinase/RTK, Target: FLT3;TAM Receptor, Biological_Activity: Gilteritinib hemifumarate is a potent FLT3/AXL inhibitor with IC50 of 0.29 nM/0.73 nM, respectively.
IC50 & Target: IC50: 0.29 nM (FLT3)[1] 
IC50: 0.35 nM (LTK), 0.73 nM (AXL), 1.2 nM (EML4-ALK), 230 nM (c-KIT)[2]
In Vitro: Of the 78 tyrosine kinases tested, Gilteritinib (ASP2215) inhibits FLT3, leukocyte tyrosine kinase (LTK), anaplastic lymphoma kinase (ALK), and AXL kinases by over 50% at 1 nM with an IC50 value of 0.29 nM for FLT3, approximately 800-fold more potent than for c-KIT[1]. Gilteritinib inhibits the activity of eight of the 78 tested kinases by over 50% at concentrations of either 1 nM (FLT3, LTK, ALK, and AXL) or 5 nM (TRKA, ROS, RET, and MER). The IC50s are 0.29 nM for FLT3 and 0.73 nM for AXL. Gilteritinib inhibits FLT3 at an IC50 that is approximately 800-fold more potent than the concentration required to inhibit c-KIT (230 nM). The antiproliferative activity of Gilteritinib is evaluated against MV4-11 and MOLM-13 cells, which endogenously express FLT3-ITD. After 5 days of treatment, Gilteritinib inhibits the growth of MV4-11 and MOLM-13 cells with mean IC50s of 0.92 nM (95% CI: 0.23-3.6 nM) and 2.9 nM (95% CI: 1.4-5.8 nM), respectively. Growth suppression of MV4-11 cells is accompanied by inhibition of FLT3 phosphorylation. Relative to vehicle control cells, phosphorylated FLT3 levels are 57%, 8%, and 1% after 2 h of treatment with 0.1 nM, 1 nM, and 10 nM Gilteritinib, respectively. In addition, doses as low as 0.1 nM or 1 nM result in the suppression of phosphorylated ERK, STAT5, and AKT, all of which are downstream targets of FLT3 activation. To investigate the effects of Gilteritinib on AXL inhibition, MV4-11 cells that expressed exogenous AXL are treated with Gilteritinib. At concentrations of 1 nM, 10 nM, and 100 nM for 4 h, Gilteritinib treatment decreases phosphorylated AXL levels by 38%, 29%, and 22%, respectively[2].
In Vivo: In MV4-11 xenografted-mice, the concentration of Gilteritinib (ASP2215) in tumors is more than 20-fold higher than that in plasma with oral administration of Gilteritinib at 10 mg/kg for 4 days. Treatment of Gilteritinib for 28 days results in dose-dependent inhibition of MV4-11 tumor growth and induces complete tumor regression at more than 6 mg/kg. Further, Gilteritinib decreases tumor burden in bone marrow and prolonged the survival of mice intravenously transplanted with MV4-11 cells[1].

Name: BMS-819881, CAS: 1197420-05-5, stock 13.2g, assay 98.5%, MWt: 468.95, Formula: C24H21ClN2O4S, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease;GPCR/G Protein;Neuronal Signaling, Target: Cytochrome P450;MCHR1 (GPR24);MCHR1 (GPR24), Biological_Activity: BMS-819881 is a melaninconcentrating hormone receptor 1 (MCHR1) antagonist, which binds rat MCHR1 with a Ki of 7 nM. BMS-819881 also is selective and potent for CYP3A4 activity with an EC50 of 13 μM.
IC50 & Target: Ki: 7 nM (rat MCHR1)[1] 
EC50: 13 μM (CYP3A4)[1]
In Vitro: BMS-819881 (Compound 27) is 99.8% binds to rat serum proteins and rat MCHR1 Ki is 7 nM. FLIPR-based assays establish that BMS-819881 is a potent and highly selective MCHR1 functional antagonist. BMS-819881 (Kb=32 nM) effectively blocks MCH stimulated Ca2+ mobilization in heterologous cells overexpressing MCHR1 but fails to inhibit MCH mediated Ca2+ mobilization of cells expressing MCHR2 at 10 μM. No activity is observed upon screening BMS-819881 at 10 μM versus a panel of 20 GPCRs associated with feeding homeostasis. The percent of BMS-819881 binds to serum proteins is species dependent ranging from 99.8%, 99.6%, and 99.3%, respectively, for rat, dog, and monkey. When BMS-819881 is screened for cytochrome P450 (CYP) activity, EC50 values for CYP1A2, CYP2C9, CYP2C19, CYP2D6 are >40 μM; however, the CYP3A4 EC50 is 13 μM[1].
In Vivo: BMS-819881 has moderate terminal elimination half-life (t1/2=5.7 h, 32±8 h, and 14±3 h for rat (1 mg/kg, iv), dog (1 mg/kg, iv), and cynomologous monkey (1 mg/kg, iv))[1].

Name: Teneligliptin (hydrobromide hydrate) MP-513 (hydrobromide hydrate), CAS: 1572583-29-9, stock 10.8g, assay 98.7%, MWt: 426.58, Formula: C22H30N6OS, Solubility: 10 mM in DMSO, Clinical_Informat: Launched, Pathway: Metabolic Enzyme/Protease, Target: Dipeptidyl Peptidase, Biological_Activity: Teneligliptin hydrobromide hydrate is a potent chemotype prolylthiazolidine-based DPP-4 inhibitor, which competitively inhibits human plasma, rat plasma, and human recombinant DPP-4 in vitro, with IC50s of approximately 1 nM[1].

Name: SGK1-IN-1, CAS: 1279829-87-6, stock 2.8g, assay 99%, MWt: 418.83, Formula: C17H12ClFN6O2S, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: SGK, Biological_Activity: SGK1-IN-1 is a highly active and selective inhibitor of SGK-1, with an IC50 of 1 nM.
IC50 & Target: IC50: 1 nM (SGK-1)[1][2].
In Vitro: SGK1-IN-1 (14n) shows an acceptable SGK isoform selectivity with a good activity on hSGK2 and a moderate activity on the hSGK3, with IC50s of 1, 41 nM at 10 μM and 50 μM ATP concentration, respectively. SGK1-IN-1 also displays cellular activity in a SGK1-dependent phosphorylation of GSK3β assay in U2OS cells with activities of 0.69 μM[2].

Name: Succinic anhydride, CAS: 108-30-5, stock 31.2g, assay 98.1%, MWt: 100.07, Formula: C4H4O3, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Antibody-drug Conjugate/ADC Related, Target: ADC Linker, Biological_Activity: Succinic anhydride is a cyclic anhydride and a nonclaevable ADC linker extracted from patent WO2009064913A1. Succinic anhydride can react with compound 4 of the patent to link the prodrug to an amine or hydroxy 1 group of a targeting polypeptide[1].

Name: (Z)2S,4R-Sacubitril, CAS: , stock 6.4g, assay 98.9%, MWt: 409.47, Formula: C24H27NO5, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: (Z)2S,4R-Sacubitril is the impurity of Sacubitril. Sacubitril is approved by the Food and Drug Administration for use in combination with valsartan for the treatment of patients with heart failure.

Name: LEQ506 NVP-LEQ506, CAS: 1204975-42-7, stock 11.3g, assay 98.8%, MWt: 432.56, Formula: C25H32N6O, Solubility: DMSO : ≥ 100 mg/mL (231.18 mM), Clinical_Informat: Phase 1, Pathway: Stem Cell/Wnt, Target: Smo, Biological_Activity: LEQ506 is a second-generation inhibitor of smoothened (Smo) with IC50s of 2 and 4 nM in human and mouse, respectively.
IC50 & Target: IC50: 2 nM (human smo), 4 nM (mouse smo)[1]
In Vitro: LEQ506 is a second-generation inhibitor of smoothened (Smo) with IC50s of 2 and 4 nM in human and mouse, respectively. LEQ506 inhibits Hedgehog (Hh) signaling in a human cell line (HEPM) as measured by the amount of Gli mRNA with an IC50 ~6-fold lower than that of Compound 2[1]. LEQ506 is an efficacious compound by consistently decreasing Gli1 mRNA by about 70 to 80%. LEQ506 shows a tendency to preferentially inhibit Gli1 rather than Ptch1 mRNA. LEQ506 (at 1%) is also an efficacious compound with an inhibition of 80 to 90% for Gli1 and of 60 to 70% for Ptch1[2].

Name: PF-4800567, CAS: 1188296-52-7, stock 18.9g, assay 98.5%, MWt: 359.81, Formula: C17H18ClN5O2, Solubility: DMSO : 75 mg/mL (208.44 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Stem Cell/Wnt;Cell Cycle/DNA Damage, Target: Casein Kinase;Casein Kinase, Biological_Activity: PF-4800567 is a potent and selective inhibitor of casein kinase 1ϵ (CK1ϵ), with an IC50 of 32 nM, which is greater than 20-fold selectivity over CK1δ (IC50, 711 nM).
IC50 & Target: IC50: 32 nM (CK1ϵ), 711 nM (CK1δ)[1]
In Vitro: PF-4800567 is a potent and selective inhibitor of casein kinase 1ϵ (CK1ϵ), with an IC50 of 32 nM, which is greater than 20-fold selectivity over CK1δ (IC50, 711 nM). PF-4800567 shows inhibitory activity against CK1ϵ and CK1δ in whole cells, with IC50s of 2.65 and 20.38 μM, respectively. PF-4800567 (0.01-10 μM) blocks CK1ϵ-mediated PER3 nuclear localization mediated by CK1ϵ and suppresses PER2 degradation at 1 μM. In addition, PF-4800567 has little effect on the circadian clock at 32 nM[1].
In Vivo: PF-4800567 (100 mg/kg, s.c.) is rapidly absorpted and distributed in plasma and brain of mice[1].

Name: Lanopepden GSK 1322322, CAS: 1152107-25-9, stock 9.5g, assay 98.8%, MWt: 479.55, Formula: C22H34FN7O4, Solubility: 10 mM in DMSO, Clinical_Informat: Phase 2, Pathway: Anti-infection, Target: Bacterial, Biological_Activity: Lanopepden (GSK 1322322) is a peptide deformylase inhibitor active against Staphylococcus aureus strains with MICs of 1 and 1 mg/L for ATCC 29213 and ATCC 25923 strain, respectively[1].

Name: Borrelidin Treponemycin, CAS: 7184-60-3, stock 17.8g, assay 98.7%, MWt: 489.64, Formula: C28H43NO6, Solubility: Ethanol : ≥ 100 mg/mL (204.23 mM), Clinical_Informat: No Development Reported, Pathway: Apoptosis;Cell Cycle/DNA Damage;Anti-infection, Target: Apoptosis;CDK;Parasite, Biological_Activity: Borrelidin (Treponemycin) is a bacterial and eukaryal threonyl-tRNA synthetase inhibitor which is a nitrile-containing macrolide antibiotic isolated from Streptomyces rochei[1]. Borrelidin (Treponemycin) is an inhibitor of Cdc28/Cln2 of the budding yeast, with an IC50 of 24 μM[2]. Borrelidin (Treponemycin) is a potent angiogenesis inhibitor, with an IC50 of 0.8 nM, and induces apoptosis of the tube-forming cells. Borrelidin (Treponemycin) has strong antimalarial activities, with IC50s of 1.9 nM and 1.8 nM against K1 and FCR3 strains of Plasmodium falciparum[3].
IC50 & Target: IC50：24 μM (Cdc28/Cln2)[2]
In Vitro: Borrelidin (Treponemycin) can target ALL cell lines and induce apoptosis and mediating G(1) arrest.

Name: VER-246608, CAS: 1684386-71-7, stock 12.4g, assay 98.2%, MWt: 552.96, Formula: C28H23ClF2N4O4, Solubility: DMSO : 100 mg/mL (180.84 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: PDHK, Biological_Activity: VER-246608 is a potent and ATP-competitive inhibitor of pyruvate dehydrogenase kinase (PDK) with IC50s of 35 nM, 40 nM, 84 nM, and 91 nM for PDK-1, PDK-3, PDK-2, and PDK-4, respectively.
IC50 & Target: IC50: 35 nM (PDK-1), 40 nM (PDK-3), 84 nM (PDK-2), 91 nM (PDK-4)[1]
In Vitro: VER-246608 is a novel pan-isoform ATP competitive inhibitor of PDK. VER-246608 demonstrates similar potency across all four PDK isoforms in a DELFIA-based enzyme functional assay in the sub 100 nM range. In terms of cellular biomarker modulation, VER-246608 suppresses the phosphorylation of the Ser293 residue of E1α (phosphorylated by all four PDK isozymes) with IC50 values of 266 nM. Treatment of PC-3 cells with 9 μM and 27 μM VER-246608 results in a 21% and 42% reduction, respectively, in media L-lactate levels following a 1 h incubation. VER-246608 also decreases D-glucose consumption at the same concentrations that result in reduced L-lactate production. An approximately 50% reduction in spheroid volume is achieved at concentrations of 10 μM and above, suggesting an increase in VER-246608 potency compared to monolayer growth[1].

Name: Astemizole R 43512, CAS: 68844-77-9, stock 3.7g, assay 98.1%, MWt: 458.57, Formula: C28H31FN4O, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Immunology/Inflammation;GPCR/G Protein;Membrane Transporter/Ion Channel;Neuronal Signaling, Target: Histamine Receptor;Histamine Receptor;Potassium Channel;Histamine Receptor, Biological_Activity: Astemizole (R 43512), a second-generation antihistamine drug to diminish allergic symptoms with a long duration of action, is a histamine H1-receptor antagonist, with an IC50 of 4 nM. Astemizole also shows potent hERG K+ channel blocking activity with an IC50 of 0.9 nM. Astemizole has antipruritic effects[1][2].

Name: GNF-2, CAS: 778270-11-4, stock 12g, assay 98%, MWt: 374.32, Formula: C18H13F3N4O2, Solubility: DMSO : ≥ 45 mg/mL (120.22 mM), Clinical_Informat: No Development Reported, Pathway: Protein Tyrosine Kinase/RTK, Target: Bcr-Abl, Biological_Activity: GNF-2 is a highly selective non-ATP competitive inhibitor of oncogenic Bcr-Abl activity (IC50 = 0.14 μM).
IC50 value: 0.14 uM [1]
Target: Bcr-Abl
in vitro: Ba/F3 cells harboring native or T315I mutated Bcr-Abl constructs were treated with GNF-2 and AKIs. We monitored the effect of GNF-2 with AKIs on the proliferation and clonigenicity of the different Ba/F3 cells. In addition, we monitored the auto-phosphorylation activity of Bcr-Abl and JAK2 in cells treated with GNF-2 and AKIs [2]. GNF-2 increased the effects of AKIs on unmutated BCR/ABL. Interestingly, the combination of Dasatinib and GNF-2 overcame resistance of BCR/ABL-T315I in all models used in a synergistic manner [3].GNF-2 dose-dependently inhibited the proliferation of osteoclast precursors through the suppression of the M-CSFR c-Fms. In addition, GNF-2 accelerated osteoclast apoptosis by inducing caspase-3 and Bim expression. Furthermore, GNF-2 interfered with actin cytoskeletal organization and subsequently blocked the bone-resorbing activity of mature osteoclasts [4].
in vivo: Combining PDMP and GNF-2 eliminated transplanted-CML-T315I-mutants in vivo and dose dependently sensitized primary cells from CML T315I patients to GNF-2-induced proliferation inhibition and apoptosis[5].

Name: PF-5190457, CAS: 1334782-79-4, stock 6.6g, assay 98.3%, MWt: 512.67, Formula: C29H32N6OS, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein, Target: GHSR, Biological_Activity: PF-5190457 is a potent and selective ghrelin receptor inverse agonist with a pKi of 8.36.
IC50 & Target: pKi: 8.36 (Humnan ghrelin receptor)[1]
In Vitro: PF-5190457 has a superior balance of ghrelin receptor pharmacology and off-target selectivity[1].
In Vivo: PF-5190457 has excellent selectivity and demonstrates robust increases in glucose-stimulated insulin secretion in human whole and dispersed islets[1].

Name: AM-4668, CAS: 1011531-27-3, stock 31.7g, assay 98.7%, MWt: 488.48, Formula: C24H19F3N2O4S, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein, Target: GPR40, Biological_Activity: AM-4668 is a GPR40 agonist for type 2 diabetes. EC50s of 3.6 nM and 36 nM for GPR40 in A9 cells (GPR40 IP3 assay) and CHO cells (GPR40 aequorin assay), respectively[1].
IC50 & Target: EC50: 3.6 nM (GPR40, in A9 cells), 36 nM (GPR40, in CHO cells)[1]

Name: Lomerizine dihydrochloride KB-2796, CAS: 101477-54-7, stock 26.9g, assay 98.9%, MWt: 541.46, Formula: C27H32Cl2F2N2O3, Solubility: DMSO : 100 mg/mL (184.69 mM; Need ultrasonic), Clinical_Informat: Launched, Pathway: Membrane Transporter/Ion Channel;Neuronal Signaling, Target: Calcium Channel;Calcium Channel, Biological_Activity: Lomerizine dihydrochloride is an antagonist of L- and T-type voltagegated calcium channels.
IC50 & Target: L- and T-type calcium channel[1]
In Vitro: Lomerizine is an antagonist of L- and T-type voltagegated calcium channels and transient receptor potential channel 5 transient receptor potential channels. Lomerizine is a dual L/T-type channel blocker used for prophylaxis of migraine. To demonstrate the effectiveness of Lomerizine in limiting intracellular [Ca2+], its ability to inhibit glutamate-induced death of motor neurons and the associated rise in cytosolic [Ca2+] is evaluated. Lomerizine inhibits the low- and high-voltage activated Ca2+ currents in dissociated rat brain neurons at a threshold concentration of 0.01 μM and IC50 of 1.9 μM and H2O2-induced Ca2+ influx in hippocampal neurons is inhibited by 1 μM Lomerizine. Pre-treatment with 1 μM Lomerizine significantly reduces acute death of motor neurons in spinal cord-DRG cultures exposed to 50 μM glutamate, a concentration that kills approximately 40% of motor neurons in the culture by 6 h, and inhibits the rise in cytosolic [Ca2+] that occurs with glutamate treatment. 0.5 μM Lomerizine is sufficient to significantly prevent the mitochondrial fragmentation of mitochondria induced by SOD1G93A[1]. Lomerizine increases the cytotoxicity of Adriamycin (ADM) and the apoptosis induced by ADM or Vincristine (VCR) in K562/ADM cells. At the concentration of 3, 10 and 30μM, Lomerizine reduces the IC50 value of ADM from 79.03 μM to 28.14, 8.16 and 3.16 μM, respectively. Lomerizine increases the intracellular accumulation of ADM and inhibits the efflux of Rh123 in K562/ ADM cells. No change in P-gp expression is observed after the treatment of Lomerizine for 72 h. Lomerizine has strong reversal effect on MDR in K562/ADM cells by inhibiting P-gp function[2].
In Vivo: To determine whether Ca2+ signaling molecules mediate NMDA-induced neurotoxicity in p50-deficient mice, the neuroprotective effects of chemical reagents are examined, which act on the Ca2+-signaling pathway including CaN activation, on NMDA-induced RGC death. The p50-deficient mice at 2 months of age, showing normal RGC survival, undergo intraperitoneal pretreatments with a NMDA antagonist, MK801 or Memantine; calcium blocker, Lomerizine; and CaN inhibitor, Tacrolimus, daily for 1 week before the injection of 5 nM NMDA. The chronic administration of Lomerizine or Tacrolimus to KO mice for 6 months results in an increase in surviving RGC numbers (p<0.0001)[3]. Lomerizine (KB-2796; 0.3 and 1 mg/kg, i.v.) dose-dependently increases cerebral blood flow significantly at 30 min and 15 min, respectively, after its administration. Lomerizine (1 mg/kg, i.v.) significantly attenuates the expression of c-Fos-like immunoreactivity in the ipsilateral frontoparietal cortex[4].

Name: GNE 2861, CAS: 1394121-05-1, stock 8.1g, assay 98.5%, MWt: 406.48, Formula: C22H26N6O2, Solubility: DMSO : 270 mg/mL (664.24 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Cytoskeleton;Cell Cycle/DNA Damage, Target: PAK;PAK, Biological_Activity: GNE 2861 is a PAK inhibitor that displays group II selectivity. GNE 2861 inhibits PAK4, PAK5 and PAK6 with IC50s of 7.5, 36, 126 nM, respectively.
IC50 & Target: IC50: 7.5 nM (PAK4), 36 nM (PAK5), 126 nM (PAK6)[1]
In Vitro: GNE 2861 is compound 4 from the reference[1].

Name: AF64394, CAS: 1637300-25-4, stock 4.6g, assay 98.5%, MWt: 393.87, Formula: C21H20ClN5O, Solubility: DMSO : ≥ 125 mg/mL (317.36 mM); H2O : < 0.1 mg/mL (insoluble), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: AF64394 is a GPR3 inverse agonist, with a pIC50 of 7.3.
IC50 & Target: pIC50: 7.3 (GPR3)[1].
In Vitro: AF64394 is a GPR3 inverse agonist, with a pIC50 of 7.3. AF34394 and related compounds are only of modest potency and are relatively lipophilic (e.g., AF34394 clogP=5.2, LLE=2.1, and 14b clog P=3.1 and LLE=3.2) the series shows promising SAR and represents an excellent start point for further optimization[1].

Name: Thymus factor X TFX-Jelfa, CAS: 78310-77-7, stock 29.7g, assay 98.5%, MWt: 1000, Formula: N/A, Solubility: H2O, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Thymic factor X (TFX-Jelfa) is an aqueous extract from juvenile calf thymuses and a natural stimulator of lymphocyte function[1][2].
In Vivo: The percentage of necrotic lymphocytes in the spleen in Group I (infected with T. spiralis and treated with Thymus factor X (TFX)) is significantly lower than in the control group on day 7, and approximately the same as in the control group for the rest of the experiment. The percentage of necrotic lymphocytes in muscle tissue in Group I is approximately the same as in the control group on day 7, significantly lower on days 14 and 21 (p<0.0002), approximately the same on days 28 and 35, significantly lower on day 42, and significantly higher on day 60 (p<0.005)[1].

Name: PRN694, CAS: 1575818-46-0, stock 33.7g, assay 98.5%, MWt: 543.67, Formula: C28H35F2N5O2S, Solubility: DMSO : 125 mg/mL (229.92 mM; Need ultrasonic and warming), Clinical_Informat: No Development Reported, Pathway: Protein Tyrosine Kinase/RTK, Target: Itk, Biological_Activity: PRN694 is an irreversible, highly selective and potent covalent interleukin-2-inducible T-cell kinase (ITK) and resting lymphocyte kinase (RLK) dual inhibitor with IC50s of 0.3 nM and 1.4 nM, respectively. PRN694 exhibits extended target residence time on ITK and RLK, enabling durable attenuation of effector cells in vitro and in vivo[1].
IC50 & Target: IC50: 0.3 nM (ITK), 1.4 nM (RLK), 3.3 nM (TEC), 17 nM (BTK), 17 nM (BMX), 30 nM (JAK3), 125 nM (BLK)[1]
In Vitro: PRN694 inhibits TEC, BTK, BMX, BLK, JAK3 with IC50s of 3.3, 17, 17, 125, 30 nM, respectively[1]. 
Immunoblot analysis of TCR activation pathways reveales that PRN694 blocks activation or nuclear translocation of NFAT1, JunB, pIκBα, and pERK. Results reveal inhibition of Ca2+ signaling with PRN694 at all concentrations above 1 nM. PRN694 significantly attenuates NK cell FcR-induced killing at concentrations exceeding 0.37 μM[1]. 
Day 6 flow cytometry analysis reveals that PRN694 significantly inhibits the anti-CD3/CD28-induced proliferation of both CD4 and CD8 T-cells (p<0.01)[1].
In Vivo: The PRN694 occupancy of ITK is 98, 95, and 54% at 1, 6, and 14 h, respectively. The concentrations of PRN694 in the plasma are 2.8, 0.66, and 0.027 μM at 1, 6, and 14 h, respectively. At 14 h, the plasma level of PRN694 is over 10 fold lower than the IC50 in whole blood. RN694 treatment also results in significantly lower weights relative to vehicle (p<0.05)[1]. 
Colitis studies show reduced numbers of CD4+ T cells present in the colonic epithelium of PRN694-treated mice compare with controls[2].

Name: 5Z-7-Oxozeaenol FR148083;L783279;LL-Z 1640-2, CAS: 253863-19-3, stock 19.6g, assay 98.9%, MWt: 362.37, Formula: C19H22O7, Solubility: DMSO : 50 mg/mL (137.98 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Protein Tyrosine Kinase/RTK;MAPK/ERK Pathway, Target: VEGFR;MAP3K, Biological_Activity: 5Z-7-Oxozeaenol is a natural anti-protozoan compound from fungal origin, acting as a potent irreversible and selective inhibitor of TAK1 and VEGF-R2, with IC50s of 8 nM and 52 nM, respectively.
IC50 & Target: IC50: 8 nM (TAK1)[1], 52 nM (VEGF-R2)[2]
In Vitro: 5Z-7-Oxozeaenol is a potent irreversible and selective inhibitor of transforming growth factor (TGF)-β-activated kinase 1 (TAK1, IC50, 8.1 nM), less active on MEK1 (IC50, 411 nM). 5Z-7-Oxozeaenol prevents inflammation by inhibiting the catalytic activity of TAK1 MAPK kinase kinase[1]. 5Z-7-Oxozeaenol is also an inhibitor of VEGF-R2, with an IC50 of 52 nM. 5Z-7-Oxozeaenol has inhibitory activity against VEGF-R3, FLT3, PDGFR-β, B-RAF VE and SRC, with IC50s of 110, 170, 340, 6300 and 6600 nM, respectively[2]. 5Z-7-Oxozeaenol inhibits JNK/p38 paythway, but it is not a direct inhibitor and is signal specific. 5Z-7-Oxozeaenol suppresses the PMA-induced AP-1 activity almost to the basal level in the KT cells, but has no effects on IL-1-induced NF-kB activity in the KK cells[3].

Name: KSI-3716, CAS: 1151813-61-4, stock 39.9g, assay 98.4%, MWt: 426.09, Formula: C17H11BrCl2N2O2, Solubility: DMSO : 5 mg/mL (11.73 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Apoptosis;Autophagy, Target: c-Myc;Autophagy, Biological_Activity: KSI-3716 is a c-Myc inhibitor.
IC50 & Target: c-Myc[1]
In Vitro: KSI-3716 blocks c-MYC/MAX from forming a complex with target gene promoters. KSI-3716 effectively blocks complex formation in a dose dependent manner (IC50=0.84 μM). c-MYC mediated transcriptional activity is inhibited by KSI-3716 at concentrations as low as 1 μM. The expression of c-MYC target genes, such as cyclin D2, CDK4 and hTERT, is markedly decreased. KSI-3716 exerts cytotoxic effects on bladder cancer cells by inducing cell cycle arrest and apoptosis[1].
In Vivo: Intravesical instillation of KSI-3716 at a dose of 5 mg/kg significantly suppresses tumor growth with minimal systemic toxicity[1].

Name: Tautomycin, CAS: 109946-35-2, stock 32.1g, assay 98.4%, MWt: 766.96, Formula: C41H66O13, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Phosphatase, Biological_Activity: Tautomycin, an antifungal antibiotic isolated from the bacterium Streptomyces verticillatus, is a potent and specific inhibitor of protein phosphatases 1 and 2A and induces contraction of smooth muscle under Ca2+-free conditions, with Kiapp values of 0.16 nM and 0.4 nM for PP1 and PP2A, respectively[1][2].
IC50 & Target: Kiapp: 0.16 nM (PP1), 0.4 nM (PP2A)[1].
In Vitro: MTC cell growth is inhibited in a dose-dependent manner by Tautomycin (0-1000 nM, 48 hours)[2]. 
NE markers ASCL1 and CgA in human MTC cells are decreased in a dose-dependent manner by Tautomycin (0-1000 nM, 48 hours)[2].

Name: Sarolaner PF-6450567, CAS: 1398609-39-6, stock 34.2g, assay 98.4%, MWt: 581.36, Formula: C23H18Cl2F4N2O5S, Solubility: H2O : < 0.1 mg/mL (insoluble); DMSO : 150 mg/mL (258.02 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Anti-infection, Target: Parasite, Biological_Activity: Sarolaner (PF-6450567) is an orally active, broad-spectrum ectoparasiticide, has efficacy against fleas and ticks on dogs, with LC80 of 0.3 μg/mL against C. felis and an LC100 of 0.003 μg/mL against O. turicata[1].
IC50 & Target: LC80: 0.3μg/mL (C. felis)[1] 
LC100: 0.003 μg/mL (O. turicata)[1]

Name: Ralinepag APD811, CAS: 1187856-49-0, stock 35.6g, assay 98.7%, MWt: 431.91, Formula: C23H26ClNO5, Solubility: DMSO : 125 mg/mL (289.41 mM; Need ultrasonic and warming), Clinical_Informat: Phase 3, Pathway: GPCR/G Protein, Target: Prostaglandin Receptor, Biological_Activity: Ralinepag is a potent, orally bioavailable and non-prostanoid prostacyclin (IP) receptor agonist, with EC50s of 8.5 nM, 530 nM and 850 nM for human and rat IP receptor and human DP1 receptor, respectively.
IC50 & Target: EC50: 8.5 nM (Human IP receptor), 530 nM (Rat IP receptor), 850 nM (Human DP1 receptor)[1]
In Vitro: Ralinepag is a potent non-prostanoid prostacyclin receptor agonist, with EC50s of 8.5 nM, 530 nM and 850 nM for human and rat IP receptor and human DP1 receptor, respectively. Ralinepag (5c) has potent receptor binding affinity at prostaglandin receptor, with Kis of 1.2 nM, 3 nM, 76 nM, and 256 nM for monkey, human, rat, and dog IP receptor (ligand, [3H]-iloprost), and 2.6 μM, 9.6 μM, 610 nM, 143 nM, and 678 nM for human DP1, EP1, EP2, EP3v6 and EP4 receptors (ligand, [3H]-PGE2), respectively. Moreover, Ralinepag shows no effect on cytochrome P450 enzymes (IC50 > 50 μM for CYPs 1A2, 2D6, 3A4 2C8, 2C9, and 2C19) or hERG channel functional activity in a patch clamp assay (IC50 > 30 μM). Ralinepag also inhibits the ADP-induced human platelet aggregation, with an IC50 of 38 nM[1].
In Vivo: Ralinepag (30 mg/kg, p.o.) markedly reduces the monocrotaline (MCT)-induced increase in pulmonary arterial pressure and pulmonary vessel wall thickness in rats[1].

Name: Losartan Carboxylic Acid E-3174;EXP-3174, CAS: 124750-92-1, stock 28.2g, assay 98.9%, MWt: 436.89, Formula: C22H21ClN6O2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein, Target: Angiotensin Receptor, Biological_Activity: Losartan Carboxylic Acid (E-3174), an active carboxylic acid metabolite of Losartan, is an angiotensin II receptor type 1 (AT1) antagonist. The Ki values are 0.97, 0.57, 0.67 nM for rat AT1B/AT1A and human AT1, respectively. Losartan Carboxylic Acid blocks the angiotensin II-induced responses in vascular smoothmuscle cells (VSMC). Losartan Carboxylic Acid elevates plasma renin activities and reduces mean arterial pressure[1][2][3][4].
IC50 & Target: Angiotensin II receptor type 1[1]
In Vitro: The specific binding of [125I]-angiotensin II to VSMC is inhibited by Losartan Carboxylic Acid (E-3174) with an IC50 of 1.1 nM. Losartan Carboxylic Acid abolishes the angiotensin II-induced formation of inositolphosphates in VSMC. Losartan Carboxylic Acid inhibits the angiotensin II-induced elevation of intracellular cytosolic Ca2+ concentration with an IC50 of 5 nM. Losartan Carboxylic Acid is more effective than losartan in blocking the angiotensin II-induced increase in Egr-1 mRNA. Losartan Carboxylic Acid inhibits the angiotensin II-induced cell protein synthesis with an IC50 of 3 nM[1].
In Vivo: Losartan Carboxylic Acid (E-3174) (0.1 mg/kg; i.v. followed by 0.02 mg/kg/h for 5.5 h) induces a similar level of inhibition (87±4%) of the pressor responses to angiotensin I[3]. 
Intravenous Losartan Carboxylic Acid (0.1 mg/kg+0.01 mg/kg/min) is infused in anesthetized dogs with recent (8.1±0.4 days) anterior myocardial infarction. Electrolytic injury of the left circumflex coronary artery to induce thrombotic occlusion and posterolateral ischemia is initiated 1 h after the start of treatment[4].

Name: Artefenomel OZ439, CAS: 1029939-86-3, stock 3.1g, assay 98.1%, MWt: 469.61, Formula: C28H39NO5, Solubility: DMSO : 4.2 mg/mL (8.94 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Anti-infection;Apoptosis, Target: Parasite;Ferroptosis, Biological_Activity: Artefenomel (OZ439) is a synthetic antimalarial agent with the artemisinin pharmacophore. Artefenomel (OZ439) is a long-acting artemisinin-related agent[1].

Name: Atrial Natriuretic Peptide (ANP) (1-28), human, porcine (Acetate), CAS: 1366000-58-9, stock 36.8g, assay 99%, MWt: 3140.50, Formula: C127H203N45O39S3.C2H4O2, Solubility: H2O, Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein, Target: Endothelin Receptor, Biological_Activity: Atrial Natriuretic Peptide (ANP) (1-28), human, porcine Acetate is a 28-amino acid hormone, that is normally produced and secreted by the human heart in response to cardiac injury and mechanical stretch. ANP (1-28) inhibits endothelin-1 secretion in a dose-dependent way.
IC50 & Target: Endothelin-1[1]
In Vitro: Atrial natriuretic peptide (ANP) is a diuretic, natriuretic, and vasodilatory peptide hormone originally isolated from mammalian hearts. In cultured porcine endothelial cells the inhibition by porcine ANP (1-28) of immunoreactive endothelin-1 secretion after stimulation with Angiotensin II (Ang II) is paralleled by an increase in the cellular cGMP level. Porcine ANP (1-28) strongly inhibits immunoreactive endothelin-1 secretion in porcine aorta after stimulation with Ang II[1]. ANP is a cardiac hormone involved in electrolyte and fluid homeostasis. The inhibition by ANP of endothelin-1 secretion stimulated by angiotensin II (ANGII) and thrombin using cultured human umbilical-vein endothelial cells. Human ANP (1-28) inhibits immunoreactive (ir)-endothelin-1 secretion and increases cyclic GMP in the human umbilical-vein endothelial cells[2]. In glomeruli from normal rats, Human 125I-ANP (1-28) binds to a single population of high affinity receptors with a mean equilibrium dissociation constant of 0.46 nM. Human ANP (1-28) binds to the glomerular ANP receptor with high affinity stimulated cGMP accumulation. Human ANP (1-28) markedly stimulates cGMP generation, but not cAMP generation in normal rat glomeruli[3].

Name: Gemilukast ONO-6950, CAS: 1232861-58-3, stock 13.1g, assay 98.1%, MWt: 601.68, Formula: C36H37F2NO5, Solubility: DMSO : 250 mg/mL (415.50 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein, Target: Leukotriene Receptor, Biological_Activity: Gemilukast is an orally active and potent dual cysteinyl leukotriene 1 and 2 receptors (CysLT1 and CysLT2) antagonist, with IC50s of 1.7, 25 nM for human CysLT1 and CysLT2, respectively.
IC50 & Target: IC50: 1.7 nM (human CysLT1), 25 nM (human CysLT2)[1].
In Vitro: Gemilukast is an orally active and potent dual cysteinyl leukotriene 1 and 2 receptors (CysLT1 and CysLT2) antagonist, with IC50s of 1.7, 25 nM for human CysLT1 and CysLT2, respectively[1]. Both Gemilukast (ONO-6950) and montelukast inhibit human CysLT1 receptor-mediated calcium response with IC50 values of 1.7 and 0.46 nM, respectively[2].
In Vivo: Gemilukast at 0.03 to 10 mg/kg, p.o. dose-dependently attenuates LTC4-induced bronchoconstriction with almost complete inhibition at 3 mg/kg. The inhibitory effect of Gemilukast on LTC4-induced bronchoconstriction is significantly stronger than that of montelukast at the dose of 1 mg/kg or more. Gemilukast (0.03 to 1 mg/kg, p.o.) dose-dependently attenuates LTD4-induced airway vascular hyperpermeability with complete inhibition at 0.3 mg/kg. Gemilukast at 0.1 to 3 mg/kg, p.o. dose-dependently inhibits OVA-induced bronchoconstriction. The inhibitory effect of Gemilukast at 3 mg/kg is significantly greater than that of montelukast alone and comparable to that of combination therapy with montelukast and BayCysLT2RA[2].

Name: Somatostatin, CAS: 51110-01-1, stock 9.1g, assay 98.8%, MWt: 1637.88, Formula: N/A, Solubility: H2O : 50 mg/mL (30.53 mM; Need ultrasonic), Clinical_Informat: Phase 4, Pathway: Others, Target: Others, Biological_Activity: Somatostatin is a tetradecapeptide which can suppress the growth hormone (GH) secretion and control the pituitary hormone secretion in human CNS.
In Vitro: Somatostatin is a tetradecapeptide which can suppress the growth hormone (GH) secretion and control the pituitary hormone secretion in human CNS. Somatostatin has two biologically active forms: the predominant form is the 14 amino-acid long Somatostatin-14 while the more potent form is the amino-terminus extended Somatostatin-28. The biological roles of the two Somatostatin isoforms very strongly overlap and the relative proportions of Somatostatin-14 to Somatostatin-28 vary between different tissues. Somatostatin can reduce adhesion of carcinosarcoma cells to the blood vessels and thus attenuate the metastatic potential of these tumours. Somatostatin can also inhibit monocyte chemotactic migration[1].

Name: Pexmetinib ARRY-614, CAS: 945614-12-0, stock 2.5g, assay 98.4%, MWt: 556.63, Formula: C31H33FN6O3, Solubility: DMSO : ≥ 125 mg/mL (224.57 mM), Clinical_Informat: No Development Reported, Pathway: MAPK/ERK Pathway;Autophagy, Target: p38 MAPK;Autophagy, Biological_Activity: Pexmetinib is a potent Tie-2 and p38 MAPK dual inhibitor, with IC50s of 1 nM, 35 nM and 26 nM for Tie-2, p38α and p38β, respectively, and can be used in the research of acute myeloid leukemia.
IC50 & Target: IC50: 1 nM (Tie-2), 35 nM (p38α), 26 nM (p38β)[1]
In Vitro: Pexmetinib is a Tie-2 and p38 MAPK dual inhibitor, with IC50s of 1 nM, 35 nM and 26 nM for Tie-2, p38α and p38β, respectively. Pexmetinib also shows IC50s of 4 nM (Abl), 10 nM (Arg), 28 nM (FGFR1), 47 nM (Flt1), 42 nM (Flt4), 41 nM (Fyn), 26 nM (Hck), 25 nM (Lyn), and 26 nM (MINK), respectively. Pexmetinib (0.5, 1 μM) blocks leukemic cell proliferation and stimulates hematopoietic activity in myelodysplastic syndromes[1].

Name: Amfenac Sodium Hydrate, CAS: 61618-27-7, stock 9g, assay 98.1%, MWt: 295.27, Formula: C15H14NNaO4, Solubility: DMSO : 150 mg/mL (508.01 mM; Need ultrasonic and warming), Clinical_Informat: Launched, Pathway: Immunology/Inflammation, Target: COX, Biological_Activity: Amfenac Sodium Hydrate is a COX-2 inhibitor.
IC50 & Target: COX-2[1]
In Vitro: Cells transfected to express COX-2 have a higher proliferation rate than those do not. The addition of Amfenac Sodium Hydrate significantly decreases the proliferation rate of all cell lines. Nitric oxide production by macrophages is inhibited by the addition of melanoma conditioned medium, the addition of Amfenac Sodium Hydrate partially overcomes this inhibition[1]. Results show that Amfenac Sodium Hydrate inhibits the release of B-glucuronidase: 5×10-4 M Amfenac Sodium Hydrate inhibits the release of the enzyme 35.3 and 16.3% in the presence of 10-8, and 10-7 M FMLP, respectively. Addition of 10-4 M Amfenac Sodium Hydrate causes 28.3% inhibition of aggregation of polgmorphonuclear leukocgtes (PMNs) during incubation for 16 min with 10-8 M FMLP[2].

Name: VAS2870, CAS: 722456-31-7, stock 2.3g, assay 98.6%, MWt: 360.39, Formula: C18H12N6OS, Solubility: DMSO : 83.3 mg/mL (231.14 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: NADPH Oxidase, Biological_Activity: VAS2870 is a NADPH oxidase (NOX) inhibitor.
IC50 & Target: Target: NADPH oxidase[1]
In Vitro: VAS2870 is effective to suppress PDGF-BB-dependent activation of NADPH oxidase and subsequent production of intracellular ROS. Furthermore, VAS2870 suppresses PDGF-BB-dependent chemotaxis, but not DNA synthesis. Preincubation with VAS2870 (10 and 20 μM) completely abolishes PDGF-mediated NADPH oxidase activation and ROS production. Preincubation with VAS2870 (0.1-20 μM) does not affect PDGF-induced cell cycle progression. However, it abolishes PDGF-dependent chemotaxis of VSMC in a concentration-dependent manner (100% inhibition at 10 μM)[1]. VAS2870 inhibits dose-dependently autocrine increase of cell number in FaO rat hepatoma cells, and almost completely blocked ROS production and thymidine incorporation when used at 25 mM. VAS2870 blocks serum-dependent cell growth of FaO rat hepatoma cells. VAS2870 inhibits proliferation of different human hepatocellular carcinoma (HCC) cell lines. VAS2870 pretreatment enhances TGF-b-mediated apoptosis of FaO rat hepatoma cells[2].

Name: ML171 2-Acetylphenothiazine;2-APT, CAS: 6631-94-3, stock 21.6g, assay 98.5%, MWt: 241.31, Formula: C14H11NOS, Solubility: DMSO : ≥ 64 mg/mL (265.22 mM), Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: NADPH Oxidase, Biological_Activity: ML171 (2-Acetylphenothiazine;2-APT) is a potent and selective NADPH oxidase 1 (Nox1) inhibitor that blocks Nox1-dependent ROS generation, with an IC50 of 0.25 μM in HEK293-Nox1 confirmatory assay.
IC50 & Target: IC50: 0.25 μM (HEK293-Nox1), 0.129 μM (HT29)[1]
In Vitro: Nox1-dependent ROS generation has been shown to play a pivotal role in cell signaling, cell growth, angiogenesis, motility and blood pressure regulation. ML171 strongly blocks ROS generation in HT29 cells (IC50=0.129 μM) and only increasing over-expression of Nox1 can overcome the blockage of ROS generation caused by ML171 treatment in HEK293 cell system reconstituted with all the components required Nox1-dependent ROS generation. ML171 efficiently blocks ROS production measured by carboxy-H2-DCFDA staining as well as DPI used as a positive control. When ML171 is tested in HEK293-Nox1 reconstituted cell system, higher potency in blocking Nox1-dependent ROS generation is observed compared with the parental compound[1].

Name: Diethyl oxalpropionate, CAS: 759-65-9, stock 13.1g, assay 98.2%, MWt: 202.20, Formula: C9H14O5, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: Diethyl oxalpropionate is an intermediate for poly((R,S)-3,3-dimethylmalic acid) (PDMMLA) derivative synthesis. PDMMLA derivative can be used in synthesis of nanoparticles and study of warfarin encapsulation and controlled release[1].

Name: Ro 64-6198, CAS: 280783-56-4, stock 3.6g, assay 98.4%, MWt: 401.54, Formula: C26H31N3O, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein;Neuronal Signaling, Target: Opioid Receptor;Opioid Receptor, Biological_Activity: Ro 64-6198 is a potent, selective, nonpeptide, high-affinity, high cellular permeability and brain penetration N/OFQ receptor (NOP) agonist with an EC50 value of 25.6 nM. Ro 64-6198 is at least 100 times more selective for the NOP receptor over the classic opioid receptors. Ro 64-6198 can be used to treat stress and anxiety, addiction, neuropathic pain, cough, and anorexia[1][2].
IC50 & Target: Nociceptin receptor[1]
In Vitro: Ro 64-6198 also produces rapid desensitization of the NOP receptor. In vitro studies shows that treatment with Ro 64-6198 results in a functional desensitization of the receptor, a loss in binding sites, and an apparent decrease in binding affinity. The desensitization produced by Ro 64-6198 is not reversed by acidic washes[1]. 
Ro 64-6198 does recruit both arrestin3 (EC50 of 0.912 µM) and arrestin2 (EC50 of 1.20 µM) to the NOP receptor in a concentration-dependent manner comparably with N/OFQ[2].
In Vivo: At low doses Ro 64-6198 is anxiolytic in several neophobic tests, including the marble burying test in mice, the elevated plus maze in rats and the open field test in rats. In the marble burying test, at 1 mg/kg, i.p., Ro 64-6198 produces a decrease in the number of marbles buried, without altering locomotor activity, indicating a decrease in neophobia and anxiety. Ro 64-6198 selectively increases the number of open arm transitions and time spent in the open arms of the elevated plus maze at doses of 0.32-3 mg/kg, i.p., without affecting closed arm transitions or locomotor activity in the closed arms. In the open field test, Ro 64-6198, at doses of 0.32-3 mg/kg, attenuates the inhibition of exploration that results from the stress of a novel environment[1].

Name: Dasotraline SEP 225289, CAS: 675126-05-3, stock 15.5g, assay 98.6%, MWt: 292.20, Formula: C16H15Cl2N, Solubility: DMSO : ≥ 31 mg/mL (106.09 mM), Clinical_Informat: Phase 3, Pathway: Neuronal Signaling;Neuronal Signaling, Target: Dopamine Transporter;Serotonin Transporter, Biological_Activity: Dasotraline is a triple reuptake inhibitor that blocks dopamine, norepinephrine, and serotonin transporters with IC50 values of 4, 6, and 11 nM, respectively.
IC50 & Target: IC50: 4 nM (dopamine transporter), 6 nM (norepinephrine transporter),11 nM (5-HT transporter)[1]
In Vivo: The present in-vivoelectrophysiological study is undertaken to determine the effects of the triple reuptake inhibitor Dasotraline (SEP-225289) on the neuronal activities of locus coeruleus (LC) NE, ventral tegmental area (VTA) DA and dorsal raphe (DR) 5-HT neurons. Administered acutely, Dasotraline dose-dependently decreases the spontaneous firing rate of LC NE, VTA DA and DR 5-HT neurons through the activation of α2, D2 and 5-HT1A autoreceptors, respectively. Dasotraline predominantly inhibits the firing rate of LC NE neurons while producing only a partial decrease in VTA DA and DR 5-HT neuronal discharge. Dasotraline is equipotent at inhibiting 5-HT and NE transporters since it prolongs to the same extent the time required for a 50% recovery (RT50) of the firing activity of dorsal hippocampus CA3 pyramidal neurons from the inhibition induced by microiontophoretic application of 5-HT and NE. The recovery time (RT), from the suppression of hippocampus pyramidal neuron firing activity following microiontophoresis application of 5-HT and NE, is assessed by determining the RT50 values before and after the acute intravenous administration of cumulative doses of Dasotraline (1–8 mg/kg). Although Dasotraline (1 and 2 mg/kg) does not modify the firing activity of CA3 pyramidal neurons, a significant reduction (∼50%) is detected with the highest dose (8 mg/kg). In rats pre-treated with WAY100635, Dasotraline (0.5-2 mg/kg i.v.) elicits a significant increase in DR 5-HT firing rate. In rats pre-treated with WAY100635, Dasotralinesignificantly increases the number of single spikes and bursts[1].

Name: IWP-4, CAS: 686772-17-8, stock 2.1g, assay 98.3%, MWt: 496.62, Formula: C23H20N4O3S3, Solubility: DMSO : 5 mg/mL (10.07 mM; Need ultrasonic and warming), Clinical_Informat: No Development Reported, Pathway: Stem Cell/Wnt, Target: Wnt, Biological_Activity: IWP-4 is a small molecule Wnt inhibitor with an IC50 of 25 nM.
IC50 & Target: IC50: 25 nM (Wnt)[1]
In Vitro: IWP-4 is a small molecule Wnt inhibitor with an IC50 of 25 nM. IWP-4 induces the expression of cardiac markers, including cardiac troponin I (CTNI) and cardiac myosin heavy chain bright cells (MYHhi +). IWP-4 also results in the appearance of beating foci (0.44±0.10 SEM beats per second), which is absent in all cultures not receiving IWP-4. Further, flow cytometric analysis shows that there are significantly more MYHlo + cells in IWP-4 treated cultures (P<0.0002) compare with untreated cultures at day 16, being 17.0±1.3 SD% and 5.4±1.4 SD%, respectively. Quantification of NKX2-5 protein expression shows that 63% (481/817) of IWP-4 treated cells display nuclear NKX2-5 expression[1]. Mesenchymal precursor cells (MPCs) treated with IWP-4 show no significant changes in the expression of AXIN2, CTNNB1 and GSK3B as compare to osteogenic medium alone on day 7, but MPCs treated with IWP-4 express elevates levels of DKK1 and GSK3β on day 21. IWP-4 also causes a significant down regulation of SPARC and COL1A1[2].

Name: KDU691, CAS: 1513879-19-0, stock 7.2g, assay 98.2%, MWt: 419.86, Formula: C22H18ClN5O2, Solubility: DMSO : 150 mg/mL (357.26 mM; Need ultrasonic and warming), Clinical_Informat: No Development Reported, Pathway: PI3K/Akt/mTOR;Anti-infection, Target: PI4K;Parasite, Biological_Activity: KDU691 is a PI4K inhibitor.
IC50 & Target: PI4K[1]
In Vivo: During the 5 days of dosing, no major weight changes are observed in the animals that receive KDU691 as prophylactic treatment (group 691-proph). From the fourth day of dosing, the animals that are treated with KDU691 show a transient yellow skin color. The KDU691 radical-cure group (group 691-RC) becomes blood-stage positive again at 31.8±0.5 days p.i. (range, 31 to 32 days). Clinical chemistry analysis of the group 691-RC monkeys reveals that bilirubin levels accumulate during the 5-day radical-cure treatment with KDU691[1].

Name: AMG 579, CAS: 1227067-61-9, stock 7.2g, assay 98.8%, MWt: 441.48, Formula: C25H23N5O3, Solubility: DMSO : 41.67 mg/mL (94.39 mM; Need ultrasonic), Clinical_Informat: Phase 1, Pathway: Metabolic Enzyme/Protease, Target: Phosphodiesterase (PDE), Biological_Activity: AMG 579 is a potent, selective, and efficacious inhibitor of phosphodiesterase 10A (PDE10A) with an IC50 of 0.1 nM.
IC50 & Target: IC50: 0.1 nM (Phosphodiesterase 10A)[1]
In Vivo: AMG 579 shows statistically significant reduction of PCP induced behavior in rats over the 2 h period. Minimum effective doses for efficacy in PCP-LMA model is determined to be 0.3 mg/kg for AMG 579. In dog, 5 exhibits superior oral bioavailability of 72%[1].

Name: NITD008 7-Deaza-2'-C-acetylene-adenosine, CAS: 1044589-82-3, stock 30.1g, assay 98.4%, MWt: 290.27, Formula: C13H14N4O4, Solubility: DMSO : ≥ 50 mg/mL (172.25 mM), Clinical_Informat: No Development Reported, Pathway: Cell Cycle/DNA Damage, Target: DNA/RNA Synthesis, Biological_Activity: NITD008 is a potent and selective flaviviruse inhibitor which can inhibit Dengue Virus Type 2 (DENV-2) with an EC50 of 0.64 μM.
IC50 & Target: EC50: 0.64 μM (DENV-2)[1]
In Vitro: NITD008 potently inhibits other, including Dengue virus (DENV), West Nile virus, yellow fever virus, and Poissan virus. NITD008 inhibits DENV-2 in a dose-responsive manner, with an EC50 value of 0.64 μM; treatment with 9 μM compound reduces viral titer by >104-fold[1]. NITD008 also inhibits a luciferase-reporting replicon of hepatitis C virus (HCV, genotype 1b), a member from the genus Hepacivirus, with an EC50 value of 0.11 μM[1].
In Vivo: NITD008 is orally bioavailable and has good pharmacokinetic properties. NITD008 exhibits the best pharmacokinetic parameters when formulated using 6 N of HCl (1.5 equimolar amount), 1 N of NaOH (pH adjusted to 3.5), and 100 mM citrate buffer (pH 3.5). Following i.v. injection, NITD008 has a high volume of distribution (3.71 L/kg) and a low systemic clearance (31.11 mL/min per kg), resulting in a long elimination half-life (t1/2=4.99 h). After p.o. dosing, NITD008 is rapidly absorbed (time of peak plasma concentration=0.5 h), with a maximal plasma concentration of 3 μM and bioavailability of 48%. Treatment of the mice immediately after viral infection with 1 mg/kg of NITD008 does not reduce mortality, but treatment with 3 mg/kg partially protects and treatment with ≥10 mg/kg completely protects the infected mice from death. NITD008 can suppress peak viremia, decrease cytokine elevation, and prevent death[1].

Name: Nitenpyram, CAS: 150824-47-8, stock 5.9g, assay 98.8%, MWt: 270.72, Formula: C11H15ClN4O2, Solubility: DMSO : 250 mg/mL (923.46 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Neuronal Signaling;Membrane Transporter/Ion Channel, Target: nAChR;nAChR, Biological_Activity: Nitenpyram is a calss of neonicotinoid and an insect nicotinic acetylcholine receptor (nAChR) agonist with an IC50 of 14 nM. Nitenpyram is an oral fast-acting insecticide used to suppress sucking insects on companion animals[1][2].
In Vivo: Nitenpyram is administered orally (1 mg/kg) for the short-term control of fleas in dogs and cats. Fleas start to fall from the animals 30 minutes post-administration and one dose can protect animals for 1-2 days[1]. 
Since Nitenpyram is highly lipophilic, it is administered orally after the meal in order to induce bile flow to help dissolve the chemical, thereby increasing GI absorption of the drug. It is rapidly and completely absorbed from the GI tract in less than 90 minutes and is completely excreted in urine within 48 hours after oral administration to dogs and cats. Nitenpyram undergoes hydroxylation, followed by conjugation in the liver. The conjugates of Nitenpyram are excreted in the urine and Nitenpyram is not accumulated in body tissues. The plasma half-life of Nitenpyram in dogs and cats are 3 and 8 hours, respectively. It is likely that animals with liver and/or kidney problems may have longer plasma half-life of Nitenpyram[1].

Name: Thiophanate-Methyl, CAS: 23564-05-8, stock 2.8g, assay 98.3%, MWt: 342.39, Formula: C12H14N4O4S2, Solubility: DMSO : 300 mg/mL (876.19 mM; Need ultrasonic); H2O : < 0.1 mg/mL (insoluble), Clinical_Informat: No Development Reported, Pathway: Anti-infection, Target: Fungal, Biological_Activity: Thiophanate-Methyl is a systematic fungicide[1].

Name: Tricyclazole, CAS: 41814-78-2, stock 15.6g, assay 98.8%, MWt: 189.24, Formula: C9H7N3S, Solubility: DMSO : 125 mg/mL (660.54 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Anti-infection, Target: Bacterial, Biological_Activity: Tricyclazole is a pentaketide-derived melanin biosynthesis inhibitor and a unique fungicide for control of Pyricularia oryzae on rice[1][2].
IC50 & Target: Pentaketide-derived melanin biosynthesis[1]

Name: Mancozeb, CAS: 8018-01-7, stock 16.6g, assay 98.9%, MWt: 661.36, Formula: C8H12Mn2N4S8Zn2 2-, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Anti-infection, Target: Fungal, Biological_Activity: Mancozeb is an ethylene-bis-dithiocarbamate fungicide[1].

Name: Pimozide R6238, CAS: 2062-78-4, stock 1.2g, assay 98.1%, MWt: 461.55, Formula: C28H29F2N3O, Solubility: DMSO : 33.33 mg/mL (72.21 mM; Need ultrasonic); H2O : < 0.1 mg/mL (insoluble), Clinical_Informat: Launched, Pathway: GPCR/G Protein;Neuronal Signaling;GPCR/G Protein;JAK/STAT Signaling;Stem Cell/Wnt;Neuronal Signaling, Target: Dopamine Receptor;Dopamine Receptor;Adrenergic Receptor;STAT;STAT;Adrenergic Receptor, Biological_Activity: Pimozide is a dopamine receptor antagonist, with Kis of 1.4 nM, 2.5 nM and 588 nM for dopamine D2, D3 and D1 receptors, respectively, and also has affinity at α1-adrenoceptor, with a Ki of 39 nM; Pimozide also inhibits STAT3 and STAT5.
IC50 & Target: Ki: 1.4 nM (Dopamine D2 receptor), 2.5 nM (Dopamine D3 receptor), 588 nM (Dopamine D1 receptor), 39 nM (α1-adrenoceptor), 310 nM (5-HT1A)[1] 
STAT3[2], STAT5[3]
In Vitro: Pimozide is a dopamine receptor antagonist, with Kis of 1.4 nM, 2.5 nM and 588 nM for dopamine D2, D3 and D1 receptors, respectively; also has affinity at α1-adrenoceptor and 5-HT1A, with Kis of 39 nM and 310 nM, respectively[1]. Pimozide acts as an inhibitor of STAT3. Pimozide (0-15 μM) shows inhibitory of the proliferation of U2OS cells, with IC50 value at 24, 48, and 72 h of 22.16 ± 2.54, 17.49 ± 1.14 and 13.78 ± 0.34 μM, respectively. Pimozide (10 μM) inhibits the colony- and sphere-forming abilities of osteosarcoma cells. Pimozide (15 μM) induces G0/G1 phase cell cycle arrest, suppresses the extracellular signal-regulated kinase (Erk) signaling to inhibit cell viability, and produces ROS generation through inhibiting antioxidant enzyme gene catalase expression in osteosarcoma cells[2]. Pimozide acts as an inhibitor of STAT5. Pimozide reduces the expression of endogenous STAT5 target genes, and decreases STAT5 tyrosine phosphorylation[3].

Name: C527, CAS: 192718-06-2, stock 9.8g, assay 99%, MWt: 293.25, Formula: C17H8FNO3, Solubility: DMSO : < 1 mg/mL (insoluble or slightly soluble), Clinical_Informat: No Development Reported, Pathway: Cell Cycle/DNA Damage, Target: Deubiquitinase, Biological_Activity: C527 is a is a pan DUB enzyme inhibitor, with a high potency for the USP1/UAF1 complex (IC50=0.88 μM).
IC50 & Target: 0.88 μM (USP1)[1]
In Vitro: Pretreatment of USP1/UAF1 with C527 resulted in inhibition of its enzyme activity with an IC50 of 0.88±0.03 μM. C527 inhibits the DUB activity of the USP12/USP46 complex and other DUB enzymes in vitro. However, the IC50 of C527 for these DUB enzymes was higher in comparison with USP1/UAF1 complex. C527 has considerably less inhibitory effect on UCH-L1 and UCH-L3, a different subclass of DUB enzymes. C527 treatments causes an increase in the levels of Ub-FANCD2 and Ub-FANCI. Pretreatment of cells with the C527 causes an enhancement in the cytoxicity of mitomycin C and camptothecin. C527 treatments lead to an increase in ubiquitinated forms of FANCD2 and FANCI, cause a decrease in homologous recombination activity, and sensitize cells to DNA damaging agents[1].

Name: Leptomycin B CI 940;LMB, CAS: 87081-35-4, stock 20.3g, assay 98.2%, MWt: 540.73, Formula: C33H48O6, Solubility: 10 mM in Ethanol, Clinical_Informat: Phase 3, Pathway: Membrane Transporter/Ion Channel;Anti-infection, Target: CRM1;Fungal, Biological_Activity: Leptomycin B (CI 940; LMB) is a potent inhibitor of the nuclear export of proteins. Leptomycin B inactivates CRM1/exportin 1 by covalent modification at a cysteine residue. Leptomycin B is a potent antifungal antibiotic blocking the eukaryotic cell cycle[1].
IC50 & Target: CRM1/exportin 1[1]

Name: CK-666, CAS: 442633-00-3, stock 19.7g, assay 98.8%, MWt: 296.34, Formula: C18H17FN2O, Solubility: DMSO : 125 mg/mL (421.81 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Cytoskeleton, Target: Arp2/3 Complex, Biological_Activity: CK-666 is a cell-permeable inhibitor of actin-related protein Arp2/3 complex, and binds to Arp2/3 complex, stabilizes the inactive state of the complex, blocking movement of the Arp2 and Arp3 subunits into the activated filament-like (short pitch) conformation[1].
IC50 & Target: Arp2/3 complex[1]

Name: CK-869, CAS: 388592-44-7, stock 12g, assay 98.6%, MWt: 394.28, Formula: C17H16BrNO3S, Solubility: DMS : 75 mg/mL (190.22 mM; Need ultrasonic); H2O : < 0.1 mg/mL (insoluble), Clinical_Informat: No Development Reported, Pathway: Cytoskeleton, Target: Arp2/3 Complex, Biological_Activity: CK-869 is an Actin-Related Protein 2/3 (ARP2/3) complex inhibitor, with an IC50 of 7 μM.
IC50 & Target: IC50: 7 μM (ARP2/3)[1].
In Vitro: CK-869 is an Actin-Related Protein 2/3 (ARP2/3) complex inhibitor, with an IC50 of 7 μM[1]. CK-869 significantly inhibits MT polymerization even at a concentration of 25 μM[2].

Name: Cytochalasin B Phomin, CAS: 14930-96-2, stock 36.5g, assay 98.4%, MWt: 479.61, Formula: C29H37NO5, Solubility: DMSO : ≥ 100 mg/mL (208.50 mM); Ethanol : 25 mg/mL (52.13 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Cytoskeleton, Target: Arp2/3 Complex, Biological_Activity: Cytochalasin B is a cell-permeable mycotoxin binding to the barbed end of actin filaments, disrupting the formation of actin polymers, with Kd value of 1.4-2.2 nM for F-actin.
IC50 & Target: Kd: 2.2 nM (F-actin, with Mg2+), 1.4 nM (F-actin, with Mg2+/K+)[1]
In Vitro: Cytochalasin B is a cell-permeable mycotoxin binding to the barbed end of actin filaments, inhibits the enlongation and shortening of actin filaments, with Kds of 2.2 nM and 1.4 nM for F-actin in the presence of MgCl2 (2 mM) or MgCl2 (2 mM) plus KCl, respectively[1]. Cytochalasin B (0.1-10 μM) shows inhibitory effect on multiple murine cancer cell lines, with IC50s of 2.56 μM (M109c), 10.46 μM (B16BL6), 105.5 μM (P388/ADR), 51.9 μM (P388/S) and IC80s of 12.23 μM (M109c), 44.86 μM (B16BL6), 188.4 μM (P388/ADR), 84.1 μM (P388/S) after treatment for 3 h, with IC50s of 0.25 μM (M109c), 0.37 μM (B16F10), 0.87 μM (B16BL6), and IC80s of 0.75 μM (M109c), 1.21 μM (B16F10), 10.41 μM (B16BL6) after treatment for 4 days[2]. Cytochalasin B (6 μM) increases the myofibrillar fragmentation index (MFI), which is attributed to the intensely breaking of myofibrillar proteins into short segments. Cytochalasin B also accelerates the disruption of actin filaments. In addition, Cytochalasin B accelerates the transformation from F-actin to G-actin, lowering the content of F-actin and significantly increasing G-actin bands during postmortem conditioning[3].
In Vivo: Cytochalasin B (10, 25, 50 mg/kg, i.p.) dose-dependently increases the life expectancy of Balb/c mice bearing with P388/ADR leukemias. Cytochalasin B at 50 mg/kg produces 10 % long-term survival in the multidrug resistant P388/ADR cohort, and 40 % long-term survival in the drug sensitive P388/S cohort[2].

Name: Cytochalasin D Zygosporin A;NSC 209835, CAS: 22144-77-0, stock 3.9g, assay 98.2%, MWt: 507.62, Formula: C30H37NO6, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Cytoskeleton, Target: Arp2/3 Complex, Biological_Activity: Cytochalasin D (Zygosporin A; NSC 209835) is a potent and cell-permeable inhibitor of actin polymerization derived from fungus, inhibits the G-actin–cofilin interaction by binding to G-actin. Cytochalasin D (Zygosporin A; NSC 209835) also inhibits the binding of cofilin to F-actin and decreases the rate of both actin polymerization and depolymerization in living cells[1][2][3].
IC50 & Target: G-actin[1]

Name: L-Alanosine NSC-153353, CAS: 5854-93-3, stock 3.2g, assay 98.7%, MWt: 149.11, Formula: C3H7N3O4, Solubility: H2O : 15 mg/mL (100.60 mM; ultrasonic and adjust pH to 8 with NaOH), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: L-Alanosine (NSC-153353), an antibiotic from Streptomyces alanosinicus, has antineoplastic activity. L-Alanosine (NSC-153353) inhibits adenylosuccinate synthetase, which converts inosine monophospate (IMP) into adenylosuccinate. L-Alanosine (NSC-153353) blocks the common de novo purine biosynthesis pathway and, thereby, inhibits tumor cells with MTAP deficiency[1][2][3].

Name: 5'-Methylthioadenosine 5'-(Methylthio)-5'-deoxyadenosine;5'-Deoxy-5'-(methylthio)adenosine; 5'-S-Methyl-5'-thioadenosine, CAS: 2457-80-9, stock 1.8g, assay 98.5%, MWt: 297.33, Formula: C11H15N5O3S, Solubility: DMSO : 12.5 mg/mL (42.04 mM; Need ultrasonic); DMF : 2.5 mg/mL (8.41 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: 5'-Methylthioadenosine is produced from S-adenosylmethionine and behaves as a powful inhibitory product.
In Vitro: 5'-Methylthioadenosine (MTA) can affect cellular processes in many ways. 5'-Methylthioadenosine has been shown to influence numerous critical responses of the cell including regulation of gene expression, proliferation, differentiation and apoptosis. Although most of these responses have been observed at the pharmacological level, their specificity makes it tempting to speculate that endogenous 5'-Methylthioadenosine could play a regulatory role in the cell. Finally, observations carried out in models of liver damage and cancer demonstrate a therapeutic potential for 5'-Methylthioadenosine that deserves further consideration[1].

Name: Navitoclax ABT-263, CAS: 923564-51-6, stock 18.6g, assay 98.1%, MWt: 974.61, Formula: C47H55ClF3N5O6S3, Solubility: DMSO : 75 mg/mL (76.95 mM; Need ultrasonic); DMF : ≥ 100 mg/mL (102.61 mM); H2O : < 0.1 mg/mL (insoluble), Clinical_Informat: Phase 2, Pathway: Apoptosis, Target: Bcl-2 Family, Biological_Activity: Navitoclax (ABT-263) is a potent and orally active Bcl-2 family protein inhibitor that binds to multiple anti-apoptotic Bcl-2 family proteins, such as Bcl-xL, Bcl-2 and Bcl-w, with a Ki of less than 1 nM.
IC50 & Target: Ki: < 1 nM (Bcl-xL), < 1 nM (Bcl-2), < 1 nM (Bcl-w)
In Vitro: Navitoclax (ABT-263) is active against approximately one-half of the cell lines of the PPTP in vitro panel. The median IC50 for all of the lines in the panel is 1.91 µM[1]. Navitoclax in combination with chemotherapy agents leads most ovarian cancer cell lines a synergistic response, and enhances the caspase activation in both SK-OV-3 and IGROV-1 cell lines[2].
In Vivo: Navitoclax (100 mg/kg; orally; 21-day treatment) enhances the activity of OSI-744 in vivo. As a single agent, 100 mg/kg Navitoclax alone dosed daily has no significant antitumor activity, whereas daily dosing of OSI-744 at 50 mg/kg results in significant tumor stasis (%TGI=52) during a 21-day treatment period. Notably, the combination of Navitoclax and OSI-744 dosed daily for 21 consecutive days results in 98% TGI and durable tumor regressions in 100% of treated tumor-bearing mice[3].

Name: JNJ 303, CAS: 878489-28-2, stock 26.8g, assay 98.8%, MWt: 440.98, Formula: C21H29ClN2O4S, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Membrane Transporter/Ion Channel, Target: Potassium Channel, Biological_Activity: JNJ 303 is a potent IKs blocker with an IC50 value of 64 nM. JNJ 303 does not have any effects on other cardiac channels at concentrations of 3.3 μM for INa, Ica, Ito, and IKr. JNJ 303 induces QT-prolongations and causes unprovoked torsades de pointes (TdP)[1].
IC50 & Target: IC50: 64 nM (IKs)[1]

Name: Cinromide trans-3-Bromo-N-ethylcinnamamide, CAS: 58473-74-8, stock 18.7g, assay 98.5%, MWt: 254.12, Formula: C11H12BrNO, Solubility: DMSO : ≥ 310 mg/mL (1219.90 mM), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Cinromide is a broad-spectrum anticonvulsant agent.
In Vitro: Cinromide (10-100 μM) inhibits 5-HT-induced contractions in rat fundus strips by 46%. Cinromide (100 μM) inhibits monoamine oxidase prepared from both liver and brain of rats[1].
In Vivo: Cinromide shows electroshock convulsion and leptazol(pentetrazo1)-induced convulsion in mice, with ED50s of 60 ± 11 mg/kg, 90 ± 15 mg/kg and 80 ± 15 mg/kg, 300 ± 61 mg/kg for i.p. and oral administrion, respectively. Cinromide produces a dose-related antileptazol activity with an ED50 value of 58 ± 11 mg/kg by i.p. administration in rats. Furthermore, Cinromide (75 mg/kg) significantly elevates the amount of leptazol needed to induce clonic seizures in the intravenously infused leptazol-threshold test in rats. Cinromide (300 mg/kg, i.p) shows no sifnificant effect on the anaesthetized open-chested dogs after 4 h treatment, neither in conscious dogs after 5-h oral treatment with 300 and 600 mg/kg of Cinromide[1]. Cinromide (40 mg/kg, i.v.) depresses the response of the neuron to the unconditioned maxillary nerve stimulus, increasing the latency and decreasing the number of spikes, and depresses the response of the neuron to the unconditioned maxillary nerve stimulus, increasing the latency and decreasing the number of spikes. Cinromide (20, 40, 80 mg/kg, i.v.) increases the latency of the unconditioned response and segmental inhibition dose-dependently. Cinromide decreases periventricular inhibition and EEG[2].

Name: Mepyramine maleate Pyrilamine maleate, CAS: 59-33-6, stock 25.7g, assay 99%, MWt: 401.46, Formula: C21H27N3O5, Solubility: DMSO : ≥ 150 mg/mL (373.64 mM), Clinical_Informat: Launched, Pathway: Immunology/Inflammation;GPCR/G Protein;Neuronal Signaling, Target: Histamine Receptor;Histamine Receptor;Histamine Receptor, Biological_Activity: Mepyramine maleate, a first generation antihistamine, is an antagonist of histamine H1 receptor, with Kds of 0.8 nM, 5200 nM and >3000 nM for H1, H2, and H3 receptor, respectively, and a pKd of 9.4 for H1 receptor.
IC50 & Target: Kd: 0.8 nM (Histamine H1 receptor), 5200 nM (Histamine H2 receptor), >3000 nM (Histamine H3 receptor)[1] 
pKd: 9.4 (Histamine H1 receptor)[2]
In Vitro: Mepyramine maleate is an antagonist of histamine H1 receptor, with Kds of 0.8 nM, 5200 nM and >3000 nM for H1, H2, and H3 receptor, respectively[1], and a pKd of 9.4 for H1 receptor[2]. Mepyramine binds to the H1 receptor with different Kds in Guinea pig brain (0.8 nM), rat brain (9.1 nM) and DDT1-MF-2 and BC3H1 cell (276 nM)[1]. Mepyramine decreases the InsP levels in CHO-gpH1 cells, with log EC50 of -7.94 ± 0.11, and reduces the the maximal response to ATP in CHO-gpH1 cells[3].
In Vivo: Mepyramine obviously decreases the second phase of nociceptive response via i.p at 10 and 20 mg/kg, but shows no significant effect at 5 mg/kg in rats[4].

Name: Dimercaprol 2,3-Dimercapto-1-propanol; Dithioglycerol, CAS: 59-52-9, stock 4.1g, assay 98.9%, MWt: 124.23, Formula: C3H8OS2, Solubility: H2O : 41.67 mg/mL (335.43 mM; Need ultrasonic); 10 mM in DMSO, Clinical_Informat: Launched, Pathway: Anti-infection, Target: HIV, Biological_Activity: Dimercaprol (2,3-Dimercapto-1-propanol) is an anti-heavy metal-poisoning drug, which exhibits anti-HIV activity[1].
IC50 & Target: HIV[1]

Name: Iodipamide Adipiodone, CAS: 606-17-7, stock 19.7g, assay 98.2%, MWt: 1139.76, Formula: C20H14I6N2O6, Solubility: DMSO : 125 mg/mL (109.67 mM; Need ultrasonic); H2O : < 0.1 mg/mL (insoluble), Clinical_Informat: Launched, Pathway: Others, Target: Others, Biological_Activity: Iodipamide is a tri-iodinated benzoate derivative and ionic dimeric contrast agent used in diagnostic imaging.

Name: Zoxazolamine, CAS: 61-80-3, stock 35.5g, assay 98.5%, MWt: 168.58, Formula: C7H5ClN2O, Solubility: DMSO : 300 mg/mL (1779.57 mM; Need ultrasonic and warming), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Zoxazolamine is widely used for a pharmacologic test that serves as a convenient indicator of changes in cytochrome P-450 activity in rodents.
In Vivo: Zoxazolamine is widely used for a pharmacologic test that serves as a convenient indicator of changes in cytochrome P-450 activity in rodents. The time-averaged serum clearance determined from tested concentrations data is 7.22±1.01 mL/min/kg for Zoxazolamine. Infusion of Zoxazolamine to righting reflex (LRR) at three different rates shows increasing Zoxazolamine concentration in serum and brain at the onset of the effect with increasing infusion rates. When the Zoxazolamine infusion is continued for 5 min beyond the onset of LRR, the concentrations of Zoxazolamine in the cerebrospinal fluid (CSF) at the offset of LRR are essentially identical to the onset concentrations[1].

Name: Meclofenamate (sodium) Meclofenamic acid (sodium), CAS: 6385-02-0, stock 26.2g, assay 98.7%, MWt: 318.13, Formula: C14H10Cl2NNaO2, Solubility: DMSO : 250 mg/mL (785.84 mM; Need ultrasonic), Clinical_Informat: Launched, Pathway: Cytoskeleton, Target: Gap Junction Protein, Biological_Activity: Meclofenamic acid sodium is a nonsteroidal anti-inflammatory drug (NSAID) approved for use in arthritis (osteo and rheumatoid), analgesia (mild to moderate pain), dysmenorrhea, and heavy menstrual blood loss (menorrhagia). Meclofenamic acid sodium is a non-selective gap-junction blocker and a highly selective inhibitor of fat mass and obesity-associated (FTO) enzyme inhibitor[1][2][3].

Name: Retinol Vitamin A1;all-trans-Retinol, CAS: 68-26-8, stock 29.7g, assay 98.9%, MWt: 286.45, Formula: C20H30O, Solubility: H2O : < 0.1 mg/mL (insoluble); DMSO : < 1 mg/mL (insoluble or slightly soluble), Clinical_Informat: Launched, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: Retinol, also known as Vitamin A1, has pleiotropic functions including vison, immunity, hematopoiesis, reproduction, cell differentiation/growth, and development.
In Vitro: It is found that contribution of hepatic microsomes (RDHs) to Retinol metabolism is greater than that of cytosol (ADHs), evidenced by higher Clint (Vmax/Km) of Retinol formation in microsomes than in cytosol[1].
In Vivo: The results show that compare with control (CON) rats, high-fat diet (HFD) significantly lowers basal level of Retinol in plasma, but markedly elevates basal levels of Retinol in kidney, adipose tissue and liver. The results show that Retinol absorption in HFD rats is faster than that in CON rats, evidenced by significantly shorter Tmax (3.0±0.0 h for HFD rats vs 5.8±1.1 h for CON rats, p<0.05)[1]. The plasma Retinol levels in methionine-choline deficient diet (MCD) rats are significantly lower than in the controls while the hepatic Retinol levels in MCD rats are markedly higher. The hepatic expression of Retinol-metabolizing enzymes and binding proteins (GRBP-I, ALDH1A1, and ALDH1A2) in MCD rats is significantly higher than that in control rats[2].

Name: Ampicillin (trihydrate) D-(-)-α-Aminobenzylpenicillin (trihydrate), CAS: 7177-48-2, stock 37.7g, assay 98.1%, MWt: 403.45, Formula: C16H25N3O7S, Solubility: 10 mM in DMSO, Clinical_Informat: Launched, Pathway: Anti-infection, Target: Bacterial, Biological_Activity: Ampicillin trihydrate (D-(-)-α-Aminobenzylpenicillin trihydrate) is a broad-spectrum beta-lactam antibiotic against a variety of gram-positive and gram-negative bacteria.
In Vitro: Ampicillin trihydrate (D-(-)-α-Aminobenzylpenicillin trihydrate) inhibits the growth of E. coli of swine origin in a dose-dependent manner. The effective inhibitory concentration of Ampicillin trihydrate is 2.5 uG/mL[1].
In Vivo: Ampicillin trihydrate (D-(-)-α-Aminobenzylpenicillin trihydrate) is very effective in alleviating the symptoms of hemorrhagic enteritis in a 11-week old pig[1]. 
Ampicillin trihydrate produces maximum concentrations in bile twice as high as in serum. The peak concentration of ampicillin after an oral dose is as twice as high in portal blood as in peripheral blood[2]. 
Ampicillin trihydrate provides neuroprotection against ischemia-reperfusion brain injury. Ampicillin trihydrate reduces the activities of MMPs and increases the expression level of GLT-1. Pretreatment with Ampicillin trihydrate significantly reduces medial hippocampal cell death following global forebrain ischemia[3].

Name: Iopromide, CAS: 73334-07-3, stock 18.3g, assay 98.7%, MWt: 791.11, Formula: C18H24I3N3O8, Solubility: DMSO : ≥ 150 mg/mL (189.61 mM), Clinical_Informat: Launched, Pathway: Others, Target: Others, Biological_Activity: Iopromide is a water-soluble, non-ionic, monomeric, low-osmolar, iodine-based contrast medium for intravascular administration.
In Vivo: Contrast medium-induced nephropathy can be induced by tail intravenous administration of iopromide[1]. In randomized controlled trials, the global image quality and diagnostic quality with iobitridol does not differ from those with other low-osmolar contrast media (iohexol, iopromide, iopamidol, iomeprol and ioxaglate) or the iso-osmolar contrast medium iodixanol in adults or children undergoing radiographic imaging. Large post-marketing surveillance studies have confirmed that iobitridol produces good or excellent opacification and is an effective contrast agent in the vast majority of patients. Iobitridol is generally well tolerated and had a tolerability profile similar to that of other low-osmolar and iso-osmolar contrast media. Thus, iobitridol is an effective intravascular agent for contrast enhancement in diagnostic imaging[2].

Name: Retinyl (palmitate) Vitamin A palmitate;Retinol palmitate, CAS: 79-81-2, stock 22.5g, assay 98.1%, MWt: 524.86, Formula: C36H60O2, Solubility: Ethanol : 10 mg/mL (19.05 mM; Need ultrasonic); DMSO : 5 mg/mL (9.53 mM; Need ultrasonic), Clinical_Informat: Launched, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: Retinyl palmitate is an ester of Retinol and is the major form of vitamin A found in the epidermis. Retinyl palmitate has been widely used in pharmaceutical and cosmetic formulations.
In Vitro: Retinyl palmitate has a high molecular weight and a stable formulation. To be active, Retinyl palmitate should be enzymatically converted in the skin to retinol by cleavage of the ester linkage and must then be converted to tretinoin via oxidative processes[1].
In Vivo: The topical administration of Retinyl palmitate in rats results in increased protein and collagen and an epidermal thickening[1].

Name: Idazoxan (hydrochloride) RX 781094 (hydrochloride), CAS: 79944-56-2, stock 10.5g, assay 98.7%, MWt: 240.69, Formula: C11H13ClN2O2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein;GPCR/G Protein;Neuronal Signaling;Neuronal Signaling, Target: Adrenergic Receptor;Imidazoline Receptor;Imidazoline Receptor;Adrenergic Receptor, Biological_Activity: Idazoxan hydrochloride (RX 781094 hydrochloride) is an α2-adrenoceptor antagonist and is also a imidazoline receptors (IRs) antagonist competitively antagonized the centrally induced hypotensive effect of imidazoline-like drugs (IMs). Idazoxan hydrochloride also improves motor symptoms in Parkinson’s disease, L-DOPA-induced dyskinesias, and experimental Parkinsonism[1][2].
IC50 & Target: α2-adrenoceptor[1]; Imidazoline receptors (IRs)[2]
In Vivo: Idazoxan (0.16-5 mg/kg; subcutaneous injection; for 1 hour; male CD-COBS rats) treatment potently reverses haloperidol-induced catalepsy with an ED50 of 0.25 mg/kg. Idazoxan (0.3 and 2.5 mg/kg) has no effect on extracellular DA and do not modify the rise of extracellular DA induced by haloperidol[1].

Name: Pinacidil monohydrate, CAS: 85371-64-8, stock 20g, assay 98.9%, MWt: 263.34, Formula: C13H21N5O, Solubility: Ethanol : 50 mg/mL (189.87 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Membrane Transporter/Ion Channel, Target: Potassium Channel, Biological_Activity: Pinacidil monohydrate, an antihypertensive drug, is a potassium channel activator.
In Vitro: Pinacidil monohydrate is a potassium channel activator[1]. Pinacidil hydrate is an antihypertensive drug of the class of agents called "potassium channel openers"[2]. Pinacidil hydrate activates the ATP-modulated potassium channels of guinea pog bladder and heart with Ki values of 104 and 251 nM, respectively[3].

Name: Isosorbide dinitrate ISDN, CAS: 87-33-2, stock 22.1g, assay 98.4%, MWt: 236.14, Formula: C6H8N2O8, Solubility: 10 mM in DMSO, Clinical_Informat: Launched, Pathway: Immunology/Inflammation, Target: NO Synthase, Biological_Activity: Isosorbide dinitrate (ISDN) is an NO donor that prevents LV remodeling and degradation of cardiac function following myocardial infarction (MI)[1].
In Vivo: Isosorbide dinitrate (3 mg/kg; intratracheal; for 13 days) improves pulmonary artery pressure and ventricular remodeling in a rat model of heart failure following myocardial infarction[1]. 
Isosorbide dinitrate postconditioning exhibits a cardioprotective effect against rat myocardial ischemia-reperfusion injury in vivo[2].

Name: Eprobemide LIS 630, CAS: 87940-60-1, stock 4.8g, assay 98.7%, MWt: 282.77, Formula: C14H19ClN2O2, Solubility: DMSO : ≥ 125 mg/mL (442.06 mM), Clinical_Informat: No Development Reported, Pathway: Neuronal Signaling, Target: Monoamine Oxidase, Biological_Activity: Eprobemide is a non-competitive reversible inhibitor of monoamine oxidase A.
IC50 & Target: Monoamine oxidase A[1][2]
In Vitro: Eprobemide is a pharmaceutical drug that is used as an antidepressant. Eprobemide is a non-competitive reversible inhibitor of monoamine oxidase A that exhibits selective action on serotonin deamination[1][2].

Name: Benzthiazide, CAS: 91-33-8, stock 32.7g, assay 99%, MWt: 431.94, Formula: C15H14ClN3O4S3, Solubility: 10 mM in DMSO, Clinical_Informat: Launched, Pathway: Metabolic Enzyme/Protease, Target: Carbonic Anhydrase, Biological_Activity: Benzthiazide is a long-acting diuretic[1] and a hypertension agent. Benzthiazide is an inhibitor of carbonic anhydrase 9 (CA9), with Kis of 8.0, 8.8 and 10 nM for CA9, CA2 and CA1, respectively. Benzthiazide also suppresses proliferation of cancer cells[2].
IC50 & Target: Ki: 8.0 nM (CA9), 8.8 nM (CA2), 10 nM (CA1)[2]
In Vitro: Benzthiazide (0.4, 2, 10 μM) suppresses proliferation of cancer cell under hypoxic conditions in a dose-dependent manner . Benzthiazide is an inhibitor of carbonic anhydrase 9 (CA9), with Kis of 8.0, 8.8 and 10 nM for CA9, CA2 and CA1, respectively[2].
In Vivo: Benzthiazide (1, 1.5 mg/100 g BW) causes a marked decrease in urinary calcium excretion and the dissociation of calcium and sodium excretion in hyperprolactinemic rats[1].

Name: Canrenone Aldadiene;SC9376;SC14266, CAS: 976-71-6, stock 14g, assay 98.2%, MWt: 340.46, Formula: C22H28O3, Solubility: DMSO : ≥ 100 mg/mL (293.72 mM), Clinical_Informat: Launched, Pathway: Metabolic Enzyme/Protease, Target: Mineralocorticoid Receptor, Biological_Activity: Canrenone (Aldadiene; SC9376; SC14266) is an aldosterone antagonist extensively used as a diuretic agent.
IC50 & Target: Target: Aldosterone[1]
In Vitro: Canrenone inhibits the production of eortieosterone, 18-hydroxydesoxyeortieosterone, 18-hydroxycorticosterone and aldosterone in a dose-dependent manner[1]. Canrenone dose-dependently reduces platelet-derived growth factor–induced cell proliferation and motility. Canrenone inhibits the activity of the Na+/H+ exchanger 1 induced by platelet-derived growth factor[2].
In Vivo: Canrenone is the principal active metabolite of Spironolactone in the rat only for a limited period. During chronic treatment a difference developed between the effect of Spironolactone and Canrenone on the RAAS indicating a decrease in the anti-mineralocorticoid activity of Canrenone and an increase in the efficacy of Spironolactone[3].

Name: Ropivacaine hydrochloride, CAS: 98717-15-8, stock 38.7g, assay 98.3%, MWt: 310.86, Formula: C17H27ClN2O, Solubility: 10 mM in DMSO, Clinical_Informat: Launched, Pathway: Membrane Transporter/Ion Channel, Target: Potassium Channel, Biological_Activity: Ropivacaine hydrochloride is an inhibitor of K2P (two-pore domain potassium channel) TREK-1 with an IC50 of 402.7 μM.
IC50 & Target: IC50: 402.7 μM (K2P TREK-1)[1]
In Vitro: Ropivacaine hydrochloride shows reversible inhibition of TREK-1 channels in a concentration-dependent manner. The half-maximal inhibitory concentrations (IC50) of Ropivacaine hydrochloride is 402.7±31.8 μM.. Hill coefficient is 0.89 for Ropivacaine hydrochloride[1].
In Vivo: Epidural injections of Ropivacaine hydrochloride (60, 180 and 600 μg) produce immediate and reversible motor paralysis. The motor blockade effect is dose-dependent, with paralysis duration of 4.6, 14.6 and 29.5 mins, respectively. Epidural Ropivacaine hydrochloride sustained release suspension also produces significant blockade of mechanical allodynia and thermal hyperalgesia by 59.5% and 70.9%, respectively (P<0.05). Ropivacaine hydrochloride sustained release suspension also produces a mild antinociception (response to heat stimulus) but longer anti-allodynic and anti-hyperalgesic effects, with biological half-lives of 6.4±2.5 hrs and 6.8±2.9 hrs, respectively (P<0.05). Multiple daily epidural administration of Ropivacaine hydrochloride sustained release suspension prolongs the preemptive effects (P<0.05)[2].

Name: Baccatin III, CAS: 27548-93-2, stock 8.8g, assay 98.4%, MWt: 586.63, Formula: C31H38O11, Solubility: DMSO : 125 mg/mL (213.08 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Baccatin III is a natural product isolated from Pacific yew tree and related species. Baccatin III reduces tumor progression by inhibiting the accumulation and suppressive function of MDSCs[1].

Name: Esomeprazole magnesium (S)-Omeprazole magnesium;(-)-Omeprazole magnesium, CAS: 161973-10-0, stock 0.9g, assay 98.7%, MWt: 713.12, Formula: C34H36MgN6O6S2, Solubility: DMSO : ≥ 125 mg/mL (175.29 mM); H2O : < 0.1 mg/mL (insoluble), Clinical_Informat: Launched, Pathway: Membrane Transporter/Ion Channel, Target: Proton Pump, Biological_Activity: Esomeprazole magnesium is an inhibitor of H+, K+-ATPase, effectively used in the research of upper intestinal disorder.
IC50 & Target: H+, K+-ATPase[1]
In Vitro: Esomeprazole magnesium is an inhibitor of H+, K+-ATPase[1].
In Vivo: Esomeprazole magnesium (0.5, 5, 50 mg/kg/day, p.o.) produces increased gastric total antioxidant capacity, decreases gastric lipid peroxide levels, significantly increases superoxide dismutase levels, but shows no obvious effect on colonic lipid peroxide levels in mice[1].

Name: Licofelone ML-3000, CAS: 156897-06-2, stock 8.1g, assay 98.9%, MWt: 379.88, Formula: C23H22ClNO2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Apoptosis;Metabolic Enzyme/Protease;Immunology/Inflammation, Target: Apoptosis;Lipoxygenase;COX, Biological_Activity: Licofelone (ML-3000) is a dual COX/5-lipoxygenase (5-LOX) inhibitor (IC50=0.21/0.18 μM, respectively) for the treatment of osteoarthritis. Licofelone exerts anti-inflammatory and anti-proliferative effects. Licofelone induces apoptosis, and decreases the production of proinflammatory leukotrienes and prostaglandins[1][2][3].
In Vitro: The IC50s of human thrombocyte COX and human 5-LO are 0.16 µM and 0.23 µM, respectively[3].

Name: 8-Azaguanine, CAS: 134-58-7, stock 21.5g, assay 98.2%, MWt: 152.11, Formula: C4H4N6O, Solubility: DMSO : 2.44 mg/mL (16.04 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Cell Cycle/DNA Damage;Metabolic Enzyme/Protease, Target: Nucleoside Antimetabolite/Analog;Endogenous Metabolite, Biological_Activity: 8-Azaguanine is a purine analogue which shows antineoplastic activity.
In Vitro: 8-Azaguanine is a purine analogue which shows antineoplastic activity. The results show that cell viability decreases after incubation with 8-Azaguanine, in a dose and time dependent manner. After 24 h of treatment with 8-Azaguanine the IC50 for CEM cell line is about 100 μM while for MOLT3 cell line the IC50 is about 10 μM. CEM and MOLT3 cells surface expression of CD26 increases after treatment with 8-Azaguanine in a concentrations dependent manner[1].

Name: Serotonin hydrochloride 5-Hydroxytryptamine hydrochloride;5-HT hydrochloride, CAS: 153-98-0, stock 9.9g, assay 98.6%, MWt: 212.68, Formula: C10H13ClN2O, Solubility: DMSO : 130 mg/mL (611.25 mM; Need ultrasonic), Clinical_Informat: Launched, Pathway: Neuronal Signaling;Metabolic Enzyme/Protease;Neuronal Signaling;GPCR/G Protein;Metabolic Enzyme/Protease, Target: COMT;COMT;5-HT Receptor;5-HT Receptor;Endogenous Metabolite, Biological_Activity: Serotonin hydrochloride is a monoamine neurotransmitter in the CNS and an endogenous 5-HT receptor agonist. Serotonin hydrochloride is also a catechol O-methyltransferase (COMT) inhibitor with a Ki of 44 μM.
IC50 & Target: 5-HT receptor[1] 
Ki: 44 μM (COMT)[1]
In Vitro: Serotonin hydrochloride is a monoamine neurotransmitter in the CNS and an endogenous 5-HT receptor agonist. Serotonin hydrochloride also inhibits catechol O-methyltransferase (COMT), an enzyme that contributes to modultion the perception of pain, via non-competitive binding to the site bound by catechol substrates with a binding affinity comparable to the binding affinity of catechol itself (Ki= 44 μM). Results show that addition of 100 μM of Serotonin hydrochloride decreases the reaction velocity of COMT[1].
In Vivo: Serotonin hydrochloride produces robust hypersensitivity compare to saline-treated controls (p<0.001)[1]. A significant increase in colonic 5-HT content is observed in IL-13-/- mice receiving Serotonin hydrochloride compare to IL-13-/- receiving vehicle following induction of DSS colitis[2].

Name: Bentiromide, CAS: 37106-97-1, stock 32.6g, assay 98.2%, MWt: 404.42, Formula: C23H20N2O5, Solubility: DMSO : ≥ 250 mg/mL (618.17 mM), Clinical_Informat: Launched, Pathway: Others, Target: Others, Biological_Activity: Bentiromide is a peptide that is broken down in the pancreas by chymotrypsin.
The bentiromide test is an excellent means of confirming the diagnosis of pancreatic exocrine insufficiency by outpatient test of chymotrypsin function[1].

Name: Enrofloxacin (hydrochloride) BAY Vp 2674 (hydrochloride);PD160788 (hydrochloride), CAS: 112732-17-9, stock 6.8g, assay 98.6%, MWt: 1000, Formula: C19H22FN3O3.xHCl, Solubility: H2O : 5 mg/mL (Need ultrasonic and warming), Clinical_Informat: No Development Reported, Pathway: Anti-infection, Target: Bacterial, Biological_Activity: Enrofloxacin hydrochloride (BAY Vp 2674 hydrochloride) is an effective antibiotic with an MIC90 of 0.312 μg/mL for Mycoplasma bovis.
IC50 & Target: MIC90: 0.312 μg/mL ( Mycoplasma bovis)[1]
In Vitro: Mycoplasma bovis is a worldwide pathogen, causative agent of pneumonia, mastitis, arthritis, and a variety of other symptoms in cattle. The antibiotic susceptibility profiles of the Hungarian strains are consistent within the tested group of fluoroquinolones. Three isolates (MYC44, MYC45 and MYC46) have high MIC values (≥10 μg/mL) to Enrofloxacin, while the rest of the strains are inhibited by Enrofloxacin with MICs ≤0.312 or 0.625 μg/mL[1].
In Vivo: Mice (n=80) undergo transient middle cerebral artery occlusion (MCAo) with reperfusion after 60 minutes. After MCAo, animals are randomly assigned to receive either a daily preventive medication (n=26, Enrofloxacin) starting at the day of MCAo or a therapeutic medication (n=25; Enrofloxacin) after diagnosis of lung infection. Standard treatment started immediately after the appearance of clinical signs (general health score>6) usually between day 4 and 6 after stroke. Both, preventive and standard antibiotic treatment using Enrofloxacin improve survival in a similar way compared with placebo treatment[2].

Name: Cyclic AMP Cyclic adenosine monophosphate;Adenosine cyclic 3', 5'-monophosphate;cAMP, CAS: 60-92-4, stock 33.7g, assay 98.6%, MWt: 329.21, Formula: C10H12N5O6P, Solubility: H2O : ≥ 5 mg/mL (15.19 mM); DMSO : < 1 mg/mL (insoluble or slightly soluble), Clinical_Informat: Phase 2, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: Cyclic AMP (cAMP) is a mitogenic messenger and promotes the G1 to S phase transition in the cell cycle.

Name: α-Cyclodextrin, CAS: 10016-20-3, stock 9.4g, assay 98.1%, MWt: 972.84, Formula: C36H60O30, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: α-Cyclodextrin is a multifunctional, soluble dietary fiber marketed for use as a fiber ingredient.

Name: Aluminum Hydroxide, CAS: 21645-51-2, stock 27.4g, assay 98.4%, MWt: 78.00, Formula: AlH3O3, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Aluminum Hydroxide is a main form of aluminum used as adjuvant. Aluminum hydroxide-based adjuvant researches including the repository effect, pro-phagocytic effect, and activation of the pro-inflammatory NLRP3 pathway. Aluminum Hydroxide also acts as adjuvant to compensate low inherent immunogenicity of subunit vaccines[1][2].

Name: Anabasine (S)-Anabasine, CAS: 494-52-0, stock 26.5g, assay 98.1%, MWt: 162.23, Formula: C10H14N2, Solubility: DMSO : 100 mg/mL (616.41 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Neuronal Signaling;Membrane Transporter/Ion Channel, Target: nAChR;nAChR, Biological_Activity: Anabasine is a nicotinic receptor agonist.
IC50 & Target: nicotinic receptor[1]
In Vivo: Anabasine significantly reverses the impairment at the 0.2 mg/kg (p<0.05) and 2 mg/kg doses (p<0.025). Anabasine does not have any significant effects on response latency when administered alone. The 0.06 mg/kg Anabasine dose, in fact, significantly (p<0.05) exacerbates the dizocilpine-induced impairment. None of these Anabasine doses affects choice accuracy on their own. Individual dose comparisons show that the 0.06 mg/kg Anabasine dose plus dizocilpine (6.7±2.6) causes a significant (p<0.05) increase in non-response trials compare with dizocilpine alone (2.1±0.8)[1].

Name: Fuchsine base (monohydrochloride) Magenta base monohydrochloride;Basic Fuchsin monohydrochloride;Rosaniline Base monohydrochloride, CAS: 632-99-5, stock 28.3g, assay 99%, MWt: 337.85, Formula: C20H20ClN3, Solubility: DMSO : ≥ 75 mg/mL (221.99 mM), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Fuchsine base (monohydrochloride) is a magenta dye, which is certified for use for acid-fast staining with carbol-fuchsin.

Name: Bemesetron MDL 72222, CAS: 40796-97-2, stock 33.9g, assay 98.1%, MWt: 314.21, Formula: C15H17Cl2NO2, Solubility: DMSO : 2 mg/mL (6.37 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Neuronal Signaling;GPCR/G Protein, Target: 5-HT Receptor;5-HT Receptor, Biological_Activity: Bemesetron (MDL 72222) is a selective 5-HT3 receptor antagonist with an IC50 of 0.33 nM[1]. Neuroprotective effect[2].
In Vitro: Blockade of 5-HT3 receptor with Bemesetron (MDL7222) reduces hydrogen peroxide-induced neurotoxicity in cultured rat cortical cells. Bemesetron (0.01, 0.1 and 1 μM, 15 hours) and Y25130 (0.05, 0.5 and 5 μM) concentration-dependently reduce the H2O2-induced decrease of MTT reduction showing 74.9±2.4 and 79.0 ±2.5% with 1 μM and 5 μM, respectively, which are maximal effects[2]. 
Pretreatment (20 minutes) with Bemesetron (1 μM), Y25130 (5 μM) or MK-801 (10 μM) significantly, but not completely, inhibits the H2O2-induced elevation of [Ca2+]c[2]. 
Bemesetron (1 μM, 15 hours) significantly blocks the H2O2-induced increase of caspase-3 immunoreactivity[2]. 
In Vivo: Bemesetron (0.1, 1 and 10 mg/kg; i.p.) is used in male adult albino mice. The lowest dose do not cause any significant change in catalepsy. However, Bemesetron (1 mg/kg) causes a significant reduction of catalepsy (from 90 min after Haloperidol), while 10 mg/kg significantly potentiates the phenomenon (from 60 min after Haloperidol). The maximum inhibition of catalepsy (about 75%) occurs at 120 min, and the maximum potentiation (about 4.5-times the control value) occurs at 60 min after Haloperidol[3].

Name: Benznidazol Ro 07-1051;Ro 71051, CAS: 22994-85-0, stock 1.5g, assay 98.7%, MWt: 260.25, Formula: C12H12N4O3, Solubility: DMSO : 160 mg/mL (614.79 mM; Need ultrasonic), Clinical_Informat: Launched, Pathway: Anti-infection, Target: Parasite, Biological_Activity: Benznidazol (Ro 07-1051) is an antiparasitic medication, with an IC50 of 20.35 μM for Colombian T. cruzi strains, and has been used in the treatment of Chagas disease[1][2].
In Vivo: Benznidazole (100 mg/kg/day, p.o., 30 days) produces a decrease in electrocardiographic alterations, fewer modifications in the affinity and density of cardiac-receptors, and few isolated areas of fibrosis in the heart, in mice infected with Trypanosoma cruzi Tulahuen strain or SGO-Z12 isolate and treated at 180 days post infection (p.i.) (i.e. chronic phase) with Benznidazole[1].

Name: OICR-0547, CAS: 1801873-49-3, stock 21.7g, assay 98.7%, MWt: 542.55, Formula: C28H29F3N4O4, Solubility: DMSO : ≥ 100 mg/mL (184.31 mM), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: OICR-0547 is a closely related derivative of OICR-9429. OICR-9429 is a novel small-molecule antagonist of the Wdr5-MLL interaction, while OICR-0547 cannot bind to WDR5.

Name: Boldine, CAS: 476-70-0, stock 26.5g, assay 98.5%, MWt: 327.37, Formula: C19H21NO4, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Boldine is an aporphine isoquinoline alkaloid extracted from the root of Litsea cubeba and also possesses these properties, including antioxidant, anti-inflammatory and cytoprotective effects. Boldine suppresses osteoclastogenesis, improves bone destruction by down-regulating the OPG/RANKL/RANK signal pathway and may be a potential therapeutic agent for rheumatoid arthritis[1].
IC50 & Target: OPG/RANKL/RANK[1]

Name: (Z)-Capsaicin Zucapsaicin;Civamide;cis-Capsaicin, CAS: 25775-90-0, stock 9.3g, assay 98.6%, MWt: 305.41, Formula: C18H27NO3, Solubility: DMSO : ≥ 125 mg/mL (409.29 mM), Clinical_Informat: Launched, Pathway: Membrane Transporter/Ion Channel;Anti-infection;Neuronal Signaling, Target: TRP Channel;HSV;TRP Channel, Biological_Activity: (Z)-Capsaicin is the cis isomer of capsaicin, acts as an orally active TRPV1 agonist, and is used in the research of neuropathic pain.
IC50 & Target: TRPV1 receptor[1]
In Vitro: (Z)-Capsaicin is the cis isomer of capsaicin, acting as a TRPV1 agonist. (Z)-Capsaicin may also blocks the neruonal calcium channel[1].
In Vivo: (Z)-Capsaicin (Zucapsaicin) significantly attenuates nociceptive behavior after oral administration in rats. (Z)-Capsaicin is also tolerated in the primary or recurrent experimental genital herpes simplex virus infection in guinea pigs[1].

Name: SR2211, CAS: 1359164-11-6, stock 12.6g, assay 98.4%, MWt: 527.48, Formula: C26H24F7N3O, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: ROR, Biological_Activity: SR2211 is a potent, selective synthetic RORγ modulator and functions as an inverse agonist, with a Ki of 105 nM and an IC50 of ~320 nM.
IC50 & Target: IC50: ~320 nM (RORγ), Ki: 105 nM (RORγ)[1][2].
In Vitro: The treatment of EL4 with SR2211 represses the IL-17 gene expression. Similarly, the expression of IL-23 receptor (Il23r) is significantly inhibited by SR2211. Treatment of EL-4 cells with SR2211 results in significant inhibition of IL-17 intracellular staining as compared to vehicle treated cells[1].

Name: Ceftizoxime, CAS: 68401-81-0, stock 17.7g, assay 98.4%, MWt: 383.40, Formula: C13H13N5O5S2, Solubility: DMSO : 25 mg/mL (65.21 mM; Need ultrasonic), Clinical_Informat: Launched, Pathway: Anti-infection, Target: Bacterial, Biological_Activity: Ceftizoxime is a bacterial inhibitor which acts by interfering with bacterial cell wall synthesis and inhibiting cross-linking of the peptidoglycan.
IC50 & Target: bacterial[1]
In Vitro: Ceftizoxime is a new parenteral cephalosporin derivative which is more active against various gram-negative bacilli, including the opportunistic pathogens such as Enterobacter, Citrobacter species, and Serratia marcescens, than cephalosporins and cephamycins such as cefotiam, cefamandole, cefuroxime, cefotaxime, and cefmetazole. Ceftizoxime shows a broad spectrum of antibacterial activity against aerobic gram-positive and gram-negative bacteria[1].
In Vivo: The therapeutic effect of Ceftizoxime in mice infected with a small inoculum size is almost the same as that of cefotaxime[1]. Ceftizoxime is stable in biological fluids such as serum, urine, and tissue homogenates, but cefotaxime is unstable in rat tissue homogenates. Binding of ceftizoxime to serum protein in all species is the lowest of all the antibiotics: 31% for humans, 17% for dogs, and 32% for rats[2].

Name: Sodium citrate dihydrate Trisodium citrate dihydrate;Citric acid trisodium salt dihydrate, CAS: 6132-04-3, stock 9.2g, assay 98.1%, MWt: 294.10, Formula: C6H9Na3O9, Solubility: H2O : 125 mg/mL (425.03 mM; Need ultrasonic), Clinical_Informat: Launched, Pathway: Others, Target: Others, Biological_Activity: Sodium citrate dehydrate is an anticoagulant and also used as a buffer and food preservatives.

Name: Sodium diatrizoate Diatrizoic acid sodium salt;Sodium amidotrizoate, CAS: 737-31-5, stock 19.3g, assay 98.7%, MWt: 635.90, Formula: C11H8I3N2NaO4, Solubility: DMSO : 100 mg/mL (157.26 mM; Need ultrasonic); H2O : ≥ 50 mg/mL (78.63 mM), Clinical_Informat: Launched, Pathway: Others, Target: Others, Biological_Activity: Sodium diatrizoate is an iodinated radiocontrast agent.
In Vivo: Sodium diatrizoate is an iodinated radiocontrast agent. Histological examination of rat lung tissue shows no acute toxicity or inflammation after insufflation of Sodium diatrizoate nanoparticle agglomerates. Sodium diatrizoate nanoparticle agglomerates offers a promising radiocontrast agent for safe and effective lung visualization[1].

Name: Dibutyl phthalate, CAS: 84-74-2, stock 27.1g, assay 98.7%, MWt: 278.34, Formula: C16H22O4, Solubility: Ethanol : ≥ 50 mg/mL (179.64 mM), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Dibutyl phthalate is a commonly used plasticizer commonly found in some food packaging materials, personal care products, and the coating of oral medications[1]. May cause toxicity and adverse neurobehavioral effects[2][3].
In Vitro: Dibutyl phthalate (0.001 µg/mL-1000 µg/mL) is detrimental to follicle growth and viability and results in significant dysregulation of cell cycle and apoptosis gene expression in a dose-specific manner. But MBP does not play a role in Dibutyl phthalate toxicity in follicles exposed in vitro[1].
In Vivo: Dibutyl phthalate (200, 400, or 600 mg/kg/day) induces decrease mice weight, impairment of spermatogenesis, reduces serum follicle stimulating hormone and testosterone level, alters testicular LDH, increases LPO, and decreases the levels of enzymatic antioxidants with histopathological anomalies[2].
Dibutyl phthalate (6.25, 12.5, 25, 50, 100 and 200 mg/kg) could cause some neurobehavioral adverse effects in mice[3].

Name: Dimethyl phthalate, CAS: 131-11-3, stock 39.3g, assay 98.9%, MWt: 194.18, Formula: C10H10O4, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Dimethyl phthalate, a known endocrine disruptor and one of the phthalate esters (PAEs), is a ubiquitous pollutant. Dimethyl phthalate is commonly used as a plasticizer to impart flexibility to rigid polyvinylchloride (PVC) resins[1].

Name: Ditiocarb sodium Sodium diethyldithiocarbamate, CAS: 148-18-5, stock 18.5g, assay 98.1%, MWt: 171.26, Formula: C5H10NNaS2, Solubility: DMSO : ≥ 300 mg/mL (1751.72 mM), Clinical_Informat: No Development Reported, Pathway: Anti-infection, Target: HIV, Biological_Activity: Ditiocarb sodium (Sodium diethyldithiocarbamate) is an accelerator of the rate of copper cementation. Sodium diethyldithiocarbamate reduces the incidence of HIV infection.
IC50 & Target: HIV[2]
In Vitro: Ditiocarb sodium (Sodium diethyldithiocarbamate) reacts with the Cu2+ solution giving a complex of copper diethyldithiocarbamate, which enhances the rate of cementation[1]. Ditiocarb sodium is an agent with strong antioxidant capacity and chelating activities[2].
In Vivo: Ditiocarb sodium (Sodium diethyldithiocarbamate) improves the depressed immune responses of newborn and aged mice. Sodium diethyldithiocarbamate prevents cisplatin nephrotoxicity in animals without reducing the antitumor activity. In that AIDS model, Ditiocarb sodium reduces lymphadenopathy and hypergammaglobulinemia, restores immunocompetence, and prolongs survival[2].

Name: Emetine (dihydrochloride), CAS: 316-42-7, stock 12.1g, assay 98.2%, MWt: 553.56, Formula: C29H42Cl2N2O4, Solubility: DMSO : 50 mg/mL (90.32 mM; Need ultrasonic), Clinical_Informat: Launched, Pathway: Autophagy;Anti-infection, Target: Autophagy;Parasite, Biological_Activity: Emetine (dihydrochloride) is an anti-protozoal drug previously used for intestinal and tissue amoebiasis[1].
In Vitro: Emetine dihydrochloride is reported to have an IC50 value of 1 nM on the drug sensitive 3D7 P. falciparum parasite strains. Dose response curves are determined for both drugs using K1 resistant isolates and IC50 values of 47 nM and 2.6 nM established for emetine dihydrochloride hydrate and DHA, respectively[1]. 
After the lymphoblasts are treated with emetine dihydrochloride, the expression level of the mutant allele is elevated almost equally to the wild-type alleles by direct sequencing of the corresponding cDNA[2]. 
Emetine dihydrochloride is identified as a lead compound with significant concentration dependent suppression of PEDF-induced TNF secretion and an IC50 of 146 nM. Emetine dihydrochloride inhibits PEDF-mediated TNF release without affecting cell viability and binds to PEDF receptor ATGL with high-binding affinity (KD=14.3 nM)[3]. 
Emetine dihydrochloride reduces cell viability, induces apoptosis, promptes AML cells towards differentiation and downregulates HIF-1α[4]. 
In Vivo: Emetine dihydrochloride (0.002, 0.02, 0.2 and 2 mg/kg) not only attenuates blood glucose levels in dose-dependent way but also induces a persistent attenuation of blood glucose levels.
Daily administration of emetine dihydrochloride dose-dependently attenuates hyperglycemic response by d 21.
Consistent with this observation, administration of emetine dihydrochloride, but not the vehicle control, results in a sustained attenuation of blood glucose levels.
Emetine dihydrochloride improves disease severity in a spontaneous model of NOD T1D[3]. 
Emetine dihydrochloride (1 mg/kg) reduces both leukemia burden in an in vivo xenotransplantation mouse model and the clonogenic capacity of leukemic cells upon treatment[4].

Name: Flavin Adenine Dinucleotide FAD; NSC 112207, CAS: 146-14-5, stock 36.6g, assay 98.8%, MWt: 785.55, Formula: C27H33N9O15P2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: Flavin Adenin Dinucleotide is a redox cofactor, more specifically a prosthetic group of a protein, involved in several important enzymatic reactions in metabolism.
In Vitro: Poly(Flavin Adenin Dinucleotide, FAD) characterized by an additional polymer-type redox reaction is a highly effective electrocatalyst for NADH oxidation: operating at the lowest potentials reported for NADH transducers (0.00 V, pH 7.4), poly(FAD) is characterized by the electrochemical rate constant of 1.8 ± 0.6×10-3 cm/s, which is at the level of the NADH mass-transfer constant. Poly(FAD)-modified electrodes are characterized by the dramatically improved stability and, is the most advantageous NADH transducers for analytical chemistry[2].
In Vivo: Flavin Adenin Dinucleotide (2 mg/kg, i.v.) significantly cancels chlorpromazine (CPZ)-induced decrease in ventricular fibrillation threshold (VFT). Flavin Adenin Dinucleotide cancels the effect of CPZ on canine heart mitochondria. After injection of Flavin Adenin Dinucleotide, the dogs show a transient hypotension within 10 min, then their blood pressures recover to the initial level. Flavin Adenin Dinucleotide also prevents mitochondrial dysfunction induced by chlorpromazine[1].

Name: Fluspirilene R 6218;Redeptin, CAS: 1841-19-6, stock 19.9g, assay 98.7%, MWt: 475.57, Formula: C29H31F2N3O, Solubility: 10 mM in DMSO, Clinical_Informat: Launched, Pathway: Membrane Transporter/Ion Channel;Neuronal Signaling, Target: Calcium Channel;Calcium Channel, Biological_Activity: Fluspirilene is a non-competitive antagonist of L-type calcium channels with an IC50 of 0.03 μM. Fluspirileneis a long-acting injectable depot antipsychotic drug used for schizophrenia.
IC50 & Target: IC50: 0.03 μM (L-type calcium channel)[1]
In Vitro: Fluspirilene, at concentrations which non-competitively modify dihydropyridine binding, selectively antagonizes the effects of calcium-channel activators[1]. Fluspirilene decreases the viability and suppresses sphere-forming of glioma stem cell lines in a dose-dependent manner. Fluspirilene demonstrates the inhibition of proliferation of T98, U87 and all GSC lines at 1.25, 2.5, and 5 μM, while it inhibits the proliferation of U251 and SNB19 at 2.5 and 5 μM[2].
In Vivo: Mice treated with fluspirilene shows a remarkable reduction of the tumor size. Fluspirilene significantly prolongs survival of the TGS04 mouse model[2].

Name: (+)-Kavain, CAS: 500-64-1, stock 10.4g, assay 98.9%, MWt: 230.26, Formula: C14H14O3, Solubility: DMSO : ≥ 125 mg/mL (542.86 mM), Clinical_Informat: Launched, Pathway: Membrane Transporter/Ion Channel;Neuronal Signaling;Membrane Transporter/Ion Channel;Membrane Transporter/Ion Channel;Neuronal Signaling, Target: Calcium Channel;GABA Receptor;GABA Receptor;Sodium Channel;Calcium Channel, Biological_Activity: (+)-Kavain, a main kavalactone extracted from Piper methysticum, has anticonvulsive properties, attenuating vascular smooth muscle contraction through interactions with voltage-dependent Na+ and Ca2+ channels[1]. (+)-Kavain is shown to bind at the α4β2δ GABAA receptor and potentiate GABA efficacy[2]. (+)-Kavain is used as a treatment for inflammatory diseases, its anti-inflammatory action has been widely studied[4].
IC50 & Target: Na+, Ca2+ channel[1]. 
α4β2δ GABAA receptor[2].
In Vitro: (+)-Kavain (10-300 μM) enhances GABA-elicited responses in a concentration-dependent manner. The modulatory effect of Kavain is moderate, with only 170±23% of enhancement measured at 300 μM[2]. (+)-Kavain inhibits TNF-α secretion in cells via suppression of LITAF[4].

Name: Lofexidine, CAS: 31036-80-3, stock 11.2g, assay 98.2%, MWt: 259.13, Formula: C11H12Cl2N2O, Solubility: DMSO : 62.5 mg/mL (241.19 mM; Need ultrasonic), Clinical_Informat: Launched, Pathway: GPCR/G Protein;Neuronal Signaling, Target: Adrenergic Receptor;Adrenergic Receptor, Biological_Activity: Lofexidine is a selective α2-receptor agonist, commonly used to alleviate the physical symptoms of heroin and other types of opioid withdrawal[1][2].
IC50 & Target: α2-receptor[1][2].

Name: Mebhydrolin, CAS: 524-81-2, stock 6.4g, assay 98%, MWt: 276.38, Formula: C19H20N2, Solubility: DMSO : 83.33 mg/mL (301.51 mM; Need ultrasonic), Clinical_Informat: Launched, Pathway: Immunology/Inflammation;GPCR/G Protein;Neuronal Signaling, Target: Histamine Receptor;Histamine Receptor;Histamine Receptor, Biological_Activity: Mebhydrolin is a specific histamine H1 receptor antagonist.
IC50 & Target: Histamine H1-receptor[1]
In Vitro: Mebhydrolin is a specific histamine H1-receptor antagonist with minimal sedative properties and comparing it with the effects of chlorpromazine, the archetypical phenothiazine[1]. Mebhydrolin exerts an antihistaminic effect over the period of the ethanol interaction study[2].

Name: Mebrofenin SQ 26962, CAS: 78266-06-5, stock 14.4g, assay 98.9%, MWt: 387.23, Formula: C15H19BrN2O5, Solubility: 10 mM in DMSO, Clinical_Informat: Launched, Pathway: Others, Target: Others, Biological_Activity: Mebrofenin (SQ 26962) is a type of iminodiacetic acid (IDA). Mebrofenin is available as a ready to use the kit for radio-labeling with Tc-99m. Tc-99m Mebrofenin, a diagnostic agent, is used for hepatobiliary imaging. Tc-99m Mebrofenin is the radiopharmaceutical of choice for the evaluation of hepatic function[1][2].
In Vitro: Tc-99m Mebrofenin is a 99mTc-labeled iminodiacetic (IDA) derivate, originally used for the diagnosis of a multitude of biliary diseases and, since recently, for the assessment of liver function[3].

Name: Citicoline sodium salt, CAS: 33818-15-4, stock 9.6g, assay 99%, MWt: 511.31, Formula: C14H26N4NaO11P2, Solubility: H2O : 300 mg/mL (586.73 mM; Need ultrasonic and warming), Clinical_Informat: Launched, Pathway: Apoptosis;Metabolic Enzyme/Protease, Target: Apoptosis;Endogenous Metabolite, Biological_Activity: Cytidoline sodium salt is an intermediate in the synthesis of phosphatidylcholine which is a component of cell membranes and also exerts neuroprotective effects.

Name: Levomepromazine Methotrimeprazine, CAS: 60-99-1, stock 31.9g, assay 98.5%, MWt: 328.47, Formula: C19H24N2OS, Solubility: 10 mM in DMSO, Clinical_Informat: Launched, Pathway: Others, Target: Others, Biological_Activity: Methotrimeprazine (Levomepromazine) is an orally available neuroleptic agent, which is commonly used to relieve nausea and vomiting in palliative care settings. Levomepromazine has antagonist actions at multiple neurotransmitter receptor sites, including dopaminergic, cholinergic, serotonin and histamine receptors[1].

Name: Metrizoic acid Metrizoate, CAS: 1949-45-7, stock 18.1g, assay 98.9%, MWt: 627.94, Formula: C12H11I3N2O4, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Metrizoic acid (Metrizoate) is an ionic contrast medium. Metrizoic acid (Metrizoate) shows high osmolality and has a risk of inducing allergic reactions[1][2][3].

Name: Oxalic Acid Ethanedioic acid, CAS: 144-62-7, stock 37.5g, assay 98.6%, MWt: 90.03, Formula: C2H2O4, Solubility: 10 mM in H2O, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: Oxalic Acid is a strong dicarboxylic acid occurring in many plants and vegetables and can be used as an analytical reagent and general reducing agent.
In Vitro: Oxalic Acid, a pathogenicity factor for sclerotinia sclerotiorum, suppresses the Oxidative burst of the host plant and directly inhibits the OGA-stimulated production of H2O2 by soybean cells, even in the absence of other fungal components[1].

Name: Perflubron Perfluorooctyl bromide;PFOB, CAS: 423-55-2, stock 7g, assay 98.1%, MWt: 498.96, Formula: C8BrF17, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Perflubron(1-Bromoheptadecafluorooctane;Heptadecafluorooctyl bromide; Perfluorooctyl bromide) is a contrast medium for magnetic resonance imaging and sonography. Perflubron (1-Bromoheptadecafluorooctane;Heptadecafluorooctyl bromide; Perfluorooctyl bromide) can be emulsified with egg phospholipids (EYP) and shows exceptionally fast excretion characteristics[1][2].

Name: Phenanthrene, CAS: 85-01-8, stock 0.8g, assay 98.5%, MWt: 178.23, Formula: C14H10, Solubility: DMSO : 250 mg/mL (1402.68 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Phenanthrene is a polycyclic aromatic hydrocarbon (PAH) and has been frequently used as an indicator for monitoring PAH contaminated matrices[1]. Phenanthrene induces oxidative stress and inflammation[2].

Name: Pregnenolone monosulfate 3β-Hydroxy-5-pregnen-20-one monosulfate, CAS: 1247-64-9, stock 7.6g, assay 98.2%, MWt: 396.54, Formula: C21H32O5S, Solubility: 10 mM in DMSO, Clinical_Informat: Phase 4, Pathway: Autophagy;GPCR/G Protein;Metabolic Enzyme/Protease;Neuronal Signaling, Target: Autophagy;Cannabinoid Receptor;Endogenous Metabolite;Cannabinoid Receptor, Biological_Activity: Pregnenolone monosulfate (3β-Hydroxy-5-pregnen-20-one monosulfate) is a powerful neurosteroid, the main precursor of various steroid hormones including steroid ketones. Pregnenolone monosulfate acts as a signaling-specific inhibitor of cannabinoid CB1 receptor, inhibits the effects of tetrahydrocannabinol (THC) that are mediated by the CB1 receptors. Pregnenolone monosulfate can protect the brain from cannabis intoxication[1][2].
IC50 & Target: Cannabinoid CB1 receptor[1]
In Vitro: CB1 receptor stimulation increases brain Pregnenolone levels, which in turn exerts a negative feedback on the activity of the CB1 receptor antagonizing most of the known behavioral and somatic effects of THC. Pregnenolone likely acts as a signaling-specific negative allosteric modulator binding to a site distinct from that occupied by orthosteric ligands. Pregnenolone does not modify agonist binding but only agonist efficacy[1]. 
The effect of THC is significantly attenuated when slices are pre-treated with Pregnenolone 100 nM (15.1±1.8 % of inhibition). These effects are likely due to a pre-synaptic action of Pregnenolone. Thus, Pregnenolone blocks the increase in paired-pulse ratio (PPR) induced by THC but does not modify either the amplitude or the decay time of miniature EPSC (mEPSC)[1].
In Vivo: Pregnenolone administration (2-6 mg/kg) blocks THC-induced food-intake in Wistar rats and in C57BL/6N mice, and blunts the memory impairment induced by THC in mice, but it does not modify these behaviors per se. Injections of Pregnenolone (2 and 4mg/kg) before each self-administration session reduce the intake of WIN 55,212-2 and reduce the break-point in a progressive ratio schedule[1].

Name: Pyridoxylamine, CAS: 85-87-0, stock 36.5g, assay 98.5%, MWt: 168.19, Formula: C8H12N2O2, Solubility: H2O : 6.25 mg/mL (37.16 mM; Need ultrasonic); DMSO : 31.25 mg/mL (185.80 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: Pyridoxylamine is an advanced glycation end production (AGEs) and lipoxidation end products (ALEs) inhibitor, to protect against diabetes-induced retinal vascular lesions.
In Vitro: Pyridoxylamine (PM), a member of the B6 vitamer family, is a potent scavenger of reactive carbonyls, inhibiting the late stages of glycation reactions that lead to AGE formation[1].
In Vivo: Pyridoxylamine limits the formation of CML and CEL and cross-linking in skin collagen and, ultimately inhibits the development of nephropathy in STZ-diabetic rats. Pyridoxylamine does not appear to function as an antioxidant since it does not prevent lipid peroxidation reactions. At the same time, it does prevent protein modification by products of lipid peroxidation, including inhibiting formation of malondialdehyde and 4-hydroxynonenal adducts on protein in Zucker rats in vivo[1].

Name: Pyridoxylamine (dihydrochloride), CAS: 524-36-7, stock 1.7g, assay 98.3%, MWt: 241.11, Formula: C8H14Cl2N2O2, Solubility: , Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity:

Name: Pyrithione, CAS: 1121-30-8, stock 3.5g, assay 98.9%, MWt: 127.16, Formula: C5H5NOS, Solubility: DMSO : 125 mg/mL (983.01 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Anti-infection, Target: Bacterial, Biological_Activity: Pyrithione is a compound with antibacterial and antifungal activity[1].

Name: Quinpirole Hydrochloride (-)-LY 171555, CAS: 85798-08-9, stock 5.6g, assay 98.2%, MWt: 255.79, Formula: C13H22ClN3, Solubility: DMSO : 31.25 mg/mL (122.17 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein;Neuronal Signaling, Target: Dopamine Receptor;Dopamine Receptor, Biological_Activity: Quinpirole Hydrochloride ((-)-LY 171555) is a high-affinity agonist of dopamine D2/D3 receptor.
IC50 & Target: Dopamine D2/D3 receptor[1].
In Vivo: DA content is left brain biased across groups, and although this asymmetry appears greater in saline controls than all drug-treated groups, there is not a significant interaction between Side and Group. When each side is considered separately it can be seen that in the left brain structure, DA levels progressively decrease with chronic quinpirole treatment, with the QQ rats differing significantly from saline controls. In contrast, right cortical DA levels are only altered significantly (increased) by acute Quinpirole. It can be found that DOPAC levels are also left brain biased across groups. However, no significant Group or interaction effects are found. Rats receiving acute Quinpirole show a selective increase in DA content and decrease in turnover ratio, relative to either saline controls or the QS group. Sensitized (QQ) rats however, have elevated DOPAC levels in comparison to the acute quinpirole group. In striatum as well, all three measures of DA function differed significantly across groups (DA, F3,33=6.27, P=0.0020; DOPAC, F3,33=7.98, P=0.0004; turnover ratio, F3,33=16.85, P<0.0001). In the acute quinpirole rats, both DOPAC and turnover ratio are significantly reduced relative to all other groups. In QQ rats, DOPAC levels are significantly greater than all other groups, while for turnover ratio, both chronic quinpirole groups were increased compared to both chronic saline groups[1].

Name: Riboflavine phosphate Riboflavine 5'-phosphate, CAS: 146-17-8, stock 37.7g, assay 98.4%, MWt: 456.34, Formula: C17H21N4O9P, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: Riboflavine phosphate is a very effective NAD+-recycling agent.
In Vitro: Riboflavine phosphate (Flavin mononucleotide, FMN) is clearly a very effective NAD+-recycling agent with good yields of the cyclohexanone product accompanied by high levels of NAP turnover being achieved routinely[1].

Name: Santonin Alpha-Santonin, CAS: 481-06-1, stock 1.5g, assay 98.2%, MWt: 246.30, Formula: C15H18O3, Solubility: DMSO : 62.5 mg/mL (253.76 mM; Need ultrasonic), Clinical_Informat: Launched, Pathway: Anti-infection, Target: Parasite, Biological_Activity: Santonin is an active principle of the plant Artemisia cina, which is formely used to treat worms[1].

Name: Succimer Dimercaptosuccinic acid;DMSA, CAS: 304-55-2, stock 19.1g, assay 98.4%, MWt: 182.22, Formula: C4H6O4S2, Solubility: DMSO : 300 mg/mL (1646.36 mM; Need ultrasonic and warming), Clinical_Informat: Launched, Pathway: Others, Target: Others, Biological_Activity: Succimer is a widely used chelating agent for the treatment of Pb poisoning.
In Vivo: Succimer is a widely used chelating agent for the treatment of Pb poisoning. Red blood cells (RBCs) from lead exposed animals treated with NAC or Succimer are shown to have significantly higher glutathione (GSH) levels and diminished malondialdehyde (MDA) levels when compare to the lead group. Succimer administration also results in decreased glucose 6-phosphate dehydrogenase (G6PD) activity in RBCs from lead exposed animals[1]. Succimer treatment produces a significant reduction in blood lead levels for both lead exposure conditions: the High Pb-succ group has blood lead levels that are 27% of the blood lead levels of the High Pb group at the end of treatment. Succimer is effective in substantially reducing brain lead, as brain lead levels in the High Pb-succ group are 37% of levels in the High Pb group[2].

Name: Spermidine, CAS: 124-20-9, stock 31.1g, assay 98.3%, MWt: 145.25, Formula: C7H19N3, Solubility: DMSO : ≥ 33.33 mg/mL (229.47 mM), Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: Spermidine, a precursor of spermine, is a polyamine derived from putrescine and could help stabilize some membranes and nucleic acid structures.

Name: Spermine NSC 268508; Neuridine, CAS: 71-44-3, stock 17.2g, assay 98.1%, MWt: 202.34, Formula: C10H26N4, Solubility: H2O : 125 mg/mL (617.77 mM; Need ultrasonic), Clinical_Informat: Phase 1, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: Spermine (NSC 268508) functions directly as a free radical scabenger to protect DNA from free radical attack.
In Vitro: Spermine (NSC 268508) at physiologically relevant concentrations inhibits ROS-induced DNA damage, with maximal inhibition observed at 1 to 2 mM. These concentrations are well within the estimates for the physiological concentrations of spermine[1].

Name: Sucrose D-(+)-Saccharose, CAS: 57-50-1, stock 38.8g, assay 98.4%, MWt: 342.30, Formula: C12H22O11, Solubility: H2O : 100 mg/mL (292.14 mM; Need ultrasonic and warming), Clinical_Informat: Launched, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: Sucrose is a disaccharide which is composed of two monosaccharides, glucose and fructose.
In Vivo: Sucrose is a disaccharide which is composed of two monosaccharides, glucose and fructose. Compare to chow-feeding, high-energy (HE)-feeding results in an overall decreased preference for Sucrose solutions in both strains. Specifically, obesity-prone (OP) rats prefer 0.3 M and 1.0 M Sucrose solutions less during HE-feeding relative to chow-feeding (P=0.046 and P=0.012, respectively). As well, obesity-resistant (OR) rats exhibit decreased preferences for 0.01 M, 0.03 M, and 1.0 M Sucrose when HE-fed compare to chow-fed counterparts (P<0.0001, P=0.043, and P=0.013, respectively). Chow-fed OP rats consume significantly less of 0.03 and 0.1 M Sucrose solutions relative to OR animals (P<0.0001, for both) while HE-fed OP rats consume less of a 0.1 M Sucrose solution only (P<0.05), compare to HE-fed OR rats[1].

Name: Sulfacetamide Sulphacetamide, CAS: 144-80-9, stock 13.7g, assay 98.9%, MWt: 214.24, Formula: C8H10N2O3S, Solubility: 10 mM in DMSO, Clinical_Informat: Launched, Pathway: Anti-infection, Target: Bacterial, Biological_Activity: Sulfacetamide (Sulphacetamide), a bacteriostatic sulphonamide, is a popular antibiotic prescribed for treating ocular infections[1][2].

Name: Sulfamethazine (sodium) Sulfadimidine (sodium);Sulfadimerazine (sodium), CAS: 1981-58-4, stock 10.5g, assay 98.4%, MWt: 300.31, Formula: C12H13N4NaO2S, Solubility: 10 mM in DMSO, Clinical_Informat: Launched, Pathway: Anti-infection, Target: Bacterial, Biological_Activity: Sulfamethazine sodium (Sulfadimidine sodium) is an antimicrobial that is widely used to treat and prevent various animal diseases (such as gastrointestinal and respiratory tract infections). In China and the European Commission, the maximum residue level for Sulfamethazine sodium in animal product is set at 100 µg/kg[1][2].
IC50 & Target: Bacterial[1]
In Vivo: Sulfamethazine (80 mg/kg; intravenous injection; healthy female pigs) treatment significantly reduces α, β and AUC0->∞, significantly increases t1/2α, Vd and CIB, and upon a single intramuscular administration of 80 mg/kg of Sulfamethazine the absolute bioavailability in pigs is 1.01[1].

Name: Taurocholic acid N-Choloyltaurine, CAS: 81-24-3, stock 18.6g, assay 98.1%, MWt: 571.81, Formula: C30H53NO7S, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: Taurocholic acid (N-Choloyltaurine) is a bile acid involved in the emulsification of fats.
In Vivo: The bile acid Taurocholic acid (TCA) exerts permeation enhancing effects in vivo[1].

Name: Thymol iodide, CAS: 552-22-7, stock 37.5g, assay 98.9%, MWt: 550.21, Formula: C20H24I2O2, Solubility: DMSO : < 1 mg/mL (insoluble or slightly soluble), Clinical_Informat: No Development Reported, Pathway: Anti-infection, Target: Fungal, Biological_Activity: Thymol iodide is a compound of Iodide and Thymol. Thymol iodide acts as a substitute for iodoform[1]. Thymol iodide is an iodine derivative of Thymol (a phenol derived from thyme oil), which is mostly used as mild antiseptic and fungicide[2].

Name: Tocainide (hydrochloride), CAS: 71395-14-7, stock 13g, assay 98.4%, MWt: 228.72, Formula: C11H17ClN2O, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Membrane Transporter/Ion Channel, Target: Sodium Channel, Biological_Activity: Tocainide hydrochloride is a sodium channel blocker, it blocks the sodium channels in the pain-producing foci in the nerve membranes. Tocainide hydrochloride is a primary amine analog of lidocaine, can be used for the treatment of tinnitus[1][2].
IC50 & Target: IC50: sodium channel[1]
In Vivo: Tocainide (100 mg/kg) effectively suppresses ventricular ectopic activity in unanesthetized dogs with coronary occlusion. Termination of tocainide infusion in both digitalis toxicity and coronary occlusion models results in prompt return of ventricular ectopic activity[1].

Name: Tolonidine, CAS: 4201-22-3, stock 35.2g, assay 98.3%, MWt: 209.68, Formula: C10H12ClN3, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Tolonidine is a derivative of imidazoline. Tolonidine is orally active and has been shown to possess hypotensive and antihypertensive properties[1].
In Vivo: In the anesthetized dog, tolonidine administered i.v. decreases the amplitude of ventricular contractions, reduces aortic blood flow and increases peripheral vascular resistances[1]. 
In the bivagotomized pithed rat, tolonidine induces a long-lasting increase in blood pressure with no secondary hypotension, thus suggesting peripheral sympathomimetic properties[1].

Name: Tricaprilin Trioctanoin;Glyceryl trioctanoate, CAS: 538-23-8, stock 15.2g, assay 98.1%, MWt: 470.68, Formula: C27H50O6, Solubility: DMSO : 41.67 mg/mL (88.53 mM; Need ultrasonic), Clinical_Informat: Launched, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: Tricaprilin (Trioctanoin) is used in study for patients with mild to moderate Alzheimer's disease and has a role as an anticonvulsant and a plant metabolite[1][2].

Name: Adefovir GS-0393;PMEA, CAS: 106941-25-7, stock 17.3g, assay 98.7%, MWt: 273.19, Formula: C8H12N5O4P, Solubility: 10 mM in DMSO, Clinical_Informat: Launched, Pathway: Anti-infection;Anti-infection, Target: HBV;Reverse Transcriptase, Biological_Activity: Adefovir (GS-0393) is an adenosine monophosphate analog antiviral agent that after intracellular conversion to Adefovir diphosphate inhibits HBV DNA polymerase. Adefovir has an IC50 of 0.7 μM against HBV in the HepG2.2.15 cell line. Adefovir has good antiviral activity against several viruses, including HBV and herpesviruses[1][2][3].
IC50 & Target: HBV[1][2][3]; 
DNA polymerase[1][2]
In Vitro: Studies to elucidate the mechanism of action of Adefovir against herpesvirus replication reveals that the phosphorylation of Adefovir occurred intracellularly and is carried out by host cellular enzymes. The diphosphorylated derivatives of Adefovir targeted the viral DNA polymerase and also acted as DNA chain terminators. Adenylate kinase is shown to be responsible for the first phosphorylation, which was followed by ADP kinase and creatine kinase, forming Adefovir diphosphate[1].
In Vivo: Unaffected by food, Adefovir achieves 60% oral bioavailability. Its half-life is 12-30 hours and Adefovir undergoes renal excretion without significant metabolites. Adefovir does not substantially affect the cytochrome P450 system[3].

Name: D-Galacturonic acid (hydrate), CAS: 91510-62-2, stock 5.5g, assay 98.1%, MWt: 212.15, Formula: C6H12O8, Solubility: , Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity:

Name: AS1949490, CAS: 1203680-76-5, stock 11.3g, assay 98.4%, MWt: 371.88, Formula: C20H18ClNO2S, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Phosphatase, Biological_Activity: AS1949490 is a potent and selective SHIP-2 (SH2 domain-containing inositol 5′ phosphatase 2) inhibitor, with an IC50 of 620 nM. AS1949490 activated glucose metabolism via up-regulation of GLUT1 gene in L6 myotubes[1][2].
IC50 & Target: IC50: 620 nM (SHIP-2)[1].

Name: Dexamethasone phosphate disodium Dexamethasone 21-phosphate disodium salt, CAS: 2392-39-4, stock 13.7g, assay 98%, MWt: 516.40, Formula: C22H28FNa2O8P, Solubility: H2O : ≥ 106.67 mg/mL (206.56 mM), Clinical_Informat: Launched, Pathway: GPCR/G Protein, Target: Glucocorticoid Receptor, Biological_Activity: Dexamethasone phosphate disodium is a glucocorticoid receptor agonist.
IC50 & Target: Glucocorticoid receptor[1]
In Vitro: Dexamethasone regulates several transcription factors, including activator protein-1, nuclear factor-AT, and nuclear factor-kB, leading to the activation and repression of key genes involved in the inflammatory response[1]. Dexamethasone potently inhibits granulocyte-macrophage colony stimulating factor (GM-CSF) release from A549 cells with EC50 of 2.2 nM. Dexamethasone (EC50=36 nM) induces transcription of the β2-receptor is found to correlate with glucocorticoid receptor (GR) DNA binding and occurred at 10-100 fold higher concentrations than the inhibition of GM-CSF release. Dexamethasone (IC50=0.5 nM) inhibits a 3×κB (NF-κB, IκBα, and I-κBβ), which is associated with inhibition of GM-CSF release[2].
In Vivo: Treatment with Dexamethasone at a dose of 2×5 mg/kg efficiently inhibits lipopolysaccharide (LPS)-induced inflammation. In our experimental system, treatment with a single dose of Dexamethasone 10 mg/kg (i.p.) significantly decreases recruitment of granulocytes as well as spontaneous production of oxygen radicals compared with animals expose to LPS and injected with solvent alone (saline). The effects are statistically significant when administered both 1 h before and 1 h after inhalation of LPS. The number of granulocytes in BALF decreased to levels comparable to healthy animals (given an aerosol of water)[3]. Rats treated with Dexamethasone consume less food and weighed less than control rats. Treated rats also weigh less than pair-fed animals though their food intake is similar. Five days of Dexamethasone injection result in a significant increase in both the liver mass (+42%) and the liver to body weight ratio (+65%). The wet weight of gastrocnemius muscle decreases 20% after 5 days of treatment, but it remains unaffected relative to body weight (g/100 g body weight), indicating that muscle weight loss paralleled body weight loss[4].

Name: Prednisone acetate Prednisone 21-acetate, CAS: 125-10-0, stock 26.3g, assay 98.6%, MWt: 400.46, Formula: C23H28O6, Solubility: DMSO : 25 mg/mL (62.43 mM; Need ultrasonic), Clinical_Informat: Launched, Pathway: GPCR/G Protein, Target: Glucocorticoid Receptor, Biological_Activity: Prednisone acetate (Prednisone 21-acetate), the acetate salt form of prednisolone, is a glucocorticoid receptor agonist with anti-inflammatory and immunomodulating properties[1].
IC50 & Target: glucocorticoid receptor[1]

Name: Megestrol, CAS: 3562-63-8, stock 6.9g, assay 98.5%, MWt: 342.47, Formula: C22H30O3, Solubility: DMSO : 70 mg/mL (204.40 mM; Need ultrasonic), Clinical_Informat: Launched, Pathway: Metabolic Enzyme/Protease, Target: Drug Metabolite, Biological_Activity: Megestrol is a synthetic progestin and used for the treatment of anorexia, cachexia, or an unexplained significant weight loss in patients with an acquired immunodeficiency syndrome diagnosis[1].

Name: Mildronate Meldonium; MET-88; Quaterin, CAS: 76144-81-5, stock 30.2g, assay 98.8%, MWt: 146.19, Formula: C6H14N2O2, Solubility: 10 mM in DMSO, Clinical_Informat: Launched, Pathway: Others, Target: Others, Biological_Activity: Mildronate (Meldonium) functions as a cardioprotective drug by cpmpetetively inhibiting BBOX1 and OCTN2. Mildronate (Meldonium) exhibits IC50 values of 34-62 μM for human recombinant BBOX and an EC50 of 21 μM for human OCTN2. Mildronate (Meldonium) treatment-induced redirection of long-chain FA metabolism from mitochondria to peroxisomes[1].
IC50 & Target: IC50: 34-62 μM (human recombinant BBOX). 
EC50: 21 μM (human OCTN2).

Name: Mildronate (dihydrate) Meldonium (dihydrate); MET-88 (dihydrate); Quaterin (dihydrate), CAS: 86426-17-7, stock 11.7g, assay 98.5%, MWt: 182.22, Formula: C6H18N2O4, Solubility: 10 mM in DMSO, Clinical_Informat: Launched, Pathway: Others, Target: Others, Biological_Activity: Mildronate dihydrate (Meldonium dihydrate) functions as a cardioprotective drug by cpmpetetively inhibiting BBOX1 and OCTN2. Mildronate (Meldonium) exhibits IC50 values of 34-62 μM for human recombinant BBOX and an EC50 of 21 μM for human OCTN2. Mildronate (Meldonium) treatment-induced redirection of long-chain FA metabolism from mitochondria to peroxisomes[1].
IC50 & Target: IC50: 34-62 μM (human recombinant BBOX). 
EC50: 21 μM (human OCTN2).

Name: Fluazinam, CAS: 79622-59-6, stock 7.6g, assay 98.8%, MWt: 465.09, Formula: C13H4Cl2F6N4O4, Solubility: DMSO : 125 mg/mL (268.77 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Anti-infection, Target: Fungal, Biological_Activity: Fluazinam is a broad spectrum pyridinamine fungal inhibitor.
IC50 & Target: Fungal[1]

Name: Faltan, CAS: 133-07-3, stock 15g, assay 98.5%, MWt: 296.56, Formula: C9H4Cl3NO2S, Solubility: DMSO : 125 mg/mL (421.50 mM; Need ultrasonic); H2O : < 0.1 mg/mL (insoluble), Clinical_Informat: No Development Reported, Pathway: Anti-infection, Target: Fungal, Biological_Activity: Faltan is a dicarboximide fungicide, widely used on vines and several vegetable crops, and is also cytotoxic effect on human bronchial epithelial cells[1].

Name: Metadoxine, CAS: 74536-44-0, stock 27.4g, assay 98.9%, MWt: 298.29, Formula: C13H18N2O6, Solubility: H2O : ≥ 155 mg/mL (519.63 mM), Clinical_Informat: Launched, Pathway: Stem Cell/Wnt;Protein Tyrosine Kinase/RTK, Target: PKA;PKA, Biological_Activity: Metadoxine blocks adipocyte differentiation in association with inhibition of the protein kinase A-cAMP response element binding protein (PKA-CREB) pathway.
In Vitro: Simultaneous Metadoxine treatment notably inhibits adipogenic differentiation in a dose-dependent manner. Metadoxine treatment from day 4 through day 8 is required for inhibition of MDI-induced preadipocyte differentiation[1]. Metadoxine prevents glutathione depletion and the increase in lipid peroxidation damage caused by ethanol and acetaldehyde in HepG2 cells. In hepatic stellate cells, Metadoxine prevents the increase in collagen and attenuated TNF-α secretion caused by acetaldehyde. Thus, Metadoxine could be useful in preventing the damage produced in early stages of alcoholic liver disease as it prevents the redox imbalance of the hepatocytes and prevents TNF-α induction, one of the earliest events in hepatic damage[2].

Name: Eperisone (Hydrochloride) (±)-Eperisone hydrochloride, CAS: 56839-43-1, stock 18.5g, assay 98.9%, MWt: 295.85, Formula: C17H26ClNO, Solubility: DMSO : 31.25 mg/mL (105.63 mM; Need ultrasonic), Clinical_Informat: Launched, Pathway: Others, Target: Others, Biological_Activity: Eperisone Hydrochloride ((±)-Eperisone hydrochloride) is an antispastic agent used for treatment of diseases characterized by muscle stiffness and pain. It works by relaxing both skeletal muscles and vascularsmooth muscles, thus demonstrating avariety of effects such as reduction ofmyotonia, improvement of circulationand suppression of the pain reflex. Eperisone Hydrochloride ((±)-Eperisone hydrochloride) is a centrally acting muscle relaxant inhibiting the pain reflex pathway, having a vasodilator effect[1][2 [3].

Name: Diaveridine EGIS-5645, CAS: 5355-16-8, stock 23.4g, assay 98.9%, MWt: 260.29, Formula: C13H16N4O2, Solubility: DMSO : 32 mg/mL (122.94 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Cell Cycle/DNA Damage;Anti-infection, Target: Antifolate;Bacterial, Biological_Activity: Diaveridine (EGIS-5645) is a dihydrofolate reductase (DHFR) inhibitor with a Ki of 11.5 nM for the wild type DHFR and also an antibacterial agent.
IC50 & Target: Ki: 11.5 nM (DHFR) [1] 
Bacterial[2]
In Vitro: Diaveridine is a dihydrofolate reductase (DHFR) inhibitor with a Ki of 11.5 nM for the wild type DHFR and also an antibacterial agent[1]. Treatments with Diaveridine for 90 min have a strong bactericidal effect on S. typhimurium TA1535, and no bacterial growth is observed at 10μg/mL or more. Without metabolic activation, treatment with Diaveridine for 48 h, but not 24 h, causes a dose-dependent, significant increase in the frequency of aberrant metaphases. At 100 μg/mL, 60% of the metaphases contain chromosome aberrations[2].
In Vivo: The sperm abnormality of the Diaveridine (DVD) treatment groups at all dose levels (Diaveridine, 128 to 512 mg/kg) shows no significant differences compare with the negative control group. There are no significant differences of micronucleus between the negative control group and the Diaveridine treatment groups (Diaveridine, 128 to 512 mg/kg). The chromosome aberration of the Diaveridine treatment groups at all dose levels and the negative control group are significantly lower than those in the positive control group treated with cyclophosphamide (P<0.05), indicating that Diaveridine at the doses studied does not cause abnormal chromosome aberration. The results demonstrate that the Diaveridine administration does not produce significant changes in the ratio of organ-to-body weight, compare with the negative control group in the end period of the study[3].

Name: Rifamycin (sodium) Rifamycin SV (sodium), CAS: 14897-39-3, stock 20.4g, assay 98.9%, MWt: 719.75, Formula: C37H46NNaO12, Solubility: DMSO : 250 mg/mL (347.34 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Anti-infection, Target: Bacterial, Biological_Activity: Rifamycin sodium (Rifamycin SV monosodium) belongs to the family of ansamycin antibiotics and has been isolated from the fermentation of A. mediterranei or its mutants. Rifamycin sodium displays a broad spectrum of antibiotic activity against Gram-positive and, to a lesser extent, Gram-negative bacteria[1].

Name: Josamycin EN-141, CAS: 16846-24-5, stock 35.2g, assay 98.5%, MWt: 827.99, Formula: C42H69NO15, Solubility: H2O : 2 mg/mL (2.42 mM; ultrasonic and adjust pH to 3 with 水); DMSO : ≥ 41.67 mg/mL (50.33 mM), Clinical_Informat: Launched, Pathway: Anti-infection, Target: Bacterial, Biological_Activity: Josamycin (EN-141) is a macrolide antibiotic exhibiting antimicrobial activity against a wide spectrum of pathogens, such as bacteria. The dissociation constant Kd from ribosome for Josamycin is 5.5 nM.
IC50 & Target: Kd: 5.5 nM (ribosome)[1]
In Vitro: Studies show that the average lifetime on the ribosome is 3 h for Josamycin and that the dissociation constants for Josamycin binding to the ribosome is 5.5 nM. Josamycin slows down formation of the first peptide bond of a nascent peptide in an amino acid-dependent way and completely inhibits formation of the second or third peptide bond, depending on peptide sequence at a saturating drug concentration, synthesis of fulllength proteins is completely shut down by Josamycin. At a saturating drug concentration, synthesis of fulllength proteins is completely shut down by Josamycin[1].
In Vivo: Blood and tissue levels of Josamycin after oral administration are 200 mg/kg to rabbits. Tissue levels are generally much higher than the blood levels, and 3 h after the administration, when the blood level is very low, the tissue levels are rather higher than those 1 h after the dose. One hour after the medication, the level in the lungs is the highest of all the tissue levels[2].

Name: ABT-737, CAS: 852808-04-9, stock 37.5g, assay 98.8%, MWt: 813.43, Formula: C42H45ClN6O5S2, Solubility: DMSO : 50 mg/mL (61.47 mM; Need ultrasonic); H2O : < 0.1 mg/mL (insoluble), Clinical_Informat: No Development Reported, Pathway: Autophagy;Apoptosis;Autophagy, Target: Autophagy;Bcl-2 Family;Mitophagy, Biological_Activity: ABT-737 is a selective and BH3 mimetic Bcl-2, Bcl-xL and Bcl-w inhibitor with EC50s of 30.3 nM, 78.7 nM, and 197.8 nM, respectively.
IC50 & Target: EC50: 78.7 nM (Bcl-xL), 30.3 nM (Bcl-2), 197.8 nM (Bcl-w)[3]
In Vitro: ABT-737 and ATO inhibits proliferation and induces apoptosis in SGC-7901 and MGC-803 cells in concentration- and time-dependent manner, and shows a synergistic effect. ABT-737 disturbs the binding of B cell lymphoma (Bcl)-2 homologous antagonist killer and Bcl-extra large[1]. ABT-737 induces a BAX/BAK-dependent impairment of maximal O2 consumption rate in sensitive cells. Stable BCL-2 overexpression in MCF10A cells induces an ABT-737-sensitive primed for death state. ABT-737 induces dose-dependent impairment of maximal O2 consumption rate in B-cell lymphoma cells[2]. ABT-737 induces apoptosis and synergizes with chemotherapy,and disrups BCL-2/BAX heterodimerization and induces BAX conformational change in AML cells[3].
In Vivo: ABT-737 (50 mg/kg, i.p.) and ATO significantly suppress SGC-7901 xenograft growth, synergistically inhibit tumour growth and induce apoptosis in vivo[1]. ABT-737 suppresses the leukemia burden by 48% and 53% at the 20 and 30 mg/kg dose levels, respectively[3].

Name: Bis(2-ethylhexyl) phthalate Diplast O; ESBO-D 82; Ergoplast FDO; Ergoplast FDO-S; Etalon, CAS: 117-81-7, stock 8.5g, assay 98.1%, MWt: 390.56, Formula: C24H38O4, Solubility: DMSO : 150 mg/mL (384.06 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: Bis(2-ethylhexyl) phthalate is an endogenous metabolite.

Name: Erucic acid, CAS: 112-86-7, stock 4.6g, assay 98.8%, MWt: 338.57, Formula: C22H42O2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: PI3K/Akt/mTOR, Target: PI3K, Biological_Activity: Erucic acid, a monounsaturated fatty acid (MUFA), is isolated from the seed of Raphanus sativus L. Erucic acid can readily cross the blood-brain barrier (BBB), it has been reported to normalize the accumulation of very long-chain fatty acids in the brain. Erucic acid can improve cognitive impairment and be effective against dementia

[1].
In Vivo: Erucic acid (oral administration; 3 mg/kg) enhances the phosphorylation level of PI3K, PKCζ, ERK, CREB and Akt in the hippocampus compared with that in the vehicle-treated control group[1].

Name: Benfluralin, CAS: 1861-40-1, stock 15.9g, assay 99%, MWt: 335.28, Formula: C13H16F3N3O4, Solubility: H2O : < 0.1 mg/mL (insoluble); DMSO : 150 mg/mL (447.39 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Benfluralin is a kind of herbicide and an agrochemical which can be used as a pre-emergence herbicide used for the control of grass and other weeds in a range of food and non-food crops.

Name: L-NMMA acetate Tilarginine acetate;Methylarginine acetate, CAS: 53308-83-1, stock 28g, assay 98.3%, MWt: 248.28, Formula: C9H20N4O4, Solubility: H2O : ≥ 50 mg/mL (201.39 mM), Clinical_Informat: Phase 4, Pathway: Immunology/Inflammation, Target: NO Synthase, Biological_Activity: L-NMMA acetate is a nitric oxide synthase inhibitor of all NOS isoforms including NOS1, NOS2, and NOS3. The Ki values for nNOS (rat), eNOS (human), and iNOS (mouse) are approximately 0.18, 0.4, and 6 µM, respectively.
IC50 & Target: Ki: 0.18 µM (nNOS), 0.4 µM (eNOS), 6 µM (iNOS)[1]
In Vitro: L-NMMA, starting from 100 μM, produces a concentration-dependent inhibition of the evoked relaxations (2Hz); maximal inhibition at 1 mM averaged about 35%. The inhibitory effect of L-NMMA is unchanged by previous incubation with D-arginine while it is prevented by L-arginine (L-Arg). L-NMMA does not affect isoprenaline-induced relaxation[2]. Superfusion of L-NMMA reduces arteriolar diameter and causes dose-dependent increases in arteriolar tone. The onset of action of L-NMMA is nearly immediate. L-NMMA inhibits vasodilator responses to the endothelium-dependent vasodilator ACh but not to the endothelium-independent NP. NE induced dose-related vasoconstriction that is significantly potentiated by L-NMMA[3].

Name: Ionomycin (calcium) SQ23377 (calcium), CAS: 56092-82-1, stock 23.9g, assay 98.3%, MWt: 747.07, Formula: C41H70CaO9, Solubility: DMSO : ≥ 10 mg/mL (13.39 mM), Clinical_Informat: No Development Reported, Pathway: Apoptosis;Membrane Transporter/Ion Channel;TGF-beta/Smad;Epigenetics;Neuronal Signaling, Target: Apoptosis;Calcium Channel;PKC;PKC;Calcium Channel, Biological_Activity: Ionomycin calcium (SQ23377 calcium) is a potent, selective calcium ionophore and an antibiotic produced by Streptomyces conglobatus. Ionomycin calcium (SQ23377 calcium) is highly specific for divalent cations (Ca>Mg>Sr=Ba). Ionomycin (SQ23377) promotes apoptosis. Ionomycin calcium (SQ23377 calcium) also induces the activation of protein kinase C (PKC)[1][2][3].
IC50 & Target: Calcium ionophore[1]
In Vitro: Ionomycin is a Calcium ionophore and an antibiotic produced by Streptomyces conglobatus[1]. Addition of 2 μM Ionomycin to LCLC 103H cells causes an instantaneous increase in intracellular Ca2+ concentration from 50 to 180 nM. DNA and protein analysis in Ionomycin-treated cultures revealed DNA fragmentation and PARP cleavage to an 85-kDa fragment typical of caspase-mediated apoptosis. Necrosis could be detected in ~1-5% of the Ionomycin treated cells as supported by simultaneously positive fluorescein labeling and propidium iodide uptake. Caspase activation in whole cells was followed by monitoring the increase in activity against Ac-DEVD-amc following Ionomycin treatment[2].

Name: Androsterone 5α-Androstan-3α-ol-17-one, CAS: 53-41-8, stock 19.1g, assay 98.2%, MWt: 290.44, Formula: C19H30O2, Solubility: H2O : < 0.1 mg/mL (insoluble); DMSO : 50 mg/mL (172.15 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease;Autophagy;Metabolic Enzyme/Protease, Target: FXR;Autophagy;Endogenous Metabolite, Biological_Activity: Androsterone is a metabolic product of testosterone and can activate Farnesoid X Receptor (FXR).
IC50 & Target: FXR[1]
In Vitro: Androsterone activates both the mFXR-LBD and the hFXR-LBD, with Androsterone activating the mFXR-LBD more strongly than the hFXR-LBD. Furthermore, cotransfection studies with gal4-hFXR-LBD and SRC-1/VP16 expression plasmids demonstrate that Androsterone potentiates the interaction of SRC-1 with the hFXR-LBD. Several amino acid changes including H294S, S332V, R351H, and Y361F significantly reduce Androsterone activation[1]. Androsterone (5α, 3α-A) (10 to 100 μM) also inhibits epileptiform discharges in a concentration-dependent fashion in the in vitro slice model[2].
In Vivo: Androsterone treatment results in a significant induction of small heterodimer partner (SHP), suggesting Androsterone may activate endogenous FXR[1]. Intraperitoneal injection of Androsterone (5α, 3α-A) protects mice in a dose-dependent fashion from seizures in the following models (ED50, dose in mg/kg protecting 50% of animals): 6 Hz electrical stimulation (29.1), pentylenetetrazol (43.5), pilocarpine (105), 4-AP (215), and maximal electroshock (224)[2].

Name: Alpha-Estradiol Alfatradiol;Epiestradiol;Epiestrol, CAS: 57-91-0, stock 36g, assay 98.8%, MWt: 272.38, Formula: C18H24O2, Solubility: DMSO : 103.3 mg/mL (379.25 mM; Need ultrasonic), Clinical_Informat: Launched, Pathway: Metabolic Enzyme/Protease;Metabolic Enzyme/Protease, Target: 5 alpha Reductase;Endogenous Metabolite, Biological_Activity: Alpha-Estradiol is a weak estrogen and a 5α-reductase inhibitor which is used as a topical medication in the treatment of androgenic alopecia.
In Vitro: Alpha-Estradiol (17 alpha-Estradiol) is a 5α-reductase inhibitor, and inhibits testosterone metabolism catalyzed by 5 alpha-reductase[1]. Alpha-Estradiol (17 Alpha-estradiol, 10 μM) attenuates LPS-induced inflammatory markers in both C57BL/6J male and female mouse embryonic fibroblast (MEF) cells, primary pre-adipocytes and differentiated 3T3-L1 adipocytes in an ERα-dependent manner, and such effects are through decreased NFκB-p65 and increased ERα protein expression[2].
In Vivo: Alpha-Estradiol (17-alpha-estradiol, 0.01, 0.1, 1 μg) significantly reduces the percentage of central avascular/total retina area of the mouse pups. Alpha-Estradiol (1 μg) markedly decreasesmalondialdehyde (MDA) levels on postnatal days (PND) 9, 13, and 17 in retinas of hyperoxia-exposed pups. Alpha-Estradiol (1 μg) also decreases the number of NADPH-oxidase-positive cells, NADPH oxidase concentration and activity in retinas of the pups. In the 1.0-μg Alpha-Estradiol-treated pups, VEGF retinal concentrations are high on PND 9 but lower on PND 14 and 17. The best effect in retinas of 1.0-μg Alpha-Estradiol-treated pups is partly reversed by ICI182780 on PND 14 and 17[3].

Name: NSC-87877, CAS: 56990-57-9, stock 38g, assay 98.3%, MWt: 459.45, Formula: C19H13N3O7S2, Solubility: DMSO : 5 mg/mL (10.88 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Phosphatase, Biological_Activity: NSC-87877 is a potent inhibitor of Shp2 and Shp1 protein tyrosine phosphatases (SH-PTP2 and SH-PTP1), with IC50 values of 0.318 μM, 0.355 μM shp2 and shp1, respectively[1]. NSC-87877 also inhibits dual-specificity phosphatase 26 (DUSP26)[2].
IC50 & Target: IC50: 0.318 μM (shp2), 0.355 μM (shp1)[1].

Name: Plicamycin Mithramycin A, CAS: 18378-89-7, stock 18.9g, assay 98.3%, MWt: 1085.15, Formula: C52H76O24, Solubility: DMSO : ≥ 100 mg/mL (92.15 mM), Clinical_Informat: No Development Reported, Pathway: Cell Cycle/DNA Damage, Target: DNA/RNA Synthesis, Biological_Activity: Plicamycin is a selective specificity protein 1 (Sp1) inhibitor. Plicamycin inhibits the growth of various cancers by decreasing Sp1 protein.
IC50 & Target: Sp1 transcription factor[1]
In Vitro: Sp1 is a zinc-finger transcription factor that regulates multiple cellular functions and promotes tumor progression by controlling expression of genes involved in cell cycle, apoptosis and DNA damage. Sp1 binds to GC-rich motifs of promoters and interacts with components of the general transcriptional machinery and co-activator complexes of multiple signaling pathways. Plicamycin (Mith) decreases Sp1 protein by inducing proteasome-dependent degradation, thereby suppressing cervical cancer growth through a DR5/caspase-8/Bid signaling pathway. To assess the antiproliferative effects of Plicamycin on cervical cancer cells, two cervical cancer cell lines with different genetic backgrounds are grown with or without treatment with Plicamycin at different concentrations. Plicamycin inhibits HEp-2 and KB cell growth in a concentration-dependent manner after 48 h. Apoptotic cell death is qualitatively estimated by DAPI staining for nuclear condensation and fragmentation. Plicamycin leads to significant DNA fragmentation compared to untreated controls[1].
In Vivo: The antitumorigenic activity of Plicamycin (0.2 mg/kg/day) is determined in a xenograft model and observed reduction in tumor volume and weight. No significant mouse body weight loss is observed in Plicamycin-treatment groups, indicating that Plicamycin-associated toxicity is minimal. Plicamycin also increases TUNEL-positive cells in tumor xenografts. No notable intergroup differences are observed among organs, indicating no marked signs of systemic toxicity at the Plicamycin dose used in this study[1].

Name: LY2812223, CAS: 1311385-20-2, stock 4.2g, assay 98.8%, MWt: 284.29, Formula: C10H12N4O4S, Solubility: DMSO : 28.75 mg/mL (101.13 mM; Need ultrasonic); H2O : 50 mg/mL (175.88 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein;Neuronal Signaling, Target: mGluR;mGluR, Biological_Activity: LY2812223 is a highly potent, functionally selective mGlu2 receptor agonist with mGlu2 binding affinity for mGlu2 and mGlu3 (Ki=144 nM and 156 nM, respectively)[1].

Name: (-)-Limonene (S)-(-)-Limonene, CAS: 5989-54-8, stock 35.3g, assay 98.8%, MWt: 136.23, Formula: C10H16, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: (-)-Limonene ((S)-(-)-Limonene) is a monoterpene found in many pine-needle oils and in turpentine. (-)-Limonene can induce a mild bronchoconstrictive effect[1].

Name: 6-Thio-2'-Deoxyguanosine 6-thio-dG;β-TGdR, CAS: 789-61-7, stock 27.8g, assay 98.6%, MWt: 283.31, Formula: C10H13N5O3S, Solubility: DMSO : 100 mg/mL (352.97 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Cell Cycle/DNA Damage, Target: DNA/RNA Synthesis, Biological_Activity: 6-Thio-2'-Deoxyguanosine is a nucleoside analogue that can be incorporated into de novo-synthesized telomeres by telomerase.
IC50 & Target: DNA/RNA Synthesis[1]
In Vitro: Treatment with 6-Thio-2'-Deoxyguanosine results in rapid cell death for the vast majority of the cancer cell lines tested with IC50s of between 0.7-2.9 µM[1].
In Vivo: In A549 lung cancer cell-based mouse xenograft studies, 6-Thio-2'-Deoxyguanosine causes a decrease of the tumor growth rate, superior to that observed with 6-thioguanine treatment. Additionally, 6-Thio-2'-Deoxyguanosine increases telomere dysfunction in tumor cells in vivo[1].

Name: Indobufen Ibustrin, CAS: 63610-08-2, stock 19.3g, assay 98.1%, MWt: 295.33, Formula: C18H17NO3, Solubility: 10 mM in DMSO, Clinical_Informat: Launched, Pathway: Immunology/Inflammation, Target: COX, Biological_Activity: Indobufen is a platelet aggregation inhibitor. Indobufen is a reversible platelet cyclooxygenase (Cox) activity inhibitor. Indobufen suppresses thromboxane A2 (TxA2) synthesis. Indobufen down-regulates tissue factor (TF) in monocytes[1].
In Vitro: Indobufen does not affect both Cox-1 and Cox-2 protein, whereas Indobufen reduces TxB2 levels. Indobufen inhibits TxA2 but not PGE2 synthesis in LPS-stimulated monocytes. Indobufen reduces the extent of ERK1/2 phosphorylation, whereas the levels of phosphorylated p38 are unaltered[1].

Name: JSH-150, CAS: 2247481-21-4, stock 29.7g, assay 98.4%, MWt: 505.08, Formula: C24H33ClN6O2S, Solubility: DMSO : 16.67 mg/mL (33.00 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Cell Cycle/DNA Damage, Target: CDK, Biological_Activity: JSH-150 is a highly selective and potent CDK9 inhibitor with an IC50 of 1 nM.
IC50 & Target: IC50: 1 nM (CDK9/Cyclin T1), 292 nM (CDK16/Cyclin Y), 1.34 μM (CDK1/Cyclin B), 1.68 μM (CDK14/Cyclin Y), 1.72 μM (CDK7/Cyclin H/MNAT1), 2.86 μM (CDK2/Cyclin A), 4.64 μM (CDK5/p25)[1]
In Vitro: The antiproliferative effect of JSH-150 is examined ton a panel of established cancer cell lines. JSH-150 exhibits potent antiproliferative activities in solid tumor cell lines such as A375 (melanoma), A431 (squamous), BE(2)M17 (neuroblastoma), GIST-T1 (GIST) and COLO205 (colon cancer) with GI50 values from 0.002 to 0.044 µM. In the leukemia cell lines including acute myeloid leukemia (AML), chronic lymphocytic leukemia (CLL) and B cell lymphoma cell lines, JSH-150 also displays strong growth inhibition efficacies with GI50s ranging from single to double digit nM. In addition, JSH-150 is much less sensitive in normal CHO cells (GI50: 1.1 µM) compared with the cancer cell lines[1].
In Vivo: Treatment of JSH-150 at all dosages, i.e., 10, 20 and 30 mg/kg/day, can almost completely suppress the tumor progression in the first two weeks and does not affect the animal’s weight indicating that there is no general cytotoxicity at these doses. After stopping the treatment of JSH-150, the tumors of the animals treated with 10 mpk drug dosage start to grow again. However, this tumor recurrence is not observed in the 20 and 30 mpk dosage groups during the following week after administration of JSH-150 is stopped and p values are quantified on the 21st day, which are 0.042, 0.0035 and 0.0028, respectively. The PK properties of JSH-150 are evaluated in different species including mice, Sprague-Dawley rats and beagle dogs through intravenous injection and oral administration. JSH-150 is absorbed rapidly in dogs and mice (Tmax=1.33 h and 2.00 h respectively) but slowly in rats (Tmax=3.33 h). JSH-150 also displays different half-lives in three different species via oral administration (T1/2=1.55 h in mice, 3.37 h in rats and 20.37 h in dogs), which indicates that it is metabolized very slowly in dogs compared with mice and rats. In addition, JSH-150 exhibits acceptable bioavailability in mice, rats and dogs (F=45.01%, 45.10% and 39.15%, respectively). The PK properties indicated that JSH-150 is suitable for oral administration[1].

Name: Taurodeoxychloic Acid (sodium hydrate) Sodium taurodeoxycholate monohydrate, CAS: 110026-03-4, stock 35.9g, assay 99%, MWt: 540.71, Formula: C26H47NNaO7S+, Solubility: DMSO : 125 mg/mL (231.18 mM; Need ultrasonic), Clinical_Informat: Launched, Pathway: Apoptosis;Apoptosis, Target: Apoptosis;Caspase, Biological_Activity: Taurodeoxychloic Acid (sodium hydrate) prevents apoptosis by blocking a calcium-mediated apoptotic pathway as well as caspase-12 activation. Taurodeoxychloic Acid (sodium hydrate) is investigated for use in several conditions such as Primary Biliary Cirrhosis (PBC), insulin resistance, amyloidosis, Cystic Fibrosis, Cholestasis, and Amyotrophic Lateral Sclerosis[1].
In Vivo: Taurodeoxychloic Acid (TUDCA) is neuroprotective in a transgenic animal model of Huntington’s disease[2].

Name: c-Fms-IN-1, CAS: 885703-64-0, stock 30.3g, assay 98.4%, MWt: 393.48, Formula: C22H27N5O2, Solubility: H2O : < 0.1 mg/mL (insoluble); DMSO : 5 mg/mL (12.71 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Protein Tyrosine Kinase/RTK, Target: c-Fms, Biological_Activity: c-Fms-IN-1 is a FMS kinase inhibitor with an IC50 of 0.0008 μM[1].
IC50 & Target: FMS kinase[1]

Name: MAPK13-IN-1, CAS: 229002-10-2, stock 21.2g, assay 98.1%, MWt: 365.43, Formula: C20H23N5O2, Solubility: DMSO : ≥ 250 mg/mL (684.13 mM), Clinical_Informat: No Development Reported, Pathway: MAPK/ERK Pathway;Autophagy, Target: p38 MAPK;Autophagy, Biological_Activity: MPAK13-IN-1 is a MAPK13 (p38δ) inhibitor, with an IC50 of 620 nM.
IC50 & Target: IC50: 620 nM (MAPK13)[1].

Name: RIPK1-IN-4, CAS: 1481641-08-0, stock 11.7g, assay 98.2%, MWt: 401.46, Formula: C23H23N5O2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Apoptosis, Target: RIP kinase, Biological_Activity: RIPK1-IN-4 (compound 8) is a potent and selective type II kinase inhibitor of receptor interacting protein 1 (RIP1) kinase and binds to a DLG-out inactive form of RIP1 with an IC50s of 16 nM and 10 nM for RIP1 and ADP-Glo kinase[1].
IC50 & Target: IC50: 16 nM (RIP1) and 10 nM (ADP-Glo)[1]

Name: SKLB-23bb, CAS: 1815580-06-3, stock 5.8g, assay 98%, MWt: 396.44, Formula: C21H24N4O4, Solubility: DMSO : 32 mg/mL (80.72 mM; Need ultrasonic and warming), Clinical_Informat: No Development Reported, Pathway: Epigenetics;Cell Cycle/DNA Damage, Target: HDAC;HDAC, Biological_Activity: SKLB-23bb is a potent and selective inhibitor for HDAC6 with an IC50 of 17 nM and shows 25-fold and 200-fold selectivity relative to HDAC1 (IC50=422 nM) and HDAC8 (IC50=3398 nM), respectively.
IC50 & Target: IC50: 17 nM (HDAC6), 422 nM (HDAC1), 398 nM (HDAC8)[1]
In Vitro: SKLB-23bb (Compound 23bb) presents low nanomolar antiproliferative effects against panel of cancer cell lines. The antiproliferative activity is ton human malignant melanoma A375 cells and cervical cancer HeLa cells, SKLB-23bb shows the most potent activities with IC50 values of 50 and 49 nM on A375 and HeLa cells, respectively. The antiproliferative activities against 11 kinds of hematological tumors (myelomaU266, RPMI8226 cells, human leukemia MV4-11, K562 cells, and human B cell lymphoma Ramos cells) or solid tumors (ovarian cancer A2780s, SKOV-3 cells, breast cancer SKBR3 cells, liver cancer HepG2 cells, lung cancer H460, A549 cells, cervical cancer HeLa cells and colon cancer HCT116, HT29 cells) cell lines of SKLB-23bb are evaluated by MTT, and the SAHA and ACY-1215 are as positive control. SKLB-23bb shows significant antiproliferative potential with the IC50 values ranging from 14 to 104 nM in these tumor cell lines[1].
In Vivo: SKLB-23bb (Compound 23bb) reduces the tumor growth in both the hematological tumor MV4-11 xenograft model and solid tumor HCT116 xenograft model. The significant antitumor activities are observed by intravenous administration of SKLB-23bb at 50 mg/kg on MV4-11 and HCT116 xenograft models. The growth of MV4-11 and HCT116 cancer cell xenografts is suppressed by 55.0% and 76.3% (percent of tumor mass change [TGI] values) after iv administration of SKLB-23bb at 50 mg/kg. The HCT116 xenograft model is also established to investigate the antitumor activity of oral administration of SKLB-23bb. The TGI value of oral administration of SKLB-23bb (25 mg/kg) on HCT116 xenograft model is 60.4%, which is superior to the SAHA group (100 mg/kg, 59.2%). Additionally, the body weight decrease is acceptable and no other adverse effects are observed upon treatment with SKLB-23bb. Low clearance (CL=7.008 L/kg per hour for iv, CL=12.877 L/kg per hour for po) and long terminal half-life (t1/2=7.658 h for iv, t1/2=9.62 h for po) are observed in SKLB-23bb. The oral bioavailability of SKLB-23bb is excellent in rats and the bioavailability is up to 47.0%[1].

Name: PD 407824, CAS: 622864-54-4, stock 13.1g, assay 98.4%, MWt: 328.32, Formula: C20H12N2O3, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Cell Cycle/DNA Damage;Cell Cycle/DNA Damage, Target: Wee1;Checkpoint Kinase (Chk), Biological_Activity: PD 407824 is a checkpoint kinase Chk1 and WEE1 inhibitor with IC50s of 47 and 97 nM, respectively. PD 407824 is a chemical BMP sensitizer and increases the sensitivity of cells to sub-threshold amounts of BMP4[1][2].
IC50 & Target: IC50: 47 nM (Chk1), 97 nM (WEE1)[1]
In Vitro: PD 407824 is sufficient to block CHK1, leading to a significant down-regulation of p21, causing activation of CDK8/9, which in turn causes depletion of SMAD2/3[1]. 
PD 407824 is selective for Chk1 and WEE1 over PKC and Cdk4 with IC50s of 3.4 µM and 3.75 µM, respectively[3].

Name: Lavendustin A RG-14355, CAS: 125697-92-9, stock 9.8g, assay 98.8%, MWt: 381.38, Formula: C21H19NO6, Solubility: DMSO : ≥ 250 mg/mL (655.51 mM), Clinical_Informat: No Development Reported, Pathway: JAK/STAT Signaling;Protein Tyrosine Kinase/RTK, Target: EGFR;EGFR, Biological_Activity: Lavendustin A (RG-14355), isolated from Streptomyces Griseolavendus, is a potent, specific and ATP-competitive inhibitor of tyrosine kinase, with an IC50 of 11 ng/mL for EGFR-associated tyrosine kinase[1]. It suppresses VEGF-induced angiogenesis and blocks the induction of LTPGABA-A[2][3].
IC50 & Target: IC50: 11 ng/mL (EGFR-associated tyrosine kinase)[1].

Name: Alofanib RPT835, CAS: 1612888-66-0, stock 0.7g, assay 98.9%, MWt: 413.40, Formula: C19H15N3O6S, Solubility: DMSO : ≥ 30.1 mg/mL (72.81 mM), Clinical_Informat: No Development Reported, Pathway: Apoptosis;Protein Tyrosine Kinase/RTK, Target: Apoptosis;FGFR, Biological_Activity: Alofanib (RPT835) is a potent and selective allosteric inhibitor of fibroblast growth factor receptor 2 (FGFR2). Anticancer and antiangiogenic activity[1][2].
IC50 & Target: FGFR2[1]
In Vitro: Alofanib inhibits phosphorylation of FRS2α with IC50s of 7 and 9 nM in hFOB and SUM 52PE cells expressing different FGFR2 isoforms[1].
Alofanib (0.2-0.8 μM, 6 hours) inhibits FGF-mediated proliferation in a panel of four cell lines representing several tumour types (triple-negative breast cancer, melanoma, and ovarian cancer) with GI50s of 16-370 nM[1].
In Vivo: In a FGFR-driven human tumour xenograft model, oral administration of alofanib (30 mg/kg,
gavage, daily, 40 days, N=10) is well tolerated and results in potent antitumour activity[1].
Treatment with alofanib (10 mg/kg/d, 0, 3 and 6 d, intraperitoneally) ablates experimental FGF-induced angiogenesis in vivo[1].

Name: Bictegravir GS-9883, CAS: 1611493-60-7, stock 10.3g, assay 99%, MWt: 449.38, Formula: C21H18F3N3O5, Solubility: DMSO : 83.3 mg/mL (185.37 mM; Need ultrasonic and warming), Clinical_Informat: Launched, Pathway: Metabolic Enzyme/Protease;Anti-infection, Target: HIV Integrase;HIV, Biological_Activity: Bictegravir is a novel, potent inhibitor of HIV-1 integrase with an IC50 of 7.5 nM.
IC50 & Target: IC50: 7.5 nM (HIV-1 integrase)[1]
In Vitro: Bictegravir (BIC) inhibits the strand transfer activity with an IC50 of 7.5± 0.3 nM. Relative to its inhibition of strand transfer activity, Bictegravir is a much weaker inhibitor of 3′-processing activity of HIV-1 IN, with an IC50 of 241±51 nM. Bictegravir enhances the accumulation of 2-LTR circles ~5-fold relative to the mock-treated control and reduces the amount of authentic integration products in infected cells by 100-fold. Bictegravir potently inhibits HIV-1 replication in both MT-2 and MT-4 cells with EC50s of 1.5 and 2.4 nM, respectively. Bictegravir exhibits potent antiviral effects in both primary CD4+ T lymphocytes and monocyte-derived macrophages, with EC50s of 1.5±0.3 nM and 6.6±4.1 nM, respectively, which are comparable to values obtained in T-cell lines[1].

Name: Etripamil MSP-2017; (-)-MSP-2017, CAS: 1593673-23-4, stock 24.3g, assay 98.4%, MWt: 452.59, Formula: C27H36N2O4, Solubility: 10 mM in DMSO, Clinical_Informat: Launched, Pathway: Membrane Transporter/Ion Channel;Neuronal Signaling, Target: Calcium Channel;Calcium Channel, Biological_Activity: Etripamil (MSP-2017) is a short-acting L-type calcium-channel antagonist with a rapid onset of action designed for intranasal administration, used to treat Paroxysmal Supraventricular Tachycardia (PSVT). Etripamil (MSP-2017) slows atrioventricular nodal conduction and prolongs atrioventricular nodal refractory periods by inhibiting calcium ion influx through the calcium slow channels in the atrioventricular node cells[1][2].
IC50 & Target: L-type calcium-channel[1].

Name: Evenamide NW-3509, CAS: 1092977-61-1, stock 25.3g, assay 98.4%, MWt: 278.39, Formula: C16H26N2O2, Solubility: DMSO : 290 mg/mL (1041.70 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Membrane Transporter/Ion Channel, Target: Sodium Channel, Biological_Activity: Evenamide (NW-3509), a sodium channel blocker, shows efficacy in a broad spectrum of rodent models of psychosis, mania, depression, and aggressiveness[1].
IC50 & Target: Sodium channel[1]

Name: Evocalcet KHK7580, CAS: 870964-67-3, stock 30.3g, assay 98%, MWt: 374.48, Formula: C24H26N2O2, Solubility: DMSO : 30 mg/mL (80.11 mM; Need ultrasonic and warming), Clinical_Informat: Phase 3, Pathway: GPCR/G Protein, Target: CaSR, Biological_Activity: Evocalcet has an activating effect on calcium sensing receptor (CaSR) extracted from patent WO 2017061621 A1, compound A.
IC50 & Target: CaSR[1]

Name: Fenclozine, CAS: 75626-98-1, stock 30.8g, assay 98.2%, MWt: 611.17, Formula: C37H39ClN2O4, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Fenclozine is a non-steroidal antiinflammatory drug extracted from patent WO 2012112690 A2.

Name: Siguazodan SKF 94836, CAS: 115344-47-3, stock 3.5g, assay 98.5%, MWt: 284.32, Formula: C14H16N6O, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Phosphodiesterase (PDE), Biological_Activity: Siguazodan (SKF 94836) is a potent, selective and orally active phosphodiesterase III (PDE-III) inhibitor with an IC50 of 117 nM. Siguazodan increases cAMP accumulation in intact platelets with an EC50 of 18.88 μM. Siguazodan also inhibits phenylephrine-induced 5-HT release with an IC50 value of 4.2 μM[1][2][3].
IC50 & Target: IC50: 117 nM (phosphodiesterase III)[1]
In Vitro: Siguazodan selectively inhibits the major cyclic AMP-hydrolysing PDE in human platelet supernatants. The inhibited enzyme has been variously termed cyclic GMP-inhibited PDE or PDE-III. In platelet-rich plasma (PRP), Siguazodan inhibits U46619-induced aggregation more potently than that induced by adenosine 5'-diphosphate (ADP), and collagen. Treatment of the PRP with Aspirin has no effect on the potency of Siguazodan. In washed platelets, Siguazodan increases cyclic AMP levels and reduces cytoplasmic free calcium. ADP decreases the ability of Siguazodan to raise cyclic AMP and this may explain its lower potency in inhibiting responses to ADP. Siguazodan has anti-platelet actions over the same concentration range that it is an inotrope and vasodilator[2].
In Vivo: Siguazodan is a potent, selective inhibitor of phosphodiesterase III that has positive inotropic and vasodilating actions in various laboratory animals and is orally active with a long duration of action in conscious dogs[2].

Name: Trombodipine PCA-4230, CAS: 113658-85-8, stock 27.1g, assay 98.2%, MWt: 448.49, Formula: C21H24N2O7S, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Trombodipine is an antithrombotic agent.
In Vitro: Trombodipine is an antithrombotic agent. Exposure to 50 μM Trombodipine reveals an important stasis of growth. The percentage of inhibition exerted by 1 μM Trombodipine on day 3, 5 and 7 of the growth curve is 22.0±4.5, 32.0±3.0 and 29.4±6.0%, respectively (P<0.05). The inhibitory effect of Trombodipine on cell proliferation is reversible and after removal of Trombodipine the proliferation of the cells is resumed[1]. Addition of Trombodipine reduces cell number in a dose-dependent manner over a period of 4 to 6 days in culture. When compare to control cultures at the latest time points investigated, 5 μM Trombodipine decreases the number of E19P cells and human VSMCs by 25 and 21%, respectively, whereas 50 μM Trombodipine reduces E19P and human VSMC number by 85 and 74%, respectively[2].

Name: KB-5246, CAS: 119474-55-4, stock 10g, assay 98.7%, MWt: 425.86, Formula: C18H17ClFN3O4S, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Anti-infection, Target: Bacterial, Biological_Activity: KB-5246 is a tetracyclic quinolone and displays antibacterial activities.
IC50 & Target: Bacterial[1]
In Vitro: KB-5246 is a tetracyclic quinolone and displays antibacterial activities. The MICs for 90% of isolates tested (MIC90s) of KB-5246 against gram-positive microorganisms such as Staphylococcus aureus, including methicillin-resistant S. aureus, Staphylococcus epidermidis, Streptococcus pneumoniae, and Streptococcus pyogenes, are 0.39 μg/mL. KB5246 inhibits 90% of isolates of Escherichia coli, Klebsiella pneumoniae, Klebsiella oxytoca at a concentration of 0.10 μg/mL or less. When a concentration of KB-5246 at the MIC or higher is added, no regrowth after 24 h of incubation is observed[1].
In Vivo: The 50% effective dose values of KB-5246 against S. pneumoniae 2132 infections are 50.5 mg/kg of body weight. The activities of KB-5246 against S. aureus Smith, P. aeruginosa GN11189, and Serratia marcescens GN7577 infections are comparable to those of ofloxacin and greater than those of norfloxacin[1].

Name: KW-6055, CAS: 63233-46-5, stock 35.9g, assay 98.5%, MWt: 299.32, Formula: C16H17N3O3, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: KW-6055 is a benzylpyridine derivative and has anti-amnesic activity.
In Vivo: KW-6055 is a benzylpyridine derivative and has anti-amnesic activity. KW-6055 (40, 160 mg/kg, p.o.) increases the extracellular level of ACh in normal rats (257±23, 202±24%). In basal forebrain-lesioned rats, KW-6055 (40 mg/kg, p.o.) significantly increases the extracellular level of ACh (251±22%) for more than 2 hr, which is longer than in normal rats[1].

Name: TG4-155, CAS: 1164462-05-8, stock 24.5g, assay 98.5%, MWt: 394.46, Formula: C23H26N2O4, Solubility: H2O : < 0.1 mg/mL (insoluble); DMSO : 125 mg/mL (316.89 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein, Target: Prostaglandin Receptor, Biological_Activity: TG4-155 is a potent, brain-permeant and selective EP2 receptor antagonist with a Ki of 9.9 nM[1][2]. TG4-155 shows low nanomolar antagonist activity against only EP2 and DP1[1]. TG4-155 has an EP2 Schild KB of 2.4 nM and displays 550-4750-fold selectivity for EP2 over EP1, EP3, EP4 and IP, but only 14-fold selectivity against the DP1 receptor[2].
In Vitro: TG4-155 inhibits the serotonin 5-HT2B receptor with IC50=2.6 µM and hERG (human Ether-à-go-go-Related Gene) with IC50=12 µM[1]. 
PGE2 (0.1-10 μM) stimulation significantly enhances human prostate cancer cell line PC3 cell growth in a concentration-dependent manner with a maximal response being obtained at approximately 1 µM. This PGE2-induced cancer cell proliferation is significantly suppressed by TG4-155 (0.01-1μM ; 48 hours) in a concentration-dependent manner[1].
In Vivo: Administration of TG4-155 (5 mg/kg, i.p.; at 1 and 12 h) significantly reduces status epilepticus (SE)-induced neurodegeneration scores in C57BL/6 mice[3]. 
TG4-155 (3 mg/kg; i.p.) displays a bioavailability of 61% (i.p. route compared with i.v.), a plasma half-life (t1/2) of 0.6 h, and a brain/plasma ratio of 0.3 in C57BL/6 mice[3].

Name: Heparin Lithium salt, CAS: 9045-22-1, stock 8.3g, assay 98.2%, MWt: 1000, Formula: (C14H25NO20S3)n.xLi, Solubility: H2O : 125 mg/mL (Need ultrasonic), Clinical_Informat: Phase 4, Pathway: Autophagy, Target: Autophagy, Biological_Activity: Heparin Lithium salt is an anticoagulant which binds reversibly to antithrombin III (ATIII).
IC50 & Target: Antithrombin III[1]
In Vitro: Heparin is a potent anticoagulant drug based on its ability to accelerate the rate at which antithrombin inhibits serine proteases in the blood coagulation cascade. Heparin interactes most tightly with peptides containing a complementary binding site of high positive charge density. Heparin resembles DNA as both are highly charged linear polymers that behave as polyelectrolytes. Heparin is believed to function as an anticoagulant primarily through its interaction with AT III by enhancing AT-III-mediated inhibition of blood coagulation factors, including thrombin and factor Xa. Heparin binds to AT III and thrombin in a ternary complex, increasing the bimolecular rate constant for the inhibition of thrombin by a factor of 2000. Heparin is principally located in the granules of tissue mast cells that are closely associated with the immune response. Heparin makes numerous contacts with both FGF-2 and FGFR-1 stabilizing FGF–FGFR binding. Heparin also makes contacts with the FGFR-1 of the adjacent FGF–FGFR complex, thus seeming to promote FGFR dimerization[1].

Name: N-Ethylmaleimide NEM, CAS: 128-53-0, stock 5.3g, assay 98.5%, MWt: 125.13, Formula: C6H7NO2, Solubility: DMSO : 50 mg/mL (399.58 mM; Need ultrasonic); H2O : 50 mg/mL (399.58 mM; Need ultrasonic), Clinical_Informat: Phase 2, Pathway: Metabolic Enzyme/Protease, Target: Cathepsin, Biological_Activity: N-Ethylmaleimide (NEM), a reagent that alkylates free sulfhydryl groups, is a cysteine protease inhibitor[1]. N-ethylmaleimide specific inhibits phosphate transport in mitochondria[2].
IC50 & Target: Cysteine protease[1]

Name: Dp44mT, CAS: 152095-12-0, stock 11.6g, assay 98.9%, MWt: 285.37, Formula: C14H15N5S, Solubility: DMSO : 100 mg/mL (350.42 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Apoptosis;Apoptosis, Target: Apoptosis;Ferroptosis, Biological_Activity: Dp44mT is an iron chelator with selective anticancer activity.
IC50 & Target: Target: Iron chelator[1]
In Vitro: Dp44mT is cytotoxic to breast cancer cells, at least in part, due to selective inhibition of top2α. Dp44mT alone induced selective cell killing in the breast cancer cell line MDA-MB-231 when compared with healthy mammary epithelial cells (MCF-12A). It induces G1 cell cycle arrest and reduces cancer cell clonogenic growth at nanomolar concentrations. Dp44mT, but not the iron chelator desferal, induces DNA double-strand breaks quantified as S139 phosphorylated histone foci (γ-H2AX) and Comet tails induced in MDA-MB-231 cells. Doxorubicin-induced cytotoxicity and DNA damage are both enhanced significantly in the presence of low concentrations of Dp44mT. The chelator caused selective poisoning of DNA topoisomerase IIα (top2α) as measured by an in vitro DNA cleavage assay and cellular topoisomerase-DNA complex formation[1]. Dp44mT targets lysosome integrity through copper binding. Copper binding is essential for the potent antitumor activity of Dp44mT, as coincubation with nontoxic copper chelators markedly attenuated its cytotoxicity[2].

Name: Rottlerin Mallotoxin; NSC 56346; NSC 94525, CAS: 82-08-6, stock 16.8g, assay 98.4%, MWt: 516.54, Formula: C30H28O8, Solubility: H2O : < 0.1 mg/mL (insoluble); DMSO : 2 mg/mL (3.87 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Apoptosis;TGF-beta/Smad;Epigenetics;Autophagy, Target: Apoptosis;PKC;PKC;Autophagy, Biological_Activity: Rottlerin, a natural product purified from Mallotus Philippinensis, is a specific PKC inhibitor, with IC50 values for PKCδ of 3-6 μM, PKCα,β,γ of 30-42 μM, PKCε,η,ζ of 80-100 μM. Rottlerin acts as a direct mitochondrial uncoupler, and stimulates autophagy by targeting a signaling cascade upstream of mTORC1. Rottlerin induces apoptosis via caspase 3 activation[1][2][3].
IC50 & Target: IC50: 3-6 μM (PKCδ), 30-42 μM (PKCα,β,γ), 80-100 μM (PKCε,η,ζ)[1].
In Vitro: Rottlerin (20 μM, 2/6/24 hours) dramatically decreases the cyclin D-1 mRNA levels in a time-dependent manner in primary HMVEC[2]. 
Rottlerin (20 μM) exhibits cell proliferation in HMVEC[2]. 
In Vivo: Rottlerin (20 mg/kg, gavage 5 days per week, once daily, for 6 weeks) inhibits AsPC-1 pancreatic tumor growth in Balb C nude mice with no toxicity[3]. 
Rottlerin inhibits tumor cell proliferation, and induces apoptosis through activation of caspase-3 and cleavage of poly(ADP-ribose) polymerase (PARP)[3].

Name: Decursin (+)-Decursin, CAS: 5928-25-6, stock 1.6g, assay 98.2%, MWt: 328.36, Formula: C19H20O5, Solubility: DMSO : 125 mg/mL (380.68 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Decursin is an anticancer agent, with potential anti-inflammatory activity.
In Vitro: Decursin (25-100 μM) shows a strong dose- and time-dependent inhibition of cell growth, accounting for 22% to 51%, 21% to 68%, 9% to 72%, and 42% to 90% growth inhibition after 24, 48, 72, and 96 hours of treatment, respectively. Furthermore, it is observed that both Decursin and Decursinol have cytotoxic effect on DU145 cells, in which similar treatment (25-100 μM for 24, 48, 72, and 96 hours) with Decursin cause 15% to 45% cell death versus 11% to 12% in controls[1]. Decursin blocks tumor progression by suppression of angiopoietin-2, angiopoietin receptor Tie-2, and endothelial nitric oxide synthase (eNOS) in endothelial progenitor cells. Decursin has the ability to inhibit vascular endothelial growth factor (VEGF)-induced proliferation, metastasis, and tube formation in human umbilical vein endothelial cells (HUVECs). Decursin inhibits pro-inflammatory molecules, such as chemokines, cytokines, and enzymes such as Cyclooxygenase-2 (COX-2) and MMPs[2].

Name: K-252a SF2370; Antibiotic K 252a; Antibiotic SF 2370, CAS: 99533-80-9, stock 0.2g, assay 98.2%, MWt: 467.47, Formula: C27H21N3O5, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Stem Cell/Wnt;Protein Tyrosine Kinase/RTK;TGF-beta/Smad;Epigenetics;Neuronal Signaling;Autophagy;Protein Tyrosine Kinase/RTK;Neuronal Signaling, Target: PKA;PKA;PKC;PKC;CaMK;Autophagy;Trk Receptor;Trk Receptor, Biological_Activity: K-252a, a staurosporine analog isolated from Nocardiopsis sp. soil fungi, inhibits protein kinase, with IC50 values of 470 nM, 140 nM, 270 nM, and 1.7 nM for PKC, PKA, Ca2+/calmodulin-dependent kinase type II, and phosphorylase kinase, respectively[1][2]. K-252a is a potent inhibitor (IC50 of 3 nM) of the tyrosine protein kinase (TRK) activity of the NGF receptor gp140trk, the product of the trk protooncogene[3].
IC50 & Target: IC50: 470 nM (PKC), 140 nM (PKA), 270 nM (Ca2+/calmodulin-dependent kinase type II), 1.7 nM (phosphorylase kinase)[1][2].

Name: Phorbol 12,13-dibutyrate Phorbol dibutyrate;PDBu, CAS: 37558-16-0, stock 11.2g, assay 98.5%, MWt: 504.61, Formula: C28H40O8, Solubility: DMSO : ≥ 125 mg/mL (247.72 mM), Clinical_Informat: No Development Reported, Pathway: TGF-beta/Smad;Epigenetics, Target: PKC;PKC, Biological_Activity: Phorbol 12,13-dibutyrate (Phorbol dibutyrate) is a PKC activator and a potent skin tumor promoter[1][2].
IC50 & Target: PKC[1]
In Vitro: Phorbol 12,13-dibutyrate (Phorbol dibutyrate) (1 MM) activates PKC and inhibited Na/K-ATPase transport activity in OK cells[3].

Name: Duocarmycin MA, CAS: 1613286-57-9, stock 15.2g, assay 98.3%, MWt: 611.09, Formula: C34H31ClN4O5, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Cell Cycle/DNA Damage;Antibody-drug Conjugate/ADC Related, Target: DNA Alkylator/Crosslinker;ADC Cytotoxin, Biological_Activity: Duocarmycin MA is an antibody drug conjugates (ADCs) toxin. Duocarmycin is a DNA alkylating agent that binds in the minor groove. Duocarmycin MA can be used against multi-drug resistant cell lines.

Name: Z-321, CAS: 130849-58-0, stock 8.4g, assay 98.8%, MWt: 344.47, Formula: C19H24N2O2S, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Z-321 is a prolylendopeptidase (PEP) inhibitor.
IC50 & Target: PEP[1]
In Vivo: Z-321 is a prolylendopeptidase (PEP) inhibitor. In the 100 or 200 mg/kg Z-321-treated groups, mean lordosis quotient (LQ) decreases after administration. However, there is no statistical difference among the values before and after. In contrast, the mean LQ in the 300 mg/kg Z-321-treated females is lower than that before injection (P<0.005). Furthermore, when compare to that in the vehicle-treated control group, mean LQ is also significantly lower (p<0.05). The incidence of soliciting behavior decreases after treatment with 300 mg/kg Z-321, when compare to that before treatment, but there is no statistical difference. The present study also demonstrates that 300 mg/kg Z-321 is effective in inhibiting lordosis behavior without disturbance of locomotor activity[1].

Name: Perzinfotel EAA-090, CAS: 144912-63-0, stock 29.9g, assay 98.9%, MWt: 260.18, Formula: C9H13N2O5P, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Membrane Transporter/Ion Channel;Neuronal Signaling, Target: iGluR;iGluR, Biological_Activity: Perzinfotel (EAA-090) is a potent, selective, and competitive NMDA receptor antagonist with neuroprotective effects. Perzinfotel (EAA-090) shows high affinity (IC50=30 nM) for the glutamate site[1][2].
IC50 & Target: NMDA receptor[1]
In Vitro: Perzinfotel blocks NMDA-induced currents with an IC50 of 0.48 μM and glutamate-induced neurotoxicity with an IC50 of 1.6 μM[1].

Name: E-5324, CAS: 141799-76-0, stock 33.3g, assay 98.1%, MWt: 434.57, Formula: C26H34N4O2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Acyltransferase, Biological_Activity: E-5324 is potent inhibitor of acyl-CoA:cholesterol acyltransferase (ACAT) with IC50s of 44 to 190 nM.
IC50 & Target: IC50: 44 to 190 nM (ACAT)[1]
In Vitro: E-5324 is a potent ACAT inhibitor with IC50s of 44 to 190 nM in microsomes. E-5324 shows no effect on triglyceride synthesis up to 10 μM. E-5324 also has no effect on bovine pancreatic cholesterol esterase or lecithin: cholesterol acyltransferase (LCAT) up to 10 μM. E-5324 inhibits the incorporation of [3H]oleate into cholesteryl [3H]oleate in a concentration-dependent manner with an IC50 of 0.44 μM. E-5324 also inhibits [3H]cholesteryl ester synthesis with an IC50 of 0.41 μM[1].
In Vivo: The areas under the cholesterol-time curves for duration of this study (AUC) for control, E-5324 0.02% and E-5324 0.1% are 104985±4411, 106096±4476 and 105231±4 348 mg×day/dL, respectively. The high dose of E-5324 (0.1%) significantly reduces the surface involvement by 34% and 54% in the aortic arch and thoracic aorta, respectively. E-5324 treatment significantly reduces the wet weight and protein content. In the aortic arch, the high dose of E-5324 (0.1%) significantly reduces both cholesteryl ester and total cholesterol by 60% and 59%, respectively. The high dose of E-5324 (0.1%) markedly reduces the ACAT activities in the aortic arch and thoracic aorta by 35% and 44%, respectively[2].

Name: Zinc phthalocyanine ZnPc, CAS: 14320-04-8, stock 15.5g, assay 98.9%, MWt: 577.90, Formula: C32H16N8Zn, Solubility: DMF : < 1 mg/mL (insoluble); DMSO : < 1 mg/mL (insoluble or slightly soluble), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Zinc phthalocyanine is commonly applied in industry (catalysts, photoconductors) and biomedical (photodynamic therapy, PDT)[1]. Zinc phthalocyanine can be used to photooxidise cyclohexane[2].

Name: Pumaprazole BY-841, CAS: 158364-59-1, stock 19.7g, assay 99%, MWt: 338.40, Formula: C19H22N4O2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Membrane Transporter/Ion Channel, Target: Proton Pump, Biological_Activity: Pumaprazole is a reversible proton pump antagonist.
IC50 & Target: proton pump[1]
In Vivo: Pumaprazole is a reversible proton pump antagonist. Basal acid secretion in the Ghosh-Schild rat is inhibited by Pumaprazole with a higher efficacy compare to ranitidine. Pumaprazole displays identical ID50 values on day 1 (11 μmol/kg, 95% confidence limits of 5 and 23) and on day 7 (10 μmol/kg, 95% confidence limits of 4 and 23) of a repeated dose study in this model. The lower dose of Pumaprazole (27 μmol/kg) rapidly elevates luminal pH up to almost neutrality, the higher dose (54 μmol/kg) further prolongs this pH-elevating effect[1].

Name: PNU-103017, CAS: 166335-18-8, stock 0.3g, assay 98.3%, MWt: 504.60, Formula: C28H28N2O5S, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease;Anti-infection, Target: HIV Protease;HIV, Biological_Activity: PNU-103017 is an HIV protease inhibitor.
IC50 & Target: HIV protease[1]
In Vivo: PNU-103017 is a selective HIV aspartyl protease inhibitor under evaluation as a potential oral treatment of Acquired Immunodeficiency Diseases. PNU-103017 is a racemic mixture of two enantiomers, designated PNU-103264 (R-) and PNU-103265 (S-). The Cmax (P≤0.0349), Cmin (P≤0.0168), and Cav (P≤0.0118) are significantly higher for the (R)- than the (S)-enantiomer, showing enantioselective pharmacokinetics of PNU-103017 in the dog[1].

Name: Ibrutinib PCI-32765, CAS: 936563-96-1, stock 30.1g, assay 98.8%, MWt: 440.50, Formula: C25H24N6O2, Solubility: DMSO : ≥ 30 mg/mL (68.10 mM); H2O : < 0.1 mg/mL (insoluble), Clinical_Informat: Launched, Pathway: Protein Tyrosine Kinase/RTK, Target: Btk, Biological_Activity: Ibrutinib (PCI-32765) is a selective, irreversible Btk inhibitor with an IC50 of 0.5 nM.
IC50 & Target: IC50: 0.5 nM (Btk)
In Vitro: Ibrutinib (PCI-32765) selectively inhibits B-cell signaling and activation. It inhibits autophosphorylation of Btk (IC50=11 nM), phosphorylation of Btk's physiological substrate PLCγ (IC50=29 nM), and phosphorylation of a further downstream kinase, ERK (IC50=13 nM)[1]. Ibrutinib (PCI-32765) inhibits BCR-activated primary B cell proliferation (IC50=8 nM). Following FcγR stimulation, Ibrutinib (PCI-32765) inhibits TNFα, IL-1β and IL-6 production in primary monocytes (IC50=2.6, 0.5, 3.9 nM, respectively)[3].
In Vivo: Ibrutinib (PCI-32765) (3.125-50 mg/kg, p.o.) reduces the level of circulating autoantibodies and completely suppresses disease in mice with collagen-induced arthritis. Ibrutinib (PCI-32765) inhibits autoantibody production and the development of kidney disease in the MRL-Fas(lpr) lupus model. Ibrutinib (PCI-32765) (3.125-50 mg/kg, p.o.) reduces renal disease and autoantibody production in MRL-Fas(lpr) mice[1]. Ibrutinib (PCI-32765) (0.1 μM) inhibits activation-induced proliferation of CLL cells, induces selective cytotoxicity in B cells compared with T cells, but alters activation induced T-cell cytokine production[2]. Ibrutinib (PCI-32765) dose-dependently and potently reverses arthritic inflammation in a therapeutic CIA model with an ED50 of 2.6 mg/kg/day. Ibrutinib (PCI-32765) also prevents clinical arthritis in CAIA models[3].

Name: Rimeporide EMD-87580, CAS: 187870-78-6, stock 0.6g, assay 98.2%, MWt: 333.38, Formula: C11H15N3O5S2, Solubility: DMSO : 20 mg/mL (59.99 mM; Need ultrasonic and warming), Clinical_Informat: Phase 1, Pathway: Membrane Transporter/Ion Channel, Target: Sodium Channel, Biological_Activity: Rimeporide (EMD-87580) is a potent and selective inhibitor of the Na+/H+ exchanger (NHE-1).
IC50 & Target: NHE1[1]
In Vitro: Blocking NHE-1 activity has been shown to decrease intracellular Na+ and Ca2+ overload and pH and Rimeporide (EMD-87580) represents a new therapeutic option for duchenne muscular dystrophy (DMD). Rimeporide (EMD-87580) is expected to act as a muscle-sparing agent and its mode of action means that it is mutation independent[1].

Name: S-8921, CAS: 151165-96-7, stock 33.6g, assay 98.4%, MWt: 540.60, Formula: C30H36O9, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: S-8921 is an ileal Na+/bile acid cotransporter (IBAT) inhibitor.
IC50 & Target: IBAT[1]
In Vitro: S-8921 is an ileal Na+/bile acid cotransporter (IBAT) inhibitor. S-8921 inhibits the uptake velocity of 60 μM [3H] taurocholate dose-dependently in IBAT-COS cells, and the IC50 value of S-8921 is 66±8 μM[1].
In Vivo: Seven-day treatment with S-8921 causes a dramatic decrease of serum cholesterol concentrations in hamsters. The hypocholesterolemic effects of S-8921 are dose-dependent, but S-8921 does not affect body weight. An increase of fecal bile acid excretion is observed especially at higher doses of S-8921[1]. S-8921 treatment for 1 to 2 weeks causes a decrease in serum total cholesterol concentrations, with 0.01% S-8921 (4.0 to 4.6 mg/kg) being almost maximally effective[2].

Name: Lauric acid, CAS: 143-07-7, stock 28.7g, assay 98.5%, MWt: 200.32, Formula: C12H24O2, Solubility: DMSO : ≥ 250 mg/mL (1248.00 mM), Clinical_Informat: No Development Reported, Pathway: Anti-infection;Metabolic Enzyme/Protease, Target: Bacterial;Endogenous Metabolite, Biological_Activity: Lauric acid is a middle chain-free fatty acid with strong bactericidal properties. The EC50s for P. acnes, S.aureus, S. epidermidis, are 2, 6, 4 μg/mL, respectively.
IC50 & Target: EC50: 2 μg/mL (P. acnes), 6 μg/mL (S.aureus), 6 μg/mL (S. epidermidis)[1].

Name: Maleic Acid, CAS: 110-16-7, stock 11.6g, assay 98.1%, MWt: 116.07, Formula: C4H4O4, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Anti-infection;Metabolic Enzyme/Protease, Target: Bacterial;Endogenous Metabolite, Biological_Activity: Maleic Acid is a Glutamate Decarboxylase (GAD) inhibitor of E. coli and L. monocytogenes.
IC50 & Target: GAD[1][2].
In Vitro: The MICs of WT 10403S for the acids (e.g., Maleic Acid) are 34 mM, 25 mM, 31 mM and 30 mM which correspond to pH values prior to growth of 4.84, 5.14, 5.32 and 5.02 respectively. Of all compounds tested, Maleic Acid is the least inhibitory despite acting at a lower pH (4.84). The most acid resistant (10403S) and the weakest (EGD-e) strain are challenged with 8.6 mM and 4.3 mM of each organic acid at pH 3 and 3.3 respectively. On both strains, Maleic Acid is the most bactericidal[2].

Name: Dulcite Dulcitol; Melampyrit; NSC 1944, CAS: 608-66-2, stock 25.8g, assay 98.8%, MWt: 182.17, Formula: C6H14O6, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: Dulcite is a sugar alcohol with a slightly sweet taste which is a metabolic breakdown product of galactose.

Name: TES, CAS: 7365-44-8, stock 1.2g, assay 98.2%, MWt: 229.25, Formula: C6H15NO6S, Solubility: H2O : 125 mg/mL (545.26 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: TES is used to make buffer solutions. TES has a pKa value of 7.550 (at 25°C). TES can be used to make buffer solutions in the pH range 6.8-8.2[1].

Name: Silvestrol aglycone (enantiomer), CAS: 1112993-18-6, stock 4.8g, assay 98.3%, MWt: 478.49, Formula: C27H26O8, Solubility: DMSO : ≥ 114 mg/mL (238.25 mM), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Silvestrol aglycone enantiomer is a cyclopenta benzofuran core phenol[1].

Name: Disodium 5'-inosinate IMP (disodium salt);Disodium inosinate, CAS: 4691-65-0, stock 3.5g, assay 98.2%, MWt: 392.17, Formula: C10H11N4Na2O8P, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Disodium 5'-inosinate, obtained from bacterial fermentation of sugars, is as a food additive and often found in a variety of other snacks.

Name: Glycylglycine, CAS: 556-50-3, stock 38.5g, assay 98.2%, MWt: 132.12, Formula: C4H8N2O3, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: Glycylglycine is the simplest of all peptides and could function as a gamma-glutamyl acceptor.

Name: NSP-SA-NHS, CAS: 199293-83-9, stock 1.4g, assay 98.1%, MWt: 681.73, Formula: C32H31N3O10S2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: NSP-SA-NHS is a chemiluminescent acridinium ester.

Name: WZB117, CAS: 1223397-11-2, stock 28.9g, assay 98.8%, MWt: 368.31, Formula: C20H13FO6, Solubility: DMSO : ≥ 150 mg/mL (407.27 mM), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: WZB117 is a glucose transporter 1 (Glut1) inhibitor, which downregulates glycolysis, induces cell-cycle arrest, and inhibits cancer cell growth in vitro and in vivo.
IC50 & Target: Glut1[1]
In Vitro: Glucose uptake assays show that WZB117 inhibits glucose transport in cancer cells in a dose-dependent manner. The inhibition of glucose transport induced by WZB117 occurres within 1 minute after the assay started, suggesting that the inhibitory activity is likely to be via a direct and fast mechanism. Cell viability assay shows that WZB117 inhibits cancer cell proliferation with an IC50 of approximately 10 μM. The inhibitory activity of WZB117 on cancer cell growth is also confirmed with a clonogenic assay, which also indicates that the inhibition is irreversible in nature. WZB117 treatment results in significantly more cell growth inhibition in lung cancer A549 cells than in nontumorigenic lung NL20 cells. Similar results are also observed in breast cancer MCF7 cells and their nontumorigenic MCF12A cells. When WZB117 is added to cancer cells grown under hypoxic conditions, more cell growth inhibition is observed than under normoxic conditions[1].
In Vivo: The animal study shows that after daily intraperitoneal injection of WZB117 at 10 mg/kg body weight, the sizes of the compound-treated tumors are on average more than 70% smaller than those of the mock (PBS/DMSO)-treated tumors. Notably, 2 of the 10 compound-treated tumors disappear during the treatment and never grow back even at the end of the study. Body weight measurement and analysis reveal that the mice treated with WZB117 lost about 1 to 2 grams of body weight compared with the mock-treated mice with most of the weight loss in the fat tissue. Blood counts and analysis of mice at the end of the study show that lymphocytes and platelets are changed in the compound-treated mice compared with the vehicle-treated mice, but the cell counts remained in the normal ranges. One of the concerns for using glucose transport inhibitors is that the inhibitor might produce hyperglycemia in the treated mice[1].

Name: L-Lactic acid (S)-2-Hydroxypropanoic acid, CAS: 79-33-4, stock 21.3g, assay 98.7%, MWt: 90.08, Formula: C3H6O3, Solubility: DMSO : ≥ 125 mg/mL (1387.66 mM), Clinical_Informat: Launched, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: L-Lactic acid is a buildiing block which can be used as a precursor for the production of the bioplastic polymer poly-lactic acid.

Name: BAZ2-ICR, CAS: 1665195-94-7, stock 3.6g, assay 98.2%, MWt: 357.41, Formula: C20H19N7, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Epigenetics, Target: Epigenetic Reader Domain, Biological_Activity: BAZ2-ICR is a potent, selective, cell active and orally active BAZ2A/B bromodomains inhibitor with IC50s of 130 nM and 180 nM, and Kds of 109 nM and 170 nM, respectively. BAZ2-ICR shows 10-15-fold selectivity for binding BAZ2A/B over CECR2 and >100-fold selectivity over all other bromodomains. BAZ2-ICR is an epigenetic chemical probe[1].
IC50 & Target: IC50: 130 nM (BAZ2A) and 180 nM (BAZ2B); Kd: 109 nM (BAZ2A) and 170 nM (BAZ2A)[1]
In Vitro: To investigate whether BAZ2-ICR (Compound 13) can displace BAZ2 bromodomains from chromatin in living cells, a fluorescence recovery after photobleaching (FRAP) assay utilizing GFP-tagged BAZ2A full length protein transfected into human osteosarcoma cells (U2OS) are tested. 1 μM BAZ2-ICR reduces the recovery time of the wild-type (wt) construct to a level similar to the dominant negative mutant, confirming that BAZ2-ICR inhibits BAZ2A in cells[1].
In Vivo: BAZ2-ICR (Compound 13) shows very high solubility (25 mM in D2O), a measured log D of 1.05, high stability in mouse microsomes, and permeation in the CaCo-2 model and thus a suitable profile for oral and intravenous gavage. BAZ2-ICR (5 mg/kg) shows 70% bioavailability and moderate clearance (∼50% of mouse liver blood flow) and volume of distribution[1].

Name: DL-Serine, CAS: 302-84-1, stock 20.5g, assay 98.3%, MWt: 105.09, Formula: C3H7NO3, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: DL-Serine is a mixture of D-Serine and L-Serine.
In Vivo: Subcutaneous injection of DL-serine increases the number and size of renal tubular cell tumors in male W rats treated with 500 or 1,000 ppm N-ethyl-N-hydroxyethylnitrosamine[1].

Name: D-Gluconic acid, CAS: 526-95-4, stock 1.9g, assay 98.1%, MWt: 196.16, Formula: C6H12O7, Solubility: 10 mM in DMSO, Clinical_Informat: Phase 4, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: D-Gluconic acid is the carboxylic acid by the oxidation with antiseptic and chelating properties.
In Vitro: D-gluconic acid, a simple sugar acid, is the most significant antifungal metabolite produced by Pseudomonas. str. AN5 against the take-all fungal pathogen in biocontrol protection[1].

Name: NVP-2, CAS: 1263373-43-8, stock 31.7g, assay 98.5%, MWt: 513.07, Formula: C27H37ClN6O2, Solubility: DMSO : ≥ 100 mg/mL (194.91 mM), Clinical_Informat: No Development Reported, Pathway: Cell Cycle/DNA Damage, Target: CDK, Biological_Activity: NVP-2 is a selective ATP-competitive CDK9 inhibitor with an IC50 of 0.5 nM.
IC50 & Target: IC50: 0.5 nM (CDK9)[1]

Name: E3330 APX-3330, CAS: 136164-66-4, stock 21.2g, assay 98.9%, MWt: 378.46, Formula: C21H30O6, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Cell Cycle/DNA Damage, Target: DNA/RNA Synthesis, Biological_Activity: E3330 (APX-3330) is a direct, orally active AP endonuclease 1 (APE1; also known as REF-1) inhibitor, which suppresses NF-κB DNA-binding activity. E3330 (APX-3330) blocks TNF-α-induced activation of IL-8 production in liver cancer cell lines. E3330 (APX-3330) shows anticancer properties, such as inhibition of cancer cell growth and migration[1-4].
IC50 & Target: DNA Synthesis, APE1[1-4]

Name: 2-Methyl-5-HT 2-Methyl-5-hydroxytryptamine; 2-Methylserotonin;2-Me-5-HT, CAS: 78263-90-8, stock 28.9g, assay 98.8%, MWt: 190.24, Formula: C11H14N2O, Solubility: DMSO : 125 mg/mL (657.06 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Neuronal Signaling;GPCR/G Protein, Target: 5-HT Receptor;5-HT Receptor, Biological_Activity: 2-Methyl-5-HT (2-Methyl-5-hydroxytryptamine) is a potent and selective 5-HT3 receptor agonist. 2-Methyl-5-HT is shown to display anti-depressive-like effects[1].
In Vivo: 2-Methyl-5-HT (2-Methyl-5-hydroxytryptamine) significantly decreases time of immobility thus showing anti-depressive-like effects[1].

Name: THZ531, CAS: 1702809-17-3, stock 18.9g, assay 98.9%, MWt: 558.07, Formula: C30H32ClN7O2, Solubility: DMSO : 16 mg/mL (28.67 mM; Need ultrasonic and warming); H2O : < 0.1 mg/mL (insoluble), Clinical_Informat: No Development Reported, Pathway: Cell Cycle/DNA Damage, Target: CDK, Biological_Activity: THZ531 is a covalent inhibitor of both CDK12 and CDK13 with IC50s of 158 nM and 69 nM, respectively.
IC50 & Target: IC50: 158 nM (CDK12), 69 nM (CDK13)
In Vitro: The results from Kinase assays demonstrate that THZ531 potently inhibits CDK12 and CDK13 with IC50s of 158 nM and 69 nM, respectively; whereas inhibition of CDK7 and CDK9 is more than 50-fold weaker with IC50s of 8.5 and 10.5 µM, respectively. THZ531 treatment leads to a dramatic and irreversible decrease in Jurkat cell proliferation with an IC50 of 50 nM. FACS cell cycle analysis following treatment with escalating doses of THZ531 displays a dose and time-dependent increase in the number of cells exhibiting sub-G1 content. At 50 nM THZ531, no increase in the percentage of apoptotic cells is observed over DMSO control for the time course of the experiment. Higher doses of THZ531 leads to pronounced Annexin V signal with 30 to 40% annexin V-positively stained cells by 72 hrs. A dramatic reduction in elongating Pol II following THZ531 treatment is also observed[1].

Name: UK-240455, CAS: 178908-09-3, stock 39.4g, assay 98.3%, MWt: 368.19, Formula: C11H11Cl2N3O5S, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Membrane Transporter/Ion Channel;Neuronal Signaling, Target: iGluR;iGluR, Biological_Activity: UK-240455 is a potent and selective N-methyl D-aspartate (NMDA) glycine site antagonist.
IC50 & Target: NMDA[1]
In Vivo: UK-240455 is a potent and selective N-methyl D-aspartate (NMDA) glycine site antagonist. Following i.v. administration of UK-240455 to male rats, UK-240455 has a clearance of 12 mL/min/kg and a volume of distribution of 0.4 L/kg. The plasma concentration of UK-240455 decreases with an apparent half-life of 0.4 h. Analysis of urine (0 to 24 h) for unchanged UK-240455 indicates that 57% of the dose administered is excreted unchanged in the urine. The urinary clearance of UK-240455 in the rat is therefore 7 mL/min/kg. Following oral administration of UK-240455 to male rats, the apparent elimination half-life of UK-240455 from plasma following oral administration is 1.6 h[1].

Name: Ingliforib CP 368296;GPi 296, CAS: 186392-65-4, stock 19.8g, assay 98.4%, MWt: 457.91, Formula: C23H24ClN3O5, Solubility: DMSO : 130 mg/mL (283.90 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Ingliforib is a glycogen phosphorylase inhibitor, with IC50s of 52, 352 and 150 nM for liver, muscle and brain glycogen phosphorylase, and has cardioprotective activity.
IC50 & Target: IC50: 52 nM (liver Glycogen phosphorylase), 352 nM (Muscle Glycogen phosphorylase), 150 nM (Barin Glycogen phosphorylase)[1]
In Vitro: Ingliforib is a glycogen phosphorylase inhibitor, and inhibits the myocardial GP isoforms (muscle and brain) with IC50s of 352 and 150 nM, respectively, also a potent inhibitor of the liver isoform (IC50 of 52 nM). Ingliforib (0.1, 1, 10 μM) dose-dependently reduces infarct size in the isolated rabbit hearts[1].
In Vivo: Ingliforib (15 mg/kg) potently reduces infarct size by 52%, and decreases plasma glucose and lactate concentrations in openchest anesthetized rabbits. Ingliforib (15 mg/kg) also inhibits myocardial glycogen phosphorylase a (GPa) and total glycogen phosphorylase (GP) activity in anesthetized rabbits[1].

Name: Solabegron GW 427353, CAS: 252920-94-8, stock 8.2g, assay 98.6%, MWt: 410.89, Formula: C23H23ClN2O3, Solubility: 10 mM in DMSO, Clinical_Informat: Phase 2, Pathway: GPCR/G Protein;Neuronal Signaling, Target: Adrenergic Receptor;Adrenergic Receptor, Biological_Activity: Solabegron (GW 427353) is a selective β3-adrenergic receptor agonist, stimulating cAMP accumulation in Chinese hamster ovary cells expressing the human β3-AR, with an EC50 value of 22 nM[1]. Solabegron (GW 427353) is being developed for the treatment of overactive bladder and irritable bowel syndrome[1].
IC50 & Target: EC50: 22 nM (β3-AR in cells)[1].
In Vivo: Solabegron (GW427353) at 3 mg/kg i.v. evokes an increase in micturition volume threshold that prevented the acetic acid-evoked decreases in dogs. The low dose (1 mg/kg) shows no significant activity[1].

Name: Esonarimod KE-298, CAS: 101973-77-7, stock 18.9g, assay 98.2%, MWt: 280.34, Formula: C14H16O4S, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Esonarimod is an antirheumatic drug.
In Vitro: Esonarimod (KE-298) (10 to 300 μg/mL) suppresses the production of NO by RAW264.7 cells in a dose dependent manner. The IC50 of Esonarimod is 117.5 μg/mL. Esonarimod does not affect cellular viability at these tested doses. Esonarimod has no direct effect on NOS activity in cell-free extracts of RAW264.7 cells[1].
In Vivo: After repeated oral administration of Esonarimod (14C-KE-298), the radioactivity decreases rapidly and no tendency towards accumulation is found[2].

Name: Besifovir LB80331, CAS: 441785-25-7, stock 37.5g, assay 98.3%, MWt: 299.22, Formula: C10H14N5O4P, Solubility: DMSO : 250 mg/mL (835.51 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Anti-infection, Target: HBV, Biological_Activity: Besifovir (LB80331), a parent drug converted by LB80380, further metabolizes to its active form, LB80317. LB80380 is potent antiviral agent against hepatitis B virus (HBV) [1][2].

Name: ERB-196 WAY-202196, CAS: 550997-55-2, stock 7.6g, assay 98.9%, MWt: 279.27, Formula: C17H10FNO2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Estrogen Receptor/ERR, Biological_Activity: ERB-196 is a nonsteroidal selective estrogen receptor-β (ERβ) agonist.
IC50 & Target: ERβ[1]
In Vivo: ERB-196 is a nonsteroidal selective estrogen receptor-β (ERβ) agonist. ERB-196 significantly reduces histopathologic evidence of injury to the gastrointestinal mucosal surface (0.7±0.1 vs. 2.3±0.2 for control; p<0.05). The mucosal mass of 10-cm segments of small bowel mucosa shows better preservation of mucosal mass than control treatment (63±20 [ERB-196] vs. 31±24 [control]), but this difference fails to reach statistical significance (p<0.06). The administration of ERB-196 is highly effective in the prevention of lethality. Consistent with the neutropenic rat model, ERB-196 significantly increases survival when compare with vehicle control[1].

Name: XL-784, CAS: 1224964-36-6, stock 34.8g, assay 98.7%, MWt: 549.93, Formula: C21H22ClF2N3O8S, Solubility: 10 mM in DMSO, Clinical_Informat: Phase 2, Pathway: Metabolic Enzyme/Protease, Target: MMP, Biological_Activity: XL-784 is a selective matrix metalloproteinases (MMP) inhibitor, with IC50s of ~1900, 0.81, 120, 10.8, 18, 0.56 nM for MMP-1，MMP-2，MMP-3，MMP-8，MMP-9，MMP-13，respectively.
IC50 & Target: MMP[1].
In Vitro: XL-784 is a highly potent, low-molecular-weight (1,122 g/mol) inhibitor of MMPs that has very limited aqueous solubility (20 μg/mL). XL-784 potently inhibits MMP-2, MMP-13, and
ADAM10 [TNF-α-converting enzyme (TACE)] activity in vitro, with IC50 values in the range of 1-2 nM. XL-784 also inhibits MMP-9 (IC50 ~20 nM) activity and ADAM17 (IC50 ~70 nM) also known as TACE. However, it exhibits low potency for inhibition of MMP-1 (IC50 ~2,000 nM)[1].
In Vivo: All mice tolerate the treatments similarly. Control mice all developed aneurysms with a mean %△AD of 158.5%±4.3%. Treatment with all doses of XL-784 and doxycycline are effective in inhibiting aortic dilatation. There is a clear dose-response relationship between XL-784 and reductions in aortic dilatation at harvest (50 mg/kg 140.4% ±3.2%; 125 mg/kg 129.3% ±5.1%; 250 mg/kg 119.2%±3.5%; all Ps<0.01 compared to control). This continues with the higher doses (375 mg/kg 88.6%±4.4%; 500 mg/kg 76.0%±3.5%). The highest 2 doses of XL-784 tested are more effective than doxycycline (112.2%±2.0%, P<0.05) in inhibiting maximal dilatation of the aorta after elastase perfusion[2].

Name: Artemisone Artemifone;BAY 44-9585, CAS: 255730-18-8, stock 11.6g, assay 98.7%, MWt: 401.52, Formula: C19H31NO6S, Solubility: DMSO : 130 mg/mL (323.77 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Anti-infection, Target: Parasite, Biological_Activity: Artemisone (Artemifone) is a potent and semi-synthetic antimalarial, inhibits P. falciparum strains, with a mean IC50 of 0.83 nM[1].
IC50 & Target: IC50: 0.83 nM (P. falciparum)[1]
In Vitro: Artemisone inhibits 3D7 and K1 P. falciparum, with IC50s of 0.88±0.59 and 1.23±0.64 nM, respectively[1].
In Vivo: Artemisone is effectve at inhibiting the parasitaemia in the P. berghei NY susceptible strain, with an ED50 of 9.62 mg/kg via subcutaneous route and 11.67 mg/kg via oral administration[1]. 
Artemisone (3, 1, 0.3 and 0.1 mg/kg, s.c.) in combination with ohter antimalarials has enhanced effect against the chloroquine-resistant line P. yoelii NS[1]

Name: GSK2018682, CAS: 1034688-30-6, stock 19g, assay 98.7%, MWt: 440.88, Formula: C22H21ClN4O4, Solubility: DMS : ≥ 125 mg/mL (283.52 mM); H2O : < 0.1 mg/mL (insoluble), Clinical_Informat: Phase 1, Pathway: GPCR/G Protein, Target: LPL Receptor, Biological_Activity: GSK2018682 is an agonist for S1P1 and S1P5 receptor with pEC50s of 7.7 and 7.2, respectively, and has no agonist activity towards human S1P2, S1P3, or S1P4. GSK2018682 is used in the research of multiple sclerosis.
IC50 & Target: pEC50: 7.7 (S1P1 receptor), 7.2 (S1P5 receptor)[1]
In Vitro: GSK2018682 is an agonist for S1P1 and S1P5 receptor with pEC50s of 7.7 and 7.2, respectively, and has no agonist activity towards human S1P2, S1P3, or S1P4[1].

Name: ACH-806 GS9132, CAS: 870142-71-5, stock 30.1g, assay 98.6%, MWt: 411.44, Formula: C19H20F3N3O2S, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease;Anti-infection, Target: HCV Protease;HCV, Biological_Activity: ACH-806 is an NS4A antagonist which can inhibit Hepatitis C Virus (HCV) replication with an EC50 of 14 nM.
IC50 & Target: NS4A[1]
EC50: 14 nM (HCV)[1]
In Vitro: ACH-806 is an NS4A antagonist which can inhibit Hepatitis C Virus (HCV) replication with an EC50 of 14 nM. ACH-806 treatment results in significant reductions of both NS3 and NS4A in the transfected cells. This finding is reminiscent of ACH-806-treated replicon cells in which the amounts of NS3 and NS4A are also both decreased. The total amount of NS3 in the ACH-806-treated sample is reduced by ~6-fold (100/16) and causes a reduction of NS4A-bound NS3 ~29-fold (261/9). The levels of labeled NS3 and NS4A immunoprecipitated by anti-NS3 antibody are apparently reduced after the treatment of ACH-806. ACH-806 also induces significant decreases of NS3 and NS4A and promotes p14 formation in the parental replicon cells but not in the ACH-806-resistant replicon cells[1].

Name: Latanoprostene bunod NCX116;LBN, CAS: 860005-21-6, stock 17.5g, assay 99%, MWt: 507.62, Formula: C27H41NO8, Solubility: DMSO : 250 mg/mL (492.49 mM; Need ultrasonic), Clinical_Informat: Launched, Pathway: Others, Target: Others, Biological_Activity: Latanoprostene bunod (LBN), a nitric oxide (NO)-donating prostaglandin F2a analog, is a topical ophthalmic therapeutic for the reduction of intraocular pressure (IOP) in patients with open-angle glaucoma or ocular hypertension (OHT) [1].

Name: Seladelpar MBX-8025, CAS: 851528-79-5, stock 33.7g, assay 98.8%, MWt: 444.46, Formula: C21H23F3O5S, Solubility: 10 mM in DMSO, Clinical_Informat: Phase 3, Pathway: Cell Cycle/DNA Damage, Target: PPAR, Biological_Activity: Seladelpar (MBX-8025) is an orally active, potent (50% effect concentration EC50 2 nM), and specific PPAR-δ agonist.
IC50 & Target: EC50: 2 nM (PPAR-δ)[1][2] 
EC50: 1600 nM (PPAR-α)[2] 
In Vitro: Seladelpar (MBX-8025) is an orally active, potent (2 nM), and specific (>750-fold and >2500-fold compared with PPAR-α or PPAR-γ receptors, respectively) PPAR-δ agonist being developed as a lipid-altering agent[1]. Seladelpar is a potent, and selective PPAR-δ agonist (50% effect concentration human PPAR-δ=2 nM, PPAR-α=1,600 nM) that demonstrates favorable effects on insulin resistance, diabetes, and atherogenic dyslipidemia[2].
In Vivo: From weaning, female Alms1 mutant (foz/foz) mice and wild-type littermates are fed an atherogenic diet for 16 weeks; groups (n=8-12) are then randomized to receive Seladelpar (10 mg/kg) or vehicle (1% methylcellulose) by gavage for 8 weeks. Despite minimally altering body weight, Seladelpar normalizes hyperglycemia, hyperinsulinemia, and glucose disposal in foz/foz mice. Serum alanine aminotransferase ranges 300-600 U/L in vehicle-treated foz/foz mice; Seladelpar reduces alanine aminotransferase by 50%. In addition, Seladelpar normalizes serum lipids and hepatic levels of free cholesterol and other lipotoxic lipids that are increased in vehicle-treated foz/foz versus wild-type mice. This abolished hepatocyte ballooning and apoptosis, substantially reduce steatosis and liver inflammation, and improve liver fibrosis. In vehicle-treated foz/foz mice, the mean nonalcoholic fatty liver disease activity score is 6.9, indicating nonalcoholic steatohepatitis (NASH); Seladelpar reverses NASH in all foz/foz mice (nonalcoholic fatty liver disease activity score 3.13). In atherogenic diet-fed Wt mice, administration of Seladelpar reduces body weight by ∼18% (P<0.05). In contrast, Seladelpar produces minimal effect on body weight in atherogenic diet–fed foz/foz mice. These animals develope severe hyperglycemia, hyperinsulinemia, and whole-body insulin resistance after 16 weeks (P<0.05); Seladelpar strikingly improves these indices (P<0.05). After intraperitoneal glucose injection, blood glucose reaches ~32 mM in vehicle-treated versus ~14 mM in Seladelpar-treated foz/foz mice (P<0.05); the area under the blood glucose disappearance curve is correspondingly lower in Seladelpar-treated foz/foz mice (P<0.05). Seladelpar produces a proportionally similar effect on glucose handling in atherogenic diet–fed Wt mice (P<0.05)[2].

Name: SAH SAH (S-Adenosylhomocysteine), CAS: 979-92-0, stock 33g, assay 98.7%, MWt: 384.41, Formula: C14H20N6O5S, Solubility: DMSO : 130 mg/mL (338.18 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: SAH is an amino acid derivative and a modulartor in several metabolic pathways. It is an intermediate in the synthesis of cysteine and adenosine[1]. SAH is an inhibitor for METTL3-METTL14 heterodimer complex (METTL3-14) with an IC50 of 0.9 µM[2].

Name: Z-VAD-FMK Z-VAD(OH)-FMK, CAS: 161401-82-7, stock 31.3g, assay 98.6%, MWt: 453.46, Formula: C21H28FN3O7, Solubility: DMSO : 100 mg/mL (220.53 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Apoptosis, Target: Caspase, Biological_Activity: Z-VAD-FMK (Z-VAD(OH)-FMK) is a well-know pan caspase inhibitor, which does not inhibit ubiquitin carboxy-terminal hydrolase L1 (UCHL1) activity even at concentrations as high as 440 μM[1].
In Vitro: Z-VAD-FMK (40 μM) reverses the apoptotic effect exerted by total saponin of Solanum lyratum Thunb (TSSLT) in Hela cells. HeLa cells are pretreated with Z-VAD-FMK (40 μM) for 30 min and exposed to TSSLT (6 μg/mL) for 48 h[2].

Name: NI-57, CAS: 1883548-89-7, stock 14.9g, assay 99%, MWt: 383.42, Formula: C19H17N3O4S, Solubility: DMSO : ≥ 83.3 mg/mL (217.26 mM), Clinical_Informat: No Development Reported, Pathway: Epigenetics, Target: Epigenetic Reader Domain, Biological_Activity: NI-57 is an inhibitor of bromodomain and plant homeodomain finger-containing (BRPF) famlily of proteins, with IC50s of 3.1, 46 and 140 nM for BRPF1, BRPF2 (BRD1) and BRPF3, respectively.
IC50 & Target: IC50: 3.1 nM (BRPF1), 46 nM (BRPF2 (BRD1)), 140 nM (BRPF3)[1]
In Vitro: NI-57 is an inhibitor of bromodomain and plant homeodomain finger-containing (BRPF), with IC50s of 3.1, 46 and 140 nM for BRPF1, BRPF2 (BRD1) and BRPF3, respectively. NI-57 binds the BRD of BRPF1 with a Kd of 31 ± 2 nM, BRD1 with a Kd of 110 ± 13 nM, and BRPF3 with a Kd of 410 ± 47 nM, whereas binding to BRD9 is weaker (Kd 1000 ± 130 nM) measured by isothermal titration calorimetry. NI-57 shows less active effect on BRD9 (IC50, 520 nM) and BRD4 (BD1) (IC50, 3700 nM), TRIM24 (IC50, 1600 nM). NI-57 also inhibits BRPF BRDs in the nucleus, but shows little effect on the proliferation of many cancer cell lines with GI50s of 10.4 μM (NCI-H1703 cells), 14.7 μM (DMS114), 15.6 μM (HRA-19), and 16.6 μM (RERF-LC-Sq1). Furthermore, Inhibition on BRPF1 of NI-57 (10 μM) reduces the gene expression of CCL-22 by 27.7 ± 9.4%[1].
In Vivo: NI-57 has favorable oral bioavailability in mice[1].

Name: Seco Rapamycin Secorapamycin A, CAS: 147438-27-5, stock 1.7g, assay 98.2%, MWt: 914.17, Formula: C51H79NO13, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Seco Rapamycin is the ring-opened product of Rapamycin. Seco-rapamycin is reported not to affect the mTOR function.
In Vitro: Disposition of Seco Rapamycin in Human Tissue Homogenates and Caco-2 Cell Monolayers. To determine whether Seco Rapamycin (D2) can be metabolized to dihydro Sirolimus (M2), 20μM Seco Rapamycin is incubated with human liver, jejunal mucosal, and Caco-2 homogenates. All of these homogenates produced M2 in an NADPH-dependent manner. Ketoconazole, at a high concentration (100μM), has no effect on the formation of M2 in any of the homogenates examined. To determine whether Seco Rapamycin can be metabolized to M2 in intact cells, 20μM Seco Rapamycin is added to Caco-2 cell monolayers. When applied to the apical compartment, little Seco Rapamycin is detected in the basolateral compartment and in the cellular fraction after 4 h. In addition, little M2 is detected. LY335979 has little effect on the distribution of Seco Rapamycin after an apical dose, although M2 became detectable in the apical compartment. In contrast, when Seco Rapamycin is applied to the basolateral compartment, both Seco Rapamycin and M2 are readily detected in the apical compartment; LY335679 decreases the flux of Seco Rapamycin to the apical compartment and increases the amount of M2 in both apical and basolateral compartments[1].

Name: BAY-598, CAS: 1906919-67-2, stock 4.3g, assay 98.9%, MWt: 525.34, Formula: C22H20Cl2F2N6O3, Solubility: DMSO : 125 mg/mL (237.94 mM; Need ultrasonic); H2O : < 0.1 mg/mL (insoluble), Clinical_Informat: No Development Reported, Pathway: Epigenetics, Target: Histone Methyltransferase, Biological_Activity: BAY-598 is selective small molecule inhibitor of SMYD2 with an IC50 of 27 nM[1][2].
IC50 & Target: IC50: 27 nM (SMYD2)[2]
In Vitro: BAY-598 treatment blocks in vitro methylation of MAPKAPK3 by SMYD2 but has no activity against the SMYD2-related KMT SMYD3. BAY-598 treatment reduces the growth of Kras;p53 mutant PDAC cells after 9 d in culture but has little impact on the growth of Kras;p53;Smyd2 mutant cells[1].

Name: Swainsonine Tridolgosir, CAS: 72741-87-8, stock 13.5g, assay 98.7%, MWt: 173.21, Formula: C8H15NO3, Solubility: DMSO : 10 mg/mL (57.73 mM; Need ultrasonic and warming); DMSO : 10 mg/mL (57.73 mM; Need ultrasonic and warming); Ethanol : 10 mg/mL (57.73 mM; Need ultrasonic and warming), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Swainsonine is an alkaloid isolated from Astragalus, acts as an inhibitor of α-mannosidase, with anti-tumor activity[1].

Name: JNJ-46778212 VU 0409551, CAS: 1363281-27-9, stock 26.5g, assay 99%, MWt: 352.36, Formula: C20H17FN2O3, Solubility: DMSO : ≥ 125 mg/mL (354.75 mM), Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein;Neuronal Signaling, Target: mGluR;mGluR, Biological_Activity: JNJ-46778212 (VU 0409551) is an mGlu5 positive allosteric modulator with an EC50 of 260 nM.
IC50 & Target: EC50: 260 nM (mGlu5)[1]
In Vivo: In oral brain/plasma studies, JNJ-46778212 displays excellent CNS penetration[1]. JNJ-46778212 enhances NMDAR function and rescues long-term potentiation in hippocampal slices obtained from SR−/− mice. The administration of JNJ-46778212 to SR−/− mice reverses their deficits in several neuroplasticity signaling pathways and improves their contextual fear memory[2].

Name: NS 11021, CAS: 956014-19-0, stock 3.4g, assay 98.3%, MWt: 511.24, Formula: C16H9BrF6N6S, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Membrane Transporter/Ion Channel, Target: Potassium Channel, Biological_Activity: NS 11021 is a potent and specific Ca2-activated big-conductance K＋ Channels (KCa1.1 channels) activator. NS 11021 at concentrations above 0.3 μM activates KCa1.1 in a concentration-dependent manner by parallelshifting the channel activation curves to more negative potentials[1].
IC50 & Target: Ca2＋-activated big-conductance K＋ Channels[1]

Name: Sodium carboxymethyl cellulose (Viscosity:800-1200 mPa.s) CMC-Na (Viscosity:800-1200 mPa.s), CAS: 9004-32-4, stock 25.4g, assay 98.8%, MWt: 1000, Formula: N/A, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Sodium carboxymethyl cellulose (Viscosity:800-1200 mPa.s) is the sodium salt of cellulose arboxymethyl and frequently used as viscous agent, paste and barrier agent.

Name: Cuminaldehyde, CAS: 122-03-2, stock 29.3g, assay 99%, MWt: 148.20, Formula: C10H12O, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Cuminaldehyde is the major component of Cuminum cyminum, a natural aldehyde with inhibitory effect on alpha-synuclein fibrillation and cytotoxicity. Cuminaldehyde shows anticancer activity[1].

Name: 2,6-Dihydroxybenzoic acid, CAS: 303-07-1, stock 26g, assay 98.7%, MWt: 154.12, Formula: C7H6O4, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: 2,6-Dihydroxybenzoic acid is a secondary metabolite of salicylic acid which has been hydrolyzed by liver enzymes during phase I metabolism.

Name: PK 11195 RP 52028, CAS: 85532-75-8, stock 12.3g, assay 98.3%, MWt: 352.86, Formula: C21H21ClN2O, Solubility: DMSO : 62.5 mg/mL (177.12 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Anti-infection, Target: Parasite, Biological_Activity: PK 11195 (RP 52028) is a ligand of translocator protein (TSPO), which targets Leishmania chemotherapy, with IC50s of 14.2 μM, 8.2 μM, 3.5 μM for L. amazonensis, L. major and L. braziliensis, respectively.
IC50 & Target: IC50: 14.2 μM (L. amazonensis), 8.2 μM (L. major), 3.5 μM (L. braziliensis)[1].
In Vitro: Median IC50 values for PK 11195 are 14.2 μM for L. amazonensis, 8.2 μM for L. major, and 3.5 μM for L. braziliensis. The selective index value for L. amazonensis is 13.7, indicating the safety of PK 11195 for future testing in mammals. Time-and dose-dependent reductions in the percentage of infected macrophages, the number of parasites per infected macrophage, and the number of viable intracellular parasites are observed. Electron microscopy reveals some morphological alterations suggestive of autophagy. Interestingly, MCP-1 and superoxide levels are reduced in L. amazonensis-infected macrophages treated with PK 11195[1].

Name: Diethyl succinate Diethyl Butanedioate, CAS: 123-25-1, stock 24.8g, assay 98.4%, MWt: 174.19, Formula: C8H14O4, Solubility: DMSO : ≥ 250 mg/mL (1435.21 mM), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Diethyl succinate (Diethyl Butanedioate) is used at physiological pH and crosses biological membranes, incorporates into cells in tissue culture and is metabolized by the TCA cycle. Diethyl succinate is known to be non-toxic and used in fragrances and flavoring[1].

Name: Levulinic acid 4-Oxovaleric acid; NSC 3716;, CAS: 123-76-2, stock 22.1g, assay 98.6%, MWt: 116.12, Formula: C5H8O3, Solubility: 10 mM in DMSO, Clinical_Informat: Phase 3, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: Levulinic acid is a precursor for the synthesis of biofuels, such as ethyl levulinate.

Name: Formamide Methanamide;Formimidic acid, CAS: 75-12-7, stock 20.7g, assay 98.8%, MWt: 45.04, Formula: CH3NO, Solubility: DMSO : 100 mg/mL (2220.25 mM; Need ultrasonic); H2O : 100 mg/mL (2220.25 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Formamide is an amide derived from formic acid and has been used as solvent for many ionic compounds.

Name: PEG300 Glycols polyethylene, CAS: 25322-68-3, stock 28.2g, assay 98.7%, MWt: 104.15, Formula: C5H12O2, Solubility: H2O : ≥ 50 mg/mL (480.08 mM); DMSO : 100 mg/mL (960.15 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: PEG300 is a neutral and biocompatible hydrophilic polymer.

Name: FPR Agonist 43, CAS: 903895-98-7, stock 28.1g, assay 98.9%, MWt: 384.86, Formula: C20H21ClN4O2, Solubility: H2O : < 0.1 mg/mL (insoluble); DMSO : 125 mg/mL (324.79 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: FPR Agonist 43 (compound 43) is a dual formyl peptide receptor 1 (FPR1) and formyl peptide receptor 2 (FPR2)/ALX agonist[1][2].
IC50 & Target: FPR1, FPR2/ALX[1]
In Vitro: FPR Agonist 43 (10-5-107 nM) is actively potent in the cAMP assay in FPR2/ALX over-expressing CHO cells[1]. 
FPR Agonist 43 is also active in the GTPγ binding assay (IC50=207±51 nM)[1]. 
FPR1 is the preferred receptor for FPR Agonist 43 in in both human neutrophils and possibly also in mouse cells[2].

Name: (±)-1,2-Propanediol 1,2-(RS)-Propanediol; 1,2-Dihydroxypropane; 1,2-Propylene glycol, CAS: 57-55-6, stock 3.6g, assay 98.4%, MWt: 76.09, Formula: C3H8O2, Solubility: H2O : ≥ 50 mg/mL (657.12 mM), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: (±)-1,2-Propanediol is an aliphatic alcohol and frequently used as an excipient in many drug formulations to increase the solubility and stability of drugs.

Name: 4-Hydroxycoumarin, CAS: 1076-38-6, stock 7.4g, assay 98%, MWt: 162.14, Formula: C9H6O3, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: 4-Hydroxycoumarin, a coumarin derivative, is one of the most versatile heterocyclic scaffolds and is frequently applied in the synthesis of various organic compounds. 4-Hydroxycoumarin possesses both electrophilic and nucleophilic properties. 4-Hydroxycoumarin derivatives are employed as the anticoagulant, antibacterial, antifungal, antiviral, antitumor, antiprotozoal, insecticidal, antimycobacterial, antimutagenic, antioxidant, anti-inflammatory agents, HIV protease inhibitors and tyrosine kinase inhibitors[1].

Name: Acetamide, CAS: 60-35-5, stock 19.4g, assay 98.7%, MWt: 59.07, Formula: C2H5NO, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: Acetamide is used primarily as a solvent and a plasticizer.

Name: Acetophenone 1-Phenylethan-1-One, CAS: 98-86-2, stock 11.4g, assay 99%, MWt: 120.15, Formula: C8H8O, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Acetophenone is an organic compound with simple structure[1].

Name: NVP-ACC789 ACC-789;ZK202650, CAS: 300842-64-2, stock 5.1g, assay 98.6%, MWt: 405.29, Formula: C21H17BrN4, Solubility: DMSO : 25 mg/mL (61.68 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Protein Tyrosine Kinase/RTK;Protein Tyrosine Kinase/RTK, Target: VEGFR;PDGFR, Biological_Activity: NVP-ACC789 is an inhibitor of human VEGFR-1, VEGFR-2 (mouse VEGFR-2), VEGFR-3 and PDGFR-β with IC50s of 0.38, 0.02 (0.23), 0.18, 1.4 μM, respectively.
IC50 & Target: IC50: 0.38 μM (human VEGFR-1), 0.02 μM (human VEGFR-2), 0.23 μM (mouse VEGFR-2), 0.18 μM (human VEGFR-3), 1.4 μM (human PDGFR-β)[1]
In Vitro: The enzymatic kinase assays demonstrate that NVP-ACC789 is an inhibitor of human VEGFR-1, VEGFR-2 (mouse VEGFR-2), VEGFR-3 and PDGFR-β with IC50s of 0.38, 0.02 (0.23), 0.18, 1.4 μM, respectively. In VEGF-treated cultures, addition of the VEGFR-2 inhibitor NVP-ACC789 reduces BME cell number to baseline levels from 1 μM. Likewise, bFGF-induced BME cell proliferation is reduced markedly by NVP-ACC789 from 1 to 10 μM, without however reaching basal levels. NVP-ACC789 is found to be a potent inhibitor of VEGF-induced HUVE cell proliferation with an IC50 of 1.6 nM. NVP-ACC789 also completely inhibits VEGF-induced BME and BAE cell invasion and VEGF-C-induced BAE cell invasion. The inhibition is dose-dependent in both cell types with a maximal effect from 1 μM[1].
In Vivo: NVP-ACC789 which is given in daily oral doses for 6 days blocks VEGF-induced angiogenesis in a dose-dependent manner. NVP-ACC789 also inhibits the response to bFGF to some extent, but the dose-response curve is not linear for NVP-ACC789[1].

Name: Seliciclib Roscovitine;CYC202;R-roscovitine, CAS: 186692-46-6, stock 39g, assay 98.7%, MWt: 354.45, Formula: C19H26N6O, Solubility: DMSO : ≥ 100 mg/mL (282.13 mM), Clinical_Informat: Phase 2, Pathway: Cell Cycle/DNA Damage, Target: CDK, Biological_Activity: Seliciclib (Roscovitine) is an orally bioavailable and selective CDKs inhibitor with IC50s of 0.2 μM, 0.65 μM, and 0.7 μM for CDK5, Cdc2, and CDK2, respectively.
IC50 & Target: IC50: 0.2 μM (CDK5), 0.65 μM (Cdc2), 0.7 μM (CDK2)[1]
In Vitro: Seliciclib (Roscovitine) displays high efficiency and high selectivity towards some cyclin-dependent kinases. The kinase specificity of Seliciclib is investigated with 25 highly purified kinases (including protein kinase A, G and C isoforms, myosin light-chain kinase, casein kinase 2, IR tyrosine kinase, c-src, v-abl). Most kinases are not significantly inhibited by Seliciclib (Roscovitine). Cdc2, Cdk2, and Cdk5 only are substantially inhibited (IC50 values of 0.65, 0.7, and 0.2 μM, respectively). Cdk4k and Cdk6 are very poorly inhibited by Seliciclib (Roscovitine) (IC50>100 μM). Extracellular regulated kinases erk1 and erk2 are inhibited with an IC50 of 34 μM and 14 μM, respectively. Seliciclib (Roscovitine) inhibits the proliferation of mammalian cell lines with an average IC50 of 16 μM[1]. Seliciclib decreases the level of CDK5 and p35 with upregulation of E-cadherin, but downregulation of Vimentin and Collagen IV. Moreover, Seliciclib (Roscovitine) inhibits the ability of high glucose cultured NRK52E cells to migrate and invade[2].
In Vivo: Compare with normal controls, Seliciclib (Roscovitine) downregulates phosphorylated ERK1/2 and PPARγ with concomitant increase in E-cadherin, but decrease in Vimentin and Collagen IV. Correspondingly, Seliciclib decreases renal tubulointerstitial fibrosis of diabetic rats. Seliciclib (Roscovitine) is effective in decreasing tubulointerstitial fibrosis via the ERK1/2/PPARγ pathway in diabetic rats[2]. Seliciclib (Roscovitine) (16.5 mg/kg) significantly reduces the rate of tumor growth and increases survival of treated mice. Strikingly, Seliciclib (Roscovitine) treatment leads to complete tumor disappearance in one mouse (25%); moreover, no tumor regrowth in this mouse is found 5 months after completion of the treatment. Mouse weights do not differ significantly between mice treated with Seliciclib and control mice, and behavioral differences between the two groups are also negligible. These results suggest that Seliciclib can be used effectively as a selective tumor growth inhibitor in HPV+ head and neck cancer[3].

Name: 3-Ethoxy-3-oxopropanoic acid, CAS: 1071-46-1, stock 27.5g, assay 98.6%, MWt: 132.11, Formula: C5H8O4, Solubility: , Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity:

Name: NSC23925, CAS: 858474-14-3, stock 27.7g, assay 98.7%, MWt: 421.36, Formula: C22H26Cl2N2O2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Membrane Transporter/Ion Channel, Target: P-glycoprotein, Biological_Activity: NSC23925 is a novel, selective and effective P-glycoprotein (Pgp) inhibitor.
IC50 & Target: P-glycoprotein[1]
In Vitro: NSC23925 is a novel, selective and effective P-glycoprotein (Pgp) inhibitor. SKOV-3 cells with long-term exposure of 1 μM NSC23925 show stable growth in culture medium. NSC23925 specifically inhibits Pgp overexpression to prevent the emergence of paclitaxel resistance during paclitaxel treatment[1]. NSC23925 reverses chemoresistance in a wide variety of tumor types where Multidrug resistance 1 (MDR1) is highly expressed. Maximal reversal of MDR is typically seen in NSC23925 doses between 0.5 and 1 µM. The IC50 for NSC23925 is 8 µM in SKOV-3/SKOV-3TR and 25 µM in OVCAR8/OVCAR8TR cell lines, whereas the mean concentration of NSC23925 required for maximal reversal of resistance in SKOV-3TR or OVCAR8TR to cytotoxic drugs is 0.5 µM to 1 µM[2].
In Vivo: Both saline alone and NSC23925 alone treated tumors grow progressively. The usage of NSC23925 in paclitaxel chemotherapy significantly prolongs anticancer efficacy of paclitaxel[1].

Name: 1-(3,4-Dimethoxycinnamoyl)piperidine, CAS: 128261-84-7, stock 12.1g, assay 98.9%, MWt: 275.34, Formula: C16H21NO3, Solubility: , Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: 1-(3,4-Dimethoxycinnamoyl)piperidine, a synthesized piperidine analog, possesses antimicrobial and antioxidant activity[1].

Name: GSK598809, CAS: 863680-45-9, stock 20.4g, assay 98.8%, MWt: 481.51, Formula: C22H23F4N5OS, Solubility: DMSO : 83.33 mg/mL (173.06 mM; Need ultrasonic), Clinical_Informat: Phase 2, Pathway: GPCR/G Protein;Neuronal Signaling, Target: Dopamine Receptor;Dopamine Receptor, Biological_Activity: GSK598809 is a potent and selective dopamine D3 Receptor (DRD3) antagonist, with a pKi of 8.9.
IC50 & Target: pKi: DRD3[1][2].
In Vivo: Cocaine and GSK598809 each increases peak mean arterial blood pressure. Least square mean differences are significant for both doses of cocaine compared with its vehicle. Likewise, least square mean differences are significant for both doses of GSK598809 as compared with its vehicle. The experimental question of interest, that is, whether GSK598809 significantly increases cocaine effects on peak mean arterial blood pressure, is probed by a prior it tests on the means of the fitted regression model. The dose of 3 mg/kg GSK598809 significantly increases the pressor effects of 5.6 mg/kg cocaine and of 1.7 mg/kg cocaine[1].

Name: Oxypurinol Oxipurinol, CAS: 2465-59-0, stock 13.7g, assay 98.5%, MWt: 152.11, Formula: C5H4N4O2, Solubility: DMSO : 12.5 mg/mL (82.18 mM; Need ultrasonic), Clinical_Informat: Phase 3, Pathway: Metabolic Enzyme/Protease;Metabolic Enzyme/Protease, Target: Xanthine Oxidase;Endogenous Metabolite, Biological_Activity: Oxipurinol (Oxipurinol), the major active metabolite of Allopurinol, is an inhibitor of xanthine oxidase. Oxipurinol can be used to regulate blood urate levels and treat gout[1].
IC50 & Target: Xanthine oxidoreductase[1]
In Vitro: Allopurinol is rapidly metabolized (half-life approximately 1 h) to its active metabolite oxypurinol. Oxypurinol is an inhibitor of xanthine oxidoreductase and has a considerably longer elimination half-life (approximately 23 h)[1].

Name: Tecadenoson CVT-510, CAS: 204512-90-3, stock 25.7g, assay 98%, MWt: 337.33, Formula: C14H19N5O5, Solubility: DMSO : ≥ 155 mg/mL (459.49 mM), Clinical_Informat: Phase 2, Pathway: GPCR/G Protein, Target: Adenosine Receptor, Biological_Activity: Tecadenoson (CVT-510) is a selective A1 adenosine receptor agonist.
IC50 & Target: Target: A1 adenosine receptor[1]
In Vitro: In the atrial-paced isolated heart, Tecadenoson is approximately 5 fold more potent to prolong the stimulus-to-His bundle (S-H interval), a measure of slowing AV nodal conduction (EC50=41 nM) than to increase coronary conductance (EC50=200 nM). At concentrations of Tecadenoson (40 nM) and diltiazem (1 μM) that causes equal prolongation of S-H interval (∼10 ms), diltiazem, but not Tecadenoson, significantly reduces left ventricular developed pressure (LVP) and markedly increases coronary conductance. Tecadenoson shortens atrial (EC50=73 nM) but not the ventricular monophasic action potentials (MAP)[1].
In Vivo: In atrial-paced anaesthetized guinea-pigs, intravenous infusions of Tecadenoson and diltiazem causes nearly equal prolongations of P-R interval[1]. Tecadenoson (2, 5, 20 μg/kg i.p.) causes a rapid and sustained dose-dependent decrease in NEFA at doses that do not cause bradycardia. Tecadenoson given at 50 μg/kg causes a significant bradycardia (50% decrease in heart rate at 25 min[2].

Name: Pranidipine OPC-13340, CAS: 99522-79-9, stock 27.8g, assay 98.2%, MWt: 448.47, Formula: C25H24N2O6, Solubility: DMSO : 270 mg/mL (602.05 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Membrane Transporter/Ion Channel;Neuronal Signaling, Target: Calcium Channel;Calcium Channel, Biological_Activity: Pranidipine (OPC-13340) is a potent, long acting 1,4-dihydropyridine calcium channel blocker with antihypertensive activity[1].
IC50 & Target: Calcium channel[1]

Name: Lirimilast BAY 19-8004, CAS: 329306-27-6, stock 8.4g, assay 98.9%, MWt: 443.26, Formula: C17H12Cl2N2O6S, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Phosphodiesterase (PDE), Biological_Activity: Lirimilast (BAY 19-8004) is a potent, selective and orally active phosphodiesterase-4 (PDE4) inhibitor with an IC50 value of 49 nM. Lirimilast can be used for the treatment of asthma or chronic obstructive pulmonary disease (COPD). Lirimilast has potently anti-inflammatory properties[1][2].
In Vitro: In PDE4 assays Lirimilast (BAY 19-8004) is reported to be 5-fold more potent than Cilomilast and equipotent with CDP-840 using freshly prepared PDE4 from human PMNL[1].
In Vivo: Since Lirimilast (BAY 19-8004) is orally active in the guinea-pig at 3 mg/kg and, more critically, in primates at 0.1 mg/kg/day it appears to have a good therapeutic ratio. In addition Lirimilast is found to be 3-fold more potent than Cilomilast when compared in a rat model of lung neutrophilic inflammation[2].

Name: Naproxen etemesil LT-NS 001;MX 1094, CAS: 385800-16-8, stock 8.2g, assay 98.9%, MWt: 336.40, Formula: C17H20O5S, Solubility: 10 mM in DMSO, Clinical_Informat: Phase 3, Pathway: Immunology/Inflammation, Target: COX, Biological_Activity: Naproxen etemesil is a lipophilic, non-acidic, inactive prodrug of naproxen that is hydrolysed to pharmacologically active Naproxen once absorbed. Naproxen is a COX-1 and COX-2 inhibitor with IC50s of 8.72 and 5.15 μM, respectively in cell assay.
IC50 & Target: IC50: 8.72 μM (COX-1), 5.15 μM (COX-2)[1]
In Vitro: Naproxen etemesil is a lipophilic, non-acidic, inactive prodrug of naproxen that is hydrolysed to pharmacologically active Naproxen once absorbed. Naproxen is a well known nonsteroidal anti-inflammatory drug. Naproxen is approximately equipotent inhibitor of COX-1 and COX-2 in intact cells with IC50s of 2.2 μg/mL and 1.3 μg/mL, respectively[1].
In Vivo: Naproxen exerts an anti-inflammatory and antifibrotic effect in mouse model of bleomycin-induced lung fibrosis. Naproxen also downregulates TGF-β levels and Smad3/4 complex formation[2]. Naproxen is shown to inhibit the time-courses of pain, fever and PGE2 with similar potencies (IC50=27, 40, 13 μM)[3].

Name: Tauroursodeoxycholate TUDCA;UR 906;Taurolite, CAS: 14605-22-2, stock 9.9g, assay 98.2%, MWt: 499.70, Formula: C26H45NO6S, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Apoptosis;Apoptosis;Stem Cell/Wnt;MAPK/ERK Pathway;Metabolic Enzyme/Protease, Target: Apoptosis;Caspase;ERK;ERK;Endogenous Metabolite, Biological_Activity: Tauroursodeoxycholate (TUDCA; UR 906; Taurolite) is an endoplasmic reticulum (ER) stress inhibitor. Tauroursodeoxycholate significantly reduces expression of apoptosis molecules, such as caspase-3 and caspase-12. Tauroursodeoxycholate also inhibits ERK.
IC50 & Target: ERK[1] 
Caspase-3, Caspase-12[2]
In Vitro: Tauroursodeoxycholate (TUDCA) suppresses both viability and migration of vascular smooth muscle cells (VSMCs) through inhibition of ERK phosphorylation, by induction of mitogen-activated protein kinase phosphatase-1 (MKP-1) via PKCα. Tauroursodeoxycholate inhibits both the proliferation and migration of VSMCs via inhibition of ERK, through Ca2+-dependent PKCα translocation. Tauroursodeoxycholate prevents platelet-derived growth factor (PDGF) and vascular injury-induced MMP-9 expression. The knock-down of MKP-1 using specific si-RNA restores the reduced VSMC viability by Tauroursodeoxycholate (200 μM), which suggests that anti-proliferative effect of Tauroursodeoxycholate depended on the MKP-1 expression[1].
In Vivo: The effects of Tauroursodeoxycholate (TUDCA) on proliferation and apoptosis of VSMCs in vivo are examined using immunohistochemistry for proliferating cell nuclear antigen (PCNA) and the transferase dUTP nick-end labelling (TUNEL) assay. Tauroursodeoxycholate (10, 50, and 100 mg/kg) increases the caspase 3 activity of injured tissues in a dose-dependent manner, indicating that Tauroursodeoxycholate induces apoptosis of VSMCs in the neointima. Using the injured tissues, further examination and comparison of the phosphorylation level of ERK and MMP-9 expression is performed at 1 week after injury, compared with normal controls. Balloon injury increased both the phosphorylation of ERK and expression of MMP-9 in the tissues. Tauroursodeoxycholate (10, 50, and 100 mg/kg) inhibits phosphorylation of ERK and MMP-9 expression in a dose-dependent manner[1]. Tauroursodeoxycholate (TUDCA) is a hydrophilic bile acid. Tauroursodeoxycholate as a cytoprotective agent improves liver function and can prevent hepatocellular carcinoma by reducing ER stress and apoptosis. Tauroursodeoxycholate significantly reduces expression of apoptosis molecules, such as caspase-3, caspase-12, C/EBP homologous protein, c-Jun N-terminal kinase (JNK), activating transcription factor 4 (ATF4), X-box binding protein (XBP), and eukaryotic initiation factor 2α (eIF2α) in Ang II induced ApoE-/- mice (p<0.05). Tauroursodeoxycholate reduces Angiotensin (Ang) II induced abdominal aortic aneurysm (AAA) formation in ApoE-/- mice. Tauroursodeoxycholate is used at a dose of 0.5 g/kg/day in treating Ang II induced ApoE-/- mice (ER stress inhibitor group). Systolic blood pressure (141.3±5.6 mmHg vs 145.9±8.9 mmHg; p>0.05) and total cholesterol levels (663.6±88.7 mg/dL vs 655.7±65.4 mg/dL; p>0 .05) do not differ between the AAA model group and Tauroursodeoxycholate group. In addition, maximum aortic diameter is significantly smaller in those in Tauroursodeoxycholate group compared with those in the AAA model group (0.95±0.03 mm vs 1.79±0.04 mm; p<0.05). AAA lesion areas are also smaller in those in Tauroursodeoxycholate group than in those in the AAA model group (0.37±0.03 mm2 vs 1.51±0.06 mm2; p<0.05)[2].

Name: trans-Zeatin, CAS: 1637-39-4, stock 6.6g, assay 98.3%, MWt: 219.24, Formula: C10H13N5O, Solubility: DMSO : ≥ 60 mg/mL (273.67 mM), Clinical_Informat: No Development Reported, Pathway: Stem Cell/Wnt;MAPK/ERK Pathway;MAPK/ERK Pathway, Target: ERK;ERK;MEK, Biological_Activity: trans-Zeatin is a plant cytokinin, which plays an important role in cell growth, differentiation, and division; trans-Zeatin also inhibits UV-induced MEK/ERK activation.
IC50 & Target: MEK/ERK[2]
In Vitro: trans-Zeatin is a plant cytokinin, which plays an important role in cell growth, differentiation, and division[1]. trans-Zeatin (20, 40 or 80 μM) inhibits UV-induced MEK/ERK activation, upregulates AQP3 in a time- and dose-dependent manner, and attenuates UV induced loss of AQP3 in keratinocytes (HaCaT cells). UV-induced AQP3 downregulation is blocked by MEK/ERK inhibitors. Trans-Zeatin (80 μM) attenuates UV-induced downregulation of wound healing and water permeability in HaCaT cells[2].

Name: Xanthohumol D, CAS: 274675-25-1, stock 32.5g, assay 98.3%, MWt: 370.40, Formula: C21H22O6, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Xanthohumol D, isolated from hops, is an inhibitor of quinone reductase-2 (QR-2) with the IC50 value of 110 μM, and binds to the active site of QR-2. Xanthohumol D shows antiproliferative activity on human cancer cell lines in vitro[1][2].
IC50 & Target: IC50: 110 μM (Quinone reductase-2)[1]

Name: Wilforgine, CAS: 37239-47-7, stock 25.3g, assay 98.5%, MWt: 857.81, Formula: C41H47NO19, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Wilforgine is a bioactive sesquiterpene alkaloid in Tripterygium wilfordii Hook. F. Wilforgine can induce microstructural and ultrastructural changes in the muscles of Mythimna separata larvae, and the sites of action are proposed to be calcium receptors or channels in the muscular system[1][2].

Name: D-(+)-Trehalose D-Trehalose; α,α-Trehalose, CAS: 99-20-7, stock 21.9g, assay 98.2%, MWt: 342.30, Formula: C12H22O11, Solubility: H2O : 125 mg/mL (365.18 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: D-(+)-Trehalose, isolated from Saccharomyces cerevisiae, can be used as a food ingredient and pharmaceutical excipient.

Name: Tokinolide B, CAS: 112966-16-2, stock 36.9g, assay 98.9%, MWt: 380.48, Formula: C24H28O4, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Tokinolide B is isolated from the rhizomes of Ligusticum porter[1].

Name: Theviridoside, CAS: 23407-76-3, stock 25.4g, assay 98.1%, MWt: 404.37, Formula: C17H24O11, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Theviridoside is a natural iridoid glucoside found in the leaves of Cerbera odollam, it has cytotoxicity.

Name: Thevetiaflavone Apigenin-5-methyl ether, CAS: 29376-68-9, stock 4.6g, assay 98.7%, MWt: 284.26, Formula: C16H12O5, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Apoptosis;Apoptosis, Target: Caspase;Bcl-2 Family, Biological_Activity: Thevetiaflavone could upregulate the expression of Bcl‑2 and downregulate that of Bax and caspase‑3.
In Vitro: Thevetiaflavone, a natural flavonoid obtained from Wikstroemia indica, could improve cell viability and suppresses the leakage of lactate dehydrogenase from the cytoplasm. Further investigation of the mechanisms demonstrated that Thevetiaflavone decreases overproduction of ROS and ameliorates ROS‑mediated mitochondrial dysfunction, including collapse of mitochondrial membrane potential and mitochondrial permeability transition pore opening. Thevetiaflavone reduces the intracellular Ca2+ level, which is closely associated with mitochondrial function and interplays with ROS. Furthermore, Thevetiaflavone inhibits apoptosis in PC12 cells through upregulating the expression of Bcl‑2 and downregulating that of Bax and caspase‑3 in addition to increasing the activity of caspase‑3. These results further indicate the protective effects of thevetiaflavone in vivo and its application in the clinic[1].

Name: Taraxasterol, CAS: 1059-14-9, stock 9.5g, assay 99%, MWt: 426.72, Formula: C30H50O, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Taraxasterol is a pentacyclic triterpenoid isolated from Taraxacum officinale. Taraxasterol has a role as a metabolite and an anti-inflammatory agent[1].

Name: Syzalterin, CAS: 94451-48-6, stock 29g, assay 99%, MWt: 298.29, Formula: C17H14O5, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Immunology/Inflammation, Target: NO Synthase, Biological_Activity: Syzalterin is an inhibitor of NO production with an IC50 of 1.87 μg/mL.
IC50 & Target: IC50: 1.87 μg/mL (NO)[1].

Name: Stigmasterol glucoside, CAS: 19716-26-8, stock 15.5g, assay 98.3%, MWt: 574.83, Formula: C35H58O6, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: 5 alpha Reductase, Biological_Activity: Stigmasterol glucoside is a sterol isolated from P. urinaria with high antioxidant and anti-inflammatory activities[1], act as an inhibitor of 5α-reductase with an IC50 of 27.2 µM[2].
IC50 & Target: IC50：27.2 µM (5α-reductase)[2]

Name: Etiracetam UCB 6474, CAS: 33996-58-6, stock 11g, assay 99%, MWt: 170.21, Formula: C8H14N2O2, Solubility: DMSO : ≥ 125 mg/mL (734.39 mM), Clinical_Informat: No Development Reported, Pathway: Membrane Transporter/Ion Channel;Neuronal Signaling, Target: Calcium Channel;Calcium Channel, Biological_Activity: Etiracetam (UCB 6474) is an acetylcholine agonist and a nootropic drug of the racetam family. Less active than its S-enantiomer Levetiracetam (UCB L059)[1].
IC50 & Target: Acetylcholine[1].

Name: Voruciclib (hydrochloride), CAS: 1000023-05-1, stock 39.7g, assay 98.7%, MWt: 506.30, Formula: C22H20Cl2F3NO5, Solubility: DMSO : ≥ 250 mg/mL (493.78 mM), Clinical_Informat: Phase 1, Pathway: Cell Cycle/DNA Damage, Target: CDK, Biological_Activity: Voruciclib hydrochloride is a clinical stage orally active and selective CDK inhibitor with Ki values of 0.626 nM-9.1 nM. Voruciclib hydrochloride potently blocks CDK9, the transcriptional regulator of MCL-1. Voruciclib hydrochloride represses expression of MCL-1 in multiple models of diffuse large B-cell lymphoma (DLBCL)[1].
In Vitro: Voruciclib hydrochloride (0.5-5 µM; 6 hours) shows targeted downregulation of MCL-1 in both ABC and GCB subtypes[1]. 
Ki values for each target such as CDK9/cyc T2, CDK9/cyc T1, CDK6/cyc D1, CDK4/cyc D1, CDK1/cyc B, and CDK1/cyc A for Voruciclib hydrochloride are 0.626 nM, 1.68 nM, 2.92 nM, 3.96 nM, 5.4 nM, 9.1 nM, respectively[1].
In Vivo: Combination of Voruciclib hydrochloride (200 mpk; Oral gavage) and Venetoclax (10 mpk, 1 mpk, 50 mpk, 25 mpk in U2932, RIVA, SU-DHL-4 and NU-DHL-1, respectively) leads to enhance tumor growth inhibition compared to either drug alone in U2932, RIVA, SU-DHL-4 (six days per week for 4 weeks), and NU-DHL-1 models (five days per week for 3 weeks) of DLBCL[1].

Name: Octanoic acid, CAS: 124-07-2, stock 11.5g, assay 98.4%, MWt: 144.21, Formula: C8H16O2, Solubility: 10 mM in DMSO, Clinical_Informat: Phase 2, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: Octanoic acid is an oily liquid with a slightly unpleasant rancid taste and used commercially in the production of esters used in perfumery and also in the manufacture of dyes.

Name: TAK-448 MVT-602, CAS: 1234319-68-6, stock 4.6g, assay 98.9%, MWt: 1225.36, Formula: C58H80N16O14, Solubility: H2O, Clinical_Informat: Phase 2, Pathway: Others, Target: Others, Biological_Activity: TAK-448 (MVT-602) is a potent and full KISS1R agonist with an IC50 of 460 pM and an EC50 of 632 pM[1].
IC50 & Target: IC50: 460 pM (KISS1R)[1] 
EC50: 632 pM (KISS1R)[1]
In Vivo: TAK-448 (0.01-3 mg/kg; given i.h.; dosings on day 0 and 28) has greater anti-tumor effects in VCaP xenograft model[2].

Name: OTX008 Calixarene 0118;PTX008, CAS: 286936-40-1, stock 25.4g, assay 98.5%, MWt: 937.18, Formula: C52H72N8O8, Solubility: Ethanol : ≥ 33.33 mg/mL (35.56 mM); DMSO : 10 mg/mL (10.67 mM; Need ultrasonic), Clinical_Informat: Phase 1, Pathway: Immunology/Inflammation, Target: Galectin, Biological_Activity: OTX008 is a selective inhibitor of galectin-1.
IC50 & Target: Galectin-1[1].
In Vitro: Growth inhibitory concentrations (GI50) of OTX008 in a large panel of human solid tumour cell lines ranges from 3 to 500 μM. A significant correlation between OTX008 GI50 values and Gal1 mRNA (LGALS1) and protein expression levels in the panel of cancer cells is observed. In SQ20B and A2780-1A9 cells, OTX008 inhibits Gal1 expression and ERK1/2 and AKT-dependent survival pathways, and induces G2/M cell cycle arrest through CDK1. OTX008 enhances the anti-proliferative effects of Semaphorin-3A (Sema3A) in SQ20B cells and reverses invasion induced by exogenous Gal1[1]. OTX008 affects endothelial cell proliferation, motility, invasiveness, and cord formation. Tumor cell proliferation is also inhibited, with differences in sensitivity among cell lines (IC50 from 1 to 190 μM)[2].
In Vivo: OTX008 inhibits growth of A2780-1A9 xenografts. OTX008 treatment is associated with down-regulation of Gal1 and Ki67 in treated tumours, as well as decreased microvessel density and VEGFR2 expression. Finally, combination studies show OTX008 synergy with several cytotoxic and targeted therapies, principally when OTX008 is administered first[1].

Name: GNE-6468, CAS: 1677668-27-7, stock 35.6g, assay 99%, MWt: 433.84, Formula: C23H16ClN3O4, Solubility: DMSO : 5 mg/mL (11.52 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: ROR, Biological_Activity: GNE-6468 is a potent and selective RORγ(RORc) agonists with an EC50 value of 13 nM for HEK-293 cell.

Name: Squalene Super Squalene; trans-Squalene;AddaVax, CAS: 111-02-4, stock 4.6g, assay 98.8%, MWt: 410.72, Formula: C30H50, Solubility: DMSO : 16.67 mg/mL (40.59 mM; Need ultrasonic); H2O : < 0.1 mg/mL (insoluble), Clinical_Informat: Phase 1, Pathway: Metabolic Enzyme/Protease;Metabolic Enzyme/Protease;NF-κB;Immunology/Inflammation, Target: Endogenous Metabolite;Reactive Oxygen Species;Reactive Oxygen Species;Reactive Oxygen Species, Biological_Activity: Squalene is an intermediate product in the synthesis of cholesterol, and shows several pharmacological properties such as hypolipidemic, hepatoprotective, cardioprotective, antioxidant, and antitoxicant activity.

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2020年3月13日星期五

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