EOS Med Chem, Medicinal Chemical is Big: EOS Med Chem Building block stock list 2347

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
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Name: Aramchol C20-FABAC, CAS: 246529-22-6, stock 4.6g, assay 98.1%, MWt: 702.10, Formula: C44H79NO5, Solubility: H2O : < 0.1 mg/mL (insoluble); DMSO : 53.33 mg/mL (75.96 mM; Need ultrasonic), Clinical_Informat: Phase 3, Pathway: Others, Target: Others, Biological_Activity: Aramchol (C20-FABAC) is a conjugate of cholic acid and arachidic acid that could inhibit stearoyl coenzyme A desaturase 1 (SCD1) activity. Aramchol has potential use in nonalcoholic fatty liver disease (NAFLD) and nonalcoholic steatohepatitis (NASH) treatment[1].

Name: Scabertopin, CAS: 185213-52-9, stock 38.4g, assay 98.4%, MWt: 358.39, Formula: C20H22O6, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Scabertopin, isolated from the whole plant of Elephantopus scaber[1], is a sesquiterpene lactone. Scabertopin has been found to be prominent anticancer constituents[2].

Name: CVT-10216, CAS: 1005334-57-5, stock 9.7g, assay 98.4%, MWt: 465.48, Formula: C24H19NO7S, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Aldehyde Dehydrogenase (ALDH), Biological_Activity: CVT-10216 is a highly selective, reversible aldehyde dehydrogenase-2 (ALDH-2) inhibitor with an IC50 of 29 nM. CVT-10216 also has inhibitory effect of ALDH-1 with an IC50 of 1.3 μM. CVT-10216 can reduces excessive alcohol drinking in alcohol-preferring rats and exhibits anxiolytic effects[1].
IC50 & Target: IC50: 29 nM (ALDH-2)[1]
In Vivo: CVT-10216 (intraperitoneal injection; 3.75, 7.5, or 15 mg/kg) exhibits a increase in social interaction as a dose-dependent manner, punctuated by a 2-fold increase in social interaction after 15 mg/kg in Fawn-Hooded rats[1].
CVT-10216 (intraperitoneal injection; 3.75 or 15 mg/kg) are determined 5 h into the third withdrawal.It has the anxiolytic effect of 15 mg/kg CVT-10216 in this model, but has no significant effects on locomotor activity[1].

Name: Seneciphyllinine, CAS: 90341-45-0, stock 32.4g, assay 98.1%, MWt: 375.42, Formula: C20H25NO6, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Seneciphyllinine, a pyrrolizidine alkaloid, is isolated from the roots of Gynura japonica. Pyrrolizidine alkaloids are highly hepatotoxic natural chemicals that produce irreversible chronic and acute hepatotoxic effects on human beings[1].

Name: Reynoutrin Quercetin-3-D-xyloside;Reinutrin, CAS: 549-32-6, stock 6.9g, assay 98%, MWt: 434.35, Formula: C20H18O11, Solubility: DMSO : 150 mg/mL (345.34 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease;NF-κB;Immunology/Inflammation, Target: Reactive Oxygen Species;Reactive Oxygen Species;Reactive Oxygen Species, Biological_Activity: Reynoutrin (Quercetin-3-D-xyloside) is a flavonoid from Psidium cattleianum, with antioxidant and radical-scavenging activity[1].
In Vitro: Reynoutrin shows potent antioxidant activity, with pEC50 of 5.37 against fluorescein oxidation[1].

Name: Royal Jelly acid Queen Bee Acid;(E)-10-Hydroxy-2-decenoic acid, CAS: 14113-05-4, stock 8.1g, assay 98.8%, MWt: 186.25, Formula: C10H18O3, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: Royal Jelly acid (Queen Bee Acid) is a fatty acid constituent of royal jelly, promotes the growth and protection of neurons, reduces anxiety-like phenotypes[1].

Name: Isoscopoletin 6-Hydroxy-7-methoxycoumarin, CAS: 776-86-3, stock 34.3g, assay 98.1%, MWt: 192.17, Formula: C10H8O4, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Anti-infection, Target: HBV, Biological_Activity: Isoscopoletin (6-Hydroxy-7-methoxycoumarin) is an active constituent in Artemisia argyi leaves. Isoscopoletin shows substantial inhibition against cell proliferation, with IC50s of 4.0 μM and 1.6 μM for human CCRF-CEM leukaemia cells and multidrug resistant subline CEM/ADR5000, respectively[1]. Isoscopoletin (6-Hydroxy-7-methoxycoumarin) possesses inhibitory activity against HBV replication[2].

Name: Herniarin 7-Methoxycoumarin;Methyl umbelliferyl ether, CAS: 531-59-9, stock 14g, assay 98.6%, MWt: 176.17, Formula: C10H8O3, Solubility: DMSO : ≥ 125 mg/mL (709.54 mM), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Herniarin is a natural coumarin occurs in some flowering plants, with antitumor effect.
In Vitro: Herniarin is cytotoxic to breast carcinoma cell line MCF-7 with an IC50 of 207.6 µM. Herniarin (100 µM) also induces apoptosis in MCF-7 cells[1]. Herniarin alone has no obvious cytotoxicity on transitional cell carcinoma (TCC) cells, but when in combination with 5 µg/mL cisplatin, Herniarin (80 µg/mL) potently enhances the antitumor effect of cisplatin, and increases chromatin condensation[2].

Name: Clinodiside A, CAS: 916347-31-4, stock 10.6g, assay 98%, MWt: 959.12, Formula: C48H78O19, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Clinodiside A is isolated from the Chinese medicinal herb Clinopodium chinensis[1].

Name: Sophoridine, CAS: 6882-68-4, stock 4.9g, assay 98.8%, MWt: 248.36, Formula: C15H24N2O, Solubility: DMSO : 50 mg/mL (201.32 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Apoptosis, Target: Apoptosis, Biological_Activity: Sophoridine is a quinolizidine alkaloid isolated from leafs of Leguminous plant Sophora alopecuroides.L. Sophoridine induces apoptosis. Sophoridine has the potential to be a novel, potent and selective antitumor drug candidate for pancreatic cancer with well-tolerated toxicity[1].
In Vitro: Sophoridine (0-500 μM; 48 hours) exhibits remarkable inhibition effects to the growth of human pancreatic, gastric, liver, colon, gallbladder, and prostate carcinoma cells with IC50 values of about 20 μM to 200 μM[1].
Sophoridine (0-20 μM; 48 hours) increases S phase cell population from 26.23% (control) to 38.67% in Miapaca-2 cells and from 29.56% (control) to 39.16% in PANC-1 cells, about a 1.5-fold and a 1.3-fold increase, respectively[1].
Sophoridine (0-20 μM; 48 hours) significantly increases bad and bax levels, and decreases bcl-2 and bcl-xl levels in contrast, with a significant increase in Bax/Bcl-2 ratio[1].
In Vivo: Sophoridine (intraperitoneal injection; 20 or 40 mg/kg; 21 days) can inhibit the growth of xenograft pancreatic tumors[1].

Name: Cefiderocol S-649266, CAS: 1225208-94-5, stock 4.9g, assay 98.4%, MWt: 752.21, Formula: C30H34ClN7O10S2, Solubility: DMSO : 50 mg/mL (66.47 mM; Need ultrasonic), Clinical_Informat: Launched, Pathway: Anti-infection, Target: Bacterial, Biological_Activity: Cefiderocol (S-649266) is a novel siderophore cephalosporin which has a potent activity against a broad range of aerobic Gram-negative bacterial species with MIC50s of 2 μg/mL or less.
IC50 & Target: MIC50: <2 μg/mL (Gram-negative bacteria)[1]
In Vitro: Cefiderocol (S-649266), a novel parenteral siderophore cephalosporin conjugated with a catechol moiety, has a characteristic antibacterial spectrum with a potent activity against a broad range of aerobic Gram-negative bacterial species, including carbapenem-resistant strains of Enterobacteriaceae and nonfermenting bacteria such as Pseudomonas aeruginosa and Acinetobacter baumannii. Cefiderocol has affinity mainly for penicillin-binding protein 3 (PBP3) of Enterobacteriaceae and nonfermenting bacteria similar to that of ceftazidime. A deficiency of the iron transporter PiuA in P. aeruginosa or both CirA and Fiu in Escherichia coli can cause 16-fold increases in cefiderocol MICs, suggesting that these iron transporters contribute to the permeation of cefiderocol across the outer membrane. The deficiency of OmpK35/36 in Klebsiella pneumoniae and the overproduction of efflux pump MexA-MexB-OprM in P. aeruginosa show no significant impact on the activity of cefiderocol[1].

Name: Dapansutrile OLT1177, CAS: 54863-37-5, stock 15.4g, assay 98.2%, MWt: 133.17, Formula: C4H7NO2S, Solubility: DMSO : ≥ 125 mg/mL (938.65 mM), Clinical_Informat: Phase 2, Pathway: Immunology/Inflammation, Target: NOD-like Receptor (NLR), Biological_Activity: Dapansutrile (OLT1177) is a potent, selective and orally active inhibitor of NLRP3 inflammasome. Anti-inflammatory, analgesic activity[1].
IC50 & Target: NLRP3 inflammasome[1]

Name: Edasalonexent CAT-1004, CAS: 1204317-86-1, stock 18.7g, assay 98%, MWt: 490.68, Formula: C31H42N2O3, Solubility: 10 mM in DMSO, Clinical_Informat: Phase 3, Pathway: NF-κB, Target: NF-κB, Biological_Activity: Edasalonexent (CAT-1004) is an orally bioavailable NF-κB inhibitor.
IC50 & Target: NF-κB[1]
In Vitro: Edasalonexent is an orally administered small molecule in which salicylic acid and docosahexaenoic acid (DHA) are covalently conjugated through an ethylenediamine linker and that is designed to synergistically leverage the ability of both of these compounds to inhibit NF-κB. Edasalonexent significantly inhibits NF-κB p65-dependent inflammatory responses as well as downstream proinflammatory genes modulated by p65 in the golden retriever duchenne muscular dystrophy (DMD) model[2].
In Vivo: The treatment of mdx mice with Edasalonexent for 20 weeks results in reduced susceptibility of the extensor digitorum longus muscle to eccentric contraction-induced injury[1].

Name: EGFR-IN-3, CAS: 1660963-42-7, stock 12g, assay 98.4%, MWt: 530.57, Formula: C29H28F2N6O2, Solubility: DMSO : 125 mg/mL (235.60 mM; Need ultrasonic); H2O : < 0.1 mg/mL (insoluble), Clinical_Informat: No Development Reported, Pathway: JAK/STAT Signaling;Protein Tyrosine Kinase/RTK, Target: EGFR;EGFR, Biological_Activity: EGFR-IN-3 is an epidermal growth factor receptor (EGFR) inhibitor.
IC50 & Target: EGFR.

Name: 20(R)-Ginsenoside Rg3 20(R)-Propanaxadiol;R-ginsenoside Rg3, CAS: 38243-03-7, stock 2.4g, assay 98.3%, MWt: 785.01, Formula: C42H72O13, Solubility: DMSO : 41.67 mg/mL (53.08 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: 20(R)-ginsenoside Rg3 (20(R)-Propanaxadiol), one of the active compounds present in ginseng root, has a potent angiosuppressive and antitumor activities[1][2].

Name: Alpinetin, CAS: 36052-37-6, stock 38.2g, assay 98%, MWt: 270.28, Formula: C16H14O4, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Cell Cycle/DNA Damage, Target: PPAR, Biological_Activity: Alpinetin is a flavonoid isolated from Alpinia katsumadai Hayata, activates activates PPAR-γ, with potent anti-inflammatory activity[1].

Name: Nevadensin, CAS: 10176-66-6, stock 31.6g, assay 98.9%, MWt: 344.32, Formula: C18H16O7, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Anti-infection, Target: Bacterial, Biological_Activity: Nevadensin is a naturally occurring selective inhibitor of human carboxylesterase 1 (hCE1) with an IC50 of 2.64 μM. Nevadensin has a variety of pharmacological effects such as anti-mycobacterium tuberculosis activities, antitussive, anti-inflammatory and anti-hypertensive[1][2].
IC50 & Target: IC50: 2.64 μM (hCE1), 132.8 μM (hCE2)[1]

Name: Periplocin, CAS: 13137-64-9, stock 9.7g, assay 98.8%, MWt: 696.82, Formula: C36H56O13, Solubility: DMSO : 250 mg/mL (358.77 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Apoptosis, Target: Apoptosis, Biological_Activity: Periplocin is a cardiotonic steroid isolated from Periploca forrestii. Periplocin promotes tumor cell apoptosis and inhibits tumor growth. Periplocin has the potential to facilitate wound healing through the activation of Src/ERK and PI3K/Akt pathways mediated by Na/K-ATPase[1][2].
IC50 & Target: Apoptosis[2]
In Vitro: Periplocin (5-20 μM; 48 hours; L929 cells) treatment shows increased proliferation up to 131% at 20 μM[1]. 
Periplocin (5-20 μM; 30-120 minutes; L929 cells) increases phosphorylation of Src, ERK, PI3K and Akt at active sites in a dosedependent and time-dependent manner.
Periplocin (5-20 μM; 48 hours) significantly promotes migration of fibroblast cell[1]. 
Periplocin (5-20 μM; 48 hours) increases collagen production in L929 fibroblast[1]. 
Periplocin induces Na/KATPase mediates the activation of Src/ERK and PI3K/Akt pathways[1].
In Vivo: Periplocin (5-20 mg/kg; intraperitoneal injection; daily; for 14 days; female SCID mice) treatment represses the growth of hepatocellular carcinoma (HCC) in xenograft tumor model in mice[2].

Name: Asperuloside, CAS: 14259-45-1, stock 28.4g, assay 98.5%, MWt: 414.36, Formula: C18H22O11, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Immunology/Inflammation, Target: NO Synthase, Biological_Activity: Asperuloside is an iridoid isolated from Hedyotis diffusa, with anti-inflammatory activity. Asperuloside inhibits inducible nitric oxide synthase (iNOS), suppresses NF-κB and MAPK signaling pathways[1].

Name: Higenamine (hydrochloride) Norcoclaurine (hydrochloride), CAS: 11041-94-4, stock 24.3g, assay 98.7%, MWt: 307.77, Formula: C16H18ClNO3, Solubility: DMSO : 100 mg/mL (324.92 mM; Need ultrasonic); H2O : 10 mg/mL (32.49 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Apoptosis;GPCR/G Protein;Neuronal Signaling, Target: Apoptosis;Adrenergic Receptor;Adrenergic Receptor, Biological_Activity: Higenamine hydrochloride (Norcoclaurine hydrochloride), a β2-AR agonist, is a key component of the Chinese herb aconite root that prescribes for treating symptoms of heart failure in the oriental Asian countries. Higenamine hydrochloride (Norcoclaurine hydrochloride) has anti-apoptotic effects[1][2].
IC50 & Target: β2-AR[1]

Name: (Z)-Ligustilide, CAS: 81944-09-4, stock 15.7g, assay 98.2%, MWt: 190.24, Formula: C12H14O2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Anti-infection, Target: Bacterial, Biological_Activity: (Z)-Ligustilide is extracted from Ligusticum chuanxiong Hort, has antimicrobial and antifungal activity, exhibits an average antifungal score of 5.6[1].
(Z)-Ligustilide inhibits the expression of FATP5 and DGAT, inhibits fatty acid uptake and esterification in mice and has potential as therapeutics for nonalcoholic fatty liver disease (NAFLD) [2].

Name: 2-Methoxycinnamic acid, CAS: 6099-03-2, stock 26.1g, assay 98.7%, MWt: 178.18, Formula: C10H10O3, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: 2-Methoxycinnamic acid is a noncompetitive inhibitor of tyrosinase[1].

Name: 4-Methoxycinnamic acid, CAS: 830-09-1, stock 16.7g, assay 98.1%, MWt: 178.18, Formula: C10H10O3, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: 4-Methoxycinnamic acid is detected as natural phenylpropanoid in A. preissii.
In Vitro: 4-Methoxycinnamic acid is an unusual phenylpropanoid involved in phenylphenalenone biosynthesis in Anigozanthos preissii[1].

Name: Syringaldehyde, CAS: 134-96-3, stock 7.5g, assay 98.2%, MWt: 182.17, Formula: C9H10O4, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Immunology/Inflammation, Target: COX, Biological_Activity: Syringaldehyde is a polyphenolic compound belonging to the group of flavonoids and is found in different plant species like Manihot esculenta and Magnolia officinalis[1]. Syringaldehyde moderately inhibits COX-2 activity with an IC50 of 3.5 μg/mL[2]. Anti-hyperglycemic and anti-inflammatory activities[1].
In Vitro: Syringaldehyde inhibits COX-2 activity in a dosedependent manner with an IC50 of 3.5 μg/mL[2].
In Vivo: Syringaldehyde exerts anti-hyperglycemic effect in rat model of diabetes induced by streptozotocin. Apart from antioxidant capability, Syringaldehyde also has anti-inflammatory activity as it is found to have inhibitory action on cyclo-oxygenase 2 (COX-2) in mouse macrophage cell line[1].

Name: 10-Deacetyltaxol 10-Deacetylpaclitaxel, CAS: 78432-77-6, stock 2.6g, assay 98.3%, MWt: 811.87, Formula: C45H49NO13, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Cell Cycle/DNA Damage;Cytoskeleton, Target: Microtubule/Tubulin;Microtubule/Tubulin, Biological_Activity: 10-Deacetyltaxol (10-Deacetylpaclitaxel) is a taxane derivative isolated from Taxus wallichiana Zucc[1]. 10-Deacetyltaxol (10-Deacetylpaclitaxel) promotes the polymerization of tubulin and to inhibit the depolymerization of microtubules induced by cold or by calcium ions in vitro[2]. 10-Deacetyltaxol (10-Deacetylpaclitaxel) exhibits cytotoxicity in human glial and neuroblastoma cell-lines[3].
IC50 & Target: tubulin[2]

Name: Androsin, CAS: 531-28-2, stock 17.7g, assay 98.6%, MWt: 328.31, Formula: C15H20O8, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Androsin is an active compound isolated from Picrorhiza Kurroa Royle ex Benth, with anti-asthmatic effects[1].

Name: (20R)-Ginsenoside Rh1, CAS: 80952-71-2, stock 31g, assay 98.7%, MWt: 638.87, Formula: C36H62O9, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: (20R)-Ginsenoside Rh1, the R isomer of Ginsenoside Rh1 isolated from Panax Ginseng, inhibits the thrombin-induced conversion of fibrinogen to fibrin[1].

Name: 20(R)-Ginsenoside Rh2, CAS: 112246-15-8, stock 18.6g, assay 98.4%, MWt: 622.87, Formula: C36H62O8, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Apoptosis;Metabolic Enzyme/Protease, Target: Apoptosis;MMP, Biological_Activity: 20(R)-Ginsenoside Rh2, a matrix metalloproteinase (MMP) inhibitor, acts as a cell antiproliferator. It has anticancer effects via blocking cell proliferation and causing G1 phase arrest. 20(R)-Ginsenoside Rh2 induces apoptosis, and has anti-inflammatory and antioxidative activity[1][2][3].
IC50 & Target: MMP[1]

Name: Tarloxotinib (bromide) TH-4000, CAS: 1636180-98-7, stock 20.1g, assay 98.7%, MWt: 681.77, Formula: C24H24Br2ClN9O3, Solubility: DMSO : ≥ 33 mg/mL (48.40 mM), Clinical_Informat: Phase 2, Pathway: JAK/STAT Signaling;Protein Tyrosine Kinase/RTK, Target: EGFR;EGFR, Biological_Activity: Tarloxotinib bromide (TH-4000) is an irreversible EGFR/HER2 inhibitor.
IC50 & Target: EGFR/HER2[1].
In Vitro: To confirm the mechanism of action, Tarloxotinib bromide is shown to be metabolized efficiently under hypoxia using a panel of human NSCLC cell lines (rate of TKI release 0.4-2.1 nM/hr/106 cells), a process that is inhibited by oxygen (TKI release <0.002 nM/hr/106 cells). Cellular anti-proliferative and receptor phosphorylation assays demonstrate a 14-80 fold reduction of Tarloxotinib bromide activity relative to TKI. Using PC9 tumors, hyperbaric oxygen breathing suppresse release of TKI from Tarloxotinib bromide by >80% (538 vs 99 nM/kg; p<0.01) compared to air breathing controls. Collectively, these data further validate that Tarloxotinib bromide is a hypoxia-activated irreversible EGFR-TKI, and show that Tarloxotinib bromide has greater activity compared with erlotinib[2].
In Vivo: A prototypic WT EGFR driven xenograft model (A431) is used to benchmark Tarloxotinib bromide activity against each EGFR-TKI by “retrotranslation” of reported plasma exposure for each agent in human subjects back to the xenograft model. Only treatment with clinically relevant doses and schedules of Tarloxotinib bromide is associated with tumor regression and durable inhibition of WT EGFR tumor phosphorylation. Consistent with these findings, Tarloxotinib bromide treatment can also regress the WT EGFR NSCLC tumor models H125 and H1648, demonstrating Tarloxotinib bromide provides the necessary therapeutic index to inhibit WT EGFR in vivo[1].

Name: 6-Methylcoumarin, CAS: 92-48-8, stock 0.2g, assay 98.9%, MWt: 160.17, Formula: C10H8O2, Solubility: DMSO : ≥ 125 mg/mL (780.42 mM), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: 6-Methylcoumarin is a synthetic fragrance widely used in cosmetics.
In Vitro: 6-Methylcoumarin is reported to be almost nonphototoxic in epidermal tissue and cell culture phototoxicity test models. HaCaT cells are treated with 6-Methylcoumarin (1-105 nM) and/or UVA (5 J cm-2), and γ-H2AX is detected by immunofluorescence staining and western blotting 4hours after the treatments. 6-Methylcoumarin clearly produces γ-H2AX-positive cells under UVA irradiation from a concentration of 100 nM[1].

Name: Polygalaxanthone III, CAS: 162857-78-5, stock 14.5g, assay 98.5%, MWt: 568.48, Formula: C25H28O15, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Cytochrome P450, Biological_Activity: Polygalaxanthone III is extracted from polygala tenuifolia wild, has inhibitory effect towards CYP450 enzyme. Polygalaxanthone III inhibits chlorzoxazone 6-hydroxylation catalyzed by CYP2E1 with an IC50 of 50.56 μM[1].

Name: (-)-Ketoconazole (-)-Ketoconazol;(-)-R 41400, CAS: 142128-57-2, stock 29.1g, assay 98.1%, MWt: 531.43, Formula: C26H28Cl2N4O4, Solubility: DMSO : 33.33 mg/mL (62.72 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Anti-infection, Target: Fungal, Biological_Activity: (-)-Ketoconazole ((-)-R 41400) is one of the enantiomer of Ketoconazole. Ketoconazole is a racemic mixture of two enantiomers, levoketoconazole ((2S,4R)-(−)-ketoconazole) and dextroketoconazole ((2R,4S)-(+)-ketoconazole).

Name: Platycodin D, CAS: 58479-68-8, stock 34.5g, assay 98.5%, MWt: 1225.32, Formula: C57H92O28, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Epigenetics;PI3K/Akt/mTOR, Target: AMPK;AMPK, Biological_Activity: Platycodin D is a saponin isolated from Platycodi Radix, acts as an activator of AMPKα, with anti-obesity property[1].
IC50 & Target: AMPKα[1]

Name: 3',6-Disinapoylsucrose, CAS: 139891-98-8, stock 28.2g, assay 98.3%, MWt: 754.69, Formula: C34H42O19, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: 3',6-Disinapoylsucrose, the index component of Yuanzhi (Polygala tenuifolia Willd), possesses potent antioxidant activity and antidepressant effect[1][2].

Name: β-Caryophyllene (-)-(E)-Caryophyllene;(−)-β-caryophyllene;(−)-trans-Caryophyllene, CAS: 87-44-5, stock 5.5g, assay 98.5%, MWt: 204.35, Formula: C15H24, Solubility: Ethanol : ≥ 176.67 mg/mL (864.55 mM); H2O : < 0.1 mg/mL (insoluble); DMSO : < 1 mg/mL (insoluble or slightly soluble), Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein;Neuronal Signaling, Target: Cannabinoid Receptor;Cannabinoid Receptor, Biological_Activity: β-Caryophyllene is a CB2 receptor agonist.
IC50 & Target: CB2 receptor[1]
In Vitro: Among the tested cancer cells, β-Caryophyllene demonstrates selective anti-proliferative effect against three cancer cell lines, namely HCT 116 (colon cancer, IC50=19 μM), PANC-1 (pancreatic cancer, IC50=27 μM), and HT29 (colon cancer, IC50=63 μM) cells, whereas β-Caryophyllene exhibits either moderate or poor cytotoxic effects against ME-180, PC3, K562 and MCF-7. Results show that β-Caryophyllene possesses higher selectivity towards the colorectal cancer cells (HCT 116), with selectivity index (SI)=27.9, followed by PANC-1 and HT 29 cells with SI=19.6 and 8, respectively. The apoptotic index estimated for β-Caryophyllene treatment on HCT 116 cells after 24 h treatment is 64±0.04. β-Caryophyllene at 10 μM concentration, causes significant nuclei condensation after 6 h of treatment. β-caryophyllene exhibits a dose and time-dependent inhibitory effect on the motility of HCT 116 cells[2].
In Vivo: Treatment with β-Caryophyllene at different doses does not show any effects on swimming speed during the test. Oral treatment with β-Caryophyllene ameliorates the rise in β-amyloid deposition in the transgenic mice in a roughly dose-dependent manner, and the two higher doses exhibit almost equal effects in modifying the β-amyloid burden. The number of activated astroglial cells is higher in vehicle-treated mouse brains than in β-Caryophyllene-treated mouse brains with different doses. β-Caryophyllene is effective at reducing the enhancement of the COX-2 protein level found in vehicle-treated APP/PS1 mice[1]. Animals treated with β-Caryophyllene display higher values of object recognition index than their vehicle-treated counterparts [t(14)=4.204, P<0.05]. The total time spent in object exploration during the test trial is not significantly different between β-Caryophyllene-treated and vehicle-treated animals (t(14)=0.5874, P>0.05). Treatment with β-Caryophyllene does not significantly alter these seizure-induced neurochemical changes[3].

Name: Sesamol, CAS: 533-31-3, stock 35.8g, assay 98.8%, MWt: 138.12, Formula: C7H6O3, Solubility: DMSO : ≥ 100 mg/mL (724.01 mM); Ethanol : ≥ 100 mg/mL (724.01 mM), Clinical_Informat: No Development Reported, Pathway: Apoptosis, Target: Apoptosis, Biological_Activity: Sesamol is a constituent of sesame oil. Sesamol shows a free radical scavenging activity. Sesamol shows an IC50=5.95±0.56 μg/mL in the DPPH assay. Anti-oxidant activities[1]. Anticancer activities[2].
In Vitro: Sesamol has also been shown to be a classical inhibitor of lipid peroxidation[1]. 
Sesamol (0-1 mM) efficiently induces the apoptosis of human liver hepatocellular carcinoma (HepG2) cells[2]. 
Sesamol suppresses cell proliferation and induces intrinsic and extrinsic apoptosis in HepG2 cells[2]. 
Sesamol treatment elicites mitochondrial dysfunction by inducing a loss of mitochondrial membrane potential. Sesamol inhibits mitophagy and autophagy through impeding the PI3K Class III/Belin-1 pathway. Sesamol decreases the expression of anti-apoptotic protein Bcl-2, but shows no effect on the expression of apoptotic signal Bax. Sesamol improves the protein expression of Fas/FasL, and activates tBid and caspase-8 which are all involved in the extrinsic apoptosis pathway[2].
In Vivo: Sesamol treatment for 35 days does not significantly impact body weight, although the tumor volume is dramatically inhibited (40.56% size inhibitory rate with Sesamol at 200 mg/kg compared to the control group). However, a lower dose (100 mg/kg Sesamol) only has significant anti-tumor growth effect up to 27 days after the first treatment[2]. 
The Bcl-2/Bax ratio in tumor tissues is also decreased. Moreover, in the Sesamol treatment group, levels of the cell proliferation marker Ki76 are down-regulated, and levels of the cell apoptosis marker cleaved-caspase 3 are increased when compared to control. The expression of LC3 protein is remarkably decreased by Sesamol in a dose-dependent manner[2].

Name: NSC117079, CAS: 500363-63-3, stock 21.6g, assay 98.2%, MWt: 473.48, Formula: C20H15N3O7S2, Solubility: DMSO : ≥ 150 mg/mL (316.80 mM), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: NSC117079 is a novel PHLPP inhibitor.
IC50 & Target: PHLPP[1]
In Vitro: NSC-117079 at 30 μM induces neutrophil adhesion to plated fibrinogen from 9.0±2.4% to 27.0±8.0% and enhanced neutrophil adhesion caused by 50 ng/mL GM-CSF from 22.9±6.0% to 47.6±10.9%. Neutrophil adhesion is followed by neutrophil transendothelial migration. Results suggest that PHLPP inhibitor NSC-117079 is effective in preventing Akt from dephosphorylation in neutrophils, and Akt phosphatase PHLPP serves to attenuate neutrophil adhesion but not migration[2].
In Vivo: A single intraarticular injection of the Phlpp inhibitor NSC117079 attenuates mechanical allodynia and slows articular cartilage degradation in joints with a destabilized meniscus. Animals treated with the Phlpp inhibitor seven weeks after injury maintain normal activity levels, while those in the control group travel shorter distances and are less active three months after the joint injury. NSC117079 also increases production of cartilage extracellular matrix components (glycosaminoglycans and aggrecan) in over 90% of human articular cartilage explants from osteoarthritis patients and increased phosphorylation of Phlpp1 substrates (AKT2, ERK1/2 and PKC) in human articular chondrocytes[1].

Name: Hecogenin, CAS: 467-55-0, stock 25.8g, assay 98.6%, MWt: 430.62, Formula: C27H42O4, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Hecogenin is a steroid saponin isolated from Agave sisalana and is a selective inhibitor of human UDP-glucuronosyltransferases. Hecogenin has a wide spectrum of pharmacological activities, including anti-inflammatory, antifungal and gastroprotective effects[1].
IC50 & Target: Human UDP-glucuronosyltransferases[1]
In Vivo: Hecogenin (3.1-90 mg/kg; oral administration; for 15 hours; male Swiss mice) acutely administered, before ethanol, exhibits a potent gastroprotective effect. The Hecogenin pretreatment normalizes GSH levels and significantly reduces lipid peroxidation and nitrite levels in the stomach, as evaluated by the ethanol-induced gastric lesion model. Hecogenin also decreases MPO release and significantly protects the gastric mucosa[1].

Name: Raspberry ketone Frambione;4-(4-Hydroxyphenyl)-2-butanone, CAS: 5471-51-2, stock 18.4g, assay 98.4%, MWt: 164.20, Formula: C10H12O2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Cell Cycle/DNA Damage, Target: PPAR, Biological_Activity: Raspberry ketone is a major aromatic compound of red raspberry, widely used as a fragrance in cosmetics and as a flavoring agent in foodstuff; also shows PPAR-α agonistic activity.
IC50 & Target: PPAR-α[3]
In Vitro: Raspberry ketone (1, 10, 20, and 50 μM) suppresses adipogenesis and lipid accumulation in 3T3-L1 pre-adipocytes. Raspberry ketone (10 µM) significantly blocks C/EBPα, PPARγ, and aP2 expression and increases the expression of ATGL and HSL, and CPT1B[1].
In Vivo: Raspberry ketone (0.5%, 1%, or 2%) increasses the levels of total cholesterol (TC), triglycerides (TG), low-density lipoprotein cholesterol contents (LDL-C), ISI (insulin-sensitivr index), PPAR-α and LDLR, decreases the serum levels of AST (aspartate aminotransferase), ALT (alanine aminotransferase), ALP (alkaline phosphatase), IRI (insulin resistance index), GLU (glucose), INS (insulin-sensitivr index), LEP (leptin), and TNF-α in rats compared with a high-fat diet-induced NASH model. Raspberry ketone also causes increased SOD activities[2]. Raspberry ketone shows cardioprotective action against isoproterenol-induced myocardial infarction in rats, and the effects may be due to its PPAR-α agonistic activity[3].

Name: Glycodeoxycholate (Sodium) Sodium glycyldeoxycholate, CAS: 16409-34-0, stock 35.8g, assay 98.9%, MWt: 472.61, Formula: C26H43NNaO5, Solubility: DMSO : ≥ 150 mg/mL (317.39 mM), Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: Glycodeoxycholate Sodium is a bile salt.

Name: Tabersonine, CAS: 4429-63-4, stock 35.1g, assay 98.6%, MWt: 336.43, Formula: C21H24N2O2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Tabersonine is an indole alkaloid mainly isolated from Catharanthus roseus. Tabersonine disrupts Aβ(1-42) aggregation and ameliorates Aβ aggregate-induced cytotoxicity. Tabersonine has anti-inflammatory activities and acts as a potential therapeutic candidate for the treatment of ALI/ARDS[1].

Name: Phytolaccagenin, CAS: 1802-12-6, stock 39.6g, assay 98.6%, MWt: 532.71, Formula: C31H48O7, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Anti-infection, Target: Bacterial, Biological_Activity: Phytolaccagenin, a triterpenoid saponin, is the active component of Radix Phytolaccae. Phytolcaccagenin has antifungal activity, anti-inflammatory activity and lower toxicity[1]

Name: Oroxin B, CAS: 114482-86-9, stock 22.7g, assay 98.1%, MWt: 594.52, Formula: C27H30O15, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: PI3K/Akt/mTOR;Apoptosis;PI3K/Akt/mTOR;Autophagy, Target: PI3K;Apoptosis;PTEN;Autophagy, Biological_Activity: Oroxin B (OB) is a flavonoid isolated from traditional Chinese herbal medicine Oroxylum indicum (L.) Vent.
Oroxin B (OB) possesses obvious inhibitory effect and induces early apoptosis rather than late apoptosis on liver cancer cells through upregulation of PTEN, down regulation of COX-2, VEGF, PI3K, and p-AKT[1].
Oroxin B (OB) selectively induces tumor-suppressive ER stress in malignant lymphoma cells[2].

Name: L-(+)-Abrine L-Abrine;L-N-Methyltryptophan;N-α-Methyl-L-tryptophan, CAS: 526-31-8, stock 10.2g, assay 98.6%, MWt: 218.25, Formula: C12H14N2O2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: L-(+)-Abrine, a lethal albumin found in Abrus precatorius seeds, is an acute toxic alkaloid and chemical marker for abrin.
In Vitro: L-(+)-Abrine is a marker for abrin poisoning. A strong indication for abrin poisoning is the presence of the chemical maker L-(+)-Abrine, which can survive metabolism in significant amounts making it detectable in human urine[1].
In Vivo: Abrin is a toxic protein found in the jequirity seed. L-(+)-Abrine (L-Abrine) is also found in the jequirity seed and can be used as a biomarker for abrin exposure. An animal study is designed to monitor the excretion and recovery of L-(+)-Abrine in 20 rats. The animals are exposed to one of three concentrations of L-(+)-Abrine, a single high concentration of L-tryptophan, or no agent (control). The low L-(+)-Abrine dose corresponds to 0.63 LD50 i.p. abrin in mice, assuming a concentration ratio of 1:4 of abrin to L-(+)-Abrine and an LD50 for abrin of 20 μg/kg. The mid and high L-(+)-Abrine (250 and 400 μg/kg) doses are included to ensure that the target analyte can be detected and tracked over the course of the experiment[2].

Name: Hydroxygenkwanin 7-O-Methylluteolin, CAS: 20243-59-8, stock 2.7g, assay 98.2%, MWt: 300.26, Formula: C16H12O6, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Hydroxygenkwanin (7-O-Methylluteolin), a natural flavonoid compound, is one of the main components of Lilac Daphne. Hydroxygenkwanin has anti-oxidant ability, anti-glioma ability and anticancer effect[1][2].
In Vitro: Hydroxygenkwanin (7-O-Methylluteolin) inhibits C6 glioma cell proliferation in a dose dependent manner[1]. 
Hydroxygenkwanin induces the cell cycle arrest by flow cytometry and inhibits colony formation ability and cell movement. Hydroxygenkwanin induces cell cycle arrest through p21 activation and causes intrinsic cell apoptosis pathway[2].

Name: Gypsogenin-3-O-glucuronide, CAS: 96553-02-5, stock 28.1g, assay 98.2%, MWt: 660.83, Formula: C37H56O10, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Gypsogenin-3-O-glucuronide is a ubiquitous saponin precursor in plants of the genus Gypsophila[1].
In Vitro: Treatment of suspended G. paniculata cells with gypsogenin 3,O-glucuronide 24 hours before administration of [14C]acetate results in a marked reduction in the incorporation of radioactivity into saponins and their precursors but not into sterols and steryl glucosides[1].

Name: Koumine, CAS: 1358-76-5, stock 8.8g, assay 98.1%, MWt: 306.40, Formula: C20H22N2O, Solubility: DMSO : 31.25 mg/mL (101.99 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Koumine is an alkaloid separated from Gelsemium elegans, shows potent anti-tumor activity. Koumine up-regulates the Bax/Bcl-2 ratio and caspase-3 expression in human breast cancer cells[1]. Koumine has anxiolytic, antistress, antipsoriatic, and analgesic activities[3], protects against the development of arthritis in Rheumatoid arthritis (RA) animal models[2].
In Vitro: Koumine (0.5, 1 and 2 mg/mL) dose- and time-dependently inhibits the proliferation of MCF-7 cells, with an IC50 of 124 µg/mL at 72 h. Koumine induces apoptosis, causes cell cycle arrest at G2/M phase[1]. 
Koumine (0.5, 1 and 2 mg/mL) up-regulates the Bax/Bcl-2 ratio and caspase-3 expression in a dose-dependent manner in MCF-7 Cells[1]. 
Koumine (25, 50, 100, and 200 μM) decreases the protein and mRNA levels of microglia M1 polarization factors in LPS-induced BV2 cells[3].
In Vivo: Koumine is less toxic, with the median lethal dose (LD50) of 300.0 mg/kg on Wistar rats. Koumine (0.6, 3, or 15 mg/kg/per, p.o.) exhibits antirheumatic properties in rats with adjuvant-induced arthritis (AIA) and collagen-induced arthritis (CIA)[2]. 
Koumine inhibits the increase in cytokines in joint tissue and TNF-α level in serum at 15 mg/kg, and suppresses the increase in the serum level of IL-1β at 3 and 15 mg/kg[2]. 
Koumine (0.28, 7 mg/kg, s.c.) significantly reduces neuropathic pain after nerve injury. Koumine suppresses the increased Iba-1 protein level[3].

Name: Afzelin Kaempferol-3-O-rhamnoside, CAS: 482-39-3, stock 26.9g, assay 98.7%, MWt: 432.38, Formula: C21H20O10, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: PI3K/Akt/mTOR;Autophagy;Metabolic Enzyme/Protease, Target: PTEN;Autophagy;Mitochondrial Metabolism, Biological_Activity: Afzelin (Kaempferol-3-O-rhamnoside) is is a flavonol glycoside found in Houttuynia cordata Thunberg and is widely used in the preparation of antibacterial and antipyretic agents, detoxicants and for the treatment of inflammation. Afzelin attenuates the mitochondrial damage, enhances mitochondrial biogenesis and decreases the level of mitophagy-related proteins, parkin and PTEN-induced putative kinase 1. Afzelin improves the survival rate and reduces the serum levels of alanine aminotransferase and pro-inflammatory cytokines in D-galactosamine (GalN)/LPS -treated mice[1].

Name: Isoquercetin Quercetin 3-glucoside, CAS: 482-35-9, stock 12.3g, assay 98.9%, MWt: 464.38, Formula: C21H20O12, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Immunology/Inflammation;NF-κB, Target: NO Synthase;NF-κB, Biological_Activity: Isoquercetin (Quercetin 3-glucoside) is a naturally occurring polyphenol that has antioxidant, anti-proliferative, and anti-inflammatory properties. Isoquercetin alleviates ethanol-induced hepatotoxicity, oxidative stress, and inflammatory responses via the Nrf2/ARE antioxidant signaling pathway[1]. Isoquercetin regulates the expression of nitric oxide synthase 2 (NO2) via modulating the nuclear factor-κB (NF-κB) transcription regulation system. Isoquercetin has high bioavailability and low toxicity, is a promising candidate agent to prevent birth defects in diabetic pregnancies[2].
In Vitro: Isoquercetin (Quercetin 3-glucoside; 5-20 μM; 24 hours) substantially reduces ethanol-induced cytotoxicity , protects hepatic cells against ethanol-stimulated liver injury[1].
Isoquercetin (10 μM; pre-treat 1 hour) dramatically downregulates the levels of ethanol-induced iNOS protein expression in HepG2 cells[1].

Name: Oleic acid 9-cis-Octadecenoic acid; 9Z-Octadecenoic acid, CAS: 112-80-1, stock 21.5g, assay 98.4%, MWt: 282.46, Formula: C18H34O2, Solubility: DMSO : ≥ 62.5 mg/mL (221.27 mM), Clinical_Informat: Phase 2, Pathway: Apoptosis;Membrane Transporter/Ion Channel;Metabolic Enzyme/Protease, Target: Apoptosis;Na+/K+ ATPase;Endogenous Metabolite, Biological_Activity: Oleic acid is an abundant monounsaturated fatty acid[1]. Oleic acid is a Na+/K+ ATPase activator[2].
IC50 & Target: Na+/K+ ATPase[2]
In Vitro: Oleic acid is the most common monounsaturated fatty acids (FA) in human adipocytes and other tissues. Oleic acid prompts cell proliferation and migration in high metastatic cancer cells via enhancing β-oxidation mediated by AMPK activation. Oleic acid inhibits cancer cell growth and survival in low metastatic carcinoma cells, such as gastric carcinoma SGC7901 and breast carcinoma MCF-7 cell lines[1].

Name: Sudan III Sudan Red III;Tetrazobenzene-β-naphthol;111440 Red, CAS: 85-86-9, stock 12.8g, assay 98.1%, MWt: 352.39, Formula: C22H16N4O, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Sudan III is a hydrophobic bisazo dye[1].
In Vitro: Sudan III changes its color from orange to blue against a small volume of sulfuric acid, and the acetonitrile solution of Sudan III is the most suitable for observing the color-change phenomenon. H-NMR and UV-Vis spectroscopic studies show that the color-change mechanism of Sudan III against sulfuric acid is due to the protonation of the dye by sulfuric acid[1].

Name: Aristolochic acid C, CAS: 4849-90-5, stock 19.2g, assay 98.5%, MWt: 327.25, Formula: C16H9NO7, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Phospholipase, Biological_Activity: Aristolochic acid C is a derivative of Aristolochic acid. Aristolochic acid is a phospholipase A2 (PLA2) inhibitor, which disrupts cortical microtubule arrays and root growth in Arabidopsis[1].

Name: Hypocrellin B, CAS: 123940-54-5, stock 39.7g, assay 98.3%, MWt: 528.51, Formula: C30H24O9, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Apoptosis, Target: Apoptosis, Biological_Activity: Hypocrellin B, a pigment isolated from the fungi Hypocrella bambusae and Shiraia bambusicola, is an apoptosis inducer. Hypocrellin B can be used as a photosensitizer for photodynamic therapy of cancer. Hypocrellin B also has antimicrobial and antileishmanial activities[1][2][3].

Name: Apigenin-7-glucuronide Apigenin 7-O-glucuronide, CAS: 29741-09-1, stock 21.4g, assay 98.8%, MWt: 446.36, Formula: C21H18O11, Solubility: DMSO : 65 mg/mL (145.62 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: MMP, Biological_Activity: Apigenin-7-glucuronide could inhibit Matrix Metalloproteinases (MMP) activities, with IC50s of 12.87, 22.39, 17.52, 0.27 μM for MMP-3, MMP-8, MMP-9, MMP-13, respectively.
In Vitro: Apigenin-7-Oglucuronide could inhibit Matrix Metalloproteinases (MMP) activities, with IC50s of 12.87, 22.39, 17.52, 0.27 μM for MMP-3, MMP-8, MMP-9, MMP-13, respectively [1]. Scutellarin A also inhibits the migrated capacity of ACHN and 786-O cells in a dose-dependent manner. It is also revealed that after treatment with Scutellarin A (30, 60, and 90 μM) for 24 h, the apoptosis rates in ACHN and 786-O cells are remarkably enhanced dose-dependently when compared to the control groups[2].

Name: Chrysosplenetin, CAS: 603-56-5, stock 14.3g, assay 98.5%, MWt: 374.34, Formula: C19H18O8, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Membrane Transporter/Ion Channel;Metabolic Enzyme/Protease;Apoptosis, Target: P-glycoprotein;Cytochrome P450;Ferroptosis, Biological_Activity: Chrysosplenetin is one of the polymethoxylated flavonoids in Artemisia annua L. (Compositae) and other several Chinese herbs. Chrysosplenetin inhibits P-gp activity and reverses the up-regulated P-gp and MDR1 levels induced by artemisinin (ART). Chrysosplenetin significantly augments the rat plasma level and anti-malarial efficacy of ART, partially due to the uncompetitive inhibition effect of Chrysosplenetin on rat CYP3A[1].

Name: Isoschaftoside, CAS: 52012-29-0, stock 27.3g, assay 98.7%, MWt: 564.49, Formula: C26H28O14, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Isoschaftoside, a C-glycosylflavonoid from Desmodium uncinatum root exudate, can inhibit growth of germinated S. hermonthica radicles[1][2].

Name: (E)-Ethyl p-methoxycinnamate, CAS: 24393-56-4, stock 38.6g, assay 98.4%, MWt: 206.24, Formula: C12H14O3, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Immunology/Inflammation, Target: COX, Biological_Activity: (E)-Ethyl p-methoxycinnamate is a natural product found in Kaempferia galangal with anti-inflammatory, anti-neoplastic and anti-microbial effects. (E)-Ethyl p-methoxycinnamate inhibits COX-1 and COX-2 in vitro with IC50s of 1.12 and 0.83 μM, respectively[1].

Name: Dihydrodaidzein (±)-Dihydrodaidzein, CAS: 17238-05-0, stock 34.1g, assay 98.7%, MWt: 256.25, Formula: C15H12O4, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: Dihydrodaidzein is one of the most prominent dietary phytoestrogens.

Name: Atractyloside (potassium salt), CAS: 102130-43-8, stock 27.9g, assay 98.5%, MWt: 802.99, Formula: C30H44K2O16S2, Solubility: DMSO : 250 mg/mL (311.34 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Atractyloside potassium salt is a toxic diterpenoid glycoside isolated from the fruits of Xanthium sibiricum. Atractyloside potassium salt is a powerful and specific inhibitor of mitochondrial ADP/ATP transport. Atractyloside potassium salt inhibits chloride channels from mitochondrial membranes of rat heart[1][2][3].

Name: Luteolin 7-O-glucuronide Luteolin 7-glucuronide, CAS: 29741-10-4, stock 28.1g, assay 98.5%, MWt: 462.36, Formula: C21H18O12, Solubility: DMSO : 130 mg/mL (281.17 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: MMP, Biological_Activity: Luteolin 7-O-glucuronide could inhibit Matrix Metalloproteinases (MMP) activities, with IC50s of 17.63, 7.99, 11.42, 12.85, 0.03 μM for MMP-1, MMP-3, MMP-8, MMP-9, MMP-13, respectively.
IC50 & Target: MMP[1].

Name: Aristolochic acid D, CAS: 17413-38-6, stock 33.2g, assay 98.6%, MWt: 357.27, Formula: C17H11NO8, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Aristolochic acid D is an aristolochic acid derivative isolated from stems of Aristolochia indica. Aristolochic acid is nephrotoxin and carcinogen[1].

Name: Oteseconazole VT-1161, CAS: 1340593-59-0, stock 26.1g, assay 98.5%, MWt: 527.39, Formula: C23H16F7N5O2, Solubility: 10 mM in DMSO, Clinical_Informat: Phase 3, Pathway: Anti-infection;Metabolic Enzyme/Protease, Target: Fungal;Cytochrome P450, Biological_Activity: Oteseconazole (VT-1161) is an orally active anti-fungal agent, potently binds to and inhibits Candida albicans CYP51 (Kd, <39 nM), shows no obvious effect on human CYP51[1][2].

Name: Verdiperstat AZD3241, CAS: 890655-80-8, stock 20.1g, assay 98.4%, MWt: 253.32, Formula: C11H15N3O2S, Solubility: DMSO : 150 mg/mL (592.14 mM; Need ultrasonic), Clinical_Informat: Phase 3, Pathway: Metabolic Enzyme/Protease, Target: Glutathione Peroxidase, Biological_Activity: Verdiperstat (AZD3241) is a selective, irreversible and orally active myeloperoxidase inhibitor, with an IC50 of 630 nM, and can be used in the research of neurodegenerative brain disorders.
IC50 & Target: IC50: 630 nM (Myeloperoxidase)[1]
In Vitro: Verdiperstat (AZD3241) is a myeloperoxidase (MPO) inhibitor, with an IC50 of 630 nM, and is used in the research of neurodegenerative brain disorders[1]. Verdiperstat (AZD3241) selectively and irreversibly inhibits myeloperoxidase, and may involves reduction of oxidative stress leading to reduction of sustained neuroinflammation[2].

Name: Zoliflodacin ETX0914;AZD0914, CAS: 1620458-09-4, stock 28.4g, assay 98.7%, MWt: 487.44, Formula: C22H22FN5O7, Solubility: DMSO : 140 mg/mL (287.21 mM; Need ultrasonic), Clinical_Informat: Phase 3, Pathway: Anti-infection;Cell Cycle/DNA Damage, Target: Bacterial;DNA/RNA Synthesis, Biological_Activity: Zoliflodacin (ETX0914;AZD0914) is a novel spiropyrimidinetrione bacterial DNA gyrase/topoisomerase inhibitor. Zoliflodacin has potent in vitro antibacterial activity against Gram-positive and Gram-negative organisms, including S. aureus with the MIC90 of 0.25 μg/mL.
IC50 & Target: MIC90: 0.25 μg/mL (S. aureus)[1]
In Vitro: Zoliflodacin has antibacterial activity against key Gram-positive (Staphylococcus aureus, Staphylococcus epidermidis, Streptococcus pneumoniae, Streptococcus pyogenes, and Streptococcus agalactiae), fastidious Gram-negative (Haemophilus influenzae, Neisseria gonorrhoeae), atypical (Legionella pneumophila), and anaerobic (Clostridium difficile) bacterial species, including isolates with known resistance to fluoroquinolones. The antibacterial activity of Zoliflodacin is shown to be via inhibition of DNA biosynthesis and accumulation of double-strand cleavages; this mechanism of action differs from those of other marketed antibacterial compounds, including fluoroquinolones. Zoliflodacin stabilizes and arrests the cleaved covalent complex of gyrase with double-strand broken DNA under permissive conditions and thus blocks religation of the double-strand cleaved DNA to form fused circular DNA[1].

Name: JTK-853, CAS: 954389-09-4, stock 32.6g, assay 98.4%, MWt: 704.64, Formula: C28H23F7N6O4S2, Solubility: 10 mM in DMSO, Clinical_Informat: Phase 1, Pathway: Anti-infection, Target: HCV, Biological_Activity: JTK-853 is a novel, non-nucleoside Hepatitis C Virus (HCV) polymerase inhibitor which shows effective antiviral activity in HCV replicon cells with EC50s of 0.38 and 0.035 µM in genotype 1a H77 and 1b Con1 strains, respectively.
IC50 & Target: HCV polymerase[1]
EC50: 0.38 μM (1a H77 HCV), 0.035 μM (1b Con1 HCV)[1]
In Vitro: JTK-853 is a novel, non-nucleoside Hepatitis C Virus Polymerase inhibitor which shows effective antiviral activity in HCV replicon cells with EC50s of 0.38 and 0.035 µM in genotype 1a H77 and 1b Con1 strains, respectively. When JTK-853 is incubated with the replicon cells for 48 h, it shows antiviral activity against genotype 1a H77 and 1b Con1 replicon cells with EC90 values of 6.5±0.5 and 0.34±0.05 µM, respectively. At 10 µM, JTK-853 induces apparent Huh-7.5 cell death in 2-week culture. JTK-853 suppresses the drug-resistant colony formation in the genotype 1a replicon cells, and the numbers of JTK-853-resistant colonies are much lower than those of GS-9190-resistant colonies for both genotypes[1].

Name: Acoziborole SCYX-7158;AN5568, CAS: 1266084-51-8, stock 17.8g, assay 99%, MWt: 367.10, Formula: C17H14BF4NO3, Solubility: DMSO : ≥ 125 mg/mL (340.51 mM), Clinical_Informat: Phase 3, Pathway: Anti-infection, Target: Parasite, Biological_Activity: Acoziborole (SCYX-7158) is an effective, safe and orally active treatment for human african trypanosomiasis (HAT). In the T. b. brucei S427 strain, the MIC value for SCYX-7158 is 0.6 µg/mL.
In Vitro: Acoziborole is active in vitro against relevant strains of Trypanosoma brucei, including T. b. rhodesiense and T. b. gambiense.In whole cell assays, Acoziborole exhibits potent activity against representative T. b. brucei, T. b. rhodesiense and T. b. gambiense strains. IC50 values for Acoziborole are approximately 0.07 µg/mL to 0.37 µg/mL following incubation of the parasite strains with Acoziborole for 72 h. In the T. b. brucei S427 strain, the MIC value for Acoziborole is 0.6 µg/mL, approximately two times the IC50 measured for this strain. In contrast to the potent activity of Acoziborole against trypanosomes, no significant inhibition of cell proliferation is observed in an in vitro mammalian cell (L929 mouse cell line) assay at drug concentrations up to 50 µg/mL. The potential for Acoziborole to inhibit cytochrome P450 (CYP) enzymes is evaluated using P450-Glo assays for the human isoforms CYP3A4, CYP1A2, CYP2C19, CYP2C9 and CYP2D6. The IC50 values for Acoziborole in these assays are all above 10 µM[1].
In Vivo: In uninfected mice, 4.3 mg/kg intravenous dose of Acoziborole show an apparent elimination half-life (t1/2) of 26.6 h; systemic clearance (CL) of 0.089 L/h/kg; a volume of distribution (Vdss) of 1.69 L/kg and area under the concentration-time curve (AUC0-24 h) of 48 h•μg/mL. Following an oral dose of 13.4 mg/kg, which corresponds to the lowest efficacious dose in the murine stage 2 HAT model, Acoziborole is rapidly absorbed, as a Cmax of 6.96 µg/mL is achieved in plasma at 6 h after dose, with an oral clearance (Cl/F) value of 0.163 L/h/kg, an AUC0-24 h of 82 h•μg/mL and absolute oral bioavailability of 55%. After a 26 mg/kg oral dose, which corresponds to the dose giving a 100% cure rate in the murine stage 2 HAT model, Cmax increases to 9.8 µg/mL and the AUC0-24 h is 113 h•μg/mL. In uninfected rats, following oral administration of Acoziborole at a nominal dose of 25 mg/kg (dose affording a 100% cure rate in mice), Cmax increases approximately 2 fold more than that in mice (Cmax=18.2 µg/mL) and AUC0-24 h, and hence oral clearance, improves approximately 4 fold (AUC0-24 h 291 h•μg/mL and CL/F=0.092 L/kg/h). The time to maximum concentration is similar to that in mice (tmax=8 h). Uninfected male and female cynomolgus monkeys are treated with Acoziborole at 2 mg/kg (IV) on study day 1 and 10 mg/kg (NG) on study day 8. Acoziborole exhibits excellent plasma pharmacokinetics, with CL of 0.022 L/h/kg; Vdss of 0.656 L/kg and area under the concentration-time curve 78.8 h•μg/mL, and 94.4 for AUC0-24 h and AUC0-inf, respectively, following intravenous administration[1].

Name: BAY-85-8501, CAS: 1161921-82-9, stock 15.4g, assay 98.6%, MWt: 474.46, Formula: C22H17F3N4O3S, Solubility: 10 mM in DMSO, Clinical_Informat: Phase 2, Pathway: Metabolic Enzyme/Protease, Target: Elastase, Biological_Activity: BAY-85-8501 is a selective, reversible and potent inhibitor of Human Neutrophil Elastase (HNE), with an IC50 of 65 pM.
IC50 & Target: IC50: 65 pM (HNE)[1].
In Vivo: In this model the exogenous HNE noxa is the primary cause of injury and lung hemorrhage. Based on picomolar potency against HNE as well as single digit potency versus MNE, BAY-85-8501 (29) completely prevents the development of lung injury and subsequent inflammation when administered 1 h prior to the HNE noxa. In the 0.01 mg/kg dose group, hemoglobin concentration is already significantly decreased. At a dose of 0.1 mg/kg, a significant effect on neutrophil count is observed. In this setup, efficacy is predominantly driven by potency against HNE (Ki=0.08 nM). As the highly HNE-selective inhibitor BAY 85-8501 has no effect on PPE, BAY-85-8501 could not prevent the primary lung injury in this setup. Nevertheless, BAY-85-8501 could inhibit MNE, the endogenous driver of inflammation and secondary injury, although with decreased potency. Consequently, the effects of BAY-85-8501 on inflammation and secondary injury are weaker at this point, and only observed at 30-fold higher doses. Efficacy is predominantly driven by potency against MNE (Ki=6 nM) in this second setup[1].

Name: ITX5061, CAS: 1252679-52-9, stock 35.5g, assay 98.7%, MWt: 620.16, Formula: C30H38ClN3O7S, Solubility: DMSO : ≥ 83.3 mg/mL (134.32 mM), Clinical_Informat: Phase 1, Pathway: MAPK/ERK Pathway;Autophagy;Anti-infection, Target: p38 MAPK;Autophagy;HCV, Biological_Activity: ITX5061 is a type II inhibitor of p38 MAPK and also an antagonist of scavenger receptor B1 (SR-B1).
IC50 & Target: p38 MAPK, SR-B1[1]
In Vivo: ITX5061 is a type II inhibitor of p38 MAPK and also an antagonist of scavenger receptor B1 (SR-B1). Treatment of ITX5061 (30 mg/kg/day) for mice results in a 50% increase in HDL-C levels compare to baseline. ApoA-I levels are moderately (+15 %) but significantly increased in ITX5061-treated HuAITg mice, compare to mice receive vehicle. ITX5061 significantly decreases HDL-CE catabolism with an FCR of 1.86±0.40 pools/d vs 2.47±0.26 pools/d in the control group (P<0.05), while calculated production rates are identical in both groups (129±24 μg/g/d vs 129±16 μg/g/d). Moreover, accumulation of [3H] CE in the liver is significantly lower in ITX5061-treated mice indicating that increased HDL-CE levels are due to reduced uptake by the liver[1].

Name: JNJ-18038683, CAS: 851376-05-1, stock 18.2g, assay 98.3%, MWt: 529.97, Formula: C26H28ClN3O7, Solubility: 10 mM in DMSO, Clinical_Informat: Phase 2, Pathway: Neuronal Signaling;GPCR/G Protein, Target: 5-HT Receptor;5-HT Receptor, Biological_Activity: JNJ-18038683 is a 5-Hydroxytryptamine Type 7 (5-HT7) receptor antagonist, with pKis of 8.19, 8.20 for rat and human 5-HT7 in HEK293 cells, respectively.
IC50 & Target: pKi: 8.19 (rat 5-HT7 receptor), 8.20 (human 5-HT7 receptor)[1].
In Vitro: JNJ-18038683 displaced, with high affinity, specific [3H]5-CT binding sites from rat and human 5-HT7 receptor express in HEK293 cells (pKi=8.19±0.02 and 8.20±0.01, respectively). Similar values are obtained on the native 5-HT7 in membranes from rat thalamus (pKi=8.50±0.20). Hill slope values are close to unity, suggesting one-site competitive binding. Antagonist potency of JNJ-18038683 is determined by the measurement of adenylate cyclase activity in HEK293 cells expressing the human or rat 5-HT7 receptor. 5-HT stimulates adenylyl cyclase activity in rat and human 5-HT7/HEK293 cells with a pEC50 of 8.09 and 8.12, respectively. JNJ-18038683 produces a concentration-dependent decrease of 5-HT (100 nM)-stimulated adenylyl cyclase. The pKB values determined for JNJ-18038683 are in good agreement with the corresponding Ki values determined from [3H]5-CT binding studies[1].
In Vivo: JNJ-18038683 dose-dependently suppresses REM sleep mainly during the first 4 h after the treatment. The duration of REM sleep is significantly decreased from the dose of 1 mg/kg onward (P<0.05) during the first 4 h after oral administration. Concomitantly, the REM sleep latency tends to be prolonged in a dose-related manner with a significant increase in REM latency occurring only at the highest dose tested (10 mg/kg; P<0.05). These alterations in REM sleep seem to be state-specific. A separate study is conducted to determine whether repeated administration of JNJ-18038683 for 7 days would result in an adaptation of the EEG sleep response in particular on REM sleep in rats during the course of the treatment and after its discontinuation. JNJ-18038683 is administered for 7 consecutive days (1 mg/kg s.c. per day) at 2 h into the light phase. On the first day of treatment, JNJ-18038683 produces a significant decrease in the time spent in REM sleep during the first 8 h after the injection and a prolongation of the REM sleep latency. The REM sleep latency is increased during the 7-day repeated treatment and is normalized on the first recovery day after cessation of treatment. The significant decrease in REM sleep time is maintained during the 7-day repeated treatment, with a rebound occurring on the first recovery day after treatment discontinuation. The NREM sleep latency and the total NREM sleep time are not affected during the entire treatment[1].

Name: Agarotetrol, CAS: 69809-22-9, stock 35.7g, assay 98.2%, MWt: 318.32, Formula: C17H18O6, Solubility: DMSO : ≥ 250 mg/mL (785.37 mM), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Agarotetrol is a chromone derivative isolated from Agarwood.
In Vitro: Agarotetrol is a chromone derivative isolated from Agarwood, shows no inhibitory activity against phosphodiesterase (PDE) 3A (IC50, >100 μM).

Name: Kaurenoic acid, CAS: 6730-83-2, stock 37.1g, assay 98.7%, MWt: 302.45, Formula: C20H30O2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Kaurenoic acid is a diterpene from Sphagneticola trilobata, inhibits Inflammatory Pain by the inhibition of cytokine production and activation of the NO–cyclic GMP–PKG–ATP-sensitive potassium channel signaling pathway[1].

Name: Tilapertin AMG747, CAS: 1000690-85-6, stock 25.5g, assay 98.6%, MWt: 378.39, Formula: C20H21F3N2O2, Solubility: 10 mM in DMSO, Clinical_Informat: Phase 2, Pathway: Neuronal Signaling;Membrane Transporter/Ion Channel, Target: GlyT;GlyT, Biological_Activity: Tilapertin is an oral inhibitor of glycine transporter type-1 (GlyT1).
IC50 & Target: GlyT1[1]
In Vivo: Tilapertin is a nanomolar potent, orally bioavailable and selective GlyT1 inhibitor. Oral administration of Tilapertin dose-dependently increases cerebrospinal fluid (CSF) glycine concentration in rats[1].

Name: F 16915, CAS: 92510-91-3, stock 29.9g, assay 98.9%, MWt: 419.60, Formula: C28H37NO2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: F 16915 is a docosahexaenoic acid derivative which can prevent heart failure-induced atrial fibrillation.
In Vivo: F 16915 is a docosahexaenoic acid derivative which can prevent heart failure-induced atrial fibrillation. Time-dependent changes in blood concentrations of total docosahexaenoic acid (DHA) and nicotinyl alcohol are followed after a single oral administration of F 16915 (300 mg/kg) to male rats. Treatment with F 16915 has no significant effect on body weight: 27.7±2.9 kg and 28.1±1.0 kg before surgery versus 29.2±3.4 kg and 28.8±1.7 kg after in the 1 and 5 g/day groups, respectively. F 16915 administered at 5 g/day for 4 weeks significantly reduces the mean duration of Atrial fibrillation (AF) induced by burst pacing but has no significant effect at 1 g/day. The duration of AF is significantly reduced from 989±111 s in the placebo group to 79±59 s in the presence of F 16915 at 5 g/day. Treatment of 2 months with 100 mg/kg F 16915 also significantly reduces the infarct size[1].

Name: Picfeltarraenin IA, CAS: 97230-47-2, stock 17.8g, assay 98.3%, MWt: 762.92, Formula: C41H62O13, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Neuronal Signaling, Target: AChE, Biological_Activity: Picfeltarraenin IA, a triterpenoid obtained from Picriafel-terrae Lour (P.fel-terrae), is an acetylcholinesterase (AChE) inhibitor. Picfeltarraenin IA can be used for the treatment of herpes infections, cancer and inflammation[1].
IC50 & Target: AChE[1]

Name: Nicotiflorin, CAS: 17650-84-9, stock 29.7g, assay 98.4%, MWt: 594.52, Formula: C27H30O15, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Nicotiflorin is a flavonoid glycoside extracted from a traditional Chinese medicine Flos Carthami. Nicotiflorin shows potent antiglycation activity and neuroprotection effects.
IC50 & Target: Antiglycation[1]
In Vitro: For primarily cultured neurons suffered 2 h hypoxia followed by 24 h reoxygenation, nicotiflorin significantly attenuates cell death and reduces LDH release. Morphological observation also directly confirms its protective effect on neuron[2]. After total 4 h hypoxia and 12 h reoxygenation, eNOS activity, mRNA and protein levels in the primarily cultured rat cerebral blood vessel endothelial cells treated with nicotiflorin (25-100 g/mL) 2 h after onset of hypoxia are significantly higher than eNOS activity, mRNA and protein levels in the pure H-R cells and also higher than eNOS activity, mRNA and protein levels in cells cultured under normoxic conditions[3].
In Vivo: At doses of 2.5, 5 and 10 mg/kg, nicotiflorin administered immediately after the onset of ischemia markedly reduces brain infarct volume and neurological deficits[2]. Nicotiflorin (2.5-10 mg/kg) administered after onset of ischemia markedly reduces brain infarct volume by 24.5-63.2% and neurological deficits[3].

Name: LY2922470, CAS: 1423018-12-5, stock 0.7g, assay 98.3%, MWt: 475.60, Formula: C28H29NO4S, Solubility: DMSO : ≥ 125 mg/mL (262.83 mM), Clinical_Informat: Phase 1, Pathway: GPCR/G Protein, Target: GPR40, Biological_Activity: LY2922470 is a potent, selective and orally available agonist of the G protein-coupled receptor 40 (GPR40), with EC50s of 7 nM, 1 nM and 3 nM for human GPR40, mouse GPR40 and rat GPR40, respectively. LY2922470 reduces glucose levels along with significant increases in insulin and GLP-1, is potential for the treatment of type 2 diabetes mellitus (T2DM)[1].
IC50 & Target: EC50：7 nM (human GPR40), 1 nM (mouse GPR40), 3 nM (rat GPR40)[1]

Name: Heterophyllin B, CAS: 145459-19-4, stock 32.1g, assay 98.4%, MWt: 778.94, Formula: C40H58N8O8, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: PI3K/Akt/mTOR, Target: PI3K, Biological_Activity: Heterophyllin B is an active cyclic peptide isolated from Pseudostellaria heterophylla. Heterophyllin B provides a novel strategy for the treatment of esophageal cancer[1].
In Vitro: Heterophyllin B (0-200 µM; 12-48 hours) reduces cell viability in the 75, 100 and 200 µM groups, has no effect on 5, 10, 25 and 50 µM groups[1].
Heterophyllin B (0-50 µM; 6 hours) suppresses the expression levels of p-PI3K, p-AKT and β-catenin in a dose-dependent manner in ECA-109 cells[1].

Name: Dencichine Dencichin;ODAP, CAS: 5302-45-4, stock 25.8g, assay 98.3%, MWt: 176.13, Formula: C5H8N2O5, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: HIF/HIF Prolyl-Hydroxylase, Biological_Activity: Dencichin is a non-protein amino acid originally extracted from Panax notoginseng, and can inhibit HIF-prolyl hydroxylase-2 (PHD-2) activity.
IC50 & Target: PHD-2[1]
In Vitro: Dencichin (β-ODAP, 10 μM, 50 μM, 100 μM and 200 μM) increases HRE expression by 1.3±0.09, 2.5±0.07, 4.2±0.15 and 1.3±0.07 fold respectively compared to control. Dencichin has intermolecular interactions with PHD-2[1]. Dencichin (10 μM, 100 μM, 1 mM) significantly inhibits cell proliferation and extracellular matrix (ECM) proteins accumulation of HBZY-1 cells, and reduces the secretion of collagen I (Col I), collagen IV (Col IV), and fibronectin (FN)[2].
In Vivo: Dencichin improves metabolism disorder in diabetic nephropathy (DN) secondary to type II diabetes mellitus (DM) model. Dencichin (80, 160 mg/kg/day, p.o.) significantly prevents the up-regulation of TCH, TG, LDL, and HbAlc and the down-regulation of HDL in DN rats induced by STZ injection. Dencichin also attenuates renal injury induced in the DN secondary to type II DM model. Dencichin alleviates pancreas damage in the STZ-induced DN model. Dencichin regulates protein expression in the TGF-β/Smad signalling pathway in STZ-induced DN models[2].

Name: Gardenoside, CAS: 24512-62-7, stock 32.6g, assay 98.1%, MWt: 404.37, Formula: C17H24O11, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Gardenoside is a natural compound found in Gardenia fruits, with hepatoprotective properties. Gardenoside suppresses the pain of chronic constriction injury by regulating the P2X3 and P2X7 receptors. Gardenoside has an inhibitory effect on free fatty acids (FFA)-induced cellular steatosis[1][2].

Name: Polygalic acid, CAS: 1260-04-4, stock 35.8g, assay 98.5%, MWt: 488.66, Formula: C29H44O6, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Polygalic acid, a triterpenoid saponin, is considered one of the major active constituents of Polygala tenuifolia[1].

Name: (-)-Fucose 6-Desoxygalactose; L-(-)-Fucose; L-Galactomethylose, CAS: 2438-80-4, stock 2.5g, assay 98.6%, MWt: 164.16, Formula: C6H12O5, Solubility: 10 mM in H2O, Clinical_Informat: Phase 2, Pathway: Anti-infection;Metabolic Enzyme/Protease, Target: Parasite;Endogenous Metabolite, Biological_Activity: (-)-Fucose is classified as a member of the hexoses, plays a role in A and B blood group antigen substructure determination, selectin-mediated leukocyte-endothelial adhesion, and host-microbe interactions.

Name: AT7519, CAS: 844442-38-2, stock 27.9g, assay 98.8%, MWt: 382.24, Formula: C16H17Cl2N5O2, Solubility: DMSO : ≥ 50 mg/mL (130.81 mM), Clinical_Informat: Phase 1, Pathway: Apoptosis;Cell Cycle/DNA Damage, Target: Apoptosis;CDK, Biological_Activity: AT7519 as a potent inhibitor of CDKs, with IC50s of 210, 47, 100, 13, 170, and <10 nM for CDK1, CDK2, CDK4 to CDK6, and CDK9, respectively.
IC50 & Target: IC50: <10 nM (CDK9), 13 nM (CDK5), 47 nM (CDK2), 100 nM (CDK4), 170 nM (CDK6), 210 nM (CDK1)[2]
In Vitro: AT7519 (0-4 μM) results in dose-dependent cytotoxicity with IC50s ranging from 0.5 to 2 μM in MM cells, and this induced cytotoxicity is associated with GSK-3β activation independent of transcriptional inhibition. AT7519 overcomes proliferative advantage conferred by cytokines and the protective effect of BMSC. AT7519 (0.5 μM) induces apoptosis of MM cells in a time-dependent manner. Moreover, AT7519 (0.5 μM) inhibits phosphorylation of RNA polymerase II CTD and partially inhibits RNA synthesis in MM.1S cells[1]. AT7519 (250 nM) inhibits cell cycle progression in human tumor cell lines. AT7519 also induces apoptosis of human tumor cell lines[2]. AT7519 (100-700 nM) induces apoptosis in leukemia cell lines. AT7519 also inhibits transcription in human tumor cell lines. Furthermore, AT7519 inhibits RNA polymerase II and reduces antiapoptotic protein levels[3].
In Vivo: AT7519 inhibits tumor growth in a human MM xenograft mouse model[1]. AT7519 (4.6 and 9.1 mg/kg/dose) inhibits the growth of early-stage HCT116 tumor xenografts. AT7519 (10 mg/kg, i.p.) also inhibits the target CDKs in HCT116 tumor-bearing BALB/c nude mice[2].

Name: MK-0941, CAS: 1137916-97-2, stock 28.1g, assay 99%, MWt: 556.61, Formula: C22H28N4O9S2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Glucokinase, Biological_Activity: MK-0941 is a potent, orally active and allosteric glucokinase activator, with EC50s of 240 and 65 nM for recombinant human glucokinase in the presence of 2.5 and 10 mM glucose, respectively. MK-0941 has potential in the treatment of type 2 diabetes[1].
IC50 & Target: EC50: 240 nM (Recombinant human glucokinase, 2.5 mM glucose), 65 nM (Recombinant human glucokinase, 10 mM glucose)[1]

Name: Astramembrangenin Cyclosieversigenin, CAS: 78574-94-4, stock 36.3g, assay 98.5%, MWt: 490.72, Formula: C30H50O5, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Apoptosis, Target: Apoptosis, Biological_Activity: Astramembrangenin (Cycloastragenol) is a triterpenoid saponin compound and a hydrolysis product of the main active ingredient in Astragalus membranaceus (Fisch.) Bunge[1].
Astramembrangenin is orally safe and has broad Extensive pharmacological effects, including telomerase activation, telomere elongation, anti-inflammatory and anti-oxidative properties[2].
Astramembrangenin has antiaging properties, CAG stimulates telomerase activity in human neonatal keratinocytes and rat neuronal cells, and induces CREB activation followed by tert and bcl2 expression. Cycloastragenol (CAG) may have a novel therapeutic role in depression[2].
In Vitro: Astramembrangenin (0-10 µM; 3-6 days) increases cell growth compared to the vehicle control in HEK cultures[1].
Astramembrangenin (0.3 µM; 5-90 mins) induces CREB phosphorylation in primary cortical neurons, total CREB expression is unaltered by CAG in both cell type[1].
Astramembrangenin (3 µM; 6-48 hours) may promotes prosurvival signaling in neurons, increases tert mRNA expression, exhibits increased bcl2 mRNA expression[1].

Name: VX-984 M9831, CAS: 1476074-39-1, stock 31g, assay 98.7%, MWt: 415.49, Formula: C23H21D2N7O, Solubility: DMSO : 10 mg/mL (24.07 mM; Need ultrasonic), Clinical_Informat: Phase 1, Pathway: PI3K/Akt/mTOR;Cell Cycle/DNA Damage, Target: DNA-PK;DNA-PK, Biological_Activity: VX-984 is a potent DNA-PK inhibitor.

Name: Maltopentaose Maltopentose, CAS: 34620-76-3, stock 8.4g, assay 98.7%, MWt: 828.72, Formula: C30H52O26, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Maltopentaose is the shortest chain oligosaccharide that can be classified as maltodextrin and is also used in a study to investigate glycation and phosphorylation of α-lactalbumin.

Name: Plumbagin 2-Methyljuglone, CAS: 481-42-5, stock 28.3g, assay 98.4%, MWt: 188.18, Formula: C11H8O3, Solubility: H2O : < 0.1 mg/mL (insoluble); DMSO : ≥ 150 mg/mL (797.11 mM), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Plumbagin (2-Methyljuglone) is a naphthoquinone isolated from Plumbago zeylanica L, exhibits anticancer and antiproliferative activities[1].
In Vitro: Plumbagin (0, 5, 10, and 15 μM) induces apoptosis of prostate cancer cell lines, such as DU145, CWR22rv1 and LNCaP, in a dose-dependent manner[1]. 
Plumbagin (5, 20 μM) obviously inhibits the invasion of PC3, DU145, and CWR22rv1 cells[1].
In Vivo: Plumbagin (2 mg/kg, i.p., five days a week for 11 weeks) inhibits the growth of tumor in male athymic nude mice[1]. 
Plumbagin (2 mg/kg, i.p., five days a week for 11 weeks) inhibits expression of PKCε, suppresses JAK-2 and Stat3 phosphorylation, and activates Stat3, PCNA, VEGF and MMP-9 in mice[1].

Name: Nystose, CAS: 13133-07-8, stock 34.1g, assay 98.8%, MWt: 666.58, Formula: C24H42O21, Solubility: H2O : 300 mg/mL (450.06 mM; Need ultrasonic and warming), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Nystose is a tetrasaccharide with two fructose molecules linked via beta (1→2) bonds to the fructosyl moiety of sucrose.

Name: Pulegone, CAS: 89-82-7, stock 11.8g, assay 98.9%, MWt: 152.23, Formula: C10H16O, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Membrane Transporter/Ion Channel;Neuronal Signaling, Target: TRP Channel;TRP Channel, Biological_Activity: Pulegone, the major chemical constituent of Calamintha nepeta (L.) Savi essential oil which is an aromatic herb with a mint-oregano flavor, is one of avian repellents[1]. The molecular target for the repellent action of Pulegone in avian species is nociceptive TRP ankyrin 1 (TRPA1). Pulegone stimulates both TRPM8 and TRPA1 channel in chicken sensory neurons and suppresses the former but not the latter at high concentrations[2].

Name: Methyl deacetylasperulosidate 6α-Hydroxygeniposide; Deacetylasperulosidic acid methyl ester, CAS: 52613-28-2, stock 2.2g, assay 98.8%, MWt: 404.37, Formula: C17H24O11, Solubility: Methanol : ≥ 125 mg/mL (309.12 mM), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Methyl deacetylasperulosidate is an iridoid isolated from Borreria and Spermacoce species.

Name: Ecliptasaponin A, CAS: 78285-90-2, stock 6.8g, assay 99%, MWt: 634.84, Formula: C36H58O9, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Ecliptasaponin A , a pentacyclic triterpenoid saponin, is one of major compounds separated from Eclipta prostrate[1]. Eclipta prostrate is considered as a nourishing herbal medicine with pleiotropic effects, including anti-inflammatory, hepatoprotective, antioxidant, and immunomodulatory[2].

Name: Kaempferol 3-O-gentiobioside, CAS: 22149-35-5, stock 30.2g, assay 98.6%, MWt: 610.52, Formula: C27H30O16, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Glucosidase, Biological_Activity: Kaempferol 3-O-gentiobioside is a flavonoid isolated from C. alata leaves with antidiabetic activity. Kaempferol 3-O-gentiobioside possesses activity against α-glucosidase and displays carbohydrate enzyme inhibitory effect with an IC50 of 50.0 µM[1].

Name: Ganoderic acid D, CAS: 108340-60-9, stock 0.5g, assay 98.3%, MWt: 514.65, Formula: C30H42O7, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Epigenetics;Cell Cycle/DNA Damage, Target: Sirtuin;Sirtuin, Biological_Activity: Ganoderic acid D, a highly oxygenated tetracyclic triterpenoid, is the major active component of Ganoderma lucidum. Ganoderic acid D upregulates the protein expression of SIRT3 and induces the deacetylated cyclophilin D (CypD) by SIRT3. Ganoderic acid D inhibits the energy reprogramming of colon cancer cells including glucose uptake, lactate production, pyruvate and acetyl-coenzyme production in colon cancer cells[1].
IC50 & Target: SIRT3[1]
In Vitro: Ganoderic acid D can inhibit the growth of numerous cancer cell lines and it inhibits HeLa human cervical carcinoma cells with an IC50 of 17.3 mM[2].

Name: Ganoderic acid H, CAS: 98665-19-1, stock 0.8g, assay 98.8%, MWt: 572.69, Formula: C32H44O9, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Ganoderic acid H is a lanostane-type triterpene isolated from Ganoderma lucidum. Ganoderic acid H suppresses growth and invasive behavior of breast cancer cells through the inhibition of transcription factors AP-1 and NF-kappaB signaling[1].

Name: Ganoderenic acid C, CAS: 100665-42-7, stock 14.7g, assay 98.1%, MWt: 516.67, Formula: C30H44O7, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Ganoderenic acid C is a triterpenoid isolated from Ganoderma lingzhi. Ganoderenic acid C is abundant in fruit bodies at an early growth stage[1].

Name: Ganoderenic acid D, CAS: 100665-43-8, stock 12.3g, assay 98.7%, MWt: 512.63, Formula: C30H40O7, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Apoptosis, Target: Apoptosis, Biological_Activity: Ganoderenic acid D is a triterpene identified from the effective compounds of Ganoderma lucidum extract (GLE). Ganoderenic acid D inhibits the proliferation of cancer cells by inducing cell cycle arrest and apoptosis[1].

Name: Ganoderic acid C2, CAS: 103773-62-2, stock 26.4g, assay 98.5%, MWt: 518.68, Formula: C30H46O7, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Ganoderic acid C2 is a bioactive triterpenoid in Ganoderma lucidum. Ganoderic acid C2 possesses the potential anti-tumor bioactivity, antihistamine, anti-aging and cytotoxic effects. Ganoderic acid C2 exhibits high inhibitory activity against the rat lens aldose reductase (RLAR) with an IC50 of 3.8 µM[1][2].
IC50 & Target: IC50: 3.8 µM (RLAR)[2]

Name: Oxalic acid dihydrate, CAS: 6153-56-6, stock 9.4g, assay 98.7%, MWt: 126.07, Formula: C2H6O6, Solubility: , Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity:

Name: 1-Cinnamoylpyrrolidine, CAS: 52438-21-8, stock 3.5g, assay 98.1%, MWt: 201.26, Formula: C13H15NO, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others;Cell Cycle/DNA Damage, Target: Others;DNA Stain, Biological_Activity: 1-Cinnamoylpyrrolidine (Compound 3), a crude extract prepared from Piper caninum, is a DNA strand scission agent, induces the relaxation of supercoiled pBR322 plasmid DNA[1].
1-Cinnamoylpyrrolidine (Compound 4) inhibits platelet aggregation induced by PAF with an IC50 of 37.3 μM[2].
IC50 & Target: IC50: 37.3 μM (1-Cinnamoylpyrrolidine)[2]

Name: Concanamycin A Antibiotic X 4357B;Concanamycin;X 4357B, CAS: 80890-47-7, stock 33.4g, assay 98.9%, MWt: 866.09, Formula: C46H75NO14, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Membrane Transporter/Ion Channel, Target: Proton Pump, Biological_Activity: Concanamycin A (Antibiotic X 4357B) is a macrolide antibiotic and a specific vacuolar type H+-ATPase (V-ATPase) inhibitor[1].
IC50 & Target: Vacuolar type H+-ATPase[1]

Name: (2S)-2'-Methoxykurarinone 2'-O-Methylkurarinone, CAS: 270249-38-2, stock 16g, assay 98.8%, MWt: 452.54, Formula: C27H32O6, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: (2S)-2'-Methoxykurarinone, a compound isolated from the roots of Sophora flavescens, has anti-inflammatory, antipyretic, antidiabetic, and antineoplastic effects. (2S)-2'-Methoxykurarinone (MK) inhibits osteoclastogenesis and bone resorption through down-regulation of RANKL signaling. (2S)-2'-Methoxykurarinone (MK) displays cytotoxic activity against human myeloid leukemia HL-60 cells[1][2].

Name: Etofibrate, CAS: 31637-97-5, stock 28.1g, assay 98.3%, MWt: 363.79, Formula: C18H18ClNO5, Solubility: DMSO : ≥ 100 mg/mL (274.88 mM), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Etofibrate is the ethandiol-1,2 diester of the nicotinic and clofibric acids. Etofibrate has been shown to be a potent hypolipidemic agent in animal and human.
In Vivo: Etofibrate is the ethandiol-1,2 diester of the nicotinic and clofibric acids. Etofibrate has been shown to be a potent hypolipidemic agent in animal and human. After 10 days of treatment with Etofibrate, the rats show a body weight similar to that found in the control animals but their liver weight is significantly enhanced whereas plasma cholesterol and triacylglycerol levels are decreased. Etofibrate treatment increases the bile flow of the animals, the effect being especially manifest during the first 2 hr after interruption of the enterohepatic circulation and the difference with the controls becomes statistically significant at 30 and 90 min. The cumulative amount of bile secreted plotted against time shows a highly significant linear correlation for both control and Etofibrate treated rats, the slope being significantly higher for the Etofibrate group than for controls[1].

Name: N-Acetyl-D-glucosamine N-Acetyl-2-amino-2-deoxy-D-glucose, CAS: 7512-17-6, stock 4.8g, assay 98.3%, MWt: 221.21, Formula: C8H15NO6, Solubility: 10 mM in DMSO, Clinical_Informat: Phase 3, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: N-Acetyl-D-Glucosamine (N-Acetyl-2-amino-2-deoxy-D-glucose) is a monosaccharide derivative of glucose.

Name: Dimetacrine Dimethacrine, CAS: 4757-55-5, stock 17.7g, assay 98.1%, MWt: 294.43, Formula: C20H26N2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Dimetacrine is a useful antidepressant which can be used for the treatment of various types of depression.
In Vivo: Dimetacrine is a useful antidepressant which can be used for the treatment of various types of depression. Dimetacrine in the highest concentration, 10 μM, decreases the contractile force to 36.5±9.1%. Dimetacrine, 0.3 μM, causes no statistically significant decline in contractile force from the controls. Tachycardia is observed after the administration of Dimetacrine, 1 to 3 mg/kg i.v., and the maximum response is obtained in dose of 3 mg/kg i.v.. The administration of Dimetacrine, 30 mg/kg i.v., causes an abrupt fall in blood pressure with tachycardia or bradycardia followed by cardiac arrest. Respiratory rate increases 40 min after the onset of infusion of Dimetacrine. Arterial blood pressure falls 50 min after the onset of infusion of Dimetacrine[1].

Name: Ro 12-1989 all-cis-8,11,14-Eicosatrienoic acid, CAS: 1783-84-2, stock 35.7g, assay 98.6%, MWt: 306.48, Formula: C20H34O2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: Ro 12-1989 is a 20-carbon-chain omega-6 fatty acid unsaturated at positions 8, 11, and 14.

Name: Phenprocoumon, CAS: 435-97-2, stock 22.8g, assay 98.7%, MWt: 280.32, Formula: C18H16O3, Solubility: DMSO : ≥ 125 mg/mL (445.92 mM), Clinical_Informat: Launched, Pathway: Others, Target: Others, Biological_Activity: Phenprocoumon is a coumarin derivative that acts as a long acting oral anticoagulant and an antagonist of vitamin K.
IC50 & Target: Vitamin K[1].
In Vivo: After a single i.v.-dose of phenprocoumon (0.355 mg/kg) the anticoagulant effect obtained is greater in older than in younger rats. There are no differences between younger and older rats in the rate of elimination, volume of distribution and in the free fraction and free concentration values of phenprocoumon in plasma and liver. After i.v.-injection of 64.3 μg/kg [3H]vitamin K1 and different doses of phenprocoumon (0.02 to 3 mg/kg) the [3H]vitamin K1 concentration in the liver decreases and the [3H] vitamin K1-2, 3-epoxide concentration increases dependent on the dose and the liver concentration of phenprocoumon. These changes are more pronounced in the older than in the younger rats[2].

Name: ML239, CAS: 1378872-36-6, stock 6.5g, assay 98.1%, MWt: 346.60, Formula: C13H10Cl3N3O2, Solubility: DMSO : ≥ 300 mg/mL (865.55 mM), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: ML239 is a potent and selective inhibitor of breast cancer stem cells, with an IC50 of 1.16 μM.
In Vitro: ML239 (Compound 7j) is a potent and selective inhibitor of breast cancer stem cells, with an IC50 of 1.16 μM, with ∼24-fold selectivity against the control cell line[1]. ML239 inhibits breast cancer stem-like cells, most likely through activation of fatty acid desaturase 2 (FADS2). ML239 is cytotoxic to NCIH661 cells, and FADS2 knockdown reduces ML239 cytotoxicity, and furthermore, FADS2 inhibitor SC-26196 also reduces ML239 cytotoxicity in cancer cell lines (CCLs)[2].

Name: Deslanoside Deacetyllanatoside C;Desacetyllanatoside C, CAS: 17598-65-1, stock 18.9g, assay 98.3%, MWt: 943.08, Formula: C47H74O19, Solubility: 10 mM in DMSO, Clinical_Informat: Launched, Pathway: Membrane Transporter/Ion Channel;Metabolic Enzyme/Protease, Target: Na+/K+ ATPase;Drug Metabolite, Biological_Activity: Deslanoside (Desacetyllanatoside C) is a rapidly acting cardiac glycoside used to treat congestive heart failure and supraventricular arrhythmias due to reentry mechanisms, and to control ventricular rate in the treatment of chronic atrial fibrillation. Deslanoside inhibits the Na-K-ATPase membrane pump, resulting in an increase in intracellular sodium and calcium concentrations [1][2][3].
In Vitro: Deslanoside (Desacetyllanatoside C) is a metabolite of Lanatoside C[4]. Deslanoside increases forearm blood flow and cardiac index and decreased heart rate concomitant with a marked decrease in skeletal muscle sympathetic nerve activity measured as an indicator of centrally mediated sympathetic nervous system activity[1].

Name: Diflorasone, CAS: 2557-49-5, stock 24.6g, assay 98.8%, MWt: 410.45, Formula: C22H28F2O5, Solubility: DMSO : 130 mg/mL (316.73 mM; Need ultrasonic), Clinical_Informat: Launched, Pathway: Others, Target: Others, Biological_Activity: Diflorasone is a potent topical anti-inflammatory steroid.

Name: Zuclopenthixol (Z)-Clopenthixol, CAS: 53772-83-1, stock 10.6g, assay 98.6%, MWt: 400.96, Formula: C22H25ClN2OS, Solubility: DMSO : ≥ 150 mg/mL (374.10 mM), Clinical_Informat: Phase 4, Pathway: GPCR/G Protein;Neuronal Signaling, Target: Dopamine Receptor;Dopamine Receptor, Biological_Activity: Zuclopenthixol is a thioxanthene derivative which acts as a mixed dopamine D1/D2 receptor antagonist.
IC50 & Target: D1/D2 receptor[1].
In Vivo: After acute treatment, Zuclopenthixol (0.2 and 0.4 mg/kg)-treated animals exhibit ethopharmacological profiles characterized by a decrease in offensive behaviors without impairment of motor activity (0.2 mg/kg). In contrast, the antiaggressive action of the highest dose used (0.4 mg/kg) is accompanied by a marked increase of immobility. After subchronic treatment, no tolerance to Zuclopenthixol antiaggressive or motor activity is observed[1]. 
Administration of Zuclopenthixol (0.7 and 1.4 mg/kg) significantly elevate MDA level compared to respective controls. Nevertheless, there is no difference between the two dose levels with respect to their effect on rat brain MDA level. Post hoc pairwise comparisons between the means of groups (n=12) receiving different dose levels of Zuclopenthixol reveal that administration of 1.4 mg/kg of Zuclopenthixol significantly reduces GSH level compared to both vehicle-treated and Zuclopenthixol (0.7 mg/kg)-treated animals (P<0.001). Nevertheless, the lower dose of the drug does not affect rat brain GSH level. Animals receiving 0.7 or 1.4 mg/kg of Zuclopenthixol exhibits significantly higher GSH levels than SCO treated animals. Administration of 0.7 mg/kg of Zuclopenthixol significantly elevated GSHPx activity compared to vehicle treated animals[2].

Name: Glycerol phenylbutyrate HPN-100, CAS: 611168-24-2, stock 25.1g, assay 98.5%, MWt: 530.65, Formula: C33H38O6, Solubility: DMSO : ≥ 150 mg/mL (282.67 mM), Clinical_Informat: Launched, Pathway: Others, Target: Others, Biological_Activity: Glycerol phenylbutyrate is a sigma-2 (σ2) receptor ligand, with a pKi of 8.02.
IC50 & Target: σ2 receptor[1].

Name: Progabide SL 76002, CAS: 62666-20-0, stock 15.8g, assay 98.3%, MWt: 334.77, Formula: C17H16ClFN2O2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Progabide is a gamma-aminobutyric acid receptor (GABA) agonist.
IC50 & Target: GABA receptor[1]
In Vivo: Progabide is a gamma-aminobutyric acid receptor (GABA) agonist. Doses of 50, 100 and 200 mg/kg Progabide given IP to male Wistar rats increase the plasma corticosterone levels by 244, 365 and 476% respectively (t=6.44 to12.55, p<0.01). 10 mg/kg of Progabide fails to change the concentration of corticosterone in plasma (t=0.76, N.S.). The increased plasma corticosterone level induced by administration of 200 mg/kg Progabide is evident 30 (t=2.625, p<0.05), 60 (t=13.13, p<0.001) and 120 min (t=4.07, p<0.01) after drug injection, but returns to the control value 240 min after drug injection (t=0.86, N.S.). The greatest corticosterone rise (compare with the corresponding control) is reached 60 min following the administration of Progabide[1].

Name: Adenosine monophosphate AMP, CAS: 61-19-8, stock 37.2g, assay 98.6%, MWt: 347.22, Formula: C10H14N5O7P, Solubility: DMSO : 16.67 mg/mL (48.01 mM; Need ultrasonic); H2O : 1.67 mg/mL (4.81 mM; Need ultrasonic), Clinical_Informat: Phase 4, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: Adenosine monophosphate is a key cellular metabolite regulating energy homeostasis and signal transduction.
In Vitro: Adenosine monophosphate is a product of various enzymatic reactions, many of which are dysregulated during disease conditions[1].

Name: YU238259, CAS: 1943733-16-1, stock 11.2g, assay 98.7%, MWt: 459.95, Formula: C22H22ClN3O4S, Solubility: DMSO : ≥ 300 mg/mL (652.24 mM), Clinical_Informat: No Development Reported, Pathway: PI3K/Akt/mTOR;Cell Cycle/DNA Damage, Target: DNA-PK;DNA-PK, Biological_Activity: YU238259 is an inhibitor of homology-dependent DNA repair (HDR), used for cancer research.
IC50 & Target: HDR[1]
In Vitro: YU238259 is an inhibitor of homology-dependent DNA repair, with no effect on PARP activity. YU238259 shows cytotoxicity in BRCA2-deficient cells, with a low LD50 of 8.5 μM. YU238259 (0-5 μM) causes a potent, dose-dependent decrease in HDR efficiency in U2OS DR-GFP or U2OS EJ5-GFP cells, but with no effect on NHEJ frequency. YU238259 (0-10 μM) exhibits synthetic lethality with loss of frequently mutated tumor suppressors, and shows synergism with radiotherapy (IR) and DNA-damaging chemotherapy that is potentiated by BRCA2 loss[1].
In Vivo: YU238259 (3 mg/kg, i.p.) inhibits the growth of BRCA2-deficient tumor xenografts in nude mice[1].

Name: RCM-1, CAS: 339163-65-4, stock 16.4g, assay 98.6%, MWt: 424.58, Formula: C20H12N2OS4, Solubility: DMSO : 16.67 mg/mL (39.26 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: RCM-1 is a FOXM1 inhibitor.
IC50 & Target: FOXM1[1].
In Vitro: RCM-1 inhibits cellular proliferation via increasing duration of cell cycle and mitosis in human and mouse cancer cell lines in vitro. Treatment with RCM-1 increases duration of mitosis and cell cycle in the cancer cell lines. RCM-1 inhibits colony formation of cancer cells in vitro in a dose-dependent manner. RCM-1 inhibits migration of cancer cells in vitro in a dose-dependent manner. RCM-1 inhibits the initiation as well as growth of cancer cell colonies in vitro[1].
In Vivo: RCM-1 treatment reduces growth of Rd76-9 rhabdomyosarcomas in mice. RCM-1 treatment decreases tumor cell proliferation and increases apoptosis in Rd76-9 rhabdomyosarcoma tumors. The RCM-1-treated Rd76-9 tumors show reduced FOXM1 staining and decreased expression of proliferation-specific markers Ki67 and PH3. Cleaved caspase staining is increased in the RCM-1 treated tumors, indicating an increase in apoptosis. RCM-1 treatment reduces growth of the B16-FlO melanoma tumors in mice. RCM-1 decreases the B 16-FlO tumor growth as compared to the Vehicle -treated group. RCM-1 treatment decreases tumor cell proliferation and increased apoptosis in B16-FlO melanoma tumors. RCM-1 treatment reduces growth of the human H2122 lung adenocarcinoma in mice[1].

Name: Rosoxacin Acrosoxacin, CAS: 40034-42-2, stock 20.4g, assay 98%, MWt: 294.30, Formula: C17H14N2O3, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Anti-infection, Target: Bacterial, Biological_Activity: Rosoxacin (Acrosoxacin) is a potent and orally active quinolone antibiotic. Rosoxacin (Acrosoxacin) has antibacterial activities against a broad spectrum of Gram negative bacteria including Neisseria gonorrhoeae (MIC90=0.03mg/ml). Rosoxacin has the potential for urinary tract infections treatment[1].
IC50 & Target: MIC90: 0.03 mg/ml[1]

Name: Inulin, CAS: 9005-80-5, stock 0.2g, assay 98%, MWt: 1000, Formula: N/A, Solubility: 10 mM in DMSO, Clinical_Informat: Launched, Pathway: Others, Target: Others, Biological_Activity: Inulin is a water soluble storage polysaccharide and belongs to a group of non-digestible carbohydrates, fructan. Inulin is from plants of the Compositae and Lilialiaceaes families, often used as a prebiotic, fat replacer, sugar replacer, texture modifier, plays beneficial role in gastric [1].

Name: Tasosartan WAY-ANA 756, CAS: 145733-36-4, stock 20.9g, assay 98.5%, MWt: 411.46, Formula: C23H21N7O, Solubility: DMSO : 125 mg/mL (303.80 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein, Target: Angiotensin Receptor, Biological_Activity: Tasosartan is a long-acting angiotensin II (AngII) receptor antagonist.
IC50 & Target: Angiotensin II (AngII) receptor[1]
In Vitro: Tasosartan is an orally active nonpeptide AngII antagonist that has demonstrates specific and selective AT1 receptor antagonistic activity in vitro. IC50 for inhibition of specific binding of 125I-AngII to rat adrenal membrane in the absence of proteins in binding buffer is 1.2±0.6 nM[1].
In Vivo: Administration of Tasosartan at doses of 1.0 and 3.0 mg/kg (iv) significantly (p<0.05) attenuates the pressor response to angiotensin-II in rats[2].

Name: 3-Furfuryl 2-pyrrolecarboxylate, CAS: 119767-00-9, stock 32.9g, assay 98.8%, MWt: 191.18, Formula: C10H9NO3, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: 3-Furfuryl 2-pyrrolecarboxylate is isolated from the root tuber of Pseudostellaria heterophylla[1].

Name: ASP5878, CAS: 1453208-66-6, stock 36.8g, assay 98.8%, MWt: 407.37, Formula: C18H19F2N5O4, Solubility: H2O : < 0.1 mg/mL (insoluble); DMSO : ≥ 250 mg/mL (613.69 mM), Clinical_Informat: Phase 1, Pathway: Protein Tyrosine Kinase/RTK, Target: FGFR, Biological_Activity: ASP5878 is an oral active inhibitor of FGFR 1, 2, 3, and 4, with IC50 values of 0.47 nM, 0.6 nM, 0.74 nM and 3.5 nM for FGFR 1, 2, 3, and 4 kinase activity. ASP5878 has potential antineoplastic activity[1].
IC50 & Target: IC50: 0.47 nM/0.6 nM/0.74 nM/3.5 nM (FGFR1/2/3/4)[1].
In Vitro: ASP5878 shows potent antiproliferative activity in most human HCC cell lines[1]. 
ASP5878 inhibits FGFR4 phosphorylation in a concentration-dependent manner. ASP5878 treatment results in the suppression of phosphorylation, mobility shift of FRS2, and suppression of ERK phosphorylation[1]. 
In Vivo: ASP5878 (3 mg/kg, orally, once daily) shows antitumor activity in a Hep3B2.1-7 subcutaneous xenograft and HCC orthotopic xenograft mouse model[1]. 
ASP5878 induces shrinkage of FGF19-expressing HCC xenograft model[1].

Name: PF-06459988, CAS: 1428774-45-1, stock 36.1g, assay 99%, MWt: 431.88, Formula: C19H22ClN7O3, Solubility: DMSO : 50 mg/mL (115.77 mM; Need ultrasonic), Clinical_Informat: Phase 2, Pathway: JAK/STAT Signaling;Protein Tyrosine Kinase/RTK, Target: EGFR;EGFR, Biological_Activity: PF-06459988 is an irreversible inhibitor of T790M-Containing EGFR Mutants.
IC50 & Target: IC50: 45 nM (H1975 EGFR), 3.3 μM (EGFR)

Name: 4',5-Dihydroxyflavone, CAS: 6665-67-4, stock 24.1g, assay 98.7%, MWt: 254.24, Formula: C15H10O4, Solubility: H2O : < 0.1 mg/mL (insoluble); DMSO : ≥ 155 mg/mL (609.66 mM), Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease;Metabolic Enzyme/Protease, Target: Lipoxygenase;Glucosidase, Biological_Activity: 4',5-Dihydroxyflavone is a soybean LOX-1 and yeast α-Glucosidase inhibitor, with an Ki of 102.6 μM for soybean LOX-1 and an IC50 of 66 μM for yeast α-glucosidase. LOX-1 isshort for Lectin-like oxidized low-density lipoprotein receptor-1.
IC50 & Target: Ki: 102.6 μM (LOX-1)[1]. IC50: 66 μM (α-glucosidase)[2].

Name: 4',7-Di-O-methylnaringenin, CAS: 29424-96-2, stock 28.6g, assay 99%, MWt: 300.31, Formula: C17H16O5, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: 4',7-Di-O-methylnaringenin is a flavonoid found in Renealmia alpinia[1].

Name: Malic acid E 296; FDA 2018; Hydroxybutanedioic acid, CAS: 6915-15-7, stock 10g, assay 98.7%, MWt: 134.09, Formula: C4H6O5, Solubility: 10 mM in DMSO, Clinical_Informat: Phase 3, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: Malic acid is a dicarboxylic acid that is naturally found in fruits such as apples and pears. It plays a role in many sour or tart foods.

Name: N-Methylmethanamine hydrochloride Dimethylammonium chloride; N,N-Dimethylamine hydrochloride, CAS: 506-59-2, stock 22.3g, assay 98.6%, MWt: 81.54, Formula: C2H8ClN, Solubility: , Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity:

Name: 4'-O-Methylbavachalcone, CAS: 20784-60-5, stock 26.3g, assay 98.5%, MWt: 338.40, Formula: C21H22O4, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Anti-infection, Target: SARS-CoV, Biological_Activity: 4'-O-Methylbavachalcone is a chalcone isolated from Psoralea corylifolia, inhibits severe acute respiratory syndrome coronavirus (SARS-CoV) papain-like protease (PLpro) activity, with an IC50 of 10.1 μM[1].
IC50 & Target: IC50: 10.1 μM (PLpro)[1]

Name: Andropanolide, CAS: 869807-57-8, stock 30.6g, assay 98.7%, MWt: 350.45, Formula: C20H30O5, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: NF-κB, Target: NF-κB, Biological_Activity: Andrographolide (Andro) is a small antagonist for NF-κB activation by covalent modifying reduced cysteine 62 of p50. Andrographolide is a bicyclic diterpenoid lactone mainly produced from the plant Andrographis (Andrographis paniculate).
Andrographolide suppresses the activation of NF-κB in stimulated endothelial cells, which reduces the expression of cell adhesion molecule E-selectin and prevents E-selectin-mediated leukocyte adhesion, but has no effect on IκBα degradation, p50 and p65 nuclear translocation[1].
In Vitro: Andrographolide (15 μM; 12 hours) inhibited the luciferase activities induced by TNF-α in a time-dependent manner with an IC50 of 10 μM[1].

Name: Taprenepag isopropyl PF-04217329, CAS: 1005549-94-9, stock 31.3g, assay 98.3%, MWt: 520.60, Formula: C27H28N4O5S, Solubility: 10 mM in DMSO, Clinical_Informat: Phase 2, Pathway: GPCR/G Protein, Target: Prostaglandin Receptor, Biological_Activity: Taprenepag isopropyl is a highly selective EP2 receptor agonist.
IC50 & Target: EP2 receptor[1]
In Vivo: Taprenepag isopropyl is a highly selective EP2 receptor agonist. Intraocular pressure (IOP) in the left, vehicle-dosed eye typically remains within the normal range. In the right (Taprenepag isopropyl-dosed) eye, IOP is reduced in all dose groups. In the high-dose group, IOP is reduced to the extent that it cannot be measured (<4mm Hg) on Days 22 and 29. There are no clinical signs or changes in body weight observed with any dose of Taprenepag isopropyl administration, and no
ocular findings occur for animals in the low-dose group (0.75 mg/day)[1].

Name: ML-210, CAS: 1360705-96-9, stock 2.5g, assay 98.1%, MWt: 475.32, Formula: C22H20Cl2N4O4, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Apoptosis;Metabolic Enzyme/Protease, Target: Ferroptosis;Glutathione Peroxidase, Biological_Activity: ML-210，the most potent compound in the nitroisoxazole series， is a selective covalent inhibitor of glutathione peroxidase 4 (GPX4) by binding the selenocysteine residue[1]. ML-210 has IC50s of 71 nM, 272 nM and 107nM for BJeLR (HRASV12), BJeH-LT (without HRASV12) and DRD cell lines, respectively[2].
IC50 & Target: Glutathione Peroxidase 4 (GPX4)[1]

Name: NSC 8751 (E)-2-Butenoic acid; (E)-Crotonic acid; trans-2-Butenoic acid; trans-Crotonic acid, CAS: 107-93-7, stock 20.9g, assay 98.1%, MWt: 86.09, Formula: C4H6O2, Solubility: , Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity:

Name: BAY-1436032, CAS: 1803274-65-8, stock 22.8g, assay 98.1%, MWt: 489.53, Formula: C26H30F3N3O3, Solubility: DMSO : 125 mg/mL (255.35 mM; Need ultrasonic and warming); H2O : < 0.1 mg/mL (insoluble), Clinical_Informat: Phase 1, Pathway: Metabolic Enzyme/Protease, Target: Isocitrate Dehydrogenase (IDH), Biological_Activity: BAY-1436032 is a novel pan-mutant isocitrate dehydrogenase 1 (IDH1) inhibitor.
IC50 & Target: IDH1[1]
In Vitro: BAY-1436032 is a novel pan-mutant isocitrate dehydrogenase 1 (IDH1) inhibitor. BAY-1436032 inhibits intracellular (R)-2-hydroxyglutarate (R-2HG) production in mouse hematopoietic cells expressing IDH1R132H or IDH1R132C with IC50s of 60 and 45 nM, respectively. R-2HG levels are not reduced in IDH2R140Q and IDH2R172K expressing mouse hematopoietic cells by BAY-1436032 at concentrations up to 10 μM. Colony growth is inhibited by 50% at a concentration of 0.1 μM BAY-1436032, while concentrations up to 100 μM do not suppress colony growth of patient-derived IDH1 wild-type AML cells. On morphologic evaluation myelomonocytic differentiation of myeloid progenitors is strongly induced by BAY-1436032[1].
In Vivo: Long-term exposure to once daily oral BAY-1436032 reveals nearly complete suppression of (R)-2-hydroxyglutarate (R-2HG) production with 150 mg/kg BAY1436032. White blood cell counts constantly increase in vehicle-treated mice and, at a lower rate, in animals receiving 45 mg/kg BAY-1436032, while they remain constant in the 150 mg/kg cohort. Hemoglobin levels are slightly lower in the vehicle and 45 mg/kg groups as compare to the 150 mg/kg cohort at day 60, while platelet counts are significantly reduced in vehicle and 45 mg/kg BAY-1436032 treated mice compare to the 150 mg/kg cohort at day 60. All mice receiving 150 mg/kg BAY-1436032 survive with minimal hCD45+ cell load in their peripheral blood until the end of observation at day 150 after treatment start (P<0.001), while vehicle-treated animals die from leukemia with a median survival of 91 days. Mice treated with 45 mg/kg BAY-1436032 display intermediate levels of CD14/CD15 expression[1].

Name: Flavopiridol Alvocidib;L86-8275;HMR-1275, CAS: 146426-40-6, stock 15.9g, assay 98.7%, MWt: 401.84, Formula: C21H20ClNO5, Solubility: DMSO : 33.33 mg/mL (82.94 mM; Need ultrasonic), Clinical_Informat: Phase 2, Pathway: Cell Cycle/DNA Damage;Autophagy;Anti-infection, Target: CDK;Autophagy;HIV, Biological_Activity: Flavopiridol (Alvocidib) is a broad spectrum and competitive inhibitor of CDKs, inhibiting CDK1, CDK2, CDK4 with IC50s of 30, 170, 100 nM, respectively.
IC50 & Target: IC50: 30 nM (CDK1), 170 nM (CDK2), 100 nM (CDK4)[3]
In Vitro: Flavopiridol (2 μM) robustly induces a distinct pattern of ER stress in CLL cells that contributes to cell death through IRE1-mediated activation of ASK1 and possibly downstream caspases[1]. Flavopiridol results in potent upregulation of a number of PRGs in treatments lasting 4-24 h. Flavopiridol has and immediate and long-term effect on the expression of several PRGs. In serum starved cells re-stimulated with serum, flavopiridol also inhibits the expression of these genes, but subsequently, JUNB, GADD45B and EGR1 are upregulated in the presence of flavopiridol[2].

Name: 6-Hydroxybentazon 6-Hydroxybentazone, CAS: 60374-42-7, stock 32.1g, assay 98.8%, MWt: 256.28, Formula: C10H12N2O4S, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: 6-Hydroxybentazon is a phase I metabolite of bentazone, and bentazone is a chemical for use in herbicides.

Name: Dolutegravir intermediate-1, CAS: 1335210-23-5, stock 29.3g, assay 98.5%, MWt: 315.28, Formula: C13H17NO8, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Dolutegravir intermediate-1 is a novel synthetic intermediate of dolutegravir extracted from patent WO 2016125192 A2. Dolutegravir is an integrase inhibitor developed for the treatment of human immunodeficiency virus (HIV)-l infection.

Name: Vatinoxan hydrochloride MK-467 hydrochloride;L-659066 hydrochloride, CAS: 130466-38-5, stock 13.5g, assay 98.1%, MWt: 454.97, Formula: C20H27ClN4O4S, Solubility: H2O : ≥ 133 mg/mL (292.33 mM), Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein;Neuronal Signaling, Target: Adrenergic Receptor;Adrenergic Receptor, Biological_Activity: Vatinoxan hydrochloride (MK-467 hydrochloride;L-659066 hydrochloride) is a peripheral α2 adrenergic receptor antagonist.
IC50 & Target: α2 adrenergic receptor[1]
In Vivo: Vatinoxan alone increases cardiac index and tissue oxygen delivery and has no deleterious adverse effects. Vatinoxan attenuates or prevents dexmedetomidine’s systemic hemodynamic effects in a dose-dependent manner when given simultaneously i.v. but has no effect on the pulmonary outcome in conscious dogs. A 50:1 dose ratio (Vatinoxan:dexmedetomidine) induces the least alterations in cardiovascular function[1]. Vatinoxan dose-dependently attenuates the bradycardia associated with dexmedetomidine, and shortens the sedative effect without altering its quality. Vatinoxan may be useful in attenuating reductions in heart rate in conscious catsadministered dexmedetomidine[2].

Name: GLX351322, CAS: 835598-94-2, stock 9.6g, assay 98.8%, MWt: 431.51, Formula: C21H25N3O5S, Solubility: DMSO : 20 mg/mL (46.35 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: NADPH Oxidase, Biological_Activity: GLX351322 is an inhibitor of NADPH oxidase 4 (Nox4), and inhibits hydrogen peroxide production from NOX4-overexpressing cells with an IC50 of 5 μM.
IC50 & Target: IC50: 5 μ M (NOX4, cell assay), 40 μM (NOX2, cell assay)[1]
In Vitro: GLX351322 is an inhibitor of NADPH oxidase 4, and inhibits hydrogen peroxide production from NOX4-overexpressing cells with an IC50 of 5 μM. GLX351322 shows weak activity against NOX2 in hPBMC cells (IC50, 40 μM).
In Vivo: GLX351322 (3.8 mg/kg/day, p.o.) ameliorates HFD-induced hyperglycemia in mice[1].

Name: Mitoquinone MitoQ; MitoQ10, CAS: 444890-41-9, stock 28.5g, assay 98.7%, MWt: 583.72, Formula: C37H44O4P, Solubility: 10 mM in DMSO, Clinical_Informat: Phase 4, Pathway: Metabolic Enzyme/Protease;NF-κB;Immunology/Inflammation, Target: Reactive Oxygen Species;Reactive Oxygen Species;Reactive Oxygen Species, Biological_Activity: Mitoquinone (MitoQ; MitoQ10) is a TPP-based, mitochondrially targeted antioxidant in order to protect against oxidative damage[1].
In Vitro: Mitoquinone (MitoQ) is a mitochondria-targeted antioxidant.The optimal doses for Mitoquinone (MitoQ) and DecylTPP treatment are selected from dose-response experiments during 4-h cold storage (CS). The potential protective benefits of Mitoquinone treatment against CS injury are tested initially using MitoSOX Red, a mitochondrial-targeted fluorescent dye that measures mitochondrial superoxide generation. Normal rat kidney (NRK) cells exposed to CS result in a ~2-fold increase in fluorescence due to mitochondrial superoxide compared with untreated cells. Mitoquinone offers significant protection against CS-induced mitochondrial superoxide generation; whereas the control compound DecylTPP does not offer any protection. Mitoquinone treatment markedly decreases mitochondrial superoxide generation, whereas kidneys treated with DecylTPP have comparable levels of mitochondrial superoxide to kidneys exposed to CS alone[1].
In Vivo: Mitoquinone (MitoQ) treatment significantly reduces pancreatic oedema and neutrophil infiltration. MitoQ dose-dependently increases serum amylase with an approximate doubling at the higher dose. MitoQ treatment nearly doubles lung MPO activity induced by Caerulein with a significant increase of serum IL-6 levels also evident at 10 mg/kg (dose 1)[2].

Name: BW-A 78U, CAS: 101155-02-6, stock 8.5g, assay 98.3%, MWt: 257.27, Formula: C13H12FN5, Solubility: DMSO : 150 mg/mL (583.05 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Phosphodiesterase (PDE), Biological_Activity: BW-A 78U is a PDE4 inhibitor with an IC50 of 3 μM.
IC50 & Target: IC50: 3 μM (PDE4)[1]
In Vitro: BW-A 78U is a PDE4 inhibitor with an IC50 of 3 μM. BW-A 78U fails to significantly inhibit arachidonate release. BW-A 78U is ineffective to inhibit the lipopolysaccharide (LPS)-induced TNF-α release[1].

Name: Enecadin, CAS: 259525-01-4, stock 38.2g, assay 98.2%, MWt: 357.46, Formula: C21H28FN3O, Solubility: 10 mM in DMSO, Clinical_Informat: Phase 2, Pathway: Others, Target: Others, Biological_Activity: Enecadin is a neuroprotective agent extracted from patent US 8623823 B2.
In Vitro: Enecadin is a neuroprotective agent which can be useful for the treatment of stroke or other cerebrovascular accident[1].

Name: Pparδ agonist 2, CAS: 870884-12-1, stock 19.3g, assay 98.1%, MWt: 437.44, Formula: C20H18F3N3O3S, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Cell Cycle/DNA Damage, Target: PPAR, Biological_Activity: Pparδ agonist 2 is a PPARδ agonist extracted from patent WO 2016057656 A1.
IC50 & Target: PPARδ[1]

Name: Vibunazole BAY-N-7133, CAS: 80456-55-9, stock 18.5g, assay 98.7%, MWt: 309.79, Formula: C15H20ClN3O2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Anti-infection, Target: Fungal, Biological_Activity: Vibunazole is a new antifungal azole.
In Vitro: Vibunazole is an antifungal azole. Low concentrations of all three drugs inhibit Coccidioides immitis, strain Silveira, in vitro with a descending order of activity ketoconazole>Vibunazole>BAY 1 9139[1].
In Vivo: The untreated, infected mice lost weight initially and progressively, whereas treated mice gain weight after an initial loss with Vibunazole (all doses), BAY 1 9139 and ketoconazole at 2.5 mg/kg/day. With both Vibunazole and BAY 1 9139, the 5 and 10 mg/kg doses yield serum concentrations exceeding the MICs for the Coccidioides immitis test strain (0.8 and 1.5 μg/mL respectively) for periods in excess of 30 min after injection[1].

Name: Bevenopran CB-5945;ADL-5945, CAS: 676500-67-7, stock 36.7g, assay 98.7%, MWt: 386.44, Formula: C20H26N4O4, Solubility: 10 mM in DMSO, Clinical_Informat: Phase 3, Pathway: GPCR/G Protein;Neuronal Signaling, Target: Opioid Receptor;Opioid Receptor, Biological_Activity: Bevenopran is a peripheral μ-opioid receptor antagonist.
IC50 & Target: μ-opioid receptor[1]
In Vivo: Bevenopran is a peripheral μ-opioid receptor antagonist. Bevenopran is currently under investigation for the treatment of opioid-induced bowel dysfunction (OBD)[1]. Bevenopran tends to increase bowel movement (BM) frequency, especially for 0.1 mg twice daily and 4 mg daily, respectively[1].

Name: Bamaluzole, CAS: 87034-87-5, stock 14.4g, assay 98.7%, MWt: 273.72, Formula: C14H12ClN3O, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Neuronal Signaling;Membrane Transporter/Ion Channel, Target: GABA Receptor;GABA Receptor, Biological_Activity: Bamaluzole is a GABA receptor agonist extracted from patent WO 2012064642 A1.
IC50 & Target: GABA receptor[1]

Name: Timegadine SR1368, CAS: 71079-19-1, stock 30.4g, assay 98.4%, MWt: 365.50, Formula: C20H23N5S, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Immunology/Inflammation, Target: COX, Biological_Activity: Timegadine, a new antiinflammatory agent, is found to be a potent, competitive inhibitor of cyclo-oxygenase (COX) and lipo-oxygenase, with IC50s ranging from 5 nM (washed rabbit platelets) to 20 μM (rat brain) for COX and 100 μM for lipo-oxygenase both in the cytosol fraction of horse platelet homogenates, and in washed rabbit platelets.
IC50 & Target: prostaglandin synthetase, COX, lipo-oxygenase[1]
In Vitro: Timegadine, a new antiinflammatory agent, is found to be a potent, competitive inhibitor of of COX and lipo-oxygenase, with IC50s ranging from 5 nM (washed rabbit platelets) to 20 μM (rat brain) for COX and 100 μM for lipo-oxygenase both in the cytosol fraction of horse platelet homogenates, and in washed rabbit platelets[2].
In Vivo: Timegadine, a new antiinflammatory agent, is found to be a potent, competitive inhibitor of prostaglandin synthetase which also inhibits cyclo-oxygenase (COX) and lipoxygenase. Daily oral doses of 10 to 30 mg/kg of Timegadine significantly inhibit both the primary and secondary lesions of adjuvant arthritis when the treatment is initiated on the day of the disease induction and continues for 28 days. Timegadine is able specifically to prevent the development of the swelling of the non-injected paw until 28 days after the adjuvant injection when administered for 5 days prior to and 5 days after the induction of the disease, in analogy with the effect of cyclophosphamide[1].

Name: Diflumidone R807, CAS: 22736-85-2, stock 25.7g, assay 98.9%, MWt: 311.30, Formula: C14H11F2NO3S, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Diflumidone is a non-steroidal antiinflammatory drug.

Name: Ancarolol, CAS: 75748-50-4, stock 27g, assay 98.8%, MWt: 332.39, Formula: C18H24N2O4, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein;Neuronal Signaling, Target: Adrenergic Receptor;Adrenergic Receptor, Biological_Activity: Ancarolol is a beta-adrenergic blocking agent.
IC50 & Target: Adrenergic receptor

Name: Clozic ICI 55897;Clobuzarit, CAS: 22494-47-9, stock 0.5g, assay 98.8%, MWt: 304.77, Formula: C17H17ClO3, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Clozic is a potential anti-arthritic agent.
In Vitro: Clozic is a potential anti-arthritic agent. Concentrations of Clozic greater than 50 μM cause a dose-dependent decrease in the amount of matrix protein synthesized by RHMC cell cultures. Inhibition of RHMC cell culture growth by Clozic occurs in a dose-dependent manner. The anti-proliferative effect of Clozic on RHMC cell growth is reversible. Lactate dehydrogenase (LDH) levels in media taken from RHMC cell cultures exposed to 500 μM Clozic for 3 days do not significantly differ from LDH levels in control cell culture media[1].

Name: Pentiapine CGS 10746, CAS: 81382-51-6, stock 1.8g, assay 98.8%, MWt: 299.39, Formula: C15H17N5S, Solubility: DMSO : 125 mg/mL (417.52 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein;Neuronal Signaling, Target: Dopamine Receptor;Dopamine Receptor, Biological_Activity: Pentiapine is a novel dopamine release inhibitor.
IC50 & Target: Dopamine receptor[1]
In Vivo: Pentiapine is a novel dopamine release inhibitor.The results show that Pentiapine dose-dependently reduces motor activity of mice. Moreover, Pentiapine dose-dependently reduces morphine-induced hyperactivity. Newman-Keuls post-hoc comparisons indicate that the group receiving morphine plus saline presents more activity than the groups receiving morphine plus 2 (P<0.05), 4, 8, 16, 24 and 32 (P<0.01) mg/kg of Pentiapine. Moreover, the groups receiving morphine plus 0.5, 1 and 2 mg/kg of Pentiapine present more activity than the groups receiving morphine plus 4, 8, 16, 24 and 32 mg/kg of Pentiapine (P<0.01)[1]. 30 mg/kg dose of Pentiapine completely blocks the methylenedioxymethamphetamine (MDMA) conditioned place preference (CPP) and also blocks the establishment of a cocaine CPP[2].

Name: Pirozadil, CAS: 54110-25-7, stock 17.6g, assay 98.4%, MWt: 527.52, Formula: C27H29NO10, Solubility: DMSO : 62.5 mg/mL (118.48 mM; Need ultrasonic); H2O : < 0.1 mg/mL (insoluble), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Pirozadil is a hypolipidemic agent.
In Vivo: Pirozadil is a hypolipidemic agent. Pirozadil's effect on increasing cerebral blood flow is almost equal to that of papaverine, less than that of nicardipine and much greater than that of the other hypolipidemic/antiatherogenic drugs, nicotinic acid and pyridinol carbamate. Pirozadil is also shown to significantly diminish vascular cerebral resistance to a much greater degree than nicotinic acid and pyridinol carbamate[1].

Name: Prifuroline, CAS: 70833-07-7, stock 20.1g, assay 98.1%, MWt: 228.29, Formula: C14H16N2O, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Prifuroline is an antiarrhythmic agent.
In Vivo: Prifuroline is an antiarrhythmic agent. Prifuroline dose-dependently antagonizes the arrhythmogenic action of aconitine in rats, when administered either intravenously (5, 10 or 20 mg/kg) or intraduodenally (10, 20 or 50 mg/kg). Prifuroline also diminishes ventricular susceptibility to electrical stimulation in open-chest rats. The arrhythmias induced in dogs by coronary artery ligation are markedly antagonized by Prifuroline after doses of 5 and 10 mg/kg i.v. or 30 mg/kg intraduodenally. The duration of its antiarrhythmic activity in this model of arrhythmias in conscious dogs is much longer after intraduodenal than after i.v. administration[1].

Name: Pirazolac ZK-76604, CAS: 71002-09-0, stock 15g, assay 98.3%, MWt: 330.74, Formula: C17H12ClFN2O2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Pirazolac is a non-steroidal anti-inflammatory drug.
In Vitro: Pirazolac is a non-steroidal anti-inflammatory drug. Pirazolac concentration-relatedly inhibits the accumulation of prostanoids in incubates of human gastric mucosa, but this inhibition is less than that by indomethacin and other commonly used non-steroidal anti-inflammatory drugs. This difference may explain the claim that Pirazolac is less damaging to the stomach[1].

Name: ICI 211965 ZM-211965, CAS: 129424-08-4, stock 8.7g, assay 98%, MWt: 389.51, Formula: C24H23NO2S, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Lipoxygenase, Biological_Activity: ICI 211965 (ZM-211965) is a selective and orally potent 5-Lipoxygenase (5-LPO) inhibitor.
IC50 & Target: 5-LPO[1]
In Vitro: ICI 211965 (ZM-211965) is a selective and orally potent 5-Lipoxygenase (5-LPO) inhibitor. ICI 211965 reduces the leakage of lactate dehydrogenase (LD) and lipid peroxidation at concentrations related to its antioxidative effect and not to its 5-1ipoxygenase-inhibiting effect[1].

Name: Mepixanox Pimexone, CAS: 17854-59-0, stock 13.2g, assay 98.4%, MWt: 323.39, Formula: C20H21NO3, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Mepixanox (Pimexone) is an analeptic drug used in respiratory and cardiorespiratory insufficiency.

Name: RGH-5526 GYKI-11679, CAS: 69579-13-1, stock 31g, assay 98.9%, MWt: 335.40, Formula: C16H25N5O3, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: RGH-5526 (GYKI-11679) is a new antihypertensive agent.
In Vivo: RGH-5526 (GYKI-11679) is a new antihypertensive agent. Results show a sharp (61%) reduction in the hypothalamic Noradrenaline (NA) level 2 h after the administration of 10 mg/kg of RGH-5526, and this effect lasts for 4 to 6 h. It is demonstrated that RGH-5526 exerts a greater NA lowering effect in the hypothalamus than in the periphery. RGH-5526 does not influence the hypothalamic monoamine oxidase (MAO)-activity following prolonged treatment[1].

Name: Beperidium iodide SX 810, CAS: 86434-57-3, stock 26.8g, assay 98.4%, MWt: 527.44, Formula: C23H34IN3O3, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Neuronal Signaling;GPCR/G Protein, Target: mAChR;mAChR, Biological_Activity: Beperidium iodide shows a competitive antagonistic effect against acetylcholine receptor with a pA2 of 7.93.
IC50 & Target: pA2: 7.93 (Acetylcholine receptor)[1]

Name: 48740 RP RP-55778, CAS: 93363-11-2, stock 3.1g, assay 98.4%, MWt: 245.30, Formula: C12H11N3OS, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: 48740 RP (RP-55778) is a platelet-activating factor (PAF) antagonist.
IC50 & Target: PAF[1]
In Vivo: 48740 RP (RP-55778) is a platelet-activating factor (PAF) antagonist. In animals treated with 48740 RP only, the number of platelets is increased at a time corresponding to 2 and 4 h after the exposure to lipopolysaccharide (LPS) and the number of eosinophils is also slightly increased. Treatment with 48740 RP in combination with the LPS exposure does not influence the increase in neutrophils seen 2 and 4 h after exposure. At 24 h the increase in the number of neutrophils is about half that in control animals. No effects are found on the LPS-induced increase in number of platelets. In animals pretreated with 48740 RP, there is a significant reduction in capillary permeability[1].

Name: Darenzepine, CAS: 84629-61-8, stock 23.2g, assay 98.3%, MWt: 347.41, Formula: C21H21N3O2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Neuronal Signaling;GPCR/G Protein, Target: mAChR;mAChR, Biological_Activity: Darenzepine is a muscarinic receptor inhibitor extracted from patent US 20170095465 A1.
IC50 & Target: muscarinic receptor[1]
In Vitro: Darenzepine is a muscarinic receptor inhibitor which is useful for the treatment of CNS disorders[1].

Name: Ipenoxazone MLV-6976;NC-1200, CAS: 104454-71-9, stock 19.2g, assay 98.4%, MWt: 358.52, Formula: C22H34N2O2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Ipenoxazone is a potent and centrally acting muscle relaxant.
In Vivo: Ipenoxazone is a potent and centrally acting muscle relaxant[1]. An intravenous injection of 2 mg/kg Ipenoxazone causes a reduction of electromyographic activity which reaches a maximum within 3 min after the injection. Within 1 min after the injection of Ipenoxazone at a dose of 4 mg/kg, the blood pressure changes from a control level of 138±9 mmHg to a minimum level of 98±9 mmHg (n=6) but it rapidly returns to the control level within 1 to 2 min, while the rigidity is still reduced significantly at that time. High doses (greater than 30 mg/kg i.p.) of Ipenoxazone produces a transient and dose-dependent sedation in almost all mice about 5 min after its administration[2].

Name: RP 54275 2-Octadecyl-1H-indole-5-carboxylic acid, CAS: 81364-78-5, stock 39.2g, assay 98.5%, MWt: 413.64, Formula: C27H43NO2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: RP 54275 (2-Octadecyl-1H-indole-5-carboxylic acid) is a novel hypocholesterolaemic drug.

Name: CI-943 (±)-CI-943, CAS: 89239-35-0, stock 34.3g, assay 98.1%, MWt: 231.30, Formula: C12H17N5, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: CI-943 is a potential antipsychotic agent.

Name: TOK-8801, CAS: 105963-46-0, stock 39.4g, assay 98.1%, MWt: 315.43, Formula: C17H21N3OS, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: TOK-8801 is a synthesized dihydroimidazothiazole carboxamide and is under development as an immunomodulator.
In Vitro: TOK-8801 is a synthesized dihydroimidazothiazole carboxamide and is under development as an immunomodulator. TOK-8801 augments the in vitro anti-SRBC PFC response of murine splenocytes in a bell-shaped manner. The stimulatory effect of TOK-8801 is observed at concentrations of 2.5×10-7 to 2.5×10-5 M and is diminished at 10-4 M. The cell-viability is not altered during the culture with TOK-8801 at any doses used in this experiment (10-7 to 10-4 M). TOK-8801 enhances the 3H-TdR uptake of these responses in a bell-shaped manner, and effective concentrations of TOK-8801 are 10-7 to 10-5 M[1].
In Vivo: The anti-SRBC PFC response per spleen, which is prominently lowered by restraint-stress (P<0.05), is significantly restored by the administration of TOK-8801 (0.5 mg/kg, P<0.05). The number of total splenic lymphocytes in restraint-stress is decreased, but there are no significant changes in the number of total splenic lymphocytes by the treatment with TOK-8801[1]. When TOK-8801 is administered orally at doses of 0.1 to 10 mg/kg, the number of plaque forming cell (PFC) significantly decreases or tends to decrease. Treatment of TOK-8801 at doses of 0.1 to 1 mg/kg causes significant suppression in the delayed-type hypersensitivity (DTH) reaction induced in high responder[2].

Name: SDZ-MKS 492 MKS 492, CAS: 114606-56-3, stock 17.3g, assay 98.7%, MWt: 433.46, Formula: C20H27N5O6, Solubility: DMSO : 250 mg/mL (576.75 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Phosphodiesterase (PDE), Biological_Activity: SDZ-MKS 492 (MKS 492) is a selective type III isozyme inhibitor of cyclic nucleotide phosphodiesterase, effective in allergic bronchoconstriction and platelet activating factor (PAF) or LTB4-induced inflammatory reactions in animals[1].

Name: AP521, CAS: 151227-08-6, stock 3.2g, assay 98.4%, MWt: 402.89, Formula: C20H19ClN2O3S, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Neuronal Signaling;GPCR/G Protein, Target: 5-HT Receptor;5-HT Receptor, Biological_Activity: AP521 is an agonist of human 5-HT1A receptor with an IC50 of 94 nM.
IC50 & Target: IC50: 94 nM (5-HT1A (human))[1]
In Vitro: AP521 is an agonist of human 5-HT1A receptor with IC50s of 135, 94, 254, 5530, 418, 422 and 198 nM for 5-HT1A (rat), 5-HT1A (human), 5-HT1B (rat), 5-HT1B (human), 5-HT1D (human), 5-HT5a (human) and 5-HT7 (rat), respectively. AP521 also decreases the forskolin-induced cAMP accumulation from 10 nM to 10 μM[1].
In Vivo: AP521 significantly increases the number of shock acceptances [F(5,105)=4.46, P<0.01] at doses between 0.5 to 10 mg/kg. Oral administration of AP521 at 3 and 10 mg/kg significantly decreases freezing time [F(3,60)=2.89, P<0.05]. AP521 significantly increases the time spent on the open arms by approximately 2-fold as compare to the vehicle treated group [F(3, 36)=4.21, P<0.05 for AP521]. The anxiolytic-like effect of AP521 appears to be dose-related. AP521 significantly increases the extracellular 5-HT level of the medial prefrontal cortex (mPFC) at 10 mg/kg from 0.5 to 1 h after administration. AP521 at 3 mg/kg tends to increase the extracellular 5-HT level, however, this increase is not significant[1].

Name: TAK-778, CAS: 180185-61-9, stock 25.9g, assay 98.1%, MWt: 505.52, Formula: C24H28NO7PS, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: TAK-778 is a derivative of ipriflavone and has been shown to induce bone growth in in vitro and in vivo models.
In Vitro: TAK-778 is a derivative of ipriflavone and has been shown to induce bone growth in in vitro and in vivo models.
Continuous treatment with TAK-778 (10 μM) for 1 to 21 days results in an increase in the area of mineralized nodules. TAK-778 at concentrations of 1 μM and higher significantly stimulates the activity of cellular Alkaline phosphatase (ALP). TAK-778 increases slightly but significantly the DNA content of the cells at the confluence stage. Treatment with TAK-778 also results in dose-dependent increases in the amount of soluble collagen and osteocalcin secreted into culture medium from days 5 to 7. TAK-778 enhances the secretion of both TGF-β and IGF-I at every time point during the 21 days of culture. Treatment of the cells with TAK-778 does not induce ALP activity, but does result in a dose-dependent increase in the saturated cell density. TAK-778 at a concentration of 10 μM significantly reduces the saturated cell density[2].
In Vivo: Treatment with a single local application of TAK-778/PLGA-MC (0.2 to 5 mg/site) results in a dose-dependent increase in the radio-opaque area formed in the defect. Histological studies show the defect area is occupied by a bony bridge and the newly-formed radio-opaque area corresponds to a calcified bone containing bone marrow cavities surrounded by thick osteoid seams with cuboidal osteoblasts. There is no significant difference in either of the indices between placebo- or TAK-778/PLGA-MC-treated skulls. Two months after the operation, the TAK-778/PLGA-MC pellets induce radiological osseous union across the defects[2]. Oral treatment of OVX rats with TAK-778 causes a more pronounced increase in bone mineral density (BMD) of the lumbar vertebrae compare to vehicle controls[3].

Name: 5-HT4 antagonist 1, CAS: 261766-73-8, stock 8.2g, assay 98.1%, MWt: 480.62, Formula: C23H36N4O5S, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Neuronal Signaling;GPCR/G Protein, Target: 5-HT Receptor;5-HT Receptor, Biological_Activity: 5-HT4 antagonist 1 is a 5-HT4 receptor antagonist with a pKi of 9.6.
IC50 & Target: pKI: 9.6 (5-HT4 receptor)[1]
In Vitro: 5-HT4 antagonist 1 (compound 6b) is a 5-HT4 receptor antagonist with a pKi of 9.6.
In Vivo: 5-HT4 antagonist 1 (compound 6b) demonstrates good exposure and prolongs t1/2 in other species, including the mouse (t1/2 7 h), rat (t1/2 12 h) and mini-pig (t1/2 21 h). In Phase I clinical trial, it is found that 5-HT4 antagonist 1 has good oral bioavailability with a steady state plasma t1/2 of >100 h[1].

Name: PRX933 hydrochloride GW876167 hydrochloride;BVT-933 hydrochloride, CAS: 639029-42-8, stock 15.2g, assay 98.6%, MWt: 351.83, Formula: C16H22ClN5O2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Neuronal Signaling;GPCR/G Protein, Target: 5-HT Receptor;5-HT Receptor, Biological_Activity: PRX933 hydrochloride is a 5-HT2c receptor agonist extracted from patent WO 2014140631 A1.
IC50 & Target: 5-HT2c receptor[1]
In Vitro: PRX933 hydrochloride is a 5-HT2c receptor agonist which is useful for the acute treatment of hypertension.

Name: DW-1350, CAS: 491577-61-8, stock 23.4g, assay 98.7%, MWt: 453.60, Formula: C25H31N3O3S, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein, Target: Leukotriene Receptor, Biological_Activity: DW-1350 is a LTB4 receptor antagonist.
IC50 & Target: LTB4 receptor[1]
In Vitro: DW-1350 is a LTB4 receptor antagonist. DW-1350 shows inhibitory effects against osteoclast in terms of differentiation, formation, fusion and bone absorption[1].

Name: W-2429 NSC294836, CAS: 37795-69-0, stock 26.4g, assay 98.7%, MWt: 188.18, Formula: C10H8N2O2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: W-2429 is a non-narcotic analgesic agent.
In Vivo: W-2429 is a non-narcotic analgesic agent. Treatment with W-2429 is well tolerated by rats as well as dogs. In the dog, the only signs of toxicity observed are decreased appetite and salivation at 100 mg/kg/day W-2429. No other significant evidence of physical, chemical, gross or histopathologic change is observed[1].

Name: PF-4878691 3M-852A, CAS: 532959-63-0, stock 14.4g, assay 98.8%, MWt: 361.46, Formula: C17H23N5O2S, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Immunology/Inflammation, Target: Toll-like Receptor (TLR), Biological_Activity: PF-4878691 (3M-852A) is a potent, orally active, and selective Toll-like receptor 7 (TLR7) agonist modelled to dissociate its antiviral and inflammatory activities[1][2].
IC50 & Target: TLR7[1]

Name: L-Threonine derivative-1, CAS: 852055-88-0, stock 17.9g, assay 98.7%, MWt: 281.26, Formula: C13H15NO6, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: L-Threonine derivative-1 is a acetylsalicylic-L-threonine ester extracted from patent US 20060287244 A1.

Name: CX-157, CAS: 205187-53-7, stock 30.9g, assay 98.3%, MWt: 348.27, Formula: C14H8F4O4S, Solubility: 10 mM in DMSO, Clinical_Informat: Phase 2, Pathway: Neuronal Signaling, Target: Monoamine Oxidase, Biological_Activity: CX-157 is a reversible inhibitor of monoamine oxidase-A (MAO-A) with an EC50 of 19.3 ng/mL.
IC50 & Target: EC50: 19.3 ng/mL (MAO-A)[1]
In Vivo: CX-157 is a reversible inhibitor of monoamine oxidase-A (MAO-A) with an EC50 of 19.3 ng/mL. CX-157 is an investigational compound currently in development for the treatment of major depressive disorder (MDD). Mechanistic studies in animals have shown that CX-157 acts to inhibit MAO-A activity in a reversible and competitive manner, elevating brain levels of monoamine neurotransmitters[1].

Name: Delpazolid LCB01-0371, CAS: 1219707-39-7, stock 23.2g, assay 98.1%, MWt: 308.31, Formula: C14H17FN4O3, Solubility: DMSO : 30 mg/mL (97.30 mM; Need ultrasonic and warming), Clinical_Informat: Phase 2, Pathway: Anti-infection, Target: Bacterial, Biological_Activity: Delpazolid is a novel oxazolidinone antibiotic agent which can inhibit the growth of MSSA and MRSA with a MIC90 of 2 μg/mL for both of them.
IC50 & Target: MIC90: 2 μg/mL (MSSA), 2 μg/mL (MRSA)[1]
In Vitro: Delpazolid (LCB01-0371), at concentrations of 1×MIC and 2×MIC, has bacteriostatic activity against MSSA and MRSA after 24 h. At concentrations of 4×MIC and 8×MIC, Delpazolid shows bacteriostatic activity, but there is no regrowth at concentrations of 4×MIC and 8×MIC after 24 h of incubation[1]. The survival of M. abscessus is greatly decreased in the presence of Delpazolid (LCB-0371) (MIC50=1.2 μg/mL). Delpazolid dramatically decreases the number of intracellular mycobacteria present at 2 days after infection at concentrations of 0.1, 1, and 10 μg/mL[2].
In Vivo: When administered orally, Delpazolid (LCB01-0371) shows potent protective effects against systemic infections caused by Gram-positive and Gram-negative bacteria. Against infection caused by S. aureus Giorgio (MSSA), the ED50 of Delpazolid is 4.53 mg/kg of body weight. Against S. aureus p125 (MRSA), the ED50 of Delpazolid is 2.96 mg/kg[1]. When Delpazolid (LCB-0371) is administered at 100 mg/kg daily (by gavage), the colony-forming unit (CFU) counts tend to be decreased in the lungs of mice at 7 days after infection[2].

Name: PF-04991532, CAS: 1215197-37-7, stock 12g, assay 98.3%, MWt: 396.36, Formula: C18H19F3N4O3, Solubility: 10 mM in DMSO, Clinical_Informat: Phase 2, Pathway: Metabolic Enzyme/Protease, Target: Glucokinase, Biological_Activity: PF-04991532 is a potent, hepatoselective glucokinase activator with EC50s of 80 and 100 nM in human and rat, respectively.
IC50 & Target: EC50: 80 nM (glucokinase in human), 100 nM (glucokinase in rat)[1]
In Vitro: PF-04991532 is a potent, hepatoselective glucokinase activator with EC50s of 80 nM in human and 100 nM in rat and also a Phase 2 clinical candidate. Mechanistic experiments conducted in freshly isolated primary rat hepatocytes treated for 1 hour with PF-04991532 show increased 2-[14C]-deoxyglucose uptake (EC50 =1.261 µM) and increased glucose oxidation (EC50=5.769 µM). Additionally, PF-04991532 decreases the production of glucose from 1-[14C]-lactate in a dose dependent manner (EC50 =0.626 µM). In isolated rat hepatocytes, PF-04991532 increases the expression of G6Pase compare to cells treated only with 100 nM glucagon, and the greatest increase in G6Pase mRNA expression is in the presence of 25 mM glucose, 100 nM glucagon and PF-04991532[1].
In Vivo: A single dose of PF-04991532 increases the glucose infusion rate in order to maintain hyperglycemia. Despite the elevations in plasma triglycerides, surprisingly, hepatic triglycerides in rats dosed with 19 days of PF-04991532 are identical to vehicle treated GK rats. In an additional cohort treated for 28 days, identical hepatic lipid concentrations are observed between vehicle and rats dosed with PF-04991532 (Vehicle: 9.89±0.31; PF-04991532 100 mg/kg: 9.91±0.31). In rats treated with PF-04991532, there is increased expression of lipogenic gene expression such as acetyl-CoA carboxylase (ACC), ATP citrate lyase (ACLY), and fatty acid synthase (FAS)[1].

Name: BACE1-IN-1, CAS: 1310347-50-2, stock 7.9g, assay 98.8%, MWt: 389.33, Formula: C18H14F3N5O2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Neuronal Signaling, Target: Beta-secretase, Biological_Activity: BACE1-IN-1 is a potent and highly brain penetrant BACE1 inhibitor with IC50s of 32 and 47 nM for human BACE1 and BACE2, respectively.
IC50 & Target: IC50: 32 nM (human BACE1), 47 nM (human BACE2)[1]

Name: GSK2239633A, CAS: 1240516-71-5, stock 35.7g, assay 98.6%, MWt: 549.06, Formula: C24H25ClN4O5S2, Solubility: DMSO : ≥ 250 mg/mL (455.32 mM), Clinical_Informat: No Development Reported, Pathway: Immunology/Inflammation;GPCR/G Protein, Target: CCR;CCR, Biological_Activity: GSK2239633A is a CC-chemokine receptor 4 (CCR4) antagonist, which inhibits the binding of [125I]-TARC to human CCR4 with a pIC50 of 7.96 ± 0.11.
IC50 & Target: CCR4[1]
In Vitro: The GSK2239633A is an allosteric antagonist of human CCR4. GSK2239633A inhibits the binding of [125I]-TARC to human CCR4 with a pIC50 of 7.96±0.11 and also inhibits thymus- and activation-regulated chemokine-induced (TARC)-induced increases in the F-actin content of isolated human CD4+ CCR4+ T-cells with a pA2 of 7.11±0.29[1]. The effect of GSK2239633A (Compound 3) on CCL17-induced increases in the F-actin content of human CD4+ CCR4+ T cells is measured. The pEC50 value is 8.79±0.22[2].
In Vivo: Following intravenous dosing, plasma GSK2239633A displays rapid, bi-phasic distribution and slow terminal elimination (t1/2: 13.5 hours), suggesting that GSK2239633A is a low to moderate clearance drug. Following oral dosing, blood levels of GSK2239633A reach Cmax rapidly (median tmax: 1.0-1.5 hours). Estimated GSK2239633A bioavailability is low with a maximum value determined of only 16%[1]. GSK2239633A (Compound 9) demonstrates good pharmacokinetic data in preclinical animal studies (bioavailability in rats and beagle dogs 85% and 97% respectively)[3].

Name: DSM265, CAS: 1282041-94-4, stock 6.6g, assay 98.8%, MWt: 415.33, Formula: C14H12F7N5S, Solubility: H2O : < 0.1 mg/mL (insoluble); DMSO : 50 mg/mL (120.39 mM; Need ultrasonic), Clinical_Informat: Phase 2, Pathway: Anti-infection, Target: Parasite, Biological_Activity: DSM265 is a long-duration inhibitor of P. falciparum dihydroorotate dehydrogenase (PfDHODH) with an IC50 of 8.9 nM. DSM265 can also inhibit the growth of Pf3D7 parasites with an EC50 of 4.3 nM[1][2].
IC50 & Target: IC50: 8.9 nM (PfDHODH)[1] 
EC50: 4.3 nM (P. falciparum 3D7 parasites)[1]
In Vivo: DSM265 (0.5 to 75 mg/kg; Oral administration; twice daily; for 4 days; NOD-scid IL-2Rγnull (NSG) mice) has potent in vivo antimalarial activity with 90% effective dose (ED90) of 3 mg/kg per day (1.5 mg/kg twice daily). The maximum rate of parasite killing occurred at and above a dose of 13 mg/kg per day (6.4 mg/kg twice daily). 
DSM265 has moderate terminal elimination half-life (t1/2) of 2-4 hours for mice (0.5 to 75 mg/kg, oral) [2].

Name: SAR-100842, CAS: 1195941-38-8, stock 16.1g, assay 98.9%, MWt: 445.51, Formula: C27H27NO5, Solubility: DMSO : ≥ 83.3 mg/mL (186.98 mM), Clinical_Informat: Phase 2, Pathway: GPCR/G Protein, Target: LPL Receptor, Biological_Activity: SAR-100842 is a lysophaphatidic acid 1 (LPA1/Edg-2) receptor inhibitor.
IC50 & Target: LPA1/Edg-2 Receptor[1][2]
In Vitro: SAR-100842 (Compound Example 14) is an Edg-2 receptor inhibitor extracted from patent WO2009135590A1, has an IC50 of <0.1 μM[1]. SAR-100842 (SAR100842) is a lysophaphatidic acid receptor 1 (LPA1) inhibitor, which can be used for the treatment of systemic sclerosis and related fibrotic diseases[2]. In LPAR1-based in vitro inhibition of LPA-stimulated Ca2+ flux in a cell based assay, SAR-100842 (SAR100842) has an IC50 of 65 nM; and shows no activity up to 10 μM on LPA2, LPA3 or LPA5 in similar calcium assays. Increasing doses of SAR-100842 do not significantly affect proliferation of either cell line over time. There is a significant decrease in the ability of cells to migrate in a wound healing assay in a dose dependent manner, 64% reduction (p<0.0001) with 5 μM SAR-100842 after 72 hours in MDA-MB-231T and 67% reduction (p<0.0001) with 50 μM SAR-100842 after 48 hours in 4T1-Luc2. In a Boyden chamber assay for motility, 50 μM SAR100842 reduces the migration of MDA-MD-231T cells through a collagen membrane by 1.92-fold (p=0.0004) and 3.15-fold (p<0.0001) to FBS and LPA chemoattractants, respectively. In 4T1-Luc2 cells 50 μM SAR-100842 reduces migration by 10.8-fold (p=0.01) and 13.6-fold (p=0.007) to FBS and LPA, respectively[3].
In Vivo: SAR-100842 (SAR100842) has a half-life of 4.9 h and a Cmax of 5600 ng/mL after a 30 mg/kg oral dosing in mice[3].

Name: LS2265, CAS: 72678-30-9, stock 10.1g, assay 98.9%, MWt: 425.88, Formula: C19H20ClNO6S, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: LS2265 is a taurine derivative of fenofibrate and can induce proliferation of peroxisomes in liver cells of rats.

Name: Amphethinile Amphetinile;CRC 82-07, CAS: 91531-98-5, stock 27.3g, assay 98.3%, MWt: 265.33, Formula: C15H11N3S, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Cell Cycle/DNA Damage;Cytoskeleton, Target: Microtubule/Tubulin;Microtubule/Tubulin, Biological_Activity: Amphethinile is an anti-tubulin agent. The affinity constant for the association (Ka) of Amphethinile with tubulin is 1.3 μM.
IC50 & Target: Ka: 1.3 μM (Tubulin)[1]
In Vitro: Amphethinile shows a remarkable similarity to colchicine in terms of its binding to tubulin and inhibition of microtubular assembly. Amphethinile binds strongly to microtubule protein (Ka=1.3 μM). This interaction has been shown to be capable of inhibiting tubulin assembly, but shows no rapid stimulation of disassembly when added to assembled tubulin. The concentration of amphethinile required to inhibit assembly by 50% (12 μM) is very similar to that for colchicine (11 μM). Amphethinile has been shown to be capable of competing for colchicine binding sites but not for those of the vinca alkaloids. Amphethinile can also be shown to stimulate the GTPase activity of tubulin in a manner similar to that observed for combretastatin A4 and 2-methoxy-5-(2',3',4'-trimethoxyphenyl) tropolone (MTPT)[1]. Amphethinile has been shown to cause a G2/M phase block in the cell cycle. In addition, this agent has been shown to be equally toxic toward parental and daunorubicin-resistant P388 cells. Whereas resistance in this cell line is associated with decreased drug accumulation in the case of daunorubicin, vincristine and vinblastine, this effect is much less pronounced for amphethinile[2].
In Vivo: Pharmacokinetic studies in male mice are undertaken. Area under the curve values (AUC), show that levels of 313 μg/L per hour are attained at doses equivalent to the LD10. The alpha half life is 8 min after a bolus intravenous injection. The beta half life is 100 min and relatively independent of dose level[2].

Name: BMY-25271, CAS: 78441-82-4, stock 36.8g, assay 98.3%, MWt: 329.44, Formula: C12H19N5O2S2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Immunology/Inflammation;GPCR/G Protein;Neuronal Signaling, Target: Histamine Receptor;Histamine Receptor;Histamine Receptor, Biological_Activity: BMY-25271 is a histamine H2 receptor antagonist.
IC50 & Target: Histamine H2 receptor[1]
In Vivo: BMY-25271 is a histamine H2 receptor antagonist. The dose response curves are parallel and oral ED50 values derived from probit analysis are 0.093, 0.97 and 6.9 mg/kg for BMY-25271, ranitidine and cimetidine, respectively. BMY-25271, therefore, is about 10 and 74 times more potent than ranitidine and cimetidine, respectively. Pretreatment with the highest dose of BMY-25271 does not significantly affect the absorption of aspirin or the formation of its major metabolite, salicylic acid[1].

Name: FK-448 Free base, CAS: 85858-76-0, stock 6.3g, assay 98.9%, MWt: 406.52, Formula: C25H30N2O3, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Proteasome, Biological_Activity: FK-448 Free base is an effective and specific inhibitor of chymotrypsin, with an IC50 of 720 nM.
IC50 & Target: IC50: 720 nM (Chymotrypsin)[1]
In Vitro: FK-448 Free base is an effective and specific inhibitor of chymotrypsin, with an IC50 of 720 nM. FK-448 Free base slightly inhibits esterolysis of Trypsin and Thrombin, with IC50s of 780 and 35 μM, respectively, but shows no effects on esterolysis of plasmin, plasma kallikrein or pancreas kallikrein, with IC50s of all >1 mM[1]. FK-448 moderately inhibits hydrolytic activities of cathepsin G with an IC50 of 15 μM[2].
In Vivo: FK-448 (20 mg/kg, i.p.) results in a decrease in the blood glucose level, and inhibits the degradation of insulin by pancreatic enzymes in rats. FK-448 (20 mg/kg, p.o.) also decreases the blood glucose level, and increases plasma IRI level in dogs[2].

Name: FKK, CAS: 78299-79-3, stock 6.8g, assay 98.9%, MWt: 329.23, Formula: C17H17BrN2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: FKK is an indazole derivative and also a novel bronchodilator.
In Vivo: FKK is an indazole derivative and also a novel bronchodilator. FKK (0.1 to 3.0 mg/kg, i.v.) slightly increases respiratory frequency, left ventricular (LV) dp/dt max and myocardial contractile force. A slight increase followed by a decrease is observed in systemic blood pressure and LV systolic pressure. FKK causes direct vasodilation in the coronary, mesenteric and femoral vasculatures, but has no effect on the renal vasculature. It is particularly pertinent that FKK (30 mg/kg, i.d., enough to cause marked bronchodilation), unlike aminophylline (30 mg/kg, i.d.), does not significantly influence the cardiovascular system[1].

Name: Alpha-Solamarine, CAS: 20318-30-3, stock 16.3g, assay 98.7%, MWt: 884.06, Formula: C45H73NO16, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Alpha-Solamarine is a glycoalkaloid isolated from Solanum aculeastrum[1].

Name: Ajmalicine Raubasine, CAS: 483-04-5, stock 32g, assay 98.9%, MWt: 352.43, Formula: C21H24N2O3, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein;Neuronal Signaling;Neuronal Signaling, Target: Adrenergic Receptor;AChE;Adrenergic Receptor, Biological_Activity: Ajmalicine (Raubasine) is found in herbs of Catharanthus roseus, is an antihypertensive drug used in the treatment of high blood pressure, decreases peripheral resistance and blood pressure[1].
Ajmalicine (Raubasine) is an adrenolytic drug which preferentially blocks alpha 1-adrenoceptor than alpha 2-adrenoceptor[2].
Ajmalicine (Raubasine) is an reversible non-competitive nicotine receptor antagonist with an IC50 of 72.3 μM[3].
Ajmalicine (Raubasine) acts preferentially at postsynaptic sites, competitively antagonizes the effect of noradrenaline on postsynaptic alpha-adrenoceptor with a pA2 value of 6.57, blocks the inhibitory effect of clonidine with an pA2 value of 6.2[4].

Name: Edpetiline, CAS: 32685-93-1, stock 9.4g, assay 98.4%, MWt: 591.78, Formula: C33H53NO8, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Edpetiline is a principal alkaloid from P. eduardi. Edpetiline has significant antiinflammatory effects[1].

Name: Mesaconine, CAS: 6792-09-2, stock 0.1g, assay 98.7%, MWt: 485.57, Formula: C24H39NO9, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Mesaconinean, an ingredient from Aconitum carmichaelii Debx., has cardiac effect[1].

Name: Hypaconine, CAS: 63238-68-6, stock 16g, assay 98%, MWt: 469.57, Formula: C24H39NO8, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Hypaconine is a C19-diterpenoid alkaloid isolated from Aconitum and Delphinium spp. Hypaconine exhibits strong cardiac activity[1].

Name: Crassicauline A Crassicaulin A, CAS: 79592-91-9, stock 4.5g, assay 98.5%, MWt: 643.76, Formula: C35H49NO10, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Crassicauline A (Crassicaulin A) is a bioactive alkaloid found in roots of Aconitum carmichaeli. Crassicauline A (Crassicaulin A) possesses feeding deterrent activity against T. castaneum adults with an EC50 of 1134.5 ppm[1][2].

Name: Dihydrocoumarin Hydrocoumarin;Chroman-2-one, CAS: 119-84-6, stock 15.2g, assay 98.6%, MWt: 148.16, Formula: C9H8O2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Epigenetics;Cell Cycle/DNA Damage, Target: Sirtuin;Sirtuin, Biological_Activity: Dihydrocoumarin is a compound found in Melilotus officinalis. Dihydrocoumarin is a yeast Sir2p inhibitor. Dihydrocoumarin also inhibits human SIRT1 and SIRT2 with IC50s of 208 μM and 295 μM, respectively[1].
In Vitro: Dihydrocoumarin induces a concentration-dependent inhibition of SIRT1 (IC50 of 208 μM) in an in vitro enzymatic assay. A decrease in SIRT1 deacetylase activity is observed even at micromolar doses (85±5.8 and 73±13.7% activity at 1.6 μM and 8 μM, respectively). The microtubule SIRT2 deacetylase is also inhibited with a similar dose dependency (IC50 of 295 μM)[1]. 
Dihydrocoumarin (1-5 mM) increases cytotoxicity in the TK6 cell line in a dose-dependent manner following a 24-h exposure. Dihydrocoumarin (1-5 mM) increases apoptosis in a dose-dependent manner in the TK6 cell line at the 6-h time point. A 5-mM dose of Dihydrocoumarin increases apoptosis at the 6-h time point in the TK6 cell line[1]. 
Dihydrocoumarin (1-5 mM) increases p53 lysine 373 and 382 acetylation in a dose-dependent manner in the TK6 cell line following a 24-h exposure period[1].

Name: Epifriedelanol, CAS: 16844-71-6, stock 11.6g, assay 98.8%, MWt: 428.73, Formula: C30H52O, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Epifriedelanol is a triterpenoid isolated from the root bark of Ulmus davidiana, with antitumor activity[1]. Epifriedelanol inhibits cellular senescence in human primary cells[2].

Name: Bayogenin, CAS: 6989-24-8, stock 4.8g, assay 98.2%, MWt: 488.70, Formula: C30H48O5, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Bayogenin is an alfalfa saponin, shows moderate potency of glycogen phosphorylase inhibition[1][2].

Name: Allocryptopine, CAS: 485-91-6, stock 19.5g, assay 98.5%, MWt: 369.41, Formula: C21H23NO5, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Membrane Transporter/Ion Channel, Target: Potassium Channel, Biological_Activity: Allocryptopine, a derivative of tetrahydropalmatine, is extracted from Corydalis decumbens (Thunb.) Pers. Papaveraceae. Allocryptopine has antiarrhythmic effects and potently blocks human ether-a-go-go related gene (hERG) current[1][2].

Name: Dihydroberberine, CAS: 483-15-8, stock 9.4g, assay 98.7%, MWt: 337.37, Formula: C20H19NO4, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease;Cell Cycle/DNA Damage;Membrane Transporter/Ion Channel, Target: HSP;HSP;Potassium Channel, Biological_Activity: Dihydroberberine inhibits human ether-a-go-go-related gene (hERG) channels and remarkably reduces heat shock protein 90 (Hsp90) expression and its interaction with hERG. Dihydroberberine has anti-inflammatory, anti-atherosclerotic, hypolipidemic and antitumor activities[1].

Name: Icariside I Icarisid I, CAS: 56725-99-6, stock 6.3g, assay 98.7%, MWt: 530.52, Formula: C27H30O11, Solubility: DMSO : 75 mg/mL (141.37 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Icariside I is a metabolite of Icarlin, which could regulate bone remodeling and is recognized as an effective agent for the treatment of osteoporosis.

Name: β-Anhydroicaritin, CAS: 38226-86-7, stock 5.1g, assay 98.9%, MWt: 368.38, Formula: C21H20O6, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Immunology/Inflammation, Target: Interleukin Related, Biological_Activity: β-Anhydroicaritin is isolated from Boswellia carterii Birdware, has important biological and pharmacological effects, such as antiosteoporosis, estrogen regulation and antitumor properties[1]</sup.
β-Anhydroicaritin ameliorates the degradation of periodontal tissue and inhibits the synthesis and secretion of TNF-α and MMP-3 in diabetic rats[2]. β-Anhydroicaritin decreases the overproduction of NO, IL-10, TNF-α, MCP-1 and IL-6 in inperitonitis mice. β-Anhydroicaritin inhibits the elevation of intracellular Ca2+, and markedly decreases iNOS protein expression[3].

Name: Isosinensetin, CAS: 17290-70-9, stock 36.5g, assay 98.1%, MWt: 372.37, Formula: C20H20O7, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Membrane Transporter/Ion Channel, Target: P-glycoprotein, Biological_Activity: Isosinensetin, a polymethoxylated flavone extracted from pericarpium citri reticulatae viride, exhibits inhibition on P-glycoprotein (P-gp) in MDR1-MDCKII cells[1][2].
IC50 & Target: P-glycoprotein[2]

Name: 5-O-Demethylnobiletin 5-Demethylnobiletin, CAS: 2174-59-6, stock 34.2g, assay 99%, MWt: 388.37, Formula: C20H20O8, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein;Metabolic Enzyme/Protease, Target: Leukotriene Receptor;Lipoxygenase, Biological_Activity: 5-O-Demethylnobiletin (5-Demethylnobiletin), a polymethoxyflavone isolated from Sideritis tragoriganum, is a direct inhibition of 5-LOX (IC50=0.1 μM), without affecting the expression of COX-2. 5-O-Demethylnobiletin (5-Demethylnobiletin) has anti-inflammatory activity, inhibits leukotriene B (4)(LTB4) formation in rat neutrophils and elastase release in human neutrophils with an IC50 of 0.35 μM[1].
IC50 & Target: IC50: 0.1 μM (Lox 5); 0.35 μM (LTB4) (5-O-Demethylnobiletin)[1]
In Vitro: 5-O-Demethylnobiletin (5-demethylnobiletin) promotes neuritogenesis through the activation of MAPK/ERK-, PKC-, and PKA-dependent signaling pathways[2].

Name: Ailanthone Δ13-Dehydrochaparrinone, CAS: 981-15-7, stock 7.3g, assay 98.7%, MWt: 376.40, Formula: C20H24O7, Solubility: DMSO : 83.3 mg/mL (221.31 mM; Need warming), Clinical_Informat: No Development Reported, Pathway: Others, Target: Androgen Receptor, Biological_Activity: Ailanthone (Δ13-Dehydrochaparrinone) is a potent inhibitor of both full-length androgen receptor (AR) (IC50=69 nM) and constitutively active truncated AR splice variants (AR1-651 IC50=309 nM).
IC50 & Target: IC50: 69 nM (Full-length androgen receptor), 309 nM (AR1-651)[1]
In Vitro: Ailanthone is a potent inhibitor of both full-length AR (AR-FL) and constitutively active truncated AR splice variants (AR-Vs). Ailanthone binds to the co-chaperone protein p23 and prevents AR's interaction with HSP90, thus resulting in the disruption of the AR-chaperone complex followed by ubiquitin/proteasome-mediated degradation of AR as well as other p23 clients including AKT and Cdk4, and downregulates AR and its target genes in PCa cell lines and orthotopic animal tumours. In addition, Ailanthone blocks tumour growth and metastasis of CRPC[1]. Ailanthone has been shown to possess an growth-inhibitory effect against several cancer cell lines including HepG2, Hep3B, R-HepG2, Jurkat, HeLa, MCF-7, MDA-MB-231 and A549 cells. Ailanthone inhibits Huh7 cell growth through the induction of mitochondrion-mediated cell apoptosis and G0/G1 cell cycle arrest. Ailanthone-induced apoptosis is mitochondrion-mediated and involved the PI3K/AKT signaling pathway in Huh7 cells[2].
In Vivo: Not only i.p. administration but also p.o. administration of Ailanthone has excellent efficiency for blocking the growth of CRPC xenografts. In pharmacokinetic studies, Ailanthone exhibits good solubility in water and good bioavailability (>20%). In addition, Ailanthone effectively suppresses CRPC tumour growth, despite not reaching a steady state of plasma drug concentration during the course of treatment[1].

Name: Nerolidol, CAS: 7212-44-4, stock 29.1g, assay 98%, MWt: 222.37, Formula: C15H26O, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Anti-infection;Anti-infection;Anti-infection, Target: Fungal;Bacterial;Parasite, Biological_Activity: Nerolidol is a natural membrane-active sesquiterpene, with antitumor, antibacterial, antifungal and antiparasitic activity[1].

Name: Chasmanine, CAS: 5066-78-4, stock 3.2g, assay 98.6%, MWt: 451.60, Formula: C25H41NO6, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Chasmanine is an alkaloid isolated from the roots of Aconitum crassicaule[1].

Name: Gamma-Mangostin γ-Mangostin, CAS: 31271-07-5, stock 15.9g, assay 98.5%, MWt: 396.43, Formula: C23H24O6, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Neuronal Signaling;GPCR/G Protein, Target: 5-HT Receptor;5-HT Receptor, Biological_Activity: Gamma-Mangostin is a novel competitive 5-hydroxytryptamine 2A (5-HT2A) receptors antagonist, purified from the fruit hull of the medicinal plant Garcinia mangostana. Gamma-Mangostin is a inhibitor of Transthyretin (TTR) fibrillization, it binds to the thyroxine (T4)-binding sites and stabilized the TTR tetramer[2]. Gamma-Mangostin inhibits [3H] spiperone binding to cultured rat aortic myocytes (IC50=3.5 nM) and reduces The perfusion pressure response of rat coronary artery to 5-HT2A (IC50=0.32 µM) [1].
IC50 & Target: 5-hydroxytryptamine 2A (5-HT2A) receptors[1]

Name: Curzerene, CAS: 17910-09-7, stock 10.1g, assay 98.8%, MWt: 216.32, Formula: C15H20O, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Gutathione S-transferase, Biological_Activity: Curzerene is a sesquiterpene is isolated from the rhizome of Curculigo orchioides Gaertn with anti-cancer activity. Curzerene inhibits glutathione S-transferase A1 (GSTA1) mRNA and protein expression. Curzerene induces cell apoptosis[1].
IC50 & Target: GSTA1[1]
In Vitro: Curzerene (0-100 µM; 24-72 hours) indicates that cell inhibition increases in a dose- and time-dependent manner, IC50 to SPC A1 cells at 24, 48, and 72 h was 403.8 μM, 154.8 µM, and 47.01 µM, respectively[1].
Curzerene (0-100 µM; 48 hours) exhibits a higher percentage of apoptotic and necrotic cells than that of the control group in SPC-A1cells[1].
Curzerene(0-100 µM; 48 hours) indicates that the percentage of cells arrested in the G2/M phase increased from 9.26% in the control group cells to 17.57% in the cells treated with the highest dose[1].
Curzerene (6.25-100 µM; 48 hours) decreases the mRNA expression of GSTA1 in SPC A1 cells[1].
Curzerene (6.25-100 µM; 48 hours) decreases the protein expression of GSTA1 in SPC A1 cells[1].

Name: Gibberellic acid Gibberellin A3, CAS: 77-06-5, stock 26.7g, assay 98.4%, MWt: 346.37, Formula: C19H22O6, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Gibberellic Acid is named after a fungus Gibberella fujikuroi . Gibberellic Acid regulates processes of plant development and growth, including seed development and germination, stem and root growth, cell division, and flowering time[1].

Name: Dihydrocurcumin, CAS: 76474-56-1, stock 19.7g, assay 98%, MWt: 370.40, Formula: C21H22O6, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Fatty Acid Synthase (FAS), Biological_Activity: Dihydrocurcumin, a major metabolites of curcumin, reduces lipid accumulation and oxidative stress. Dihydrocurcumin regulates mRNA and protein expression levels of SREBP-1C, PNPLA3 and PPARα, increases protein expression levels of pAKT and PI3K, and reduced the levels of cellular NO and ROS via Nrf2 signaling pathways[1].

Name: Quercetin-3-O-β-D-glucose-7-O-β-D-gentiobiosiden Quercetin-3-O-beta-D-glucose-7-O-beta-D-gentiobioside, CAS: 60778-02-1, stock 32.9g, assay 98.5%, MWt: 788.66, Formula: C33H40O22, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Quercetin-3-O-β-D-glucose-7-O-β-D-gentiobiosiden is a flavonoid from Quercetin.

Name: 3,3'-Di-O-methylellagic acid 3,8-Di-O-methylellagic acid, CAS: 2239-88-5, stock 3.5g, assay 98.6%, MWt: 330.25, Formula: C16H10O8, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: 3,3'-Di-O-methylellagic acid obtained from Euphorbia adenochlora selectively inhibits the formation of acid-fastness in mycobacteria without retardation of their growth. 3,3'-di-O-methylellagic acid as a hepatoprotective compound is apparently due to its antioxidative effect[1][2].

Name: 5,7-Dihydroxychromone, CAS: 31721-94-5, stock 15.7g, assay 98.4%, MWt: 178.14, Formula: C9H6O4, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Epigenetics;Cell Cycle/DNA Damage;Apoptosis;Anti-infection;NF-κB, Target: PARP;PARP;Caspase;Arenavirus;Keap1-Nrf2, Biological_Activity: 5,7-Dihydroxychromone, the extract of Cudrania tricuspidata, activates Nrf2/ARE signal and exerts neuroprotective effects against 6-hydroxydopamine (6-OHDA)-induced oxidative stress and apoptosis. 5,7-Dihydroxychromone inhibits the expression of activated caspase-3 and caspase-9 and cleaved PARP in 6-OHDA-induced SH-SY5Y cells[1].

Name: Sennoside C, CAS: 37271-16-2, stock 26.2g, assay 98.4%, MWt: 848.76, Formula: C42H40O19, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Sennoside C is an anthraquinone glycoside, found in leaves and pods of Senna (Cassia angustifolia)[1].

Name: Sennoside D, CAS: 37271-17-3, stock 34.9g, assay 98.9%, MWt: 848.76, Formula: C42H40O19, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Sennoside D is an anthraquinone glycoside, found in leaves and pods of Senna (Cassia angustifolia)[1].

Name: Fuziline 15α-Hydroxyneoline, CAS: 80665-72-1, stock 19.9g, assay 98.5%, MWt: 453.57, Formula: C24H39NO7, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Fuziline is a alkaloid isolated from the lateral roots of Aconitum carmichaelii[1].
In Vitro: Fuziline shows activity against pentobarbital sodiuminduced cardiomyocytes damage by obviously recovering beating rhythm and increasing the cell viability[1]. 
In Vivo: Fuziline exhibits the mean half-life of 5.93 hours, 6.13 hours and 5.12 hours for 14 mg/kg, 2 4 mg/kg and 4 mg/kg, respectively, by oral administration in rat[2].

Name: (+)-(3R,8S)-Falcarindiol (3R,8S)-Falcarindiol; 3(R),8(S),9(Z)-Falcarindiol, CAS: 225110-25-8, stock 27.1g, assay 98.6%, MWt: 260.37, Formula: C17H24O2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Anti-infection, Target: Bacterial, Biological_Activity: (+)-(3R,8S)-Falcarindiol is a polyacetylene found in carrots, has antimycobacterial activity, with an IC50 of 6 μM and MIC of 24 μM against Mycobacterium tuberculosis H37Ra[1][2]. Antineoplastic and anti-inflammatory activity[2].
IC50 & Target: IC50: 6 μM (Mycobacterium tuberculosis H37Ra)[1]

Name: 3'-Methoxypuerarin, CAS: 117047-07-1, stock 24.9g, assay 98.8%, MWt: 446.40, Formula: C22H22O10, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: 3'-Methoxypuerarin (3'-MOP) is an isoflavone extracted from radix puerariae that shows neuron protection activity.
In Vivo: 3'-Methoxypuerarin increases the number of surviving neurons in the hippocampal CA1 region and markedly reduces the number of apoptotic pyramidal neurons after ischemia/reperfusion injury. 3'-Methoxypuerarin can protect hippocampal neurons against I/R injury by inhibiting apoptosis[1].

Name: 4'-Methoxypuerarin 4'-O-Methylpuerarin, CAS: 92117-94-7, stock 22.4g, assay 98.3%, MWt: 430.40, Formula: C22H22O9, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: 4'-Methoxypuerarin (4'-O-Methylpuerarin), an isoflavone diglycoside, is isolated from Pueraria lobata[1].

Name: 3'-Hydroxypuerarin, CAS: 117060-54-5, stock 19.4g, assay 98.7%, MWt: 432.38, Formula: C21H20O10, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: 3'-Hydroxypuerarin is an isoflavone isolated from the roots of Pueraria lobata (Willd.) Ohwi. 3'-Hydroxypuerarin is a antioxidant, which shows marked ONOO(-), NO•, total ROS scavenging activities[1][2][3].

Name: Triolein, CAS: 122-32-7, stock 25g, assay 98.1%, MWt: 885.43, Formula: C57H104O6, Solubility: DMSO : 125 mg/mL (141.17 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: MMP, Biological_Activity: Triolein is a symmetrical triacylglycerol, reduces MMP-1 upregulation, with strong antioxidant and anti-inflammatory properties[1].

Name: Denudatine, CAS: 26166-37-0, stock 38.4g, assay 98.8%, MWt: 343.50, Formula: C22H33NO2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Denudatine, is primarily isolated from plants of the genera Aconitum and Delphinium[1]. Denudatine has effects on action potential of ventricular fibers and inhibits arrhythmogenic action of aconitine[2].

Name: Caudatin, CAS: 38395-02-7, stock 5.1g, assay 98.8%, MWt: 490.63, Formula: C28H42O7, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Apoptosis, Target: Apoptosis, Biological_Activity: Caudatin is a steroidal cmpound found in Cynanchum auriculatum, causes cell cycle arrest and induces apoptosis, with anti-cancer and antiangiogenic properties[1].

Name: Artemisic acid Qing Hao acid; Artemisinic acid; Arteannuic acid, CAS: 80286-58-4, stock 4.8g, assay 98.3%, MWt: 234.33, Formula: C15H22O2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Artemisinic acid (Qing Hao acid), an amorphane sesquiterpene isolated from Artemisia annua L., possesses a variety of pharmacological activity, such as antimalarial activity, anti-tumor activity, antipyretic effect, antibacterial activity, allelopathy effect and anti-adipogenesis effect[1].

Name: Cucurbitacin D, CAS: 3877-86-9, stock 8.2g, assay 98.4%, MWt: 516.67, Formula: C30H44O7, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease;Cell Cycle/DNA Damage, Target: HSP;HSP, Biological_Activity: Cucurbitacin D is an active component in Cucurbita texana, disrupts interactions between Hsp90 and two co-chaperones, Cdc37 and p23. Cucurbitacin D prevents Hsp90 client (Her2, Raf, Cdk6, pAkt) maturation without induction of the heat shock response. Anti-cancer activity[1].

Name: Cucurbitacin IIb, CAS: 50298-90-3, stock 27.6g, assay 98.8%, MWt: 520.70, Formula: C30H48O7, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Apoptosis, Target: Apoptosis, Biological_Activity: Cucurbitacin IIb is an active component isolated from Hemsleya amabilis, induces apoptosis with anti-inflammatory activity. Cucurbitacin IIb inhibits phosphorylation of STAT3, JNK and Erk1/2, enhances the phosphorylation of IκB and NF-κB (p65), blocks nuclear translocation of NF-κB (p65) and decreases mRNA levels of IκBα and TNF-α[1].

Name: Cucurbitacin IIa Hemslecin A, CAS: 58546-34-2, stock 0.9g, assay 98.8%, MWt: 562.73, Formula: C32H50O8, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Apoptosis;Apoptosis, Target: Apoptosis;Survivin, Biological_Activity: Cucurbitacin IIa is a triterpene isolated from Hemsleya amalils Diels, induces apoptosis of cancer cells, reduces expression of survivin, reduces phospho-Histone H3 and increases cleaved PARP in cancer cells[1].

Name: Gypenoside XLIX, CAS: 94987-08-3, stock 8.6g, assay 98.8%, MWt: 1047.23, Formula: C52H86O21, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Cell Cycle/DNA Damage, Target: PPAR, Biological_Activity: Gypenoside XLIX, a dammarane-type glycoside, is a prominent component of G. pentaphyllum. Gypenoside XLIX is a selective peroxisome proliferator-activated receptor (PPAR)-alpha activator and inhibits cytokine-induced vascular cell adhesion molecule-1 (VCAM-1) overexpression and hyperactivity in human endothelial cells[1].

Name: Theaflavin 3,3'-digallate TF3, CAS: 30462-35-2, stock 3.7g, assay 98.2%, MWt: 868.70, Formula: C43H32O20, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Stem Cell/Wnt;MAPK/ERK Pathway;PI3K/Akt/mTOR;MAPK/ERK Pathway;NF-κB, Target: ERK;ERK;Akt;MEK;NF-κB, Biological_Activity: Theaflavin 3,3'-digallate (TF3), the typical pigment in black tea, is a good antitumor agent. Theaflavin 3,3'-digallate is generally regarded as the effective component for the inhibitory effects against carcinogenesis without adverse side effects by affecting multiple signal transduction pathways, such as upregulating p53 and p21, inhibiting phosphorylation of the cell survival protein Akt and MAPK pathway, downregulation of NF-κB, shifting the ratio between pro-/antiapoptotic proteins. Theaflavin 3,3'-digallate causes a rapid and sustained decrease in phospho-ERK1/2 and -MEK1/2 protein expression. Theaflavin 3,3'-digallate inhibits HCT116 cell growth with an IC50 of 17.26 μM[1].

Name: 5-Methyl-7-methoxyisoflavone, CAS: 82517-12-2, stock 20.1g, assay 98.7%, MWt: 266.29, Formula: C17H14O3, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: 5-Methyl-7-methoxyisoflavone is a sensational, non-steroidal anabolic isoflavone. 5-Methyl-7-methoxyisoflavone shows potency increasing muscle mass and endurance[1].

Name: Bellidifolin, CAS: 2798-25-6, stock 2.1g, assay 98.7%, MWt: 274.23, Formula: C14H10O6, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Anti-infection, Target: HIV, Biological_Activity: Bellidifolin is a xanthone isolated from the stems of Swertia punicea, with hepatoprotective, hypoglycemic, anti-oxidation, anti-inflammatory and antitumor activities[1][2][3]. Bellidifolin also acts as a viral protein R (Vpr) inhibitor[4].

Name: Araloside X, CAS: 344911-90-6, stock 10.5g, assay 98.5%, MWt: 1267.40, Formula: C60H98O28, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Araloside X (Congmunoside X) is a triterpenoid saponin isolated from Aralia elata[1].

Name: Araloside VII Congmunoside VII, CAS: 340982-22-1, stock 25.8g, assay 98.2%, MWt: 1121.26, Formula: C54H88O24, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Araloside VII (Congmunoside VII) is a saponin isolated from leaves of Aralias elate[1].

Name: D-Tetrahydropalmatine, CAS: 3520-14-7, stock 23.7g, assay 98.1%, MWt: 355.43, Formula: C21H25NO4, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein;Neuronal Signaling, Target: Dopamine Receptor;Dopamine Receptor, Biological_Activity: D-Tetrahydropalmatine is an isoquinoline alkaloid, mainly in the genus Corydalis[1]. D-Tetrahydropalmatine is a Dopamine (DA) receptor antagonist with preferential affinity toward the D1 receptors[2]. D-Tetrahydropalmatine is a potent organic cation transporter 1 (OCT1) inhibitor[3].
IC50 & Target: DA[2], OCT1[3]

Name: Veratric acid 3,4-Dimethoxybenzoic acid, CAS: 93-07-2, stock 36.3g, assay 98.5%, MWt: 182.17, Formula: C9H10O4, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Immunology/Inflammation;Metabolic Enzyme/Protease;NF-κB;Immunology/Inflammation, Target: COX;Reactive Oxygen Species;Reactive Oxygen Species;Reactive Oxygen Species, Biological_Activity: Veratric acid (3,4-Dimethoxybenzoic acid) is an orally active phenolic compound derived from vegetables and fruits, has antioxidant[1] and anti-inflammatory activities[3]. Veratric acid also acts as a protective agent against hypertension-associated cardiovascular remodelling[2]. Veratric acid reduces upregulated COX-2 expression, and levels of PGE2, IL-6 after UVB irradiation[3].
IC50 & Target: COX-2[3]
In Vitro: Veratric acid (100, 200 μM) suppresses iNOS expression in LPS-stimulated RAW264.7 cells. Veratric acid (200 μM) inhibits LPS-induced activation of the PI3K/Akt pathway, HAT activation and HDAC3 expression in RAW264.7 cells[1]. 
Veratric Acid (10-100 μg/mL) has anti-inflammatory activity, protects HaCaT cells against UVB-mediated phototoxicity, increases S-phase cells, and prevents UVB-mediated apoptosis[3]. 
Veratric acid reduces upregulated COX-2 expression, and levels of PGE2, IL-6 after UVB irradiation[3].
In Vivo: Veratric acid (40 mg/kg, p.o., b.w.) significantly promotes ventricular function, reduces lipid peroxidation and increases antioxidants in l-NAME-induced hypertensive rats[2].

Name: Methyl gallate Gallincin; NSC 363001, CAS: 99-24-1, stock 38.2g, assay 98.9%, MWt: 184.15, Formula: C8H8O5, Solubility: DMSO : ≥ 160 mg/mL (868.86 mM), Clinical_Informat: No Development Reported, Pathway: Anti-infection;Metabolic Enzyme/Protease;NF-κB;Immunology/Inflammation, Target: Bacterial;Reactive Oxygen Species;Reactive Oxygen Species;Reactive Oxygen Species, Biological_Activity: Methyl gallate is a plant phenolic with antioxidant, anticancer, and anti-inflammatory activities. Methyl gallate also shows bacterial inhibition activity.
IC50 & Target: Bacterial[1]
In Vitro: The growth of A. viscosus is inhibited completely by a low dose of Methyl gallate (MIC=1 mg/mL). S. mutans and . sobrinus show intermediate sensitivity to Methyl gallate (MIC=2-4 mg/mL), whereas the growth of Lactobacillus spp. is inhibited completely at a relatively high concentration (MIC=8 mg/mL)[1]. Methyl gallate, in a concentration of 100 mM, could alleviate lipid peroxidation of the cells exposed to a short-term H2O2 treatment. In addition, Methyl gallate-treated cells could prevent intracellular glutathione (GSH) from being depleted following an exposure of H2O2 (8.0 mM) for a 3 h period[2]. Methyl gallate inhibits Treg cell-suppressive effects on effector CD4+ T cells and Treg migration toward tumor environment. Furthermore, forkhead box P3 (Foxp3) expression is also significantly decreased by methyl gallate[3].

Name: Octyl gallate n-Octyl gallate; Stabilizer GA 8, CAS: 1034-01-1, stock 16.6g, assay 98%, MWt: 282.33, Formula: C15H22O5, Solubility: DMSO : 125 mg/mL (442.74 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Anti-infection;Metabolic Enzyme/Protease;NF-κB;Immunology/Inflammation, Target: Bacterial;Reactive Oxygen Species;Reactive Oxygen Species;Reactive Oxygen Species, Biological_Activity: Octyl gallate (Progallin O) is widely used as a food additive, with antimicrobial and antioxidant activity[1][2]. Octyl gallate (Progallin O) shows selective and sensitive fluorescent property[2].
In Vitro: Octyl gallate has antimicrobial activity over H. pylori, with a minimum inhibitory concentration (MIC) value of 125 µg/mL[1].

Name: Aristolactam I Aristololactam; Aristolactam, CAS: 13395-02-3, stock 22.7g, assay 98.2%, MWt: 293.27, Formula: C17H11NO4, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Apoptosis, Target: Caspase, Biological_Activity: Aristololactam I (AL-I), is the main metabolite of aristolochic acid I (AA-I), participates in the processes that lead to renal damage.
Aristololactam I (AL-I) directly injures renal proximal tubule cells, the cytotoxic potency of AL-I is higher than that of AA-I and that the cytotoxic effects of these molecules are mediated through the induction of apoptosis in a caspase-3-dependent pathway[1].

Name: Hastatoside, CAS: 50816-24-5, stock 25.1g, assay 98.7%, MWt: 404.37, Formula: C17H24O11, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Hastatoside is an iridoid glycoside that is isolated from Verbena officinalis and has a role in promoting sleep[1].
In Vivo: Hastatoside (0.32-0.64 mmol/kg; oral administration; for 9 hours; male rats of the Sprague-Dawley strain) treatment increases the total time of non-rapid eye movement sleep during a 9-h period, with a lag time of about 3-5 h after the administration at 20. 00 hours (lights-off time). Hastatoside also increases the delta activity during non-rapid eye movement sleep[1].

Name: Arteannuin B, CAS: 50906-56-4, stock 8.6g, assay 98.4%, MWt: 248.32, Formula: C15H20O3, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Apoptosis, Target: Ferroptosis, Biological_Activity: Arteannuin B co-occurs with artemisinin, which is the potent antimalarial principle of the Chinese medicinal herb Artemisia annua (Asteraceae)[1].

Name: Calpeptin, CAS: 117591-20-5, stock 39.3g, assay 98.1%, MWt: 362.46, Formula: C20H30N2O4, Solubility: H2O : < 0.1 mg/mL (insoluble); DMSO : ≥ 155 mg/mL (427.63 mM), Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease;Apoptosis;Metabolic Enzyme/Protease, Target: Proteasome;Apoptosis;Cathepsin, Biological_Activity: Calpeptin is a potent, cell penetrating calpain inhibitor, with an ID50 of 40 nM for Calpain I in human platelets[1]. Calpeptin is also an inhibitor of cathepsin K[2].
IC50 & Target: ID50: 40 nM (Calpain I in human platelets)[1]. 
Cthepsin K[2]
In Vitro: Calpeptin (0-100 nM, 24 hours) treatment suppresses the proliferation of both WI38 VA13 and IMR90 cells in a dose-dependent manner. Calpeptin (1000 pg/ml, 24 hours) inhibits IL-6-induced cell proliferation of lung fibroblasts[3].
In Vivo: Calpeptin with Bleo (0.04 mg/mouse, i.p., 3 times weekly, 28 days) administration significantly inhibits the collagen deposition and increases of calpain activity in the NSC-125066 treated mouse lung tissues[3].

Name: SANT-1, CAS: 304909-07-7, stock 15.1g, assay 98.8%, MWt: 373.49, Formula: C23H27N5, Solubility: DMSO : 62.5 mg/mL (167.34 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Stem Cell/Wnt;Stem Cell/Wnt, Target: Hedgehog;Smo, Biological_Activity: SANT-1 is a potent Smo antagonist, inhibits Hedgehog signaling, with IC50s of 20 nM and 30 nM in Shh-LIGHT2 and SmoA1-LIGHT2 assay, respectively[1].
IC50 & Target: IC50: 20 nM (Shh signaling), 30 nM (SmoA1)[1]
In Vitro: SANT-1 is a potent Smo antagonist, binds directly to Smo, and inhibits Hedgehog signaling, with IC50s of 20 nM and 30 nM in Shh-LIGHT2 and SmoA1-LIGHT2 cells, respectively[1]. 
SANT-1 (1 μM, for 24 or 48 hours) decreases the proliferation of medulloblastoma cells[2].

Name: ME0328, CAS: 1445251-22-8, stock 23.3g, assay 98%, MWt: 321.37, Formula: C19H19N3O2, Solubility: H2O : < 0.1 mg/mL (insoluble); DMSO : 75 mg/mL (233.38 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Epigenetics;Cell Cycle/DNA Damage, Target: PARP;PARP, Biological_Activity: ME0328 is a potent and selective ARTD3/PARP3 inhibitor with an IC50 of 0.89±0.28 μM.
IC50 & Target: IC50: 0.89±0.28 μM (ARTD3/PARP3), 6.3±0.6 μM (ARTD1/PARP1), 10.8±4.0 μM (ARTD2/PARP2), 34.3±17.0 μM (ARTD6/TNKS2), 47.3±29.0 μM (ARTD5/TNKS1), 71.3±22.0 μM (ARTD10/PARP10)[1]
In Vitro: ME0328 is a potent and selective inhibitor of ARTD3/PARP3 that is active in cells. In in vitro histone H1 modification assay, ME0328 inhibits the transferase activity of ARTD3 with an IC50 of 0.89±0.28 μM. In human A549 cells, ME0328 and ME0355 (at 10 μM) delay the resolution of γH2AX-containing foci that serve as markers for DNA double strand break repair following γ-irradiation (2 Gy). In silico and in vitro physicochemical and metabolic profiling indicated that ME0328 is soluble, cell permeable, and metabolically stable in human liver microsomes and rat hepatocytes[1].

Name: E 64c, CAS: 76684-89-4, stock 21.7g, assay 98.6%, MWt: 314.38, Formula: C15H26N2O5, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Cathepsin, Biological_Activity: E 64c is a derivative of naturally occurring epoxide inhibitor of cysteine proteases, a Calcium-activated neutral protease (CANP) inhibitor and a very weak irreversible cathepsin C inhibitor.
IC50 & Target: Cysteine proteases[1], CANP[2], Cathepsin C[3].
In Vitro: E-64c, a derivative of naturally occurring epoxide inhibitor of cysteine proteases, with papain; especially with regard to the hydrogen bonding and hydrophobic interactions of the ligands with conserved residues in the catalytic binding site[1]. E 64c (k2/Ki=140±5M-1s-1) is demonstrated to be a lead structure for the development of irreversible cathepsin C inhibitors[3].
In Vivo: The t-1/2 of plasma E-64c is 0.48 hours. The hemodynamic effects of E-64c are absent at this dose. Using two way analysis of variance, the effects of reperfusion (p=0.0016) or E-64c (p=0.0226) per se on infarct size are significant. In comparing Group A with Group B and Group C with Group D, the depletion of CPK in the E-64c treated groups (Groups A and C) is slightly less than in the vehicle-injected groups (Groups B and D). The insufficient effect of E-64c alone may be explained by the early administration and relatively short t-1/2. Since the effectiveness of NCO-700 has been established,6),7) our findings might indicate a small but beneficial effect of E-64c on infarct size and CPK content[2].

Name: ML133 (hydrochloride), CAS: 1222781-70-5, stock 29.5g, assay 98.3%, MWt: 313.82, Formula: C19H20ClNO, Solubility: DMSO : ≥ 125 mg/mL (398.32 mM), Clinical_Informat: No Development Reported, Pathway: Membrane Transporter/Ion Channel, Target: Potassium Channel, Biological_Activity: ML133 hydrochloride is a selective Kir2 family channels inhibitor, with an IC50 of 1.8 μM at pH 7.4 and 290 nM at pH 8.5[1].
IC50 & Target: IC50: 1.8 μM (Kir2 at pH 7.4), 290 nM (Kir2 at pH 8.5)[1].
In Vitro: ML133, which inhibits Kir2.1 with IC50 of 1.8 μM at pH 7.4 and 290 nM at pH 8.5, but exhibits little selectivity against other members of Kir2.x family channels[1]. 
ML133 has no effect on Kir1.1 (IC50 > 300 μM), and displays weak activity for Kir4.1 (76 μM) and Kir7.1 (33 μM), making ML133 the most selective small molecule inhibitor of the Kir family reported to date[1].

Name: Anacardic Acid Hydroginkgolic acid, CAS: 16611-84-0, stock 37.4g, assay 98.9%, MWt: 348.52, Formula: C22H36O3, Solubility: H2O : < 0.1 mg/mL (insoluble); DMSO : 100 mg/mL (286.93 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Epigenetics;Anti-infection;Epigenetics, Target: Epigenetic Reader Domain;Bacterial;Histone Acetyltransferase, Biological_Activity: Anacardic Acid, extracted from cashew nut shell liquid, is a histone acetyltransferase inhibitor, inhibits HAT activity of p300 and PCAF, with IC50s of ∼8.5 μM and ∼5 μM, respectively.
IC50 & Target: IC50: ∼8.5 μM (p300 HAT), ∼5 μM (PCAF)[1]
In Vitro: Anacardic Acid is a histone acetyltransferase, inhibits HAT activity of p300 and PCAF, with IC50s of ∼8.5 μM and ∼5 μM, respectively[1]. Anacardic Acid (300 μM) inhibits mycelial growth. Anacardic Acid (50 μM) induces apoptosis-like characteristics in M. oryzae, and the effect is caspase independent. Anacardic Acid (1-80 μM) leads to loss of mitochondrial potential. Anacardic Acid (1-60 μM) also exhibits antioxidant activity in M. oryzae[3].
In Vivo: Anacardic acid (5 mg/kg, i.p.) attenuates the binding of HATs to the promoter of MEF2A and reverse hyperacetylation of H3K9ac caused by phenylephrine in C57BL/6 mice. Anacardic acid inhibits the level of transcription on MEF2A and cardiac development-related downstream genes, attenuates the protein overexpression of cardiac downstream genes caused by phenylephrine, reverses and attenuates cardiac hypertrophy in the hearts of mice exposed to phenylephrine, and attenuates the left ventricular pressure and improves cardiac function in the cardiac hypertrophy mice[2].

Name: Antihistamine-1, CAS: 1186430-60-3, stock 20g, assay 98.2%, MWt: 389.47, Formula: C23H24FN5, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Immunology/Inflammation;GPCR/G Protein;Metabolic Enzyme/Protease;Membrane Transporter/Ion Channel;Neuronal Signaling, Target: Histamine Receptor;Histamine Receptor;Cytochrome P450;Potassium Channel;Histamine Receptor, Biological_Activity: Antihistamine-1 is a H1-antihistamine (Ki=6.9 nM) with acceptable blood-brain barrier penetration and also an inhibitor of CYP2D6 and hERG channel with IC50s of 5.4 and 0.8 μM, respectively.
IC50 & Target: Ki: 6.9 nM (H1-antihistamine)[1]
IC50: 5.4 μM (CYP2D6), 0.8 μM (hERG channel)[1]
In Vitro: Antihistamine-1 (Compound 2) is a H1-antihistamine (Ki=6.9 nM) with acceptable blood-brain barrier penetration and also an inhibitor of CYP2D6 and hERG channel with IC50s of 5.4 and 0.8 μM, respectively[1].

Name: ICI 153110, CAS: 87164-90-7, stock 32.7g, assay 98.9%, MWt: 201.22, Formula: C11H11N3O, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Phosphodiesterase (PDE), Biological_Activity: ICI 153110 is an orally active phosphodiesterase inhibitor with both vasodilating and inotropic properties which is designed for the treatment of congestive cardiac failure.
IC50 & Target: Phosphodiesterase[1]
In Vivo: ICI 153110 is an orally active phosphodiesterase inhibitor with both vasodilating and inotropic properties which is designed for the treatment of congestive cardiac failure. Fourteen animals have died as a direct or indirect consequence of ICI 153110 administration in the high-dose main test and reversibility groups. In the female rat dosed at 10 mg/kg/day ICI 153110 a mild focal arteritis is characterized by a predominantly and diffusely adventitial infiltration of mixed cells and early formation of fibrous tissue. The two rats dosed at 250 mg/kg/day ICI 153110 die prematurely from intratracheal intubation of dosing solution. Arteries from two further animals (dosed at 5 and 250 mg/kg/day ICI 153110) show minimal focal arteritis with medial necrosis, and medial and adventitial inflammation[1].

Name: Lodelaben SC-39026;Declaben, CAS: 111149-90-7, stock 37.5g, assay 98.9%, MWt: 425.04, Formula: C25H41ClO3, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Elastase, Biological_Activity: Lodelaben is a human neutrophil elastase inhibitor with an IC50 and Ki of 0.5 and 1.5 μM, respectively.
IC50 & Target: IC50: 0.5 μM (elastase)[1]
Ki: 1.5 μM (elastase)[1]
In Vitro: Lodelaben is a human neutrophil elastase inhibitor with an IC50 and Ki of 0.5 and 1.5 μM, respectively. Results indicate that the inhibition of human neutrophil elastase (HNE) by Lodelaben is non-competetive. Lodelaben is not inhibitory at 10 μM with the synthetic substrates or at 5 μM vith Azocoll. Pseudomonas aeruginosa elastase, a metallo-protease is not inhibited by Lodelaben. Cathepsin G activity, however, is inhibited by Lodelaben, with an IC50 of approximately 2.5 μM, with Azocoll as substrate[1].
In Vivo: The mean pulmonary artery pressures of the saline/vehicle and saline/Lodelaben groups are similar, 16.4±1.1 and 17.4±0.9 mm Hg, respectively. Although, mean pulmonary artery pressure in the monocrotaline/vehicle group is 27.5±0.8 mm Hg, treatment of monocrotaline rats with Lodelaben results in significantly lower values (21.00±1.6 mm Hg, p<0.05). Saline/vehicle and saline/Lodelaben rats have only a small percentage of arteries muscularized at the alveolar wall level (1.9±1.4 and 0.4±0.4%, respectively). Treatment of monocrotaline-injected rats with Lodelaben results in a decreased percentage of alveolar wall arteries muscularized (10.0±3.6%)[2].

Name: Nafocare B1 Methylfurylbutyrolactone, CAS: 93135-89-8, stock 15.9g, assay 98.6%, MWt: 256.21, Formula: C11H12O7, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Nafocare B1 is a synthetic immune biological response modifier.

Name: Mivotilate YH439, CAS: 130112-42-4, stock 37g, assay 98.5%, MWt: 330.45, Formula: C12H14N2O3S3, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Immunology/Inflammation, Target: Aryl Hydrocarbon Receptor, Biological_Activity: Mivotilate is a nontoxic, potent activator of the aryl hydrocarbon receptor (AhR), and acts as a hepatoprotective agent.
IC50 & Target: Aryl hydrocarbon receptor[1]
In Vitro: Mivotilate is a nontoxic, potent activator of the aryl hydrocarbon receptor. Mivotilate (YH439) has a novel activation mode that tolerates mutation of histidine 285 to tyrosine[1]. Mivotilate induces cytochromes P4501A1/2 (CYP1A1/2) through the aryl hydrocarbon (Ah) receptor[3].
In Vivo: Mivotilate (YH439, 150 mg/kg, p.o.) reduces CYP2E1-mediated NDMA demethylase activity in rats, but shows no obvious effect on NADPH-dependent P450 oxidoreductase activity. Mivotilate (75-300 mg/kg) rapidly decreases immunoreactive CYP2E1 protein. Mivotilate (150 mg/kg, p.o.) inhibits the transcription of CYP2E1 in rats[2].

Name: NS1652, CAS: 1566-81-0, stock 39.1g, assay 98.9%, MWt: 324.25, Formula: C15H11F3N2O3, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Membrane Transporter/Ion Channel, Target: Chloride Channel, Biological_Activity: NS1652 is a reversible anion conductance inhibitor, blocks chloride channel, with an IC50 of 1.6 μM in human and mouse red blood cells.
IC50 & Target: IC50: 1.6 μM (chloride channel, human and mouse red blood cell)[1]
In Vitro: NS1652 potently inhibits the chloride conductance (IC50, 1.6 μM) in human and mouse red blood cells, but only weakly inhibits VRAC (IC50, 125 μM) in HEK293 cells. NS1652 markedly blocks the NO production with an IC50 of 3.1 μM in BV2 cells. NS1652 also down-regulates iNOS expression at 3 μM, and completely abolishes at 10 μM in BV2 cells[1]. NS1652 (0, 1.0, 3.3, 10, and 20 μM) causes increasing hyperpolarization due to inhibition of the chloride conductance in normal erythrocytes. NS1652 lowers the net KCl loss from deoxygenated sickle cells from about 12 mM cells/h to about 4 mM cells/h. NS1652 (20 μM) completely and reversiblely inhibits the red cell Cl-conductance[2].
In Vivo: NS1652 (50 mg/kg, i.v.) blocks murine erythrocyte Cl- conductance by >90% in mice[2].

Name: OM-189, CAS: 55381-18-5, stock 22.6g, assay 98.4%, MWt: 488.65, Formula: C24H36N6O3S, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Thrombin, Biological_Activity: OM-189 is a selective synthetic thrombin inhibitor.
IC50 & Target: Thrombin[1]

Name: CI-1044 PD-189659, CAS: 197894-84-1, stock 28.6g, assay 98.7%, MWt: 397.43, Formula: C23H19N5O2, Solubility: DMSO : 125 mg/mL (314.52 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Phosphodiesterase (PDE), Biological_Activity: CI-1044 is an orally active PDE4 inhibitor with IC50s of 0.29, 0.08, 0.56, 0.09 μM for PDE4A5, PDE4B2, PDE4C2 and PDE4D3, respectively.
IC50 & Target: IC50: 0.29 μM (PDE4A5), 0.08 μM (PDE4B2), 0.56 μM (PDE4C2), 0.09 μM (PDE4D3)[1]
In Vitro: CI-1044 is an orally active PDE4 inhibitor with IC50s of 0.29, 0.08, 0.56, 0.09 μM for PDE4A5, PDE4B2, PDE4C2 and PDE4D3, respectively. CI-1044 selectively inhibits PDE4 crude extract from U937 cells with an IC50 value of 0.27±0.02 μM being threefold more potent than rolipram (IC50=0.91±0.14) and tenfold less potent than cilomilast (IC50=0.026±0.007) in the same assay. In the presence of PDE4 inhibitors, the production of TNF-α is dose dependently decreased with mean IC50 values from three separate experiments of 0.31±0.05, 0.26±0.05 and 0.11±0.01 μM, for CI-1044, cilomilast and rolipram, respectively[1].
In Vivo: TNF-α production is dose-dependently inhibited by CI-1044, rolipram and cilomilast with ID50s of 0.4, 1.4 and 1.6 mg/kg respectively following single oral administration. Following repeated administration with CI-1044, the ID50 value represents 0.5 mg/kg p.o.. CI-1044 plasma levels increase proportionally with doses ranging between 0.1 and 40 mg/kg p.o. (R2=0.878). CI-1044 dose dependently inhibits the accumulation of eosinophils in Bronchoalveolar lavages (BAL) fluids with an ID50 value of 3.25 mg/kg. A single dose treatment with CI-1044 (10 mg/kg, p.o.) 24, 8, 3 or 1 h before the antigen challenge induces 6, 56, 48 and 79% inhibition in the number of eosinophils in BAL[1].

Name: Sarmazenil Ro 15-3505, CAS: 78771-13-8, stock 20.1g, assay 98.4%, MWt: 319.74, Formula: C15H14ClN3O3, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Neuronal Signaling;Membrane Transporter/Ion Channel, Target: GABA Receptor;GABA Receptor, Biological_Activity: Sarmazenil is a benzodiazepine receptor antagonist.
IC50 & Target: Benzodiazepine receptor[1]

Name: XEN723, CAS: 1072803-08-7, stock 20g, assay 98%, MWt: 425.48, Formula: C21H20FN5O2S, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Stearoyl-CoA Desaturase (SCD), Biological_Activity: XEN723 is a novel and potent thiazolylimidazolidinone inhibitor of Stearoyl-CoA Desaturase (SCD1) with IC50s of 45 and 524 nM in mouse and HepG2 cell, respectively.
IC50 & Target: IC50: 45 nM (SCD1 in Mouse), 524 nM (SCD1 in HepG2 cell)[1]
In Vitro: XEN723 is a novel and potent thiazolylimidazolidinone inhibitor of Stearoyl-CoA Desaturase (SCD1) with IC50s of 45 and 524 nM in mouse and HepG2 cell, respectively. XEN723 demonstrates an improvement in SCD1 in vitro potency of more than 560-fold compare to the original high throughput screen (HTS) hit[1].

Name: Spirofylline, CAS: 98204-48-9, stock 16.6g, assay 98.3%, MWt: 480.52, Formula: C24H28N6O5, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Spirofylline is a bronchodilator, which can be used to treat asthma and bronchitis and emphysema.

Name: TA-7552, CAS: 104756-72-1, stock 24.2g, assay 98%, MWt: 486.47, Formula: C25H26O10, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: TA-7552 is a potent cholesterol-lowering agent.
In Vivo: TA-7552 is a potent cholesterol-lowering agent. When TA-7552 is mixed with unsupplemented CLEA CE-2 powder in a concentration of 0.05% and administered to rats for 7 days, TA-7552 does not reduce the normal level of serum cholesterol. The hypocholesterolemic effect of TA-7552 is apparent at the lowest concentration (0.01%) of the drug in the diet, corresponding to a daily dose of ~10 mg/kg body weight, and maximal at the highest concentration of 0.2% TA-7552, lowering serum total cholesterol by 72% while elevating serum HDL cholesterol by 88%. TA-7552 also dose dependently suppresses this rise of hepatic cholesterol, and its lowering rate at the maximal dose is 90%[1].

Name: TAK-024, CAS: 186971-69-7, stock 33.9g, assay 98.3%, MWt: 594.62, Formula: C27H34N10O6, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein, Target: P2Y Receptor, Biological_Activity: TAK-024 is a platelet inhibitor with IC50s of 31, 79 and 51 nM in human, monkey and guinea pig, respectively.
IC50 & Target: IC50: 31 nM (human platelet), 79 nM (monkey platelet), 51 nM (pig platelet)[1]
In Vitro: TAK-024 is a platelet inhibitor with IC50s of 31, 79 and 51 nM in human, monkey and guinea pig, respectively. In a preliminary experiment, the IC50 value of TAK-024 in the heparinized blood sample is 230 nM, 4.5-fold less potent than that in the citrated physiological blood sample. The ID50 value of TAK-024 on ex vivo ADP-induced platelet aggregation in guinea pigs is 0.18 μg/kg/min, the dissociation ratio of TAK-024 is found to be 32[1].
In Vivo: Intravenous infusion of TAK-024 (compound 12c) at 1.6 μg/mL/min completely prevents arterial thrombus formation induced by endothelial injury in guinea pigs. Results demonstrate the inhibitory effects of TAK-024 on the carotid thrombosis induced by balloon injury in guinea pigs and the ID50 value is 0.73 μg/kg/min. A single dose of TAK-024 at 100 μg/kg iv produces almost complete inhibition for 120 min, and about 40% inhibition is observed after 240 min. Dose-dependent inhibition of platelet aggregation is achieved with a single iv dose of 30 to 100 μg/kg of TAK-024[1].

Name: Tiodazosin BL-5111, CAS: 66969-81-1, stock 37g, assay 98.8%, MWt: 431.47, Formula: C18H21N7O4S, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein;Neuronal Signaling, Target: Adrenergic Receptor;Adrenergic Receptor, Biological_Activity: Tiodazosin is a potent competitive postsynaptic alpha adrenergic receptor antagonist.
IC50 & Target: alpha adrenergic receptor[1]
In Vitro: Tiodazosin is a potent competitive postsynaptic alpha adrenergic receptor antagonist. In the mesenteric artery, Tiodazosin produces a parallel shift to the right in the concentration response curves to norepinephrine. A Schild plot constructed from two concentrations of Tiodazosin results in a pA2 value of 8.66 and a slope equal to -0.99. Tiodazosin inhibits contraction to norepinephrine in the portal vein and the inhibition results in a nonparallel inhibition of the norepinephrine concentration-response curve with a marked depression of maximal norepinephrine response[1].

Name: Sodium Channel inhibitor 2, CAS: 653573-60-5, stock 3.4g, assay 98.8%, MWt: 466.40, Formula: C26H25Cl2N3O, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Membrane Transporter/Ion Channel, Target: Sodium Channel, Biological_Activity: Sodium Channel inhibitor 2 is a sodium channel blocker extracted from patent WO 2004011439 A2, compound 3c.
IC50 & Target: Sodium channel[1]
In Vitro: Sodium Channel inhibitor 2 is a sodium channel blocker which is useful for the treatment of neuronal damage following global and focal ischemia and for the treatment or prevention of neurodegenerative conditions such as amyotrophic lateral sclerosis[1].

Name: Y-9738, CAS: 59399-41-6, stock 4.3g, assay 98.8%, MWt: 309.74, Formula: C15H16ClNO4, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Y-9738 is a hypolipidemic agent.
In Vivo: Y-9738 is a hypolipidemic agent. At 100 mg/kg Y-9738 lowers the cholesterol level by 36% and clearly diminishes the intensity of the β-lipoprotein band with a tendency for the α-lipoprotein band to be intensified. Y-9738 causes a dose-dependent decrease in serum cholesterol, triglyceride and heparin-precipitable β-lipoprotein cholesterol. Furthermore, Y-9738 reduces the intensity of the β-lipoprotein band shown by electrophoresis, and increases that of the α-lipoprotein band[1].

Name: beta-L-D4A 2'3'-didehydro-2'3'-dideoxyadenosine, CAS: 7057-48-9, stock 24.5g, assay 98.9%, MWt: 233.23, Formula: C10H11N5O2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Anti-infection, Target: HIV, Biological_Activity: beta-L-D4A is a nucleoside HIV-1 reverse transcriptase inhibitor.
IC50 & Target: HIV-1 reverse transcriptase[1]
In Vitro: beta-L-D4A is a nucleoside HIV-1 reverse transcriptase inhibitor. Results confirm that the biological activity of NSC 108602 is connected with the termination of the DNA chain synthesis in the 5′-3′ direction[1].

Name: CCR5 antagonist 1, CAS: 716354-86-8, stock 27.6g, assay 98.9%, MWt: 738.33, Formula: C39H46ClF2N5O3S, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Immunology/Inflammation;GPCR/G Protein;Anti-infection, Target: CCR;CCR;HIV, Biological_Activity: CCR5 antagonist 1 is a CCR5 antagonist which can inhibit HIV replication extracted from WO 2004054974 A2.
IC50 & Target: CCR5, HIV[1]

Name: Sulfasymazine, CAS: 1984-94-7, stock 4.1g, assay 98.6%, MWt: 307.37, Formula: C13H17N5O2S, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Anti-infection, Target: Bacterial, Biological_Activity: Sulfasymazine is a sulfonamide drug and displays antibacterial properties.
IC50 & Target: Bacterial[1]
In Vivo: Sulfasymazine is a sulfonamide drug and displays antibacterial properties. On a dosage basis, Sulfasymazine is from 2 to 10 times more potent than sulfisoxazole; on a blood level basis, Sulfasymazine potency ranges from 0.3 to 1. In acute toxicity studies in mice, the sodium salt of Sulfasymazine is tolerated at 2000 mg/kg orally, and at 1000 mg/kg intraperitoneally[1].

Name: Metofenazate Methophenazine, CAS: 388-51-2, stock 21.7g, assay 98.5%, MWt: 598.15, Formula: C31H36ClN3O5S, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Neuronal Signaling;Autophagy, Target: CaMK;Autophagy, Biological_Activity: Metofenazate is a selective calmodulin inhibitor.
IC50 & Target: Calmodulin[1]

Name: Uldazepam U31920, CAS: 28546-58-9, stock 27.2g, assay 98.3%, MWt: 360.24, Formula: C18H15Cl2N3O, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Neuronal Signaling;Membrane Transporter/Ion Channel, Target: GABA Receptor;GABA Receptor, Biological_Activity: Uldazepam is a benzodiazepine derivative and can be used to treat patients with anxiety syndromes as tranquilizer.

Name: Cinperene R5046, CAS: 14796-24-8, stock 22.8g, assay 98.2%, MWt: 388.50, Formula: C25H28N2O2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Cinperene is an atropine-like drug which can block pilocarpine-induced lacrimation and salivation.

Name: Nitromifene CI628, CAS: 10448-84-7, stock 38g, assay 98.5%, MWt: 444.52, Formula: C27H28N2O4, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Estrogen Receptor/ERR, Biological_Activity: Nitromifene is an antagonist of estrogen receptor (ER).
IC50 & Target: ER[1]
In Vitro: Nitromifene is an antagonist of estrogen receptor (ER). At 0.5 μM and 1.0 μM concentrations, Nitromifene inhibits MCF 7 cell proliferation to 70% of that in drug-free controls. At higher concentrations, Nitromifene is clearly more effective than other metabolites. Specifically bound estradiol is displaced from intact MCF 7 cells by Nitromifene. Nitromifene is an effective antagonist of the ability of calmodulin (CM) to activate cyclic nucleotide phosphodiesterase[1].

Name: Chlordantoin Clodantoin, CAS: 5588-20-5, stock 0.4g, assay 98.1%, MWt: 347.69, Formula: C11H17Cl3N2O2S, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Anti-infection, Target: Fungal, Biological_Activity: Chlordantoin is an antifungal drug which can be used to treat vaginal candidiasis.
IC50 & Target: Fungal[1]

Name: Xenalamine Xenazoic acid;CV58903, CAS: 1174-11-4, stock 13.3g, assay 98.2%, MWt: 375.42, Formula: C23H21NO4, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Xenalamine is a synthetic antiviral agent.

Name: Chymase-IN-1, CAS: 862090-74-2, stock 18.4g, assay 98.6%, MWt: 431.83, Formula: C20H15ClNO4PS, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Chymase-IN-1 is a potent, selective, orally active, nonpeptide inhibitor of human mast cell chymase with an IC50 of 29 nM.
IC50 & Target: IC50: 29 nM (chymase)[1]
In Vitro: Chymase-IN-1 (compound 5f) is a potent, selective, orally active, nonpeptide inhibitor of human mast cell chymase with an IC50 of 29 nM. Results demonstrate that Chymase-IN-1 has a chymase Ki value of 36 nM and a Cat G Ki value of 9500 nM[1].
In Vivo: Chymase-IN-1 exhibits low oral bioavailability in rats (F=3%; oral t1/2=1.8 h)[1].

Name: Rho-Kinase-IN-1, CAS: 1035094-83-7, stock 4.5g, assay 98.1%, MWt: 352.50, Formula: C20H24N4S, Solubility: DMSO : 50 mg/mL (141.84 mM; ultrasonic and warming and heat to 60°C), Clinical_Informat: No Development Reported, Pathway: TGF-beta/Smad;Stem Cell/Wnt;Cell Cycle/DNA Damage, Target: ROCK;ROCK;ROCK, Biological_Activity: Rho-Kinase-IN-1 is a Rho kinase (ROCK) inhibitor (Ki values of 30.5 and 3.9 nM for ROCK1 and ROCK2, respectively) extracted from US20090325960A1, compound 1.008[1].
IC50 & Target: Ki: 30.5 nM (ROCK1), 3.9 nM (ROCK2)[1]
In Vitro: Rho-Kinase-IN-1 is a ROCK inhibitor which can be useful for treating diseases or conditions associated with excessive cell proliferation, remodeling, edema and inflammation[1].

Name: Org41841, CAS: 301847-37-0, stock 28.7g, assay 98.4%, MWt: 402.53, Formula: C19H22N4O2S2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein, Target: TSH Receptor, Biological_Activity: Org41841 is a partial agonist of both luteinizing hormone/chorionic gonadotropin receptor (LHCGR) and thyroid-stimulating hormone receptor (TSHR) with EC50s of 0.2 and 7.7 μM, respectively.
IC50 & Target: EC50: 0.2 μM (LHCGR), 7.7 μM (TSHR)[1]
In Vitro: Functional assays demonstrate that Org41841 is a partial agonist of both luteinizing hormone/chorionic gonadotropin receptor (LHCGR) and thyroid-stimulating hormone receptor (TSHR) with EC50s of 0.2 and 7.7 μM, respectively. Treatment of L570F with Org41841 reveals an improved EC50 of 800 nM. M9 responds to Org41841 with an improved EC50 of 2700 nM and a greatly improved efficacy for signaling to 99% of the maximal value observed for thyroid-stimulating hormone (TSH) stimulation of thyroid-stimulating hormone receptor (TSHR)[1].

Name: AGN 194078, CAS: 321995-62-4, stock 19.4g, assay 98.6%, MWt: 403.42, Formula: C22H23F2NO4, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease;Autophagy, Target: RAR/RXR;Autophagy, Biological_Activity: AGN 194078 is a selective RARα agonist with a Kd and EC50 of 3 and 112 nM, respectively.
IC50 & Target: Kd: 4 nM (RARα)[1]
EC50: 140 nM (RARα)[1]
In Vitro: AGN 194078 is a selective RARα agonist and binds to RARα with very high affinity, having a Kd value of 3 nM, while being unable to bind to RARβ and binding only very weakly (Kd=5600 nM) to RARγ. Furthermore, AGN 194078 maintains full transcriptional activity through RARα, with an EC50 value of 112 nM, but only activated
RARβ and RARγ with about 10% efficacy at the highest dose (1000 nM) tested[1].

Name: Adenosine antagonist-1, CAS: 431040-19-6, stock 26.9g, assay 98.9%, MWt: 359.41, Formula: C18H13N7S, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein, Target: Adenosine Receptor, Biological_Activity: Adenosine antagonist-1 is an adenosine A3 receptor (AA3R) antagonist.
IC50 & Target: AA3R[1]
In Vitro: Adenosine antagonist-1 (compound 22) is an adenosine A3 receptor (AA3R) antagonist.

Name: MK-3328, CAS: 1201323-97-8, stock 14.9g, assay 98.9%, MWt: 268.25, Formula: C14H9FN4O, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Neuronal Signaling, Target: Amyloid-β, Biological_Activity: MK-3328 is a β-Amyloid PET ligand, which exhibits high binding potency with an IC50 of 10.5 nM.
IC50 & Target: IC50: 10.5 nM (β-Amyloid)[1]
In Vitro: MK-3328 exhibits amyloid binding potency balanced with low levels of nonspecific binding[1].
In Vivo: In vivo, [18F]MK-3328 demonstrates favorable kinetics, exhibiting high brain uptake and good washout in normal rhesus monkey positron emission tomography (PET) imaging studies[1].

Name: Naminidil BMS 234303-01, CAS: 220641-11-2, stock 2.3g, assay 98.3%, MWt: 269.34, Formula: C15H19N5, Solubility: DMSO : 125 mg/mL (464.10 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Membrane Transporter/Ion Channel, Target: Potassium Channel, Biological_Activity: Naminidil is a cyanoguanidine KATP opener.
IC50 & Target: Potassium Channel[1]
In Vitro: Naminidil works through the potassium (K) channel[1].

Name: Mifobate SR-202, CAS: 76541-72-5, stock 7.3g, assay 98.1%, MWt: 358.65, Formula: C11H17ClO7P2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Cell Cycle/DNA Damage, Target: PPAR, Biological_Activity: Mifobate (SR-202) is a potent and specific PPARγ antagonist. Mifobate (SR-202) selectively inhibits Thiazolidinedione (TZD)-induced PPARγ transcriptional activity (IC50=140 μM). Mifobate (SR-202) does not affect basal or ligand-stimulated transcriptional activity of PPARα, PPARβ, or the farnesoid X receptor (FXR). Mifobate (SR-202) shows antiobesity and antidiabetic effects[1].
In Vitro: Mifobate (100-400 μM; pretreated with 24 hours) significantly inhibits BRL 49653- and hormone-induced adipocyte differentiation of 3T3-L1 cells in a dose-dependent manner after 6 days[1]. 
Mifobate is able to both interact specifically with PPARγ and inhibit its agonist-dependent interaction with the coactivator steroid receptor coactivator-1 (SRC-1). Mifobate (SR-202) inhibits TZD-stimulated recruitment of the coactivator steroid receptor coactivator-1. Mifobate blocks adipocyte differentiation induced either by thiazolidinediones or by the combination of dexamethasone, insulin, and 3-isobutyl-1-methylxanthine (IBMX)[1].
In Vivo: Mifobate (400 mg/kg; Feed for 20 days) increases insulin sensitivity in ob/ob mice[1]

Name: RMI 10874, CAS: 38020-45-0, stock 2.8g, assay 98.3%, MWt: 370.44, Formula: C21H26N2O4, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: RMI 10874 is a tilorone analogue. Tilorone is a small-molecule, orally bioavailable antiviral agent. RMI 10874 completely abolishes lung colonization of an H-2 negative (GR9.B9) MCA-induced fibrosarcoma clone.
In Vivo: The effect of RMI 10874 (RMI 10,874DA) in the abrogation of the metastatic spread of tumor cells is studied. Pre-treatment of BALB/c mice with the RMI 10,874DA completely eliminates lung colonization of an H-2-negative (GR9.B9) MCA-induced fibrosarcoma clone in an experimental metastasis assay[1]. The effect of a tilorone analogue (RMI 10,874DA) and anti-asialo GM1 serum is studied on the survival of BALB/c and C57B1/6 mice after i.v. injections of different syngeneic murine tumor cells. Natural killer (NK) cell activation in vivo by RMI 10874 prolongs survival and inhibits metastasis formation in mice, even when pretreatment consists of a single dose of the analogue[2]. Tilorone is a small-molecule, orally bioavailable drug that is used clinically as an antiviral[3].

Name: Pirolate CP-32387, CAS: 55149-05-8, stock 18.6g, assay 98%, MWt: 329.31, Formula: C16H15N3O5, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Immunology/Inflammation;GPCR/G Protein;Neuronal Signaling, Target: Histamine Receptor;Histamine Receptor;Histamine Receptor, Biological_Activity: Pirolate is a histamine H1 receptor.
IC50 & Target: Histamine H1 receptor[1]
In Vitro: Pirolate is an antihistamine compound[1].

Name: CGS 15435, CAS: 95853-92-2, stock 12.2g, assay 98.6%, MWt: 356.85, Formula: C20H21ClN2O2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein, Target: Prostaglandin Receptor, Biological_Activity: CGS 15435, a potent thromboxane (TxA2) synthetase inhibitor with an IC50 of 1 nM, has a selectivity for Tx synthetase 100000-fold greater than that for cyclooxygenase, PGI2 synthetase and lipoxygenase enzymes.
IC50 & Target: IC50: 1 nM (TxA2 synthetase), 60 μM (5-Lipoxygenase), 90 μM (PGI2 synthetase), 1200 μM (Cyclooxygenase)[1]
In Vitro: CGS 15435 is a highly specific Tx synthetase inhibitor. CGS 15435 is only weakly effective as an inhibitor of PGE2 (Cyclooxygenase, IC50=1200 μM), prostacyclin (PGI2 synthetase, IC50=90 μM) or 5-Lipoxygenase (IC50=60 μM) product formation[1].
In Vivo: CGS 15435 has a long duration of action, since the increases in the plasma levels of TxB2 are prevented even at 24 h after CGS 15435 administration. CGS 15435 significantly inhibits TxB2 formation 4, 6, 12 and 24 h after dosing. Administration of CGS 15435 0.25 or 24 h prior to Arachidonic acid (AA) produced no increase in TxB2 in the surviving animals (4/4 and 5/6, respectively). The final TxB2 levels in the CGS15435A (0.25 and 24 h pretreatment) groups are significantly lower (P<0.05) than those seen in the AA or the Dazoxiben (2 h pretreatment) groups[1].

Name: Thiazolidinone-Derivatives-1, CAS: 136272-75-8, stock 10.8g, assay 98.3%, MWt: 218.27, Formula: C11H10N2OS, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Thiazolidinone-Derivatives-1 is an antiulcer agent which inhibits the secretion of gastric acid.
In Vitro: Thiazolidinone-Derivatives-1 is extracted from patent WO/1991/008203, compound example 1. Thiazolidinone-Derivatives-1 shows a gastric acid secretion-inhibiting effect and therefore, is useful for the treatment of gastric and duodenal ulcers.

Name: RD3-0028, CAS: 3886-39-3, stock 0.3g, assay 98.9%, MWt: 168.28, Formula: C8H8S2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Anti-infection, Target: RSV, Biological_Activity: RD3-0028 is a potent and selective inhibitor of RSV replication with an EC50 of 4.5 μM.
IC50 & Target: EC50: 4.5 μM (RSV)[1]
In Vitro: RD3-0028 has a 50% effective concentration of 4.5 μM and a 50% cytotoxic concentration of 271.0μM which is superior to that of ribavirin. RD3-0028 inhibits different RSV strains at a low concentration (4.5-11.0 μM) using the MTT method. Using the MTT method, EC50 values of RD3-0028 against tested strains are lower than those of ribavirin. RD3-0028 does not inhibit the replication of measles virus, influenza A virus, herpes simplex virus types 1 and 2, or human cytomegalovirus[1].
In Vivo: Aerosols generated from reservoirs containing RD3-0028 (7 mg/mL) administered for 2 h twice daily for 3 days significantly reduces the pulmonary titer of RSV-infected mice. It is clear that the minimal effective dose of RD3-0028 for RSV-infected mice is significantly less than that of ribavirin, the only compound currently available for use against RSV disease. Furthermore, the RD3-0028 aerosol administration protect the lungs of infected, CYP-treated mice against tissue damage, as evidenced by the preservation of the lung architecture and a reduction in pulmonary inflammatory infiltrates. RD3-0028 aerosol is not toxic for mice at the therapeutic dose[2]. The plasma concentration of RD3-0028 is maintained at the same level from 5 min to 1 h, and decreases with a half-life of 2.2 h for 1±8 h. The excretion of radioactivity in the urine and faeces at 24 h after aerosol treatment is 89.3 and 4.5%, respectively, indicating that almost all the radioactivity is rapidly excreted in the urine. The excretion of total radioactivity is 98.9% within 168 h[3].

Name: MDL 19301, CAS: 89388-38-5, stock 2.2g, assay 98.9%, MWt: 279.46, Formula: C15H21NS2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: MDL 19301 is a nonsteroidal, anti-inflammatory agent.
In Vivo: Oral administration of MDL 19301 inhibits rat paw edema induced by carrageenan (ED30=4.8 mg/kg) or an Arthus reaction (ED30=8.2 mg/kg p.o.). The oral dose which induces gastric ulceration in 50% of fasted rats is greater than 1,000 mg/kg, demonstrating a more favorable therapeutic ratio than conventional nonsteroidal anti‐inflammatory agents. The anti-inflammatory activity of MDL 19301, but not that of MDL 16,861, is attenuated by co-administration of an inhibitor of drug metabolite (SKF525A). This suggests that MDL 19301 is a prodrug of MDL 16,861 and this phenomenon would explain its lack of ulcerogenicity. Additional anti-inflammatory properties of MDL 19301 include inhibition of carrageenan pleurisy, adjuvant arthritis, and HOAc-induced writhing. Other pharmacological data indicate that MDL 19301 administration results in inhibition of prostaglandin synthesis; inhibition of arachidonic acid-induced, but not prostaglandin-E2-induced, diarrhea in mice; and inhibition of ex vivo arachidonic-acid-induced, but not ADP-induced, rat platelet aggregation. MDL 19301 and MDL 16,861 are unexpectedly weak antipyretic agents in rats[1].

Name: 2-(E-2-decenoylamino)ethyl 2-(cyclohexylethyl) sulfide, CAS: 137089-36-2, stock 22.4g, assay 98.3%, MWt: 339.58, Formula: C20H37NOS, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein;Metabolic Enzyme/Protease, Target: Prostaglandin Receptor;Phospholipase, Biological_Activity: 2-(E-2-decenoylamino)ethyl 2-(cyclohexylethyl) sulfide is a compound that inhibits stress-induced ulcer and low toxicity, and can maintain the content of phospholipase A2 and prostaglandin E2 in ulcerated rats induced by water immersed restrained stress.
IC50 & Target: Prostaglandin Receptor, Phospholipase[1]
In Vivo: 2-(E-2-decenoylamino)ethyl 2-(cyclohexylethyl) sulfide (compd.III-1α, 100 mg/kg, p.o.) maintains the relative content of Fr.I hexose, lipid peroxide and phospholipase A2 (PLA2) in normal level in ulcerated rats induced by water immersed restrained stress via dosing twice a day for 3 day (b.i.d. for 3 d). 2-(E-2-decenoylamino)ethyl 2-(cyclohexylethyl) sulfide (100 mg/kg, p.o.) reduces the hexosamine content equally with the control group 4 h after the stress loading, and then markedly increases 7 h after stress loading. 2-(E-2-decenoylamino)ethyl 2-(cyclohexylethyl) sulfide (25 mg/kg, p.o.) blocks the reduction of prostaglandin E2 (PGE2) and PGI2 in early phase and accelerates the increase of PGE2 and PGI2 in the late phase of the stress. 2-(E-2-decenoylamino)ethyl 2-(cyclohexylethyl) sulfide (25 mg/kg, p.o.) also significantly accelerates the cell proliferation in fundic glands in gastric mucosa of mice[1].

Name: RP 73163 Racemate, CAS: 136609-53-5, stock 0.1g, assay 98.7%, MWt: 432.58, Formula: C25H28N4OS, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: RP 73163 Racemate is the racemate of RP 73163. RP 73163 is a potent ACAT inhibitor, with cholesterol lowering activity.

Name: MF 5137, CAS: 148927-23-5, stock 9.8g, assay 98.7%, MWt: 389.45, Formula: C23H23N3O3, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Anti-infection, Target: Bacterial, Biological_Activity: MF 5137 is a potent antibacterial agent.
IC50 & Target: Antibacterial[1]
In Vitro: MF 5137 (Compound 2) is rapidly photodegraded upon UVA irradiation, yielding a toxic photoproduct. MF 5137 rapidly decreases the emission of the protein by about 80% after irradiation for 15 min. This effect is markedly reduced in anaerobic conditions[1].

Name: 5-HT1A modulator 1, CAS: 142477-34-7, stock 20.1g, assay 98.5%, MWt: 383.51, Formula: C21H25N3O2S, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Neuronal Signaling;GPCR/G Protein, Target: 5-HT Receptor;5-HT Receptor, Biological_Activity: 5-HT1A modulator 1 displays very high affinities for the 5HT1A, adrenergic α1 and dopamine D2 receptor with IC50s of 2 ±0.3 nM, 10 ± 3 nM and 40 ±9 nM, respectively.
IC50 & Target: IC50: 2±0.3 nM (5-HT1A receptor), 300±55 nM (5-HT1B receptor), 500±75 nM (5-HT2A receptor), 4000±440 nM (5-HT2C receptor), 10±3 nM (Adrenergic α1 receptor), 40±9 nM (Dopamine D2 receptor)[1]
In Vitro: 5-HT1A modulator 1 (Compound 24) also displays affinities for the 5HT1B, 5-HT2A and 5-HT2C receptor with IC50s of 300±55 nM, 500±75 nM, and 4000±440 nM, respectively[1].
In Vivo: 5-HT1A modulator 1 (Compound 24) shows clear antagonist action at 5HT2A receptor subtype in mice. The antagonism is nearly complete at the dose of 1 mg/kg ip for 5-HT1A modulator 1 (94% of antagonism, p<0.01). 5-HT1A modulator 1 completely blocks the stereotypies and the climbing at the dose of 1 mg/kg ip (100% of antagonism). 5-HT1A modulator 1 is also tested in rats, using the same paradigm. After oral administration, 5-HT1A modulator 1 significantly (p<0.05) reduces the hyperactivity by 50% at the doses of 2 and 4 mg/kg po, respectively 63% and 58% of antagonism for 5-HT1A modulator 1; the antagonism is complete (103% and 108%) at the respective doses of 8 and 16 mg/kg po for 5-HT1A modulator 1 (p<0.01)[1].

Name: SX-3228, CAS: 156364-04-4, stock 25.8g, assay 98.8%, MWt: 338.36, Formula: C18H18N4O3, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Neuronal Signaling;Membrane Transporter/Ion Channel, Target: GABA Receptor;GABA Receptor, Biological_Activity: SX-3228 is a selective benzodiazepine1 (BZ1) receptor agonist with an IC50 of 17 nM.
IC50 & Target: IC50: 17 nM (BZ1 receptor)[1]
In Vitro: SX-3228 is a selective ligand for the BZ1 receptor. Among the BZ-receptor subtypes, SX-3228 preferentially binds to the BZ1 receptor (IC50=17 nM). It has very weak affinity for the BZ2 receptor (spinal cord: IC50=127 nM), and virtually no affinity for the peripheral type BZ receptor (kidney: IC50>10000 nM). A compound with similar selectivity, SX-3228 has been shown to bind to BZ receptors, but not to dopamine (D1, D2), serotonin (5-HT1, 5-HT2 and 5-HT3 subtypes), noradrenaline (α1, α2, β), GABA or acetylcholine (muscarinic) subtypes[1].
In Vivo: Administration of 0.5-2.5 mg/kg SX-3228 to rats during the light phase induces a significant reduction of rapid-eye-movement sleep (REMS) (P<0.05) during the third recording hour. Administration of SX-3228 (0.5-2.5 mg/kg) at the beginning of the dark period significantly and dose-dependently reduces waking (W) and increases slow wave sleep (SWS) during the 6-h recording period (P<0.05-0.01); however, significant changes during the last recording hour are restricted to the 2.5 mg/kg dose (P<0.01)[1].

Name: SL910102, CAS: 144756-71-8, stock 18.6g, assay 98.1%, MWt: 490.60, Formula: C30H30N6O, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein, Target: Angiotensin Receptor, Biological_Activity: SL910102 is a nonpeptide angiotensin AT1 receptor antagonist.
IC50 & Target: Angiotensin AT1 receptor[1]
In Vitro: SL910102 (SL 91.0102-90 DL) is a unlabelled nonpeptide AT1-antagonist, which is tested for its ability to compete with [125J](Sar1-Ile8)-angiotensin II for specific AT1-receptor sites in rat lung homogenate[1].

Name: Ruzadolane UP 26-91, CAS: 115762-17-9, stock 25g, assay 98.1%, MWt: 375.44, Formula: C18H19F2N5S, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Ruzadolane (UP 26-91) is a non-narcotic, centrally-acting analgesic agent.

Name: (4-Acetamidocyclohexyl) nitrate BM121307, CAS: 137213-91-3, stock 9.3g, assay 98.9%, MWt: 202.21, Formula: C8H14N2O4, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein, Target: Guanylate Cyclase, Biological_Activity: (4-Acetamidocyclohexyl) nitrate (BM121307) is a guanylate cyclase activator that was in phase I development for the treatment of ischaemic heart disorders. The research has been discontinued.
In Vivo: The elimination of BM121307 and its metabolites via urine and feces amount to 76.5% after oral application, and to 80.7% of the applied dose after intravenous application. The major amount of radioactivity is eliminated via urine (69.4% and 73.6% of the dose, respectively), whereas the fecal elimination is found to be negligible. Investigations of the urinary samples show that the drug is metabolized to a high percentage trans-N-(4-Hydroxycyclohexyl) acetamide is the main metabolite; 73% of the radioactive compounds (after p.o.-administration and 69% after intravenous application could be identified as the alcohol of BM121307; the amounts of the drug totaled 9% and 13%, respectively[1].

Name: Gastrofensin AN 5 free base, CAS: 89845-16-9, stock 7.4g, assay 98.1%, MWt: 344.84, Formula: C19H21ClN2O2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Gastrofensin AN 5 free base, a 4-phenyl-tetrahydroisoquinoline derivative, is an antiulcer agent.
In Vivo: Gastrofensin AN 5 supresses the formation of ulcers in all experimental models. From the broad pharmacological studies of Gastrofensin AN 5 on this model it can be seen that even a dose of 0.100 mg/kg has a high antiulcer activity. The increase of the dose leads to a regular increase of the antiulcer activity, the highest suppression of the ulcer index being reaches at a dose of 1 mg/kg (86.15%). The comparative studies with Ranitidine and Cimetidine on the same experimental models of gastric ulcers show that Gastrofensin AN 5 possesses an antiulcer activity many times higher than that of the above-mentioned drugs[1].

Name: MK-447, CAS: 58456-91-0, stock 37.6g, assay 98.3%, MWt: 305.16, Formula: C11H16INO, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein, Target: Prostaglandin Receptor, Biological_Activity: MK-447 is a free radical scavenger, also a nonsteroidal antiinflammatory agent, and enhances the formation of the endoperoxide, PGH2, and other prostaglandins.
IC50 & Target: Prostaglandin Receptor[1][2]
In Vitro: MK-447 is a free radical scavenger, reduces the accumulation of the endoperoxide, PGG2 and also enhances the formation of the endoperoxide, PGH2, and other prostaglandins[1]. MK-447 (100 μM) increases the amounts of prostaglandin I2 (PGI2). MK-447 also accelerates endogenous PGI2 generation in the isolated rat aorta[2].
In Vivo: MK-447 (20 and 50 mg/kg, p.o.) blocks gastric acid secretion in the 4 hour pylorus ligated rats, but shows no effect on gastric secretion of pepsin. MK-447 (5, 10, 20 and 40 mg/kg, p.o.) dose-dependently decreases acid output in dogs[1].

Name: Caldaret MCC-135, CAS: 133804-44-1, stock 37.2g, assay 98.7%, MWt: 256.32, Formula: C11H16N2O3S, Solubility: 10 mM in DMSO, Clinical_Informat: Phase 2, Pathway: Membrane Transporter/Ion Channel, Target: Na+/Ca2+ Exchanger, Biological_Activity: Caldaret is an intracellular Ca2+ handling modulator that acts through reverse mode Na+/Ca2+ exchanger inhibition.
IC50 & Target: Na+/Ca2+ exchanger[1]
In Vitro: Caldaret (MCC-135) is demonstrated to restore Ca2+-ATPase activity of the sarcoplasmic reticulum (SR) isolated from the myocardium acutely exposed to ischemia and reperfusion in vitro[2].
In Vivo: Caldaret, an intracellular Ca2+ handling modulator, limits infarct size of reperfused canine heart. The cardioprotective effect of Caldaret, a novel intracellular Ca2+ handling modulator that acts through reverse-mode Na+/Ca2+ exchanger inhibition and potential sarcoplasmic reticulum (SR) Ca2+ uptake enhancement, against reperfusion injury is investigated. Intravenously infused Caldaret (3 or 30 microg/kg per hour) for 30 min at left circumflex (LCX)-reperfusion markedly reduces infarct size (by 51.3% or 71.9%, respectively). The amelioration of intracellular Ca2+ handling dysfunction achieved by Caldaret leads to cardioprotective effects against reperfusion injury following prolonged ischemia[1]. Caldaret (MCC-135) is a new potent compound with beneficial effects in heart failure. In diabetic rats, Caldaret decreases TR80 significantly without significant effect on developed tension (DT). Caldaret has minimal effects on SR Ca2+ uptake in normal rats, that is observed as increased SR Ca2+ uptake at uptake time of 20 and 30 s at the highest concentration of 10 μM. In diabetic rats, Caldaret increases SR Ca2+ uptake all over the range of uptake time. Both initial rate of SR Ca2+ uptake and the amount of Ca2+ accumulated in the SR with longer uptake time are increased by Caldaret[2].

Name: RPR107393 free base, CAS: 197576-78-6, stock 38.5g, assay 98.4%, MWt: 330.42, Formula: C22H22N2O, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Farnesyl Transferase, Biological_Activity: RPR107393 free base is a selective squalene synthase inhibitor, which inhibits rat liver microsomal squalene synthase with an IC50 of 0.8±0.2 nM.
IC50 & Target: IC50: 0.8±0.2 nM (rat liver microsomal squalene synthase)[1]
In Vitro: RPR107393 is a selective squalene synthase inhibitor with subnanomolar potency. RPR107393 inhibits rat liver microsomal squalene synthase with an IC50 value of 0.8±0.2 nM (n=4)[1]. In the time-course study, cells are treated with ER-27856 (1 μM), RPR-107393 (10 μM), Atorvastatin (1 μM), or NB-598 (1 μM) for 2-24 h, and lipid biosynthesis during the last 2 h of the incubation is determined. RPR-107393 (10 μM) inhibits Cholesterol biosynthesis and reduces triglyceride biosynthesis. Similarly, 1 μM RPR-107393 inhibits Cholesterol and triglyceride biosynthesis by 82.4% and 70.0%, respectively[2].
In Vivo: One hour after RPR107393 (10 mg/kg p.o.), Cholesterol biosynthesis is reduced by 92% with an approximate ED50 value of 5 mg/kg. Six hours after RPR107393 (10 mg/kg p.o.) administration, Cholesterol biosynthesis is reduced by 74% (the time for 50% inhibition is ~7 hr). An 82% inhibition of hepatic Cholesterol biosynthesis is observed 10 hr after RPR107393 (25 mg/kg p.o.), but the effect is no longer apparent at 21 hr. Inhibition of Cholesterol biosynthesis by Zaragozic acid or RPR107393 is associated with an accumulation of radiolabeled diacid products in the liver. RPR107393 is a potent Cholesterol-lowering agent in rats. RPR107393 (30 mg/kg p.o. b.i.d.) lowers serum Cholesterol by 35% after 2 days and by nearly 50% after 3 days of treatment[1].

Name: AGN 192836, CAS: 171102-29-7, stock 35.9g, assay 98.6%, MWt: 231.25, Formula: C12H13N3O2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein;Neuronal Signaling, Target: Adrenergic Receptor;Adrenergic Receptor, Biological_Activity: AGN 192836 is a potent and selective α2 adrenergic agonist with EC50s of 8.7, 41 and 6.6 nM for α2A, α2B and α2C receptor, respectively.
IC50 & Target: EC50: 8.7 nM (α2A), 41 nM (α2B), 6.6 nM (α2C)[1]
Ki: 1.7 nM (α2A), 82 nM (α2B), 19 nM (α2C)[1]
In Vitro: Binding assays demonstrates that AGN 192836 is 1200-fold selective for the α2A-receptor relative to the α1-receptor, 50-fold selective for the α2A-receptor relative to the α2B-receptor, and 10-fold selective for the α2Areceptor relative to the α2C-receptor[1].
In Vivo: AGN 192836 is equally efficacious when compared to brimonidine for the reduction of intraocular pressure upon topical administration to the rabbit and more efficacious than brimonidine for the reduction of blood pressure upon intravenous administration to monkey[1].

Name: FR167344 free base, CAS: 215258-13-2, stock 38.8g, assay 98.7%, MWt: 673.38, Formula: C30H28BrCl2N5O4, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein, Target: Bradykinin Receptor, Biological_Activity: FR167344 free base is an orally active, nonpeptide bradykinin receptor B2 antagonist. FR167344 free base shows a high affinity binding to the B2 receptor with an IC50 value of 65 nM and no binding affinity for the B1 receptor.
IC50 & Target: IC50: 65 nM (Bradykinin receptor B2)[1]
In Vitro: In competitive experiments using membranes prepared from Chinese hamster ovary cells expressing the bradykinin receptor subtypes, FR167344 shows a high affinity binding to the B2 receptor with IC50 values of 65 nM, and no binding affinity for the B1 receptor. FR167344 inhibits the B2 receptor-mediated phosphatidylinositol (PI) hydrolysis and produces a concentration-dependent rightward shift in the dose-response curve to bradykinin. This shift is accompanied by a progressive reduction of maximal response. Estimated pA2 values for the antagonism of bradykinin induced PI hydrolysis by FR167344 is 8.0. FR167344 shows no stimulatory effects on PI hydrolysis[1].
In Vivo: Oral administration of FR167344 inhibits carrageenin-induced paw oedema in rats with an ID50 of 2.7 mg/kg at 2h after carrageenin injection. Oral administration of FR167344 inhibits kaolin-induced writhing in mice with an ID50 of 2.8 mg/kg in 10 min writhing and 4.2 mg/kg in 15 min writhing. Oral administration of FR167344 inhibits caerulein-induced pancreatic oedema with an ID50 of 13.8 mg/kg as well as increases in amylase and lipase of blood samples with ID50 of 10.3 and 7.4 mg/kg, respectively, in rats[2].

Name: FR183998 free base, CAS: 239440-20-1, stock 12.2g, assay 98.7%, MWt: 428.34, Formula: C17H19Cl2N5O2S, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Membrane Transporter/Ion Channel, Target: Sodium Channel, Biological_Activity: FR183998 free base is a potent Na+/H+-exchange inhibitor, with IC50s of 0.3 nM, 3.1 nM and 6.5 nM by measurement of pHi change in rat lymphocytes, rat and human platelets, respectively.
IC50 & Target: IC50: 0.3 nM (Na+/H+-exchange, Rat lymphocytes), 3.1 nM (Na+/H+-exchange, Human platelet), 6.5 nM (Na+/H+-exchange, Rat platelet)[1]
In Vitro: FR183998 free base is a Na+/H+-exchange inhibitor, with IC50s of 0.3 nM, 6.5 nM and 3.1 nM by measurement of pHi change in rat lymphocytes, rat and human platelets, respectively[1].
In Vivo: FR183998 (0.1 and 1.0 mg/kg, i.v.) shows no effect hemodynamic parameters, and does not affect mean blood pressure and heart rate in conscious rats. Pretreatment of 0.01, 0.032, 0.10 mg/kg FR183998 or posttreament of 0.032 and 0.10 mg/kg FR183998 via intravenous administration, dose-dependently reuces reperfusion-induced ventricular fibrillation (VF) and mortality in reperfusion-induced arrhythmias in anesthetized rats, with ED50s against VF of 0.015 mg/kg and 0.070 mg/kg, respectively. FR183998 also reduces myocardial infarct sizes, and suppresses the arrhythmias in anesthetized rats[1]. FR183998 (1 mg/kg, i.v.) reduces the increase in serum levels of alanine transaminase, aspartate transaminase, and lactate dehydrogenase induced by hepatic I/R, and prevents the incidences of hepatic necrosis, apoptosis, and neutrophil infiltration. FR183998 blocks the I/R-induced activation of the NF-κB, reduces induction of iNOS and inhibits the production of nitric oxide. FR183998 also decreases the expression of the iNOS gene antisense transcript in the liver of hepatic I/R rats[2].

Name: FR194738 free base, CAS: 204067-45-8, stock 39.9g, assay 98.8%, MWt: 439.65, Formula: C27H37NO2S, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: FR194738 free base is a squalene epoxidase inhibitor. FR194738 inhibits squalene epoxidase activity in HepG2 cell homogenates with an IC50 of 9.8 nM.
IC50 & Target: IC50: 9.8 nM (squalene epoxidase, in HepG2 cell homogenates)[1]
In Vitro: In intact HepG2 cells, FR194738 concentration-dependently inhibits the incorporation of [14C]acetate into free cholesterol and cholesteryl ester, with IC50s of 4.9 and 8.0 nM, respectively. FR194738 induces intracellular [14C]squalene accumulation. FR194738 increases the incorporation of [14C]acetate into squalene, an intermediate of cholesterol synthesis[1]. FR194738 potently inhibits squalene epoxidase (SE) in HepG2 cell homogenate and liver microsomes in dogs and rats. The inhibitory effect of FR194738 in comparison to the HMG-CoA reductase inhibitors, Simvastatin, Fluvastatin and Pravastatin, on cholesterol biosynthesis in HepG2 cells is examined. Among these compounds, FR194738 is the most potent, with an IC50 of 2.1 nM. The IC50s of Simvastatin, Fluvastatin and Pravastatin are 40, 28 and 5100 nM, respectively[2]. FR194738 inhibits hamster liver microsomal squalene epoxidase activity in a concentration-dependent manner with an IC50 of 14 nM[3].
In Vivo: Serum lipid levels in hamsters after daily administration of FR194738 and Pravastatin for 10 d are measured. FR194738 reduces the serum levels of total, non high density lipoprotein (HDL) and HDL cholesterol, and triglyceride. Treatment of hamsters with FR194738 increases HMG-CoA reductase activity by 1.3-fold at 32 mg/kg compared to the control group and does not significantly change that at 100 mg/kg[3].

Name: KW-8232 free base, CAS: 170365-25-0, stock 6.8g, assay 98.7%, MWt: 609.16, Formula: C36H37ClN4O3, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein, Target: Prostaglandin Receptor, Biological_Activity: KW-8232 free base is an anti-osteoporotic agent, and can reduces the biosynthesis of PGE2.
IC50 & Target: Prostaglandin Receptor[1]
In Vitro: KW-8232 free base is an anti-osteoporotic agent. KW-8232 reduces the biosynthesis of PGE2 in mouse osteoblastic cells[1].
In Vivo: KW-8232 (3, 10, 30 mg/kg, p.o.) potently increases the femoral bone mineral density (BMD) of immobilized legs of rats, and affects immobilization-induced abnormal bone turnovrer. KW-8232 markedly decreases urinary calcium excreation in the neurectomized rats only at 30 mg/kg, and highly reduces urinary pyridinoline and deoxypyridionline excretion which are markers of bone resorption in neurectomized rats. KW-8232 inhibits bone loss may be attributed to the lower prostaglandins (PGs)-stimulated bone resorption via regulation of PGE2 production[1].

Name: Substituted piperidines-1, CAS: 170842-46-3, stock 22.5g, assay 98.1%, MWt: 517.67, Formula: C29H39N7O2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Substituted piperidines-1 is a compound that can promote the release of growth hormone in humans and animals.
In Vitro: Substituted piperidines-1 is from patent US5721251A, Page 14, line 15 to 25.

Name: PNU-176798, CAS: 428861-91-0, stock 32.2g, assay 98.5%, MWt: 360.36, Formula: C16H13FN4O3S, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Anti-infection, Target: Bacterial, Biological_Activity: PNU-176798 is an antimicrobial agent, targeting protein synthesis in a wide spectrum of gram-positive and anaerobic bacteria.
IC50 & Target: Bacterial[1]
In Vitro: PNU-176798 is an antimicrobial agent, with a minimum inhibitory concentration (MIC) of 1.4 μM for E. coli. PNU-176798 inhibits fMet-tRNA binding to the 70S ribosomes, with an IC50 of 32 μM. PNU-176798 also blocks translation, 70S initiation with IC50s of 0.53, and 32 μM, respectively. PNU-176798 inhibits peptidyl transferase (IC50, 40 μM), and the inhibition is more pronounced in the presence of elongation factor P (EF-P). PNU-176798 markedly inhibits the EF-G-mediated translocation of fMet-tRNA (IC50, 8 μM)[1].

Name: SB-568849, CAS: 395679-53-5, stock 16.7g, assay 98.8%, MWt: 500.55, Formula: C28H31F3N2O3, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein;Neuronal Signaling, Target: MCHR1 (GPR24);MCHR1 (GPR24), Biological_Activity: SB-568849 is a melanin-concentrating hormone receptor 1 (MCH R1) antagonist with a pKi of 7.7.
IC50 & Target: MCH R1 receptor[1]
In Vitro: SB-568849 is a selective SLC-1 antagonist with a pKi of 7.7 as determined in radioligand binding displacement assays; coincubation of tissue with 1 μM SB-568849 for 45 min completely inhibits the MCH induced increase in corticotropin-releasing factor (CRF) release to basal levels without causing any effect on its own. The only reported MCH receptor in the rat is SLC-1, a G protein coupled receptor found throughout the brain and periphery[2].
In Vivo: SB-568849 (Compound 15h) possesses good receptor affinity and selectivity. SB-568849 proves to be an antagonist with stability in vivo, an acceptable brain–blood ratio and oral bioavailability. SB-568849 retains affinity, demonstrates greater in vivo stability (CLb=16 mL/min/kg) and shows an acceptable brain-blood ratio of 1. SB-568849 also shows >30-fold selectivity over a wide range of monoamine receptors and is an antagonist in the FLIPR assay with a pKb of 7.7[3].

Name: N-type calcium channel blocker-1, CAS: 241499-17-2, stock 37.4g, assay 98.1%, MWt: 461.73, Formula: C31H47N3, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Membrane Transporter/Ion Channel;Neuronal Signaling, Target: Calcium Channel;Calcium Channel, Biological_Activity: N-type calcium channel blocker-1 is an orally active analgesic agent which shows high affinity to functionally block N-type calcium channels with an IC50 of 0.7 μM in the IMR32 assay.
IC50 & Target: IC50: 0.7 μM (N-type calcium channels)[1]
In Vitro: N-type calcium channel blocker-1 shows good activities in the IMR32 assay (IC50=0.7 μM). N-type calcium channel blocker-1 is the most orally active N-type calcium channel blocker for analgesia found in a series of compounds[1].
In Vivo: N-type calcium channel blocker-1 shows good activities in the acetic acid anti-writhing model (ED50=4 mg/kg, iv). N-type calcium channel blocker-1 exhibits oral activity (ED50=12 mg/kg, po). A time course study of N-type calcium channel blocker-1 in the anti-writhing model indicates that the CF-1 mice have maximal effect at 120 min after oral dosing at 60 mg/kg. Further evaluation of N-type calcium channel blocker-1 demonstrates several important and advantageous features: the pharmacokinetic profile of N-type calcium channel blocker-1 is improved (Versus of 5.9 L/kg and CL of 26 mL/min/kg) and the logPn of 26 is favorable for CNS agent (logPn measured to be 3.20)[1].

Name: (±)-WS75624B, CAS: 188048-45-5, stock 35g, assay 98%, MWt: 380.46, Formula: C18H24N2O5S, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: (±)-WS75624B is an endothelin converting enzyme (ECE) inhibitor with an IC50 of 0.03 μg/mL.
IC50 & Target: IC50: 0.03 μg/mL (ECE)[1]
In Vitro: Endothelin converting enzyme (ECE) inhibitors, WS75624A and (±)-WS75624B, have been isolated from the fermentation broth of Saccharothrix sp. No. 75624. WS75624A and (±)-WS75624B show highly potent ECE inhibitory activity, and both have IC50s of 0.03 μg/mL. WS75624A and (±)-WS75624B also show other metalloprotease (collagenase and neutral endopeptidase) inhibitory activity with IC50 s of 1 μg/mL. (±)-WS75624B markedly inhibits ECE activity with an IC50 value of 0.03 μg/mL, while it weakly inhibit collagenase and NEP activities with IC50s of 1.0 μg/mL and 1.25 μg/mL, respectively[1].
In Vivo: (±)-WS75624B inhibits big endothelin-induced pressor effect when administered to SD rat intravenously with big ET-1. WS75624 B (30 mg/kg) markedly attenuates the hypertensive effect of big ET-1 (1 nmol/kg,iv) the inhibiting the conversion of big ET-1 to ET-1[1].

Name: YM-53601 free base, CAS: 182959-28-0, stock 1g, assay 98.1%, MWt: 336.40, Formula: C21H21FN2O, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Farnesyl Transferase, Biological_Activity: YM-53601 free base is a squalene synthetase inhibitor which suppresses lipogenic biosynthesis and lipid secretion in rodents.
IC50 & Target: Target: Squalene synthetase[1]
In Vivo: YM-53601 inhibits cholesterol biosynthesis from acetate in a dose-dependent manner in the plasma of rats. At the same time, YM-53601 inhibits both FFA and triglyceride biosynthesis in rats treated with cholestyramine over the same dose range at which it inhibits cholesterol biosynthesis. YM-53601 by single oral administration decreases the enhanced plasma triglyceride levels in hamsters induced by an injection of protamine sulfate, which inhibits lipoprotein lipase (LPL) and consequently increases plasma very low-density lipoprotein (VLDL) triglyceride levels. YM-53601 also decreases the enhanced plasma triglyceride and cholesterol levels in hamsters treated with Triton WR1339, which also inhibits the degradation of VLDL. Plasma cholesterol was significantly decreased as soon as 1 h after single administration of YM-53601 in hamsters fed a normal diet[1].

Name: BCR-ABL-IN-1, CAS: 188260-50-6, stock 17.8g, assay 98.1%, MWt: 459.44, Formula: C23H21F4N5O, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Protein Tyrosine Kinase/RTK, Target: Bcr-Abl, Biological_Activity: BCR-ABL-IN-1 is an inhibitor of BCR-ABL tyrosine kinase, with a pIC50 of 6.46, and may be used in the research of chronic myelogenous leukemia.
IC50 & Target: pIC50: 6.46 (BCR-ABL)[1]
In Vitro: BCR-ABL-IN-1 (Compound 21) is an inhibitor of BCR-ABL tyrosine kinase, with a pIC50 of 6.46, and may be used in the research of chronic myelogenous leukemia.

Name: Tyrosine kinase-IN-1, CAS: 705946-27-6, stock 31.6g, assay 98.3%, MWt: 445.53, Formula: C26H28FN5O, Solubility: DMSO : ≥ 62.5 mg/mL (140.28 mM), Clinical_Informat: No Development Reported, Pathway: Protein Tyrosine Kinase/RTK;Protein Tyrosine Kinase/RTK;Protein Tyrosine Kinase/RTK, Target: VEGFR;PDGFR;FGFR, Biological_Activity: Tyrosine kinase-IN-1 is a multi-targeted tyrosine kinase inhibitor with IC50s of 4, 20, 4, 2 nM for KDR, Flt-1, FGFR1 and PDGFRα, respectively.
IC50 & Target: IC50: 4 nM (KDR), 20 nM (Flt-1), 4 nM (FGFR1), 2 nM (PDGFRα)[1]
In Vitro: Tyrosine kinase-IN-1 is from reference (compound 8K)[1].
In Vivo: Tyrosine kinase-IN-1 shows a reasonable PK profile (AUC(0–∞)=1.9, t1/2=4.6 h). It has a favorable oral bioavailability (F=63%) in rats[1].

Name: CP-96486, CAS: 139401-45-9, stock 37.8g, assay 98%, MWt: 502.99, Formula: C31H23ClN4O, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein, Target: Leukotriene Receptor, Biological_Activity: CP-96486 is a potent and orally active leukotriene D4 (LTD4)/platelet activating factor (PAF) receptor antagonist with Kis of 20 and 24 nM, respectively.
IC50 & Target: Ki: 20 nM (LTD4 receptor), 24 nM (PAF receptor)[1]
In Vitro: CP-96486 (CP-96,486) antagonizes 3H-LTD4 binding to guinea pig lung membranes and 3H-PAF binding to rabbit platelets with Ki's of 20 and 24 nM respectively[1].
In Vivo: CP-96486 (CP-96,486) inhibits iv LTD4- and iv PAF-induced bronchoconstriction in guinea pigs with ED50's of 0.27 and 0.26 mg/kg p.o. respectively[1].

Name: NGD-4715, CAS: 476322-70-0, stock 15.7g, assay 98.2%, MWt: 422.32, Formula: C19H24BrN3O3, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein;Neuronal Signaling, Target: MCHR1 (GPR24);MCHR1 (GPR24), Biological_Activity: NGD-4715 is a selective and orally active melanin-concentrating hormone receptor 1 (MCHR1) antagonist .
In Vitro: NGD-4715 was developed for the treatment of obesity. The research has been discontinued[1].

Name: UK-157147, CAS: 162704-20-3, stock 0.7g, assay 98%, MWt: 472.51, Formula: C23H24N2O7S, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: UK-157147 is a substrate for UDP-glucuronosyltransferases (UGT1A1) with a Km value of 105 μM.
IC50 & Target: Km: 105 μM (UGT1A1)[1]
In Vitro: Glucuronidation is an important pathway for human drug metabolism. Four cloned and expressed human UDP-glucuronosyltransferases (UGT1A1, UGT1A6, UGT1A9, and UGT2B15) are used to screen a series of three potential drug substrates differing only in position of the phenol moiety. The para phenol UK-157147 (UK-157,147) is found to be a substrate for UGT1A1 with a Km value of 105 μM[1].

Name: AVE5688, CAS: 613260-13-2, stock 32.5g, assay 98.2%, MWt: 438.69, Formula: C16H8ClF5N2O5, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: AVE5688 is an inhibitor of glycogen phosphorylase (GP), with IC50s of 430 nM and 915 nM and Kds of 170 nM and 530 nM for rabbit muscle glycogen phosphorylase (rmGPb and rmGPa, respectively); AVE5688 can be used for the research of type 2 diabetes.
IC50 & Target: IC50: 430 nM (rmGPb), 915 nM (rmGPa)[1] 
Kd: 170 nM (rmGPb), 530 nM (rmGPa)[1]
In Vitro: AVE5688 is an inhibitor of glycogen phosphorylase (GP), with IC50s of 430 nM and 915 nM and Kds of 170 nM and 530 nM for rabbit muscle glycogen phosphorylase (rmGPb and rmGPa, respectively)[1].

Name: MCHr1 antagonist 2, CAS: 863115-70-2, stock 22.2g, assay 98.7%, MWt: 424.42, Formula: C23H21FN2O5, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Membrane Transporter/Ion Channel;GPCR/G Protein;Neuronal Signaling, Target: Potassium Channel;MCHR1 (GPR24);MCHR1 (GPR24), Biological_Activity: MCHr1 antagonist 2 is an antagonist of melanin concentrating hormone receptor 1, with an IC50 of 65 nM; MCHr1 antagonist 2 also inhibits hERG, with an IC50 of 4.0 nM in IMR-32 cells.
IC50 & Target: IC50: 65 nM (melanin concentrating hormone receptor 1), 4.0 nM (hERG in IMR-32 cells)[1]
In Vitro: MCHr1 antagonist 2 (Compound 30) is an antagonist of melanin concentrating hormone receptor 1, with an IC50 of 65 nM. MCHr1 antagonist 2 has inhibitory effects on Ca2+ flux, and hERG, with IC50s of 196 ± 30 nM and 4.0 ± 0.8 nM, respectively, in IMR-32 cells[1].

Name: H100, CAS: 643727-55-3, stock 38.3g, assay 99%, MWt: 388.39, Formula: C18H16N2O6S, Solubility: 10 mM in DMSO, Clinical_Informat: Phase 1, Pathway: Membrane Transporter/Ion Channel, Target: Chloride Channel, Biological_Activity: H100 is a Cl- transport inhibitor, with partial effects against both the NaK2Cl cotransporter and the Band 3 anion exchanger, but no effect against KCl cotransporter, in human erythrocytes.
IC50 & Target: Cl- transport[1]
In Vitro: H100 is a Cl- transport inhibitor, with partial effects against both the NaK2Cl cotransporter (NKCC) and the Band 3 anion exchanger (AE), but no effect against KCl cotransporter (KCC), in human erythrocytes. H100 (0.1 mM) shows 63% and 74% inhibition of NKCC and AE in human erythrocytes[1].

Name: NHE3-IN-1, CAS: 632355-68-1, stock 24.6g, assay 98.4%, MWt: 263.75, Formula: C12H10ClN3S, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Membrane Transporter/Ion Channel, Target: Sodium Channel, Biological_Activity: NHE3-IN-1 is a sodium/proton exchanger type 3 (NHE-3) inhibitor extracted from patent WO 2011019784 A1.

Name: MK-6913 Tetrahydrofluoroene 52, CAS: 1398510-92-3, stock 26.1g, assay 98.2%, MWt: 401.50, Formula: C25H27N3O2, Solubility: 10 mM in DMSO, Clinical_Informat: Phase 2, Pathway: Others, Target: Estrogen Receptor/ERR, Biological_Activity: MK-6913 (Tetrahydrofluoroene 52) is a potent and selective estrogen receptor β agonist.
IC50 & Target: Estrogen receptor β [1]
In Vitro: MK-6913 (Tetrahydrofluoroene 52), a highly substituted tetrahydrofluorene derivative, is a potent and selective estrogen receptor β agonist.

Name: CB2R-IN-1, CAS: 1257555-79-5, stock 30.8g, assay 98.7%, MWt: 608.67, Formula: C23H27F3N4O6S3, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein;Neuronal Signaling, Target: Cannabinoid Receptor;Cannabinoid Receptor, Biological_Activity: CB2R-IN-1 is a potent cannabinoid CB2 receptor inverse agonist with a Ki of 0.9 nM.
IC50 & Target: Ki: 0.9 nM (Cannabinoid CB2 receptor)[1]
In Vitro: CB2R-IN-1 (Compound 37) is a potent cannabinoid CB2 receptor ligand (Ki=0.9 nM) with excellent selectivity over the CB1 receptor (Ki=8259.3 nM)[1].

Name: CGP 65015, CAS: 189564-33-8, stock 25g, assay 99%, MWt: 261.27, Formula: C14H15NO4, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: CGP 65015 is an oral iron chelator, which can mobilize iron deposits.
In Vitro: CGP 65015 is an oral iron chelator[1].
In Vivo: CGP65015 (150 μmol IBE/kg p.o. on d0) dramatically increases the urinary and faecal iron clearance, and still enhances iron elimination during the second post-treatment day in iron-overloaded marmosets[1].

Name: MCH-1 antagonist 1, CAS: 1039825-68-7, stock 10.9g, assay 98%, MWt: 414.50, Formula: C25H26N4O2, 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: MCH-1 antagonist 1 is a potent melanin concentrating hormone (MCH-1) antagonist with a Ki of 2.6 nM. MCH-1 antagonist 1 also inhibits CYP3A4 with an IC50 of 10 μM.
IC50 & Target: Ki: 2.6 nM (MCH-1)[1] 
IC50: 10 μM (CYP3A4)[1]
In Vitro: MCH-1 antagonist 1 (Compound 1) also inhibits cytochrome P450 3A4 (CYP3A4) with an IC50 of 10 μM[1].
In Vivo: MCH-1 antagonist 1 is administered to male C57BL/6J DIO mice to assess their pharmacokinetic profile. Effect of MCH-1 antagonist 1 (dosed at 30 mg/kg, po) is measured on the body weight of DIO mice with the AUC0-6 h of 14760 h*ng/mL[1].

Name: CP 375, CAS: 752186-89-3, stock 9g, assay 98.2%, MWt: 211.26, Formula: C11H17NO3, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: CP 375 is a Fe3+ chelating agent, with a log K1 value of 14.50.
In Vitro: CP 375 is a Fe3+ chelating agent, with a log K1 value of 14.50, with the absolute deviation between the predicted and experimental values of 0.12 (14.62 vs. 14.50)[1].

Name: PF-02575799, CAS: 863491-70-7, stock 25g, assay 98.1%, MWt: 680.77, Formula: C42H37FN4O4, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: PF-02575799 is a microsomal triglyceride transfer protein (MTP) inhibitor with an IC50 of 0.77±0.29 nM.
IC50 & Target: IC50: 0.77±0.29 nM (MTP)[1]
In Vitro: PF-02575799 is compound 13 from the reference[1].
In Vivo: PF-02575799 produces appreciable triglyceride effects at its minimally effective dose (10 mg/kg). PF-02575799 significant increase alanine transaminase at 100 mg/kg[1].

Name: Pirinixil BR-931, CAS: 65089-17-0, stock 39.5g, assay 98.3%, MWt: 366.87, Formula: C16H19ClN4O2S, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Pirinixil is a hypolipidemic agent of low toxicity.
In Vivo: Pirinixil is a hypolipidemic agent of low toxicity. Total cholesterol is reduced by Pirinixi in the spleen, kidney and heart of rats. Pirinixil decreases the estimated total body cholesterol approximately 40%[1]. Pirinixil increases plasma cholesterol levels significantly without affecting plasma triglycerides. Liver cholesterol and triglycerides are markedly reduced by Pirinixil, while combined plasma and liver lipid levels decrease approximately 20%. Liver HMG-CoA reductase activity is not affected, but cholesterol 7α-hydroxylase is significantly reduced by Pirinixil[2].

Name: Oroxin A, CAS: 57396-78-8, stock 31.3g, assay 98.8%, MWt: 432.38, Formula: C21H20O10, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Epigenetics;Cell Cycle/DNA Damage;Metabolic Enzyme/Protease, Target: PARP;PARP;Glucosidase, Biological_Activity: Oroxin A is the major component of an ethanol-water Oroxylum indicum (L.) Kurz (Bignoniaceae) seed extract (OISE), activates peroxisome proliferator-activated receptor γ (PPARγ) by docking into the PPARγ protein ligand-binding domain. Oroxin A exhibits an inhibitory activity against α-glucosidase and an antioxidant capacity[1]. Oroxin A exerts anti-breast cancer effects by inducing ER stress-mediated senescence[2].
In Vitro: Oroxin A (0.5- 100 μM; 24 hours) significantly increases the PPARγ transcription level and exhibits the strongest activation with 50 μM in HEK-293t cells[1].

Name: PCI-33380, CAS: 1022899-36-0, stock 18.5g, assay 99%, MWt: 855.78, Formula: C46H52BF2N11O3, Solubility: DMSO : ≥ 50 mg/mL (58.43 mM), Clinical_Informat: No Development Reported, Pathway: Protein Tyrosine Kinase/RTK, Target: Btk, Biological_Activity: PCI-33380 is an irreversible Bruton's Tyrosine Kinase (BTK) inhibitor (fluorescent probe).
IC50 & Target: BTK[1][2].

Name: Propylparaben Propyl parahydroxybenzoate;Propyl 4-hydroxybenzoate, CAS: 94-13-3, stock 16.9g, assay 98.2%, MWt: 180.20, Formula: C10H12O3, Solubility: DMSO : 125 mg/mL (693.67 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Anti-infection;Metabolic Enzyme/Protease, Target: Bacterial;Endogenous Metabolite, Biological_Activity: Propylparaben is an antimicrobial agent, preservative, flavouring agent.

Name: Demethylwedelolactone, CAS: 6468-55-9, stock 6.5g, assay 98.6%, MWt: 300.22, Formula: C15H8O7, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Demethylwedelolactone is a naturally occurring coumestan isolated from Eclipta alba. Demethylwedelolactone is a potent trypsin inhibitor with an IC50 of 3.0 μM. Demethylwedelolactone suppresses cell motility and cell invasion of breast cancer cell[1][2].
IC50 & Target: IC50: 3.0 μM (trypsin)[1]

Name: Euphorbiasteroid, CAS: 28649-59-4, stock 25.1g, assay 98.3%, MWt: 552.66, Formula: C32H40O8, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Epigenetics;PI3K/Akt/mTOR, Target: AMPK;AMPK, Biological_Activity: Euphorbiasteroid is a tricyclic diperpene of Euphorbia lathyris L., inhibits tyrosinase, and increases the phosphorylation of AMPK, with anti-cancer, anti-virus, anti-obesity and multidrug resistance-modulating effect[1].

Name: Higenamine Norcoclaurine, CAS: 5843-65-2, stock 22.2g, assay 98.2%, MWt: 271.31, Formula: C16H17NO3, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Apoptosis;GPCR/G Protein;Neuronal Signaling, Target: Apoptosis;Adrenergic Receptor;Adrenergic Receptor, Biological_Activity: Higenamine (Norcoclaurine), a β2-AR agonist, is a key component of the Chinese herb aconite root that prescribes for treating symptoms of heart failure in the oriental Asian countries. Higenamine (Norcoclaurine) has anti-apoptotic effects[1][2].
IC50 & Target: β2-AR[1]

Name: 3,5,6,7,8,3',4'-Heptemthoxyflavone, CAS: 1178-24-1, stock 19.2g, assay 98.8%, MWt: 432.42, Formula: C22H24O9, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: 3,5,6,7,8,3',4'-heptamethoxyflavone, a flavonoid in C. unshiu peels, exhibits anti-tumor-initiating effect and Anti-neuroinflammatory activity[1][2][3]. 3,5,6,7,8,3',4'-heptamethoxyflavone inhibits collagenase activity and increased type I procollagen content in HDFn cells[1]. 3,5,6,7,8,3',4'-heptamethoxyflavone induces brain-derived neurotrophic factor (BDNF) expression via cAMP/ERK/CREB signaling and reduces phosphodiesterase activity in C6 cells[4].

Name: 20(R)-Ginsenoside Rg2, CAS: 80952-72-3, stock 5.3g, assay 98.6%, MWt: 785.01, Formula: C42H72O13, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: 20(R)-Ginsenoside Rg2, isolated from Ginseng stems and leaves, shows inhibitory effects on lung cancer NCI-H1650 cells. Anti-cancer activities[1].

Name: (20R)-Protopanaxadiol, CAS: 7755-01-3, stock 37.8g, assay 98.8%, MWt: 460.73, Formula: C30H52O3, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: (20R)-Protopanaxadiol is a triterpenoid saponin metabolite of 20(R)-ginsenoside Rg3 in black ginseng. (20R)-Protopanaxadiol exhibits anti-tumor activity and cytotoxicity, and potently inhibits the growth of Helicobacter pylori[1][2][3].

Name: Myristic acid, CAS: 544-63-8, stock 34.4g, assay 98.7%, MWt: 228.37, Formula: C14H28O2, Solubility: DMSO : ≥ 250 mg/mL (1094.71 mM), Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: Myristic acid is a saturated 14-carbon fatty acid occurring in most animal and vegetable fats, particularly butterfat and coconut, palm, and nutmeg oils.

Name: Cimigenol-3-O-α-L-arabinoside, CAS: 161207-05-2, stock 15.1g, assay 98.9%, MWt: 616.78, Formula: C35H52O9, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Cimigenol-3-O-α-L-arabinoside is a triterpenoid isolated from Cimicifuga foetida L[1].

Name: Huperzine B, CAS: 103548-82-9, stock 27.6g, assay 98.3%, MWt: 256.34, Formula: C16H20N2O, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Neuronal Signaling, Target: AChE, Biological_Activity: Huperzine B is a Lycopodium alkaloid isolated from Huperzia serrata and a highly selective acetylcholinesterase (AChE) inhibitor. Huperzine B can be uesd to can be used to improve Alzheimer's disease[1][2].
IC50 & Target: AChE[1]

Name: 20(R)-Notoginsenoside R2, CAS: 948046-15-9, stock 10.7g, assay 98.9%, MWt: 770.99, Formula: C41H70O13, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: 20(R)-Notoginsenoside R2 is an isolated notoginsenoside from Panax notoginseng[1].

Name: Zeylenone, CAS: 193410-84-3, stock 17.6g, assay 98.7%, MWt: 382.36, Formula: C21H18O7, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Apoptosis, Target: Apoptosis, Biological_Activity: Zeylenone, isolated from ethanol extract of the leaves of Uvaria grandiflora Roxb. Zeylenone, a naturally occurring cyclohexene oxide, inhibits proliferation and induces apoptosis in cervical carcinoma cells via PI3K/AKT/mTOR and MAPK/ERK pathways[1].

Name: 11-Keto-beta-boswellic acid 11-Keto-β-boswellic acid, CAS: 17019-92-0, stock 7.4g, assay 98.2%, MWt: 470.68, Formula: C30H46O4, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein;Metabolic Enzyme/Protease;NF-κB, Target: Leukotriene Receptor;Lipoxygenase;NF-κB, Biological_Activity: 11-Keto-beta-boswellic acid (11-Keto-β-boswellic acid) is a pentacyclic triterpenic acid of the oleogum resin from the bark of the Boswellia serrate tree, popularly known as Indian Frankincense. 11-Keto-beta-boswellic acid has the anti-inflammatory activity is primarily due to inhibit 5-lipoxygenase (5-LOX) and subsequent leukotriene and nuclear factor-kappa B (NF-κB) activation and tumor necrosis factor alpha generation production[1].
IC50 & Target: 5-lipoxygenase, leukotriene, NF-κB[1]

Name: Racanisodamine, CAS: 17659-49-3, stock 30.2g, assay 98.5%, MWt: 305.37, Formula: C17H23NO4, Solubility: DMSO : ≥ 125 mg/mL (409.34 mM), Clinical_Informat: Launched, Pathway: Neuronal Signaling;GPCR/G Protein, Target: mAChR;mAChR, Biological_Activity: Racanisodamine is one of the racemic isomers of anisodamine, resembles anisodamine in pharmacological effect. Racanisodamine is a non-selective muscarinic antagonist, used as a component of eye drops for myopic control[1].

Name: Withaferin A, CAS: 5119-48-2, stock 27.1g, assay 98.2%, MWt: 470.60, Formula: C28H38O6, Solubility: DMSO : 100 mg/mL (212.49 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: NF-κB;Apoptosis, Target: NF-κB;Ferroptosis, Biological_Activity: Withaferin A is a steroidal lactone isolated from Withania somnifera, inhibits NF-kB activation and targets vimentin, with potent antiinflammatory and anticancer activities.
IC50 & Target: NF-kB[1], vimentin[2]
In Vitro: Withaferin A has antiinflammatory activity, and potently inhibits NF-kB activation by preventing the TNF-induced activation of Ik-B kinase beta via a thioalkylation-sensitive redox mechanism[1]. Withaferin A also has anticancer activity. Withaferin A targets the IF protein vimentin, causes aggregation of vimentin filaments in bovine aortic endothelial cells (BAECs) at 3 μM, and induces vimentin fragmentation in endothelial cells at 10 μM[2]. Withaferin A (0.5, 1.5 μM) alone or incombination with cisplatin (CIS) dose-dependently reduces tumorigenic potential of ALDH1 positive cancer stem cells (CSCs)[3].
In Vivo: Withaferin A (2 mg/kg, i.p.) shows potent angiogenesis inhibitory activity via vimentin in mice[2]. Withaferin A (2 mg/kg) combined with cisplatin (CIS) regulates the expression of ALDH1 marker, and downregulates the expression of securin in tumors collected from mice[3].

Name: Vanillyl alcohol p-(Hydroxymethyl)guaiacol, CAS: 498-00-0, stock 15.1g, assay 98.6%, MWt: 154.16, Formula: C8H10O3, Solubility: DMSO : 125 mg/mL (810.85 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Apoptosis, Target: Apoptosis, Biological_Activity: Vanillyl alcohol (p-(Hydroxymethyl)guaiacol), derived from vanillin, is a phenolic alcohol and is used as a flavoring agent in foods and beverages[1].

Name: Didymin, CAS: 14259-47-3, stock 25g, assay 98.3%, MWt: 594.56, Formula: C28H34O14, Solubility: DMSO : 250 mg/mL (420.48 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Apoptosis, Target: Apoptosis, Biological_Activity: Didymin, a dietary flavonoid glycoside from citrus fruits, possesses antioxidant properties. Didymin induces apoptosis by inhibiting N-Myc and upregulating RKIP in neuroblastoma[1][2].

Name: Acevaltrate, CAS: 25161-41-5, stock 13.8g, assay 98.9%, MWt: 480.50, Formula: C24H32O10, Solubility: DMSO : ≥ 125 mg/mL (260.15 mM), Clinical_Informat: No Development Reported, Pathway: Membrane Transporter/Ion Channel, Target: Na+/K+ ATPase, Biological_Activity: Acevaltrate, isolated from Valeriana glechomifolia, inhibits the Na+/K+-ATPase activity in the rat kidney and brain hemispheres with IC50s of 22.8±1.1 μM and 42.3±1.0 μM, respectively[1].
IC50 & Target: IC50: 22.8±1.1 μM (Na+/K+-ATPase, in rat kidney), 42.3±1.0 μM (Na+/K+-ATPase, in rat brain hemispheres)[1]
In Vitro: Acevaltrate differentiallys inhibit the activity of rat P-type ATPases in vitro. 60.7±7.3% inhibition of the rat H+/K+-ATPase is achieved at 100 µM[1].

Name: Cedrol (+)-Cedrol;α-Cedrol, CAS: 77-53-2, stock 29.5g, assay 98.3%, MWt: 222.37, Formula: C15H26O, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Anti-infection;Metabolic Enzyme/Protease, Target: Fungal;Cytochrome P450, Biological_Activity: Cedrol is a bioactive sesquiterpene, a potent competitive inhibitor of cytochrome P-450 (CYP) enzymes. Cedrol inhibits CYP2B6-mediated bupropion hydroxylase and CYP3A4-mediated midazolam hydroxylation with Ki of 0.9 μM and 3.4 μM, respectively. Cedrol also has weak inhibitory effect on CYP2C8, CYP2C9, and CYP2C19 enzymes[1]. Cedrol is found in cedar essential oil and poetesses anti-septic, anti-inflammatory, anti-spasmodic, tonic, astringent, diuretic, sedative, insecticidal, and anti-fungal activities[2].
IC50 & Target: CYP2B6; CYP3A4; CYP2C8; CYP2C9; CYP2C19[1]

Name: Transcrocetin trans-Crocetin, CAS: 27876-94-4, stock 12.1g, assay 98.1%, MWt: 328.40, Formula: C20H24O4, Solubility: DMSO : ≥ 33 mg/mL (100.49 mM), Clinical_Informat: Phase 2, Pathway: Membrane Transporter/Ion Channel;Neuronal Signaling, Target: iGluR;iGluR, Biological_Activity: Transcrocetin (trans-Crocetin), extracted from saffron (Crocus sativus L.), acts as an NMDA receptor antagonist with high affinity[1]. Transcrocetin (trans-Crocetin) is capable of crossing the blood-brain barrier and reach the central nervous system (CNS)[2].
IC50 & Target: NMDA receptor[1]
In Vitro: Transcrocetin (trans-Crocetin), a saffron metabolite originating from the crocin apocarotenoids, has been shown to exert strong NMDA receptor affinity and is thought to be responsible for the CNS activity of saffron.To ensure unchanged viability of Caco-2 cells throughout the transport experiments, cellular mitochondrial dehydrogenase activity of Caco-2 cells is measured by MTT assay after a 24 h incubation period with the test compounds: Hydroalcoholic saffron extract saffron extract (SE, 0.5-1 mg/mL) and crocin-1 (250-1000 µM) reveal no negative significant changes in cellular viability. Transcrocetin at 10 µM level does not change viability while higher concentrations (40-160 µM) reduces significantly cellular viability[1].

Name: 3-Acetyl-beta-boswellic acid, CAS: 5968-70-7, stock 12.4g, assay 98.1%, MWt: 498.74, Formula: C32H50O4, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: 3-Acetyl-beta-boswellic acid is a boswellic acid isolated from Boswellia serrata gum resin[1].

Name: Heteroclitin D, CAS: 140369-76-2, stock 7.7g, assay 98.3%, MWt: 482.52, Formula: C27H30O8, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Membrane Transporter/Ion Channel;Neuronal Signaling, Target: Calcium Channel;Calcium Channel, Biological_Activity: Heteroclitin D is a lignin from Kadsura medicinal plants with anti-liqid peroxidation. Heteroclitin D inhibits L-type calcium channels[1].

Name: (-)-Securinine, CAS: 5610-40-2, stock 18.8g, assay 98.3%, MWt: 217.26, Formula: C13H15NO2, Solubility: DMSO : 2 mg/mL (9.21 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Neuronal Signaling;Membrane Transporter/Ion Channel, Target: GABA Receptor;GABA Receptor, Biological_Activity: (-)-Securinine is plant-derived alkaloid and also a GABAA receptor antagonist.
IC50 & Target: GABAA receptor[1]
In Vitro: (-)-Securinine is a major plant-derived alkaloid and also a GABAA receptor antagonist. (-)-Securinine is significantly potent on HeLa cells growth inhibition with IC50 values of 7.02±0.52 μg/mL (32.3 μM). (-)-Securinine induces apoptosis in a dose-dependent manner in the tested cells, increases the percentage of ROS positive cells and depolarized cells as well as stimulates the activity of ERK1/2, caspase-9 and -3/7. (-)-Securinine also induces cell cycle arrest in S phase. Real-time PCR analysis shows high expression of tumor necrosis factor receptor superfamily (TNFRSF) genes in the cells stimulated with (-)-Securinine[1].
In Vivo: In this tumor model, tumor growth is significantly impaired with (-)-Securinine treatment indicating that (-)-Securinine has potential as an Acute Myeloid Leukemia (AML) therapeutic. (-)-Securinine treated mice (n=5 mice, bilateral tumors), exhibit an average of more than 75% smaller tumors than vehicle treated mice at the end of the study period[2].

Name: Isorhamnetin 3-O-galactoside Cacticin, CAS: 6743-92-6, stock 1.3g, assay 98.7%, MWt: 478.40, Formula: C22H22O12, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Isorhamnetin 3-O-galactoside (Cacticin), a flavonoid glycoside isolated from Artemisia capillaris Thunberg, which ameliorates CCl4-induced hepatic damage by enhancing the anti-oxidative defense system and reducing the inflammatory signaling pathways. Isorhamnetin 3-O-galactoside (Cacticin) has antithrombotic and anti-inflammatory activities[1][2][3].

Name: Handelin, CAS: 62687-22-3, stock 3g, assay 98.9%, MWt: 552.66, Formula: C32H40O8, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Handelin is a guaianolide dimer from Chrysanthemum boreale that has potent anti-inflammatory activity by down-regulating NF-κB signaling and pro-inflammatory cytokine production[1].
In Vitro: Handelin (Compound 1; 10-40 μM; RAW 264.7 cells) treatment suppresses the LPS-induced (1 μg/mL) overexpression of iNOS and COX-2 protein levels in a concentration-dependent manner. Handelin also suppresseS the induction of pro-inflammatory cytokines TNF-α and IL-1β in LPS-stimulated RAW 264.7 cells. Handelin also suppresses the activation of mitogen-activated protein kinases, including ERK and JNK signaling[1]. 
Handelin (Compound 1; 10-40 μM; RAW 264.7 cells) treatment significantly reduces the iNOS and COX-2 mRNA levels in LPS- stimulated RAW 264.7 cells. The transcriptional activity of NF-κB stimulated with LPS is also suppressed by Handelin. In addition, the LPS-stimulated upregulation of miRNA-155 expression is suppressed by Handelin[1].
In Vivo: Handelin (Compound 1; 10-20 mg/kg; oral administration; for 30 mintues; male Sprague-Dawley rats) treatment inhibits acute inflammation in carrageenan-induced paw edema model. The serum level of IL-1β is also inhibited by Handelin in a carrageenan-induced paw edema model [1].

Name: Ligupurpuroside B, CAS: 147396-02-9, stock 32.7g, assay 98.8%, MWt: 738.73, Formula: C35H46O17, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Ligupurpuroside B is a glycoside isolated from Ligustrum robustum, with antioxidant activity[1].

Name: Ligupurpuroside C, CAS: 1194056-33-1, stock 30.4g, assay 98.6%, MWt: 738.73, Formula: C35H46O17, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Ligupurpuroside C is a natural phenylethanoid glycoside isolated from Kudingcha[1].

Name: Vicine, CAS: 152-93-2, stock 10.6g, assay 98.8%, MWt: 304.26, Formula: C10H16N4O7, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Vicine, an alkaloid glycoside found mainly in fava beans, is toxic in individuals and may cause haemolytic anaemia[1].

Name: Genipin 1-β-D-gentiobioside Genipin 1-gentiobioside; Genipin 1-β-gentiobioside; Genipin gentiobioside, CAS: 29307-60-6, stock 38.7g, assay 98.7%, MWt: 550.51, Formula: C23H34O15, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Genipin 1-β-D-gentiobioside (Genipin 1-gentiobioside) is one of the most abundant and bioactive iridoid glycosides in Gardenia jasminoides Ellis, which possesses hepatoprotective, anti-inflammatory, antioxidant, and antithrombotic activities.
In Vivo: Genipin 1-β-D-gentiobioside (Genipin gentiobioside) has moderate terminal elimination half-life (t1/2=1.65±0.87 h and 2.43±2.30 h for nomal rats (11.4 mg/kg) and cholestatic liver injury (CLI) rats (11.4 mg/kg), respectively)[1].

Name: Cimigenoside, CAS: 27994-11-2, stock 21.7g, assay 98.9%, MWt: 620.81, Formula: C35H56O9, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Cimigenoside is an active compound from genus Cimicifuga[1].

Name: Onjisaponin B, CAS: 35906-36-6, stock 4.9g, assay 98.5%, MWt: 1573.67, Formula: C75H112O35, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Autophagy, Target: Autophagy, Biological_Activity: Onjisaponin B is a natural product derived from Radix Polygalae. Onjisaponin B enhances autophagy and accelerates the degradation of mutant α-synuclein and huntingtin in PC-12 cells, and exbibits potential therapeutic effects on Parkinson disease and Huntington disease[1].

Name: 6'-O-beta-D-Glucosylgentiopicroside, CAS: 115713-06-9, stock 12.7g, assay 98.8%, MWt: 518.47, Formula: C22H30O14, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: 6'-O-beta-D-Glucosylgentiopicroside is a secoiridoid isolated from the roots of G. straminea. 6'-O-beta-D-Glucosylgentiopicroside strongly suppresses N-formyl-methionyl-leucyl-phenylalanine (fMLP)-induced superoxide generation[1].

Name: Tenacissoside I, CAS: 191729-44-9, stock 32.3g, assay 98.3%, MWt: 814.95, Formula: C44H62O14, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Tenacissoside I is a C21 steroid from the Marsdenia tenacissima, which is detected at relatively high level in M. tenacissima[1][2].

Name: Tenacissoside G, CAS: 191729-43-8, stock 9.9g, assay 98.8%, MWt: 792.95, Formula: C42H64O14, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Tenacissoside G is a C21 steroid from the stems of Marsdenia tenacissima. Tenacissoside G reverses multidrug resistance in P-glycoprotein (Pgp)-overexpressing multidrug-resistant cancer cells[1][2].

Name: Dehydroevodiamine, CAS: 67909-49-3, stock 12g, assay 98.4%, MWt: 301.34, Formula: C19H15N3O, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Immunology/Inflammation;Immunology/Inflammation;Immunology/Inflammation;NF-κB, Target: COX;PGE synthase;NO Synthase;NF-κB, Biological_Activity: Dehydroevodiamine is a major bioactive quinazoline alkaloid isolated from Evodiae Fructus, has an antiarrhythmic effect in guinea-pig ventricular myocytes[1]. Dehydroevodiamine inhibits LPS-induced iNOS, COX-2, prostaglandin E2 (PGE2) and nuclear factor-kappa B (NF-κB) expression in murine macrophage cells[2].
IC50 & Target: iNOS; COX-2; PGE2; NF-κB[2]
In Vitro: Dehydroevodiamine (0-50 μM; 2 hours) inhibits iNOS and COX-2 expression and prevents degradation of IκB-α in LPS induced RAW 264.7 macrophages[2].
Dehydroevodiamine (0-50 μM; 2 hours) inhibits a LPS-induced increase in the iNOS and COX-2 mRNA expression[2].

Name: 7-Ethylcamptothecin, CAS: 78287-27-1, stock 1.1g, assay 98.9%, MWt: 376.41, Formula: C22H20N2O4, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: 7-Ethylcamptothecin is one of camptothecin analogues. camptothecin (CPT), a cytotoxic alkaloid isolated from Camptotheca acuminate, is shown to have strong antitumor activity against L1210 leukemia and Walker 256 carcinosarcoma models[1].

Name: Momordicoside A, CAS: 75801-95-5, stock 12g, assay 98.3%, MWt: 817.01, Formula: C42H72O15, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Phosphatase, Biological_Activity: Momordicoside A is isolated from Momordica charantia L. Momordicoside A has the inhibitory effect on protein tyrosine phosphatase (PTP1B)[1].
IC50 & Target: Protein tyrosine phosphatase[1]

Name: Glaucocalyxin A, CAS: 79498-31-0, stock 27.7g, assay 98.9%, MWt: 332.43, Formula: C20H28O4, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: PI3K/Akt/mTOR;Apoptosis;PI3K/Akt/mTOR, Target: PI3K;Apoptosis;Akt, Biological_Activity: Glaucocalyxin A, an ent-kauranoid diterpene from Rabdosia japonica var., induces apoptosis in osteosarcoma by inhibiting nuclear translocation of Five-zinc finger Glis 1 (GLI1) via regulating PI3K/Akt signaling pathway. Glaucocalyxin A has antitumor effect[1].
In Vitro: Glaucocalyxin A induces apoptosis by mitochondrial apoptotic pathway through several steps including increasing the Bax/Bcl-2 ratio, triggering the intracellular reactive oxygen species (ROS) generation, reducing mitochondrial membrane potential (MMP), and inducing cleavage of caspase-9 and caspase-3[1].

Name: Araloside A Chikusetsusaponin IV, CAS: 7518-22-1, stock 16.2g, assay 98.4%, MWt: 927.08, Formula: C47H74O18, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Renin, Biological_Activity: Araloside A (Chikusetsusaponin IV) is a component of Panax japonicus, with low-renin-inhibitory activity, with an IC50 of 77.4 μM[1].
IC50 & Target: IC50: 77.4 μM (Renin)[1]

Name: Ginkgolic acid C17:1, CAS: 111047-30-4, stock 15.4g, assay 98.1%, MWt: 374.56, Formula: C24H38O3, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: PI3K/Akt/mTOR;Metabolic Enzyme/Protease, Target: PTEN;Phosphatase, Biological_Activity: Ginkgolic acid C17:1, extracted from Ginkgo biloba Leaves, suppresses constitutive and inducible STAT3 activation through induction of PTEN and SHP-1 tyrosine phosphatase. Ginkgolic acid C17:1 has anticancer effects[1].
IC50 & Target: PTEN; Phosphatase[1]

Name: Bilobetin, CAS: 521-32-4, stock 27.2g, assay 98.2%, MWt: 552.48, Formula: C31H20O10, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Stem Cell/Wnt;Protein Tyrosine Kinase/RTK;Cell Cycle/DNA Damage, Target: PKA;PKA;PPAR, Biological_Activity: Bilobetin, an active component of Ginkgo biloba, can reduce blood lipids and improve the effects of insulin. Bilobetin ameliorated insulin resistance, increased the hepatic uptake and oxidation of lipids, reduced very-low-density lipoprotein triglyceride secretion and blood triglyceride levels, enhanced the expression and activity of enzymes involved in β-oxidation and attenuated the accumulation of triglycerides and their metabolites in tissues. Bilobetin also increased the phosphorylation, nuclear translocation and activity of PPARα accompanied by elevated cAMP level and PKA activity[1].

Name: Neoliquiritin, CAS: 5088-75-5, stock 21.5g, assay 98.3%, MWt: 418.39, Formula: C21H22O9, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Neoliquiritin is isolated from Glycyrrhiza uralensis with an anti-inflammatory activity[1].

Name: AQ-13 dihydrochloride, CAS: 169815-40-1, stock 32.3g, assay 98.8%, MWt: 364.74, Formula: C16H24Cl3N3, Solubility: DMSO : 80 mg/mL (219.33 mM; Need ultrasonic), Clinical_Informat: Phase 2, Pathway: Anti-infection, Target: Parasite, Biological_Activity: AQ-13 dihydrochloride is an aminoquinoline antimalarial drug that is effective against chloroquine-resistant strains of Plasmodium falciparum.
In Vivo: Slight decreases in the PCE/RBC ratio are observed in male and female rats treated with CQ and in females only treated with AQ-13; however, none of these changes is statistically significant[1].

Name: Parishin B, CAS: 174972-79-3, stock 25.7g, assay 98.8%, MWt: 728.65, Formula: C32H40O19, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Parishin B, a parishin derivative isolated from Gastrodia elata, may have antioxidant property[1].

Name: Parishin C, CAS: 174972-80-6, stock 5.8g, assay 98.9%, MWt: 728.65, Formula: C32H40O19, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Parishin C, a parishin derivative isolated from Gastrodia elata, may have antioxidant property[1].

Name: Parishin E, CAS: 952068-57-4, stock 8.9g, assay 98.9%, MWt: 460.39, Formula: C19H24O13, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Parishin E, a parishin derivative isolated from Gastrodia elata, may have antioxidant property[1].

Name: Nigakinone, CAS: 18110-86-6, stock 25.8g, assay 99%, MWt: 266.25, Formula: C15H10N2O3, Solubility: DMSO : 8.33 mg/mL (31.29 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Nigakinone is one of the most abundant alkaloids responsible for the major pharmacological activities of Kumu.

Name: N-Nornuciferine, CAS: 4846-19-9, stock 19.1g, assay 98.9%, MWt: 281.35, Formula: C18H19NO2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Cytochrome P450, Biological_Activity: N-Nornuciferine is an aporphine alkaloid in lotus leaf that significantly inhibits CYP2D6 with IC50 and Ki of 3.76 and 2.34 μM, respectively.
IC50 & Target: IC50: 3.76 μM (CYP2D6)[1]
Ki: 2.34 μM (CYP2D6)[1]
In Vitro: The herb of lotus leaves is a commonly used traditional Chinese medicine with a wide range of pharmacological and physiological activities, particularly the reduction of the blood triglyceride and cholesterol levels. N-Nornuciferine strongly inhibits CYP2D6 activity but shows weak or no inhibition of the other four P450 isoenzymes (CYP2C19, CYP3A4, CYP2E1, CYP2C9). N-Nornuciferine competitively inhibits the CYP2D6-catalyzed dextromethorphan o-demethylation with apparent Ki values of 2.34 μM[1].

Name: Isosakuranetin, CAS: 480-43-3, stock 33.2g, assay 98.5%, MWt: 286.28, Formula: C16H14O5, Solubility: DMSO : 125 mg/mL (436.64 mM; Need ultrasonic and warming), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Isosakuranetin is a flavanone flavonoid which can be found in the fruit of Citrus bergamia.
In Vitro: Isosakuranetin stimulates melanin accumulation in a dose-dependent manner. In addition, Isosakuranetin at 30 μM gradually increases the expression of Tyr, TRP1, and TRP2 after 48 and 72 h. The MTT assay shows that Isosakuranetin decreases the number of cells at concentrations greater than 45 μM. Further analysis of trypan blue staining demonstrates that Isosakuranetin does not affect the viability of B16 melanocytes, but shows that Isosakuranetin decreases their proliferation rate. The tyrosinase activity of B16 melanocytes treated with 15 and 30 μM Isosakuranetin for 72 h is significantly increased by 2- and 3.2-fold, respectively, in comparison with that of the control cells[1].
In Vivo: Isosakuranetin dose-dependently increases the paw-withdrawal threshold within the dose range of 1.5 to 6 mg/kg. Post hoc analysis reveals that Isosakuranetin increases the paw-withdrawal threshold and statistical significance is seen at times 30 and 40 min for the dose of 3 mg/kg and 30 to 60 min for the dose of 6 mg/kg[2].

Name: Flavokawain B Flavokavain B, CAS: 1775-97-9, stock 33.3g, assay 98.6%, MWt: 284.31, Formula: C17H16O4, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Apoptosis, Target: Apoptosis, Biological_Activity: Flavokawain B (Flavokavain B) is a chalcone isolated from the root extracts of kava-kava plant and a potent apoptosis inducer for inhibiting the growth of various cancer cell lines. Flavokawain B (Flavokavain B) shows strong antiangiogenic activity. Flavokawain B (Flavokavain B) inhibits human brain endothelial cell (HUVEC) migration and tube formation with very low and non-toxic concentrations[1][2].

Name: Mirificin Puerarin apioside, CAS: 103654-50-8, stock 30.9g, assay 98.6%, MWt: 548.49, Formula: C26H28O13, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Mirificin (Puerarin apioside) is a isoflavone in Puerariae Lobatae Radix. Mirificin inhibits tyrosinase (TYR) with an IC50 of 12.66 μM[1].
IC50 & Target: IC50: 12.66 μM (TYR)[1]

Name: Puerarin 6''-O-Xyloside, CAS: 114240-18-5, stock 0.7g, assay 98%, MWt: 548.49, Formula: C26H28O13, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Apoptosis, Target: Apoptosis, Biological_Activity: Puerarin 6''-O-Xyloside, isolated from radix of Pueraria lobata (Willd.), possesses snti-osteoporotic and anti-tumor activity. Puerarin 6''-O-Xyloside induces the mitochondria-mediated apoptosis pathway.[1][2].

Name: Buddlejasaponin IVb, CAS: 152580-79-5, stock 1.2g, assay 98.8%, MWt: 943.12, Formula: C48H78O18, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Buddlejasaponin IVb (Compound 2), a triterpene saponin isolated from Clinopodium chinense (Benth.) O. Kuntze, Compound 2 has hemostasis efficacy, shortens thrombin time (TT) by 20.6 %[1].

Name: 3-O-beta-Allopyranosyl-(1->4)-beta-oleandropyranosyl-11-O-isobutyryl-12-O-acetyltenacigenin B, CAS: 1260252-18-3, stock 1.2g, assay 98.6%, MWt: 780.94, Formula: C41H64O14, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: 3-O-beta-Allopyranosyl-(1->4)-beta-oleandropyranosyl-11-O-isobutyryl-12-O-acetyltenacigenin B is a chemical constituent of the plant Poria cocos [1].

Name: Remetinostat SHP-141, CAS: 946150-57-8, stock 37.6g, assay 98.9%, MWt: 323.34, Formula: C16H21NO6, Solubility: DMSO : 150 mg/mL (463.91 mM; Need ultrasonic), Clinical_Informat: Phase 2, Pathway: Epigenetics;Cell Cycle/DNA Damage, Target: HDAC;HDAC, Biological_Activity: Remetinostat (SHP-141) is a hydroxamic acid-based inhibitor of histone deacetylase enzymes (HDAC) which is under development for the treatment of cutaneous T-cell lymphoma[1].
IC50 & Target: HDAC[1].

Name: Diroximel fumarate ALKS 8700;BIIB098, CAS: 1577222-14-0, stock 10.8g, assay 98%, MWt: 255.22, Formula: C11H13NO6, Solubility: DMSO : 125 mg/mL (489.77 mM; Need ultrasonic), Clinical_Informat: Phase 3, Pathway: Others, Target: Others, Biological_Activity: Diroximel fumarate (DRF) is a prodrug of monomethyl fumarate in a controlled-release formulation that rapidly and efficiently converts to MMF in the body[1].

Name: (S)-ML753286, CAS: 1699720-85-8, stock 10.6g, assay 98.2%, MWt: 355.43, Formula: C20H25N3O3, Solubility: DMSO : ≥ 50 mg/mL (140.67 mM), Clinical_Informat: No Development Reported, Pathway: Membrane Transporter/Ion Channel, Target: BCRP, Biological_Activity: (S)-ML753286 is a breast cancer resistance protein (BCRP) inhibitor with an IC50 of 0.6 μM on BCRP efflux transporter.
IC50 & Target: IC50: 0.6 μM (BCRP efflux transporter)[1]
In Vivo: (S)-ML753286 (Compound A) shows the potency and a potent pharmacokinetic (PK) profile in rats (lower clearance [1.54 L/h/kg] and higher bioavailability [123%]). XL388 has moderate terminal elimination half-life with t1/2s of 0.9 h and 2.0 h for 2 mg/kg (iv) and 20 mg/kg (po) in rats, respectively[1].

Name: Nevanimibe PD-132301;ATR-101, CAS: 133825-80-6, stock 32g, assay 98.1%, MWt: 421.62, Formula: C27H39N3O, Solubility: 10 mM in DMSO, Clinical_Informat: Phase 2, Pathway: Metabolic Enzyme/Protease, Target: Acyltransferase, Biological_Activity: Nevanimibe (PD-132301; ATR101) is a selective and potent acyl-coenzyme A:cholesterol O-acyltransferase 1 (ACAT1) inhibitor with an EC50 of 9 nM. Nevanimibe (PD-132301; ATR101) inhibits ACAT2 with an EC50 of 368 nM[1].
In Vitro: Coincubation of Nevanimibe (ATR-101; 3 nM-30 μM) and Cholesterol markedly increases toxicity in a dose-dependent manner, where 3 nM Nevanimibe in the presence of 60 μg/mL Cholesterol reduces survival by 60% after 24 hours. All doses of Nevanimibe (3 nM-30 μM) induces cytoxicity in the presence of Cholesterol, whereas treatment with Cholesterol in the absence of Nevanimibe has no effect on cell viability[1].

Name: Nevanimibe hydrochloride PD-132301 hydrochloride;ATR101 hydrochloride, CAS: 133825-81-7, stock 2.3g, assay 98.9%, MWt: 458.08, Formula: C27H40ClN3O, Solubility: DMSO : 41.67 mg/mL (90.97 mM; Need ultrasonic), Clinical_Informat: Phase 2, Pathway: Metabolic Enzyme/Protease, Target: Acyltransferase, Biological_Activity: Nevanimibe hydrochloride (PD-132301 hydrochloride; ATR101 hydrochloride) is a selective and potent acyl-coenzyme A:cholesterol O-acyltransferase 1 (ACAT1) inhibitor with an EC50 of 9 nM. Nevanimibe hydrochloride (PD-132301 hydrochloride; ATR101 hydrochloride) inhibits ACAT2 with an EC50 of 368 nM[1].
In Vitro: Coincubation of Nevanimibe (ATR-101; 3 nM-30 μM) and Cholesterol markedly increases toxicity in a dose-dependent manner, where 3 nM Nevanimibe in the presence of 60 μg/mL Cholesterol reduces survival by 60% after 24 hours. All doses of Nevanimibe (3 nM-30 μM) induces cytoxicity in the presence of Cholesterol, whereas treatment with Cholesterol in the absence of Nevanimibe has no effect on cell viability[1].

Name: K-604 dihydrochloride, CAS: 217094-32-1, stock 13.8g, assay 98.5%, MWt: 575.64, Formula: C23H32Cl2N6OS3, Solubility: 10 mM in DMSO, Clinical_Informat: Phase 2, Pathway: Metabolic Enzyme/Protease, Target: Acyltransferase, Biological_Activity: K-604 dihydrochloride is a potent and selective acyl-CoA:cholesterol acyltransferase 1 (ACAT-1) inhibitor with an IC50 of 0.45±0.06 μM.
IC50 & Target: IC50: 0.45±0.06 μM (ACAT-1), 102.85±14.33 μM (ACAT-2)[1]
In Vitro: The potency and selectivity of K-604 for human ACAT-1 and ACAT-2 is examined. The IC50 value of K-604 for human ACAT-1 is 0.45 μM and that for human ACAT-2 is 102.85 μM, indicating that K-604 is 229-fold more selective for ACAT-1 than ACAT-2. Kinetic analysis indicates that the inhibition is competitive with respect to oleoyl-coenzyme A with a Ki value of 0.378 μM. K-604 efficiently inhibits cholesterol esterification in human macrophages with IC50 value of 68 nM[1]. In cell free biochemical assays, K604 at 0.5 µM inhibits ACAT1 enzymatic activity by 70% without significantly inhibiting the ACAT2 enzyme activity. To investigate whether blocking ACAT1 increases autophagy in neuronal cells, N2a cells are treated with K604. The result shows that at 0.1 to 1 µM, K604 inhibits ACAT activity by 60-80%. Next K604 is added to N2a cells at concentrations from 0.1 to 1 µM for 24 h, and LC3 levels are examined by western blot. The result shows that K604 increases the LC3-II/LC3-I ratio, a reliable marker for autophagosome formation, in a dose-dependent manner. The number of the fluorescent LC3 puncta is significantly increased in N2a cells after K604 treatment. By western blot, K604 significantly decreases the levels of p62 in N2a cells[2].
In Vivo: Using F1B hamsters, an animal model susceptible to diet-induced hyperlipidemia and atherosclerosis, the effects of K-604 on aortic lesion areas and plasma cholesterol levels are assessed. Administration of K-604 does not affect body weight or food consumption. The plasma cholesterol levels in fat-fed hamsters are ~12-fold higher than those in chow-fed hamsters, which are significantly decreased by K-604 only at the highest dose tested (30 mg/kg) but not at lower doses (1-10 mg/kg).The fatty streak lesions stain with oil red O are markedly induced by the high-fat diet, which is significantly reduced by administration of K-604. Further, the histological analyses of the atherosclerotic lesions are performed. The fatty streak lesions in the control group are characterized by accumulation of foamy macrophages in the subendothelial space. In contrast, the areas occupied by foamy macrophages are markedly reduced by administration of K-604[1].

Name: LOC14, CAS: 877963-94-5, stock 15.8g, assay 98.7%, MWt: 317.41, Formula: C16H19N3O2S, Solubility: DMSO : 25 mg/mL (78.76 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: LOC14 is a potent Protein disulfide isomerase (PDI) inhibitor with EC50 and Kd values of 500 nM and 62 nM, respectively. LOC14 exhibits high stability in mouse liver microsomes and blood plasma, low intrinsic microsome clearance, and low plasma-protein binding[1].
LOC14 inhibits PDIA3 activity, decreases intramolecular disulfide bonds and subsequent oligomerization (maturation) of HA in lung epithelial cells[3].
IC50 & Target: Kd: 62 nM (PDI)[1]
In Vitro: LOC14 (0.01-100 μM; 24 hours) exhibits the capacity to inhibit recombinant (r)PDIA3 at an IC50 of approximately 5 μM[3].
In Vivo: LOC14 (orally administered by gavage; 20 mg/kg; once daily; 12-28 weeks) significantly improves motor function, attenuated brain atrophy and extended survival in the N171–82Q HD mice[2].

Name: Palbociclib PD 0332991, CAS: 571190-30-2, stock 32.4g, assay 98.5%, MWt: 447.53, Formula: C24H29N7O2, Solubility: H2O : < 0.1 mg/mL (insoluble); DMSO : 0.2 mg/mL (0.45 mM; Need ultrasonic and warming); 0.1 M HCL : 25 mg/mL (55.86 mM; ultrasonic and warming and heat to 60°C), Clinical_Informat: Launched, Pathway: Cell Cycle/DNA Damage, Target: CDK, Biological_Activity: Palbociclib (PD 0332991) is a selective CDK4 and CDK6 inhibitor with IC50s of 11 and 16 nM, respectively. Palbociclib can be used for the treatment of ER-positive and HER2-negative breast cancer.
IC50 & Target: IC50: 11 nM (Cdk4), 16 nM (Cdk6)[1]
In Vitro: The IC50 of Palbociclib (PD 0332991) for reduction of retinoblastoma (Rb) phosphorylation at Ser780 in MDA-MB-435 breast carcinoma cells is 66 nM. Palbociclib is equally effective at reducing Rb phosphorylation at Ser795 in this tumor with an IC50 of 63 nM, and similar effects on both Ser780 and Ser795 phosphorylation are obtained in the Colo-205 colon carcinoma[1]. The MP-MRT-AN (AN), KP-MRT-RY (RY), G401, and KP-MRT-NS (NS) cell lines are effectively inhibited by Palbociclib (PD) in a concentration-dependent manner in a WST-8 assay. The IC50s are 0.01 µM, 0.01 µM, 0.06 µM, and 0.6 µM, respectively. In contrast, the KP-MRT-YM (YM) cell line is resistant to Palbociclib (IC50>10 µM). The flow cytometry results show that Palbociclib at concentrations between 0 to 1.0 µM induces G1 arrest in the AN, RY, G401 and NS cell lines in a concentration-dependent manner, but has no effect on YM cells. The BrdU incorporation results are consistent with the WST-8 and flow cytometry results: PD reduces BrdU incorporation (indicating G1 arrest) in the AN, RY, G401 and NS cell lines, but not in the YM cell line. Palbociclib, even at a concentration of 0.05 µM, significantly reduces BrdU incorporation in the AN, RY, and G401 cell lines (p<0.05)[2].
In Vivo: Palbociclib (PD 0332991) exhibits significant antitumor efficacy against multiple human tumor xenograft models. In mice bearing Colo-205 colon carcinoma xenografts (p16 deleted), daily p.o. dosing for 14 days with Palbociclib (150 or 75 mg/kg) produces rapid tumor regressions and a corresponding tumor growth delay of ~50 days with >1 log of tumor cell kill at the highest dose tested. At 37.5 mg/kg, the tumor slowly regressed during treatment. Even at doses as low as 12.5 mg/kg, a 13-day growth delay is obtained indicating a 90% inhibition of tumor growth rate. Likewise, robust antitumor activity is seen in the MDA-MB-435 breast carcinoma (p16 deleted) where complete tumor stasis is apparent at 150 mg/kg and some cell kill is evident at the highest dose[1].

Name: iRGD peptide c(CRGDKGPDC), CAS: 1392278-76-0, stock 4.3g, assay 98.4%, MWt: 948.04, Formula: C35H57N13O14S2, Solubility: H2O : ≥ 50 mg/mL (52.74 mM), Clinical_Informat: No Development Reported, Pathway: Cytoskeleton, Target: Integrin, Biological_Activity: iRGD peptide is a 9-amino acid cyclic peptide, triggers tissue penetration of drugs by first binding to av integrins, then proteolytically cleaved in the tumor to produce CRGDK/R to interact with neuropilin-1, and has tumor-targeting and tumor-penetrating properties.
IC50 & Target: Integrin[1]
In Vitro: iRGD peptide-mediated tumor penetration occurs in three steps: binding to αv-integrins on tumor vasculature or tumor cells, exposure by proteolysis of a C-terminal motif that binds to neuropilin-1 (NRP-1) and cell internalization. iRGD peptide inserted in the ICOVIR15K fiber C terminus enhances binding and internalization only in MCF7 cells, which express NRP-1 and integrins. iRGD insertion does not impair virus infection and replication[1]. iRGD peptide alone has no obvious effect on gastric cancer cells, and when combined with 5-FU, iRGD peptide (0.3 μmol/mL) enhances the chemotherapy efficacy of 5-FU on gastric cancer cells through NRP1[2].
In Vivo: iRGD inserted in the oncolytic adenovirus ICOVIR15K (ICOVIR15K-iRGD) enhances early adenovirus dissemination through the tumor mass and elevates the antitumor effect in mice[1]. iRGD (4 mmol/kg, i.v.) in combination with 5-FU significantly suppresses the tumor growth in nude mice bearing human gastric cancer cells[2].

Name: Paquinimod ABR 25757, CAS: 248282-01-1, stock 12.9g, assay 98.2%, MWt: 350.41, Formula: C21H22N2O3, Solubility: DMSO : ≥ 125 mg/mL (356.72 mM), Clinical_Informat: Phase 2, Pathway: Others, Target: Others, Biological_Activity: Paquinimod is a S100A9 inhibitor, which prevents S100A9 binding to TLR-4.
IC50 & Target: S100A9[1]
In Vivo: S100A9 is a calcium-binding protein of the S100 family. Paquinimod is an immunomodulatory compound preventing S100A9 binding to TLR-4. Prophylactic treatment with S100A9 inhibitor Paquinimod reduces pathology in experimental collagenase-induced osteoarthritis[1]. Paquinimod is a potent inhibitor of insulitis and diabetes development in the NOD mouse. To assess the preventive efficacy of Paquinimod on diabetes development in female NOD mice, groups of mice are treated with daily doses of 0.04, 0.2, 1, and 5 mg/kg/day of Paquinimod from week 10 of age until week 20 of age. Glycosuria is analyzed on a weekly basis from 10 weeks of age until the endpoint of the experiment at 40 weeks of age. There is a clear dose-dependent reduction in diabetes development in the Paquinimod-treated mice[2].

Name: 2'-Hydroxy-4'-methylacetophenone, CAS: 6921-64-8, stock 32.6g, assay 98.2%, MWt: 150.17, Formula: C9H10O2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: 2'-Hydroxy-4'-methylacetophenone, a phenolic compound isolated from Angelicae koreana roots possesses acaricidal property[1]. It could be used in the preparation of 4’-methyl-2’-[(p-tolylsulfonyl) oxy] acetophenone[2].

Name: TAK-243 MLN7243, CAS: 1450833-55-2, stock 13.5g, assay 98%, MWt: 519.52, Formula: C19H20F3N5O5S2, Solubility: DMSO : 50 mg/mL (96.24 mM; Need ultrasonic); H2O : 1 mg/mL (1.92 mM; Need ultrasonic), Clinical_Informat: Phase 1, Pathway: Apoptosis;Metabolic Enzyme/Protease;NF-κB, Target: Apoptosis;E1/E2/E3 Enzyme;NF-κB, Biological_Activity: TAK-243 (MLN7243) is a first-in-class, selective ubiquitin activating enzyme, UAE (UBA1) inhibitor (IC50=1 nM), which blocks ubiquitin conjugation, disrupting monoubiquitin signaling as well as global protein ubiquitination. TAK-243 (MLN7243) induces endoplasmic reticulum (ER) stress, abrogates NF-κB pathway activation and promotes apoptosis[1][2].
IC50 & Target: IC50: 1 nM (UBA1)[1]
In Vitro: TAK-243 shows anti-proliferative effect on a panel of cell lines derived from hematologic and solid tumors with variable EC50 values that ranged from 0.006 µM to 1.31 µM[1]. 
TAK-243 reduces growth and viability of human AML cell lines (OCI-AML2, TEX, U937 and NB4) in a concentration- and time-dependent manner with IC50s ranging from 15-40 nM after treatment for 48 hours[3].
In Vivo: TAK-243 significantly delays tumor growth in mice (T/C=0.02) with no toxicity as evidenced by no changes in mouse body weight, serum chemistry, or organ histology. TAK-243 reduces primary AML tumor burden in both tested samples without toxicity[3].

Name: 1,4-Diaminobutane (dihydrochloride), CAS: 333-93-7, stock 4.2g, assay 98.8%, MWt: 161.07, Formula: C4H14Cl2N2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: 1,4-Diaminobutane dihydrochloride is an endogenous metabolite, acts as an indicator of pollution-induced stress in higher plants: barley and rape stressed with Cr(III) or Cr(VI) [1]. 1,4-Diaminobutane dihydrochloride is an important source of GABA[2].
IC50 & Target: Human Endogenous Metabolite[1]
In Vitro: 1,4-Diaminobutane is an important source of GABA in the postnatal rat subventricular zone. GABA synthesis from an alternative pathway uses 1,4-Butanediamine as a precursor[2].

Name: Apigenin-7-O-(2G-rhamnosyl)gentiobioside, CAS: 174284-20-9, stock 18.8g, assay 98.3%, MWt: 740.66, Formula: C33H40O19, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Apigenin-7-O-(2G-rhamnosyl)gentiobioside is a flavone glycosides from Lonicera gracilipes var. glandulosa[1].

Name: Rhodojaponin V, CAS: 37720-86-8, stock 39.4g, assay 98.4%, MWt: 410.50, Formula: C22H34O7, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Rhodojaponin V is a diterpenoid from the leaves of Rhododendron molle with anti-inflammatory activity[1].

Name: Tubuloside A, CAS: 112516-05-9, stock 12.8g, assay 99%, MWt: 828.76, Formula: C37H48O21, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Tubuloside A is a phenylethanoid glycoside with antioxidative effect and hepatoprotective activity.
In Vitro: Tubuloside A is a phenylethanoid glycoside with antioxidative effect and hepatoprotective activity[1][2]. Tubuloside A (8.6 μM) could inhibit D-GalN-induced death of hepatocytes[2].

Name: Paeonolide, CAS: 72520-92-4, stock 16g, assay 98.2%, MWt: 460.43, Formula: C20H28O12, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Paeonolide is a plant glycoside that contains a non-reducing end α-l-arabinopyranoside and is found in the roots of the widespread plant genus Paeonia[1].

Name: 7-O-Methylmangiferin, CAS: 31002-12-7, stock 33.4g, assay 98.2%, MWt: 436.37, Formula: C20H20O11, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: 7-O-Methylmangifer is isolated from the cortexes of Polygala tenuifolia[1].

Name: Lancerin, CAS: 81991-99-3, stock 30.1g, assay 98.2%, MWt: 406.34, Formula: C19H18O10, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Lancerin, isolated from the root bark of Cudraniu cochinchinensis, possesses anti-lipid peroxidation[1].

Name: 6‴-Feruloylspinosin, CAS: 77690-92-7, stock 4.6g, assay 98.1%, MWt: 784.71, Formula: C38H40O18, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: 6‴-Feruloylspinosin is a flavonoid isolated from seeds of Ziziphus jujuba. 6‴-Feruloylspinosin can across the blood-brain barrier and enhance the expression of GABAAα1, GABAAα5, and GABABR1 mRNA in rat hippocampal neurons[1].

Name: Apiopaeonoside, CAS: 100291-86-9, stock 27.7g, assay 98.3%, MWt: 460.43, Formula: C20H28O12, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Apiopaeonoside is a natural product isolated from the root of Paeonia suffruticosa[1].

Name: 12-Epinapelline, CAS: 110064-71-6, stock 13.9g, assay 98.4%, MWt: 359.50, Formula: C22H33NO3, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: 12-Epinapelline is a diterpene alkaloid isolated from Aconitum baikalense. 12-Epinapelline exhibits Anti-inflammatory activity and stimulates the growth of colonies from fibroblast precursors[1][2].

Name: 3-Deoxyaconitine, CAS: 3175-95-9, stock 39.2g, assay 98.5%, MWt: 629.74, Formula: C34H47NO10, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: 3-Deoxyaconitine is a diterpenoid alkaloid, isolated from Aconitum Carmichaeli Debx.[1].

Name: Vicenin 2, CAS: 23666-13-9, stock 14.4g, assay 98.3%, MWt: 594.52, Formula: C27H30O15, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Angiotensin-converting Enzyme (ACE), Biological_Activity: Vicenin 2 is an angiotensin-converting enzyme (ACE) inhibitor (IC50=43.83 μM) from the aerial parts of Desmodium styracifolium[1].

Name: Tomatine α-Tomatine;Lycopersicin;Tomatin, CAS: 17406-45-0, stock 30g, assay 98.6%, MWt: 1034.19, Formula: C50H83NO21, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Proteasome, Biological_Activity: Tomatine is a glycoalkaloid, found in the tomato plant (Lycopersicon esculentum Mill.). Tomatine elicits neurotoxicity in RIP1 kinase and caspase-independent manner. Tomatine promotes the upregulation of nuclear apoptosis inducing factor (AIF) in neuroblastoma cells. Tomatine also inhibits 20S proteasome activity[1].
In Vitro: Tomatine inhibits gastric carcinoma cell line (AGS), neuroblastoma cell line (SH-SY5Y) and non-small cell lung cancer cell line (A549) with IC50s of 2 µM, 1.6 µM and 1.1 µM, respectively[1].

Name: Sibiricose A5, CAS: 107912-97-0, stock 3g, assay 98.5%, MWt: 518.47, Formula: C22H30O14, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Sibiricose A5 is an oligosaccharide ester isolated from Polygalae Radix with potent antioxidant activity[1][2].

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