EOS Med Chem, Medicinal Chemical is Big: EOS Med Chem Building block stock list 2348

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

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

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

Name: Polygalasaponin V, CAS: 162857-65-0, stock 17.1g, assay 98.8%, MWt: 1223.35, Formula: C58H94O27, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Polygalasaponin V is a triterpenoid saponin isolated from the aerial parts of Polygala japonica. Polygala japonica has been a folk medicine herb used as expectorant, anti-inflammatory, antibacterial and antidepressant agents in the south of China[1].

Name: Acetylshengmanol Arabinoside, CAS: 402513-88-6, stock 1.8g, assay 99%, MWt: 662.85, Formula: C37H58O10, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Acetylshengmanol Arabinoside is isolated from Cimicifugae rhizoma.

Name: Sibiricose A6, CAS: 241125-75-7, stock 19.6g, assay 98.9%, MWt: 548.49, Formula: C23H32O15, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Sibiricose A6 is an oligosaccharide ester isolated from Polygalae Radix with potent antioxidant activity[1][2].

Name: Forsythoside E, CAS: 93675-88-8, stock 9.8g, assay 98.1%, MWt: 462.45, Formula: C20H30O12, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Forsythoside E is a phenylethanoid glycoside isolated from the fruits of forsythia suspense (thunb.) vahl[1].

Name: Cixiophiopogon A, CAS: 288143-27-1, stock 7.8g, assay 98.2%, MWt: 887.02, Formula: C44H70O18, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Cixiophiopogon A, a steroidal glycoside, obtained from the tuberous roots of Ophiopogon japonicus (Liliaceae)[1].

Name: 3-Dehydrotrametenolic acid, CAS: 29220-16-4, stock 20.8g, assay 98.7%, MWt: 454.68, Formula: C30H46O3, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Apoptosis;Metabolic Enzyme/Protease, Target: Apoptosis;Lactate Dehydrogenase, Biological_Activity: 3-Dehydrotrametenolic acid, isolated from the sclerotium of Poria cocos, is a lactate dehydrogenase (LDH) inhibitor. 3-Dehydrotrametenolic acid promotes adipocyte differentiation in vitro and acts as an insulin sensitizer in vivo. 3-Dehydrotrametenolic acid induces apoptosis and has anticancer activity[1][2].
IC50 & Target: Lactate dehydrogenase [1]

Name: Saikosaponin F, CAS: 62687-63-2, stock 31.5g, assay 98.1%, MWt: 929.14, Formula: C48H80O17, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Saikosaponin F is a component found in Bupleurum (B.) falcatum L[1].

Name: Hypaphorine, CAS: 487-58-1, stock 14.2g, assay 98.3%, MWt: 246.30, Formula: C14H18N2O2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Hypaphorine is an indole alkaloid isolated from Pisolithus tinctorius, and with neurological and glucose-lowering effects in rodents[1].

Name: Pinoresinol dimethyl ether (+)-Eudesmin, CAS: 29106-36-3, stock 21.8g, assay 98.4%, MWt: 386.44, Formula: C22H26O6, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Pinoresinol dimethyl ether ((+)-Eudesmin) is a non-phenolic furofuran lignan isolated from the stem bark of Magnolia kobus with neuritogenic activity. Pinoresinol dimethyl ether ((+)-Eudesmin) can induce neuritis outgrowth from PC12 cells by stimulating up-stream MAPK, PKC and PKA pathways[1][2].

Name: Acetylshikonin, CAS: 24502-78-1, stock 35.2g, assay 98.9%, MWt: 330.33, Formula: C18H18O6, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Neuronal Signaling;Metabolic Enzyme/Protease, Target: AChE;Cytochrome P450, Biological_Activity: Acetylshikonin, derived from the root of Lithospermum erythrorhizon, has anti-cancer and antiinflammation activity. Acetylshikonin is a non-selective cytochrome P450 inhibitor against all P450s (IC50 values range from 1.4-4.0 μM). Acetylshikonin is an AChE inhibitor and exhibits potent antiapoptosis activity[1][2][3].
IC50 & Target: IC50: 1.4-4.0 μM (all P450s)[2] 
AChE[3]

Name: Episyringaresinol 4'-O-β-D-glncopyranoside, CAS: 137038-13-2, stock 23.3g, assay 98.6%, MWt: 580.58, Formula: C28H36O13, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Episyringaresinol 4'-O-β-D-glncopyranoside (compound 22), isolated from Alhagi sparsifolia Shap, is a natural potential neuroinflammatory inhibitor[1].
In Vitro: Episyringaresinol 4'-O-β-D-glncopyranoside inhibits NO production in LPS-induced N9 microglial cells dramatically in a dose independent manner with an IC50 of 91.50 μM.

Name: Baimaside Quercetin 3-O-sophoroside, CAS: 18609-17-1, stock 2.1g, assay 98.5%, MWt: 626.52, Formula: C27H30O17, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Quercetin 3-beta-sophoroside is isolated from the flowers of A. venetum, is an scavengers of superoxide anions[1].

Name: (5R,6E)-5-Hydroxy-1,7-diphenyl-6-hepten-3-one, CAS: 87095-74-7, stock 9.2g, assay 98.8%, MWt: 280.36, Formula: C19H20O2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: (5R,6E)-5-Hydroxy-1,7-diphenyl-6-hepten-3-one is the methylene chloride extract of Alpinia nutans, has antioxidant activity[1].

Name: Deoxyshikonin, CAS: 43043-74-9, stock 39.8g, assay 98.1%, MWt: 272.30, Formula: C16H16O4, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Anti-infection;Metabolic Enzyme/Protease, Target: Bacterial;HIF/HIF Prolyl-Hydroxylase, Biological_Activity: Deoxyshikonin is isolated from Lithospermum erythrorhizon Sieb with antitumor activity. Deoxyshikonin increases the expression of VEGF-C and VEGF-A mRNA in HMVEC-dLy, promotes HIF-1α and HIF-1β subunit interaction and binds to specific DNA sequences targeted by HIF, indicates a prolymphangiogenesis as well as a proangiogenesis effect in vitro[1]. Deoxyshikonin shows significant synergic antimicrobial activity against S. pneumonia (MIC=17 μg/mL), also shows significantly inhibitory activities against MRSA[2].

Name: Swertisin, CAS: 6991-10-2, stock 37g, assay 98.1%, MWt: 446.40, Formula: C22H22O10, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein, Target: Adenosine Receptor, Biological_Activity: Swertisin, a C-glucosylflavone isolated from Swertia japonica, is known to have antidiabetic, anti-inflammatory and antioxidant effects. Swertisin is an adenosine A1 receptor antagonist[1][2].

Name: Hederagenin 28-O-beta-D-glucopyranosyl ester, CAS: 53931-25-2, stock 15.1g, assay 98.3%, MWt: 634.84, Formula: C36H58O9, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Hederagenin 28-O-beta-D-glucopyranosyl ester, a triterpenoid saponin isolated from Ilex cornuta, exhibits protective effects against H2O2-induced myocardial cell injury[1].

Name: Ecliptasaponin D, CAS: 206756-04-9, stock 8.7g, assay 98.3%, MWt: 634.84, Formula: C36H58O9, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Ecliptasaponin D is a triterpenoid glucoside isolated from Eclipta alba (L.) Hassk which is the aerial part of Eclipta prostrate. Eclipta prostrate is considered as a nourishing herbal medicine with pleiotropic effects, including anti-inflammatory, hepatoprotective, antioxidant and immunomodulatory[1,2].

Name: Hirsutine, CAS: 7729-23-9, stock 34.5g, assay 98.9%, MWt: 368.47, Formula: C22H28N2O3, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Apoptosis, Target: Apoptosis, Biological_Activity: Hirsutine, an indole alkaloid of Uncaria rhynchophylla, exhibits anti-cancer activity. Hirsutine induces apoptosis and is a potent Dengue virus inhibitor exhibiting low cytotoxicity[1][2][3].
In Vitro: Hirsutine remarkably reduces the viability of MCF-7 and MDA-MB-231 cells in a time- and dose-dependent manner with IC50 values of 447.79 and 179.06 μM, respectively. In the MDA-MB-231 cells, Hirsutine induces apoptosis and depolarization of MMP, releases Cyt C from mitochondria, and activates caspase 9 and caspase 3[2].
In Vivo: Hirsutine induces mPTP-dependent apoptosis through ROCK1/PTEN/PI3K/GSK3β pathway in human lung cancer cells[3].

Name: Bergamottin 5-Geranoxypsoralen; Bergamotine; Bergaptin, CAS: 7380-40-7, stock 2.1g, assay 98.4%, MWt: 338.40, Formula: C21H22O4, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Cytochrome P450, Biological_Activity: Bergamottin is a potent and competitive CYP1A1 inhibitor with a Ki of 10.703 nM.
IC50 & Target: Ki: 10.703 nM (CYP1A1)[1] 
IC50: 0.192±0.029 μM (CYP1A1), 5.077±0.31 μM (CYP1A2), 4.535±0.092 μM(CYP2B2), 9.495±0.979μM (CYP2B1)[1].
In Vitro: Bergamottin is a competitive inhibitor of CYP1A1. Bergamottin inhibits CYP1A1, CYP1A2, CYP2B1, and CYP2B2 with IC50s of 0.192±0.029 μM, 5.077±0.31 μM, 9.495±0.979 μM, 4.535±0.092 μM, respectively[1]. Bergamottin has potent antiproliferative effects on the A549 cells. Bergamottin shows both concentration-dependent as well as time‑dependent growth inhibitory effects against these cells. Bergamottin also inhibits the clonogenic activity of the A549 cancer cells by reducing the number of cancer colony forming cells. A reduction in clonogenicity also follows the concentration dependence on Bergamottin[2].
In Vivo: The anticancer efficacy of Bergamottin under in vivo conditions using female BALB/c nude mice (a total of 20 mice are used) is determined. Tumors are induced in the mice by injecting non-small cell lung cancer A549 cells (1×106 cells/mouse). After tumor formation, the mice are sacrificed and tumors are removed and their weights and volumes are calculated. The results show that 25, 50 and 100 mg/kg Bergamottin injection reduce the tumor weight from 1.61 g in the PBS-treated group (control) to 1.21, 0.42 and 0.15 g, respectively. Tumor weight in the nude mice is reduced much more significantly in the highest-concentration Bergamottin group (100 mg/kg body weight) compared with the vehicle group (P<0.05). Likewise, 25, 50 and 100 mg/kg Bergamottin injection reduces the tumor volume from 2.2 cm3 in the PBS-treated group (control) to 1.71, 1.1 and 0.51 cm3, respectively. The periodic measurement of the tumor xenograft volume indicates that the tumor volume in the nude mice is reduced considerably in the highest-concentration Bergamottin group (100 mg/kg body weight) compared with the vehicle group (P<0.05)[2].

Name: Hirsuteine, CAS: 35467-43-7, stock 4.7g, assay 98.3%, MWt: 366.45, Formula: C22H26N2O3, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Hirsuteine is an indole alkaloid extracted from Uncaria genus. Hirsuteine non-competitively antagonizes nicotine-mediated dopamine release by blocking ion permeation through nicotinic receptor channel complexes[1].

Name: Pseudoginsenoside RT1, CAS: 98474-74-9, stock 38.1g, assay 98.1%, MWt: 927.08, Formula: C47H74O18, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Pseudoginsenoside RT1, isolated from the fruit of Randia siamensis, exhibits acute ichthyotoxic activity[1].

Name: Vitexin2''-O-p-coumarate, CAS: 59282-55-2, stock 28.2g, assay 98%, MWt: 578.52, Formula: C30H26O12, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Vitexin2''-O-p-coumarate is isolated from fenugreek seeds. Vitexin2''-O-p-coumarate strongly promotes 2BS cell proliferation induced by H2O2[1][2].

Name: Swertiajaponin, CAS: 6980-25-2, stock 9.2g, assay 98.6%, MWt: 462.40, Formula: C22H22O11, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Tyrosinase, Biological_Activity: Swertiajaponin is a tyrosinase inhibitor, forms multiple hydrogen bonds and hydrophobic interactions with the binding pocket of tyrosinase, with an IC50 of 43.47 μM. Swertiajaponin also inhibits oxidative stress-mediated MAPK/MITF signaling, leading to decrease in tyrosinase protein level. Swertiajaponin suppresses melanin accumulation and exhibits strong anti-oxidative activity[1].
IC50 & Target: IC50: 43.47 μM (tyrosinase)[1]

Name: Esculentoside H, CAS: 66656-92-6, stock 32.7g, assay 98.8%, MWt: 989.10, Formula: C48H76O21, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: MAPK/ERK Pathway;NF-κB, Target: JNK;NF-κB, Biological_Activity: Esculentoside H (EsH) is a water-soluble saponin isolated and purified from the root extract of perennial plant Phytolacca esculenta[1].
Esculentoside H (EH) has anti-tumor activity, the mechanism is related to the capacity for TNFrelease[2].
Esculentoside H (EsH) suppresses colon cancer cell migration through blockage of the JNK1/2 and NF-κB signaling-mediated matrix metalloproteinases-9 (MMP-9) expression[1].

Name: rel-(8R,8'R)-Dimethyl-(7S,7'R)-bis(3,4-methylenedioxyphenyl)tetrahydro-furan, CAS: 178740-32-4, stock 35.5g, assay 98%, MWt: 340.37, Formula: C20H20O5, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: rel-(8R,8'R)-Dimethyl-(7S,7'R)-bis(3,4-methylenedioxyphenyl)tetrahydro-furan is a chemical constituent of the fruit of Myristica fragrans.

Name: 4-Hydroxylonchocarpin, CAS: 56083-03-5, stock 25g, assay 98.8%, MWt: 322.35, Formula: C20H18O4, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: MAPK/ERK Pathway;Autophagy, Target: p38 MAPK;Autophagy, Biological_Activity: 4-Hydroxylonchocarpin is a chalcone compound from an extract of Psoralea corylifolia. 4-Hydroxylonchocarpin increases phosphorylation of p38 MAPK, JNK and ERK. 4-Hydroxylonchocarpin has diverse pharmacological activities, including antibacterial, antifungal, anticancer, antireverse transcriptase, antitubercular, antimalarial, anti-inflammatory and antioxidant activities[1].

Name: Angeloylgomisin H, CAS: 66056-22-2, stock 14g, assay 98.5%, MWt: 500.58, Formula: C28H36O8, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Cell Cycle/DNA Damage, Target: PPAR, Biological_Activity: Angeloylgomisin H, as a major lignin extract of Schisandra rubriflora, has the potential to improve insulin-stimulated glucose uptake by activating PPAR-γ[1].

Name: 5,7,4'-Trihydroxy-8-Methylflavanone 8-Methyl-naringenine, CAS: 916917-28-7, stock 6.1g, assay 98.5%, MWt: 286.28, Formula: C16H14O5, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: 5,7,4'-Trihydroxy-8-Methylflavanone (Compound 2) is a flavanone isolated from Qualea grandiflora[1].

Name: Picfeltarraenin IB, CAS: 97230-46-1, stock 7g, assay 98.5%, MWt: 792.95, Formula: C42H64O14, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Neuronal Signaling, Target: AChE, Biological_Activity: Picfeltarraenin IB, a triterpenoid obtained from Picriafel-terrae Lour (P.fel-terrae), is an acetylcholinesterase (AChE) inhibitor. Picfeltarraenin IB can be used for the treatment of herpes infections, cancer and inflammation[1].
IC50 & Target: AChE[1]

Name: 7-O-Methylaloeresin A, CAS: 329361-25-3, stock 29.6g, assay 98.7%, MWt: 554.54, Formula: C29H30O11, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Anti-infection, Target: Bacterial, Biological_Activity: 7-O-Methylaloeresin A is 5-methylchromone glycoside isolated from Commiphora socotrana (Burseraceae)[1].
7-O-Methylaloeresin A exhibits good activity against multiple drug resistant Staphylococcus aureus (NCTC 11994) and Salmonella typhimurium (ATCC 1255) with MIC values of 0.72 and 0.18 mM, respectively[2].
7-O-Methylaloeresin A has antioxidant activities, gives IC50 values of 0.026 mM and 0.021 mM for DPPH and 2-deoxyribose degradation assay, respectively[2].

Name: Aloeresin D, CAS: 105317-67-7, stock 12.4g, assay 98.2%, MWt: 556.56, Formula: C29H32O11, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Neuronal Signaling, Target: Beta-secretase, Biological_Activity: Aloeresin D is a chromone glycoside isolated from Aloe vera, inhibits β-Secretase (BACE1) activity, with an IC50 of 39 μM[1].

Name: Rotundic acid, CAS: 20137-37-5, stock 28.7g, assay 98.5%, MWt: 488.70, Formula: C30H48O5, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: MAPK/ERK Pathway;Apoptosis;PI3K/Akt/mTOR;PI3K/Akt/mTOR, Target: p38 MAPK;Apoptosis;mTOR;Akt, Biological_Activity: Rotundic acid, a triterpenoid obtained from I. rotunda, induces DNA damage and cell apoptosis in hepatocellular carcinoma through AKT/mTOR and MAPK Pathways. Rotundic acid possesses anti-inflammatory and cardio-protective abilities[1].

Name: Jionoside B1, CAS: 120406-37-3, stock 22.6g, assay 98.6%, MWt: 814.78, Formula: C37H50O20, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Jionoside B1 is a phenylpropanoid isolated from herbs of Eriophyton wallichii.

Name: 6-Formyl-isoophiopogonanone A, CAS: 116291-82-8, stock 15.3g, assay 98.3%, MWt: 356.33, Formula: C19H16O7, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: 6-Formyl-isoophiopogonanone A is a homoisoflavonoidal extracted from Ophiopogon japonicas, with antioxidant activity[1].

Name: Guaijaverin, CAS: 22255-13-6, stock 37.5g, assay 98.1%, MWt: 434.35, Formula: C20H18O11, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Anti-infection, Target: Bacterial, Biological_Activity: Guaijaverin is a urease inhibitor with an IC50 of 120 μM. Guaijaverin shows antioxidant and anti-Streptococcus mutans activities[1][2][3].
IC50 & Target: IC50: 120 μM (Urease)[1]
In Vitro: Guaijaverin has anti-Strep.mutans activity, with MIC values of 4 and 2 mg/ml for MTCC 1943 and CLSM 001 strain of Strep. mutans, respectively[3].

Name: (-)-Epigallocatechin-3-(3''-O-methyl) gallate (-)-EGCG-3''-O-ME, CAS: 83104-87-4, stock 27.4g, assay 98.4%, MWt: 472.40, Formula: C23H20O11, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: (-)-Epigallocatechin-3-(3''-O-methyl) gallate is a natural product isolated from the tea leaf, with strong antioxidative activity. (-)-Epigallocatechin-3-(3''-O-methyl) gallate has a strong cytotoxic activity for rat cancer cells[1].

Name: Rhapontigenin, CAS: 500-65-2, stock 18.8g, assay 98.3%, MWt: 258.27, Formula: C15H14O4, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Cytochrome P450, Biological_Activity: Rhapontigenin is a natural analog of resveratrol with anticancer, antioxidant, antifungal and antibacterial activities. Rhapontigenin is amechanism-based, potent and selective cytochrome P450 1A1 inactivator (IC50
= 400 nM). Rhapontigenin exhibits 400-fold and 23-fold selectivity for P450 1A1 over P450 1A2 and P450 1B1, respectively[1].
In Vitro: Rhapontigenin (0-250 μM; 24 hours) demonstrates concentration-dependent anti-cancer activity with an IC50 115μM in HEP G2 cells[1].
Rhapontigenin (20 μM; 20 hours) pre-treatment decreases TGF-β triggered increased snail expression in diverse cancer cells[2].
Rhapontigenin (0-20 μM; 6 hours) inhibits TGF-β-induced expression of N-cadherin, vimentin, and CA9 in a dose-dependent manner[2].
Rhapontigenin inhibits ADP- and collagen-induced platelet aggregation with IC50 values of 4 and 70 μg/ml, respectively[3].
Rhapontigenin demonstrates a strong inhibitory activity on the 13-hexosaminidase release induced by DNP-BSA, it exhibits IC50 value of 0.03 mM in RBL 2H3 cells[3].
In Vivo: Rhapontigenin (intraperitoneal injection; 25mg/kg) shows significant protection from death due to pulmonary thrombosis in mice, those samples are orally administered 90 min before tail vein injection of epinephrine and collagen[3].

Name: N-p-trans-Coumaroyltyramine, CAS: 36417-86-4, stock 0.5g, assay 98.1%, MWt: 283.32, Formula: C17H17NO3, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Neuronal Signaling, Target: AChE, Biological_Activity: N-p-trans-Coumaroyltyramine is a cinnamoylphenethyl amide isolated from polygonum hyrcanicum, acts as an acetylcholinesterase (AChE) inhibitor with an an IC50 of 122 μM. N-p-trans-Coumaroyltyramine exhibits anti-trypanosomal activity with an IC50 of 13.3 µM for T. brucei rhodesiense[1][2].
IC50 & Target: IC50: 122 μM (AChE)[2]

Name: Ganolactone B, CAS: 1028449-53-7, stock 4.1g, assay 98.6%, MWt: 458.59, Formula: C27H38O6, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Ganolactone B is a lanostane-type triterpene isolated from the fruiting bodies of G. sinense[1].

Name: Piceatannol 3'-O-glucoside Quzhaqigan, CAS: 94356-26-0, stock 21.6g, assay 98.3%, MWt: 406.38, Formula: C20H22O9, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Immunology/Inflammation;Immunology/Inflammation;Metabolic Enzyme/Protease, Target: NO Synthase;Arginase;Arginase, Biological_Activity: Piceatannol 3'-O-glucoside, an active component of Rhubarb, activates endothelial nitric oxide (NO) synthase through inhibition of arginase activity with IC50s of 11.22 µM and 11.06 µM against arginase I and arginase II, respectively.
IC50 & Target: NO synthase[1] 
IC50: 11.22 μM (Arginase I), 11.06 μM (Arginase II)[1]
In Vitro: Piceatannol 3'-O-glucoside (Piceatannol-3'-O-β-D-glucopyranoside; PG) is a potent component of stilbenes, inhibits the activity of arginase I and II prepared from mouse liver and kidney lysates, respectively, in a dose-dependent manner. In human umbilical vein endothelial cells, incubation of Piceatannol 3'-O-glucoside markedly blocks arginase activity and increases nitrite and nitrate (NOx) production, as measured by Griess assay. In liver lysates, incubation of different concentrations of Piceatannol 3'-O-glucoside significantly decreases arginase I activity (75±5% at 1 µM, 72±7% at 3 µM, 62±1% at 10 µM) compared to untreated control (100±9%). In kidney lysates, the residual arginase activities after incubation of 1, 3 and 10 µM Piceatannol 3'-O-glucoside are 75±6, 74±5, and 53±8%, respectively. Arginase activity is measured in the presence of different concentration of Piceatannol 3'-O-glucoside (from 0 to 120 µM) using liver lysate and kidney lysate. The 50% inhibitory concentrations (IC50) are 11.22 µM for the liver lysate and 11.06 µM for kidney lysate. The values are obtained using the software of Graphpad prizm 4.0. Piceatannol 3'-O-glucoside inhibits arginase activity and increases NO production in HUVECs. Piceatannol 3'-O-glucoside inhibits lipoxygenase activity upto 66% at the concentration of 100 µM and IC50 value is 69 µM[1].
In Vivo: In order to ascertain whether Piceatannol 3'-O-glucoside (PG) ameliorates vascular function in wild-type (WT) and atherogenic model mice [apolipoprotein E-null mice (ApoE-/-)] and to investigate the possible underlying mechanism. Preincubation of aortic vessels from WT mice fed a normal diet (ND) with Piceatannol 3'-O-glucoside attenuates vasoconstriction response to U46619 and phenylephrine (PE), while the vasorelaxant response to acetylcholine (Ach) is markedly enhanced in an endothelium-dependent manner. Piceatannol 3'-O-glucoside treatment attenuates the phenylephrine (PE)-dependent contractile response, and significantly improves the acetylcholine (Ach)-dependent vasorelaxation response in aortic rings from ApoE-/- mice fed a high-cholesterol diet (HCD). Piceatannol 3'-O-glucoside administration in the drinking water significantly reduces fatty streak formation in ApoE-/- mice fed an HCD[2].

Name: Dipsanoside A, CAS: 889678-62-0, stock 0.7g, assay 98.7%, MWt: 1475.40, Formula: C66H90O37, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Dipsanoside A is a novel tetrairidoid glucoside from Dipsacus asper. Dipsacus asper Wall., a perennial plant widespread in China, has been used in traditional Chinese medicine for hundreds of years as a tonic for refreshment, as a fissiparism promoter of the osseous cells, and as an embryo security agent, etc[1].

Name: 6-Methoxykaempferol 3-O-Rutinoside, CAS: 403861-33-6, stock 27.5g, assay 98.1%, MWt: 624.54, Formula: C28H32O16, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: 6-Methoxykaempferol 3-O-Rutinoside is a natural product isolated from the herbs of Pilocarpus pennatifolius[1].

Name: Eupalinolide K, CAS: 108657-10-9, stock 18g, assay 98.6%, MWt: 362.42, Formula: C20H26O6, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: JAK/STAT Signaling;Stem Cell/Wnt, Target: STAT;STAT, Biological_Activity: Eupalinolide K, a sesquiterpene lactones compound from Eupatorium lindleyanum, is a STAT3 inhibitor. Eupalinolide K is a Michael reaction acceptor (MRA) [1].
IC50 & Target: STAT3[1]

Name: Hosenkoside F (+)-Hosenkoside F, CAS: 160896-45-7, stock 33.6g, assay 98.1%, MWt: 949.13, Formula: C47H80O19, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Hosenkoside F is a baccharane glycoside isolated from the seeds of impatiens balsamina.

Name: Hosenkoside G, CAS: 160896-46-8, stock 35.9g, assay 98.6%, MWt: 949.13, Formula: C47H80O19, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Hosenkoside G, a baccharane glycoside isolated from the seeds of Impatiens Balsamina L., possesses anti-tumor activity[1][2].

Name: Hosenkoside K, CAS: 160896-49-1, stock 38.6g, assay 98.5%, MWt: 1141.29, Formula: C54H92O25, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Hosenkoside K is a baccharane glycoside isolated from the seeds of impatiens balsamina.
In Vivo: The mean peak concentrations of hosenkoside K in rats after oral administration of total saponins of Semen Impatientis is 511.11±234.07 ng/mL, occurring at times of 0.46 h. The terminal half-lives of hosenkoside A is 4.96±1.75 h[1].

Name: Hosenkoside M (+)-Hosenkoside M, CAS: 161016-51-9, stock 28.4g, assay 98.6%, MWt: 1111.27, Formula: C53H90O24, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Hosenkoside M is a baccharane glycoside isolated from the seeds of impatiens balsamina.

Name: Gomisin H, CAS: 66056-20-0, stock 9.5g, assay 98%, MWt: 418.48, Formula: C23H30O7, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Gomisin H is a dibenzocyclooctadiene lignan isolated from the fruits of Schizandra chinensis BAILL[1].

Name: Hosenkoside A, CAS: 156791-82-1, stock 15.6g, assay 98.6%, MWt: 979.15, Formula: C48H82O20, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Hosenkoside A is a baccharane glycoside isolated from the seeds of impatiens balsamina.
In Vivo: The mean peak concentrations of hosenkoside A in rats after oral administration of total saponins of Semen Impatientis is 162.08±139.87 ng/mL, occurring at times of 0.67 h. The terminal half-lives of hosenkoside A is 5.39±2.06h[1].

Name: Hosenkoside B, CAS: 156764-82-8, stock 2.8g, assay 98.1%, MWt: 979.15, Formula: C48H82O20, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Hosenkoside B is a baccharane glycoside isolated from the seeds of impatiens balsamina.

Name: Tyrphostin AG 528 Tyrphostin B66;AG 528, CAS: 133550-49-9, stock 5.2g, assay 98.4%, MWt: 306.32, Formula: C18H14N2O3, Solubility: DMSO : 25 mg/mL (81.61 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: JAK/STAT Signaling;Protein Tyrosine Kinase/RTK, Target: EGFR;EGFR, Biological_Activity: Tyrphostin AG 528 is an inhibitor of EGFR and ErbB2 with IC50s of 4.9 and 2.1 μM, respectively.
Tyrphostin AG 528 (Tyrphostin B66) is a protein tyrosine kinase inhibitor, with IC50s of 4.9 μM for epidermal growth factor receptors (EGFR) and 2.1 μM for ErbB2[1]. Tyrphostin AG 528 is also an anticancer agent[2].
IC50 & Target: IC50: 4.9 μM (EGFR), 2.1 μM (ErbB2)[1]
In Vitro: In the present study, the interaction between drug Tyrphostin AG528 and CNT(6,6-6) nanotube by Density Functional Theory (DFT) calculations in solvent water has been investigated for the first time. According to the calculations, intermolecular hydrogen bonds take place between an active position of the molecule Tyrphostin AG528 and hydrogen atoms of the nanotube which play an important role in the stability of complex CNT(6,6- 6)/Tyrphostin AG528. The non-bonded interaction effects of the molecule Tyrphostin AG528 with CNT(6,6-6) nanotube on the electronic properties, chemical shift tensors and natural charge have also been detected. The natural bond orbital (NBO) analysis suggested that the molecule Tyrphostin AG528 as an electron donor and the CNT(6,6-6) nanotube play the role of an electron acceptor at the complex CNT(6,6-6)/Tyrphostin AG528[2].

Name: Crebanine, CAS: 25127-29-1, stock 31.3g, assay 98.5%, MWt: 339.39, Formula: C20H21NO4, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Apoptosis;PI3K/Akt/mTOR, Target: Apoptosis;Akt, Biological_Activity: Crebanine, an alkaloid from Stephania venosa, induces G1 arrest and apoptosis in human cancer cells. Crebanine exhibits anti-inflammatory activity via suppressing MAPKs and Akt signaling. Crebanine also possesses antiarrhythmic effect[1][2].

Name: (-)-Salutaridine, CAS: 4090-18-0, stock 35.3g, assay 98.1%, MWt: 327.37, Formula: C19H21NO4, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: (-)-Salutaridine (Salutaridine) is an alkaloid isolated from the stems of Sinomenium acutum[1].

Name: Curcumenol (+)-Curcumenol, CAS: 19431-84-6, stock 6.6g, assay 98.2%, MWt: 234.33, Formula: C15H22O2, Solubility: DMSO : 125 mg/mL (533.44 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Cytochrome P450, Biological_Activity: Curcumenol ((+)-Curcumenol) is a potent CYP3A4 inhibitor with an IC50 of 12.6 μM, which is one of constituents in the plants of medicinally important genus of Curcuma zedoaria, with neuroprotection, anti-inflammatory, anti-tumor and hepatoprotective activities. Curcumenol ((+)-Curcumenol) suppresses Akt-mediated NF-κB activation and p38 MAPK signaling pathway in LPS-stimulated BV-2 microglial cells[1][2].
IC50 & Target: IC50：12.6 μM (CYP3A4)[1]

Name: Ipecoside, CAS: 15401-60-2, stock 2.8g, assay 98.8%, MWt: 565.57, Formula: C27H35NO12, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Ipecoside is an alkaloid isolated from Psychotria[1].

Name: Aristolone, CAS: 25274-27-5, stock 21.2g, assay 98.8%, MWt: 218.33, Formula: C15H22O, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Aristolone is a sesquiterpene isolated from Aristolochia debilis[1].

Name: 8-Geranyloxypsoralen, CAS: 7437-55-0, stock 35.5g, assay 98.6%, MWt: 338.40, Formula: C21H22O4, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Cytochrome P450, Biological_Activity: 8-Geranyloxypsoralen is a furanocoumarin isolated from grapefruit, acts as a potent inhibitor of P450 3A4 (CYP3A4) with an IC50 of 3.93 μM[1].
IC50 & Target: IC50: 3.93 μM (P450 3A4)[1]

Name: Skimmin Umbelliferone glucoside, CAS: 93-39-0, stock 1.9g, assay 98.8%, MWt: 324.28, Formula: C15H16O8, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Skimmin (Umbelliferone glucoside) is a coumarin found in Hydrangea paniculata, inhibits immune complex deposition, with anti-inflammatory activity[1].

Name: Gymnemagenin, CAS: 22467-07-8, stock 9.7g, assay 98.9%, MWt: 506.71, Formula: C30H50O6, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Gymnemagenin is a triterpenoid isolated from G. sylvestre. Gymnemagenin is an agent for diabetes and obesity and also possesses antiviral properties[1][2].
In Vivo: Gymnemagenin has a poor oral bioavailability (~ 14 %) in rats[2]. 
Gymnemagenin has a short half-life and a high clearance in rats[2]. 
Gymnemagenin metabolizes rapidly with a short apparent and intrinsic half-life (~ 7 min) and high intrinsic clearance[2].

Name: Angeloylgomisin O, CAS: 83864-69-1, stock 27.3g, assay 98.1%, MWt: 498.56, Formula: C28H34O8, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Angeloylgomisin O, a lignin extract of Schisandra rubriflora. Anti-inflammatory properties[1].

Name: 23-Hydroxylongispinogenin 12-Oleanene-3β,16β,23,28-tetrol; 3β,16β-12-Oleanene-3, 16,23,28-tetrol, CAS: 42483-24-9, stock 5.8g, assay 98.8%, MWt: 474.72, Formula: C30H50O4, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: 23-Hydroxylongispinogenin (12-Oleanene-3β,16β,23,28-tetrol) is extracted from Lysimachia heterogenea Klatt. Lysimachia heterogenea Klatt is a perennial herb, which is used as a folk medicine in subduing swelling and detoxicating in China. The effective fraction LH-1 of L. heterogene has antitumor activity[1].

Name: 21-O-Tigloylgymnemagenin, CAS: 1581276-63-2, stock 29.7g, assay 98.3%, MWt: 588.81, Formula: C35H56O7, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: 21-O-Tigloylgymnemagenin (Compound 7) is a acylated triterpenes isolated from Gymnema sylvestre[1].

Name: Kushenol A Leachianone E, CAS: 99217-63-7, stock 7g, assay 98.1%, MWt: 408.49, Formula: C25H28O5, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Tyrosinase, Biological_Activity: Kushenol A is isolated from the root of Sophora flavescent, a non-competitive tyrosinase inhibitor with IC50 and Ki values of 1.1 μM and 0.4 μM, respectively[1].
Kushenol A is a flavonoid antioxidant, has inhibitory effects on alpha-glucosidase and beta-amylase[2].
Kushenol A is confirmed as potential inhibitors of enzymes targeted by cosmetics for skin whitening and aging[1].

Name: Kurarinone, CAS: 34981-26-5, stock 28.3g, assay 98.6%, MWt: 438.51, Formula: C26H30O6, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Kurarinone, a flavanoid derived from shrub Sophora flavescens, inhibits the process of experimental autoimmune encephalomyelitis via blocking Th1 and Th17 cell differentiation[1].

Name: Deltonin, CAS: 55659-75-1, stock 14.6g, assay 99%, MWt: 885.04, Formula: C45H72O17, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Stem Cell/Wnt;MAPK/ERK Pathway;PI3K/Akt/mTOR, Target: ERK;ERK;Akt, Biological_Activity: Deltonin, a steroidal saponin, isolated from Dioscorea zingiberensis Wright, with antitumor activity; Deltonin inhibits ERK1/2 and AKT activation.
IC50 & Target: ERK1/2, AKT[1][2]
In Vitro: Deltonin inhibits ERK1/2 and AKT activation. Deltonin (0.5-8 μM) significantly inhibits the proliferation of several colon cancer cell lines including SW480, SW620, LOVO and C26, with IC50s of 1.3, 1.29, 2.11 and 1.22 μM. Deltonin also causes G2-M phase arrest and induces apoptosis in C26 cells[1]. Deltonin (0-5 μM) decreases the phosphorylation of AKT and ERK1/2 levels in MDA‑MB‑231 cells. Deltonin (0.5-8 μM) also dose-dependently inhibits the proliferation, and causes apoptosis with ROS production in MDA‑MB‑231 cells[2].
In Vivo: Deltonin (20 and 40 mg/kg, p.o.) reduces the tumor growth of 37.7% and 56.7%, and causes a 50-day survival rate of 60% and 50%, respectively, in mice. Deltonin also inhibits tumor angiogenesis in mice[1].

Name: Fabiatrin, CAS: 18309-73-4, stock 32g, assay 98%, MWt: 486.42, Formula: C21H26O13, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Fabiatrin is a natural product isolated from Przewalskia tangutica[1].

Name: 2''-O-Rhamnosylicariside II, CAS: 135293-13-9, stock 22.5g, assay 98.3%, MWt: 660.66, Formula: C33H40O14, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: 2''-O-Rhamnosylicariside II is a flavonoid glycoside compound and might be beneficial for improving postmenopausal osteoporosis.

Name: Baohuoside VII, CAS: 119730-89-1, stock 1.4g, assay 98.2%, MWt: 676.66, Formula: C33H40O15, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Baohuoside VII is a flavonoid isolated from Herba Epimedii, with anti-osteoporosis activities[1].

Name: Rebaudioside G, CAS: 127345-21-5, stock 21.9g, assay 98.4%, MWt: 804.87, Formula: C38H60O18, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Rebaudioside G is the minor constituent isolated from the leaves of Stevia rebaudiana Bertoni, used for sweeteners research[1].

Name: Chrysin 7-O-beta-gentiobioside Chrysin 7-O-β-gentiobioside, CAS: 88640-89-5, stock 30.2g, assay 98.3%, MWt: 578.52, Formula: C27H30O14, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Chrysin 7-O-beta-gentiobioside (Chrysin 7-O-β-gentiobioside) is the glycosylation product of Chrysin[1].

Name: (2R,3R)-3,7-Dihydroxy-2-(4-hydroxyphenyl)-5-methoxy-8-(3-methylbut-2-en-1-yl)chroman-4-one, CAS: 204935-85-3, stock 1.5g, assay 98.9%, MWt: 370.40, Formula: C21H22O6, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: (2R,3R)-3,7,4'-Trihydroxy-5-methoxy-8-prenylflavanone can be used in a flame retardant for transparent polycarbonate products or in elevator illumination devices research[1][2].

Name: Camellianin A, CAS: 109232-77-1, stock 25.9g, assay 98.2%, MWt: 620.56, Formula: C29H32O15, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Apoptosis, Target: Apoptosis, Biological_Activity: Camellianin A, the main flavonoid in A. nitida leaves, displays anticancer activity and angiotensin converting enzyme (ACE)-inhibitory activity. Camellianin A inhibits the proliferation of the human Hep G2 and MCF-7 cell lines and induces the significant increase of the G0/G1 cell population[1][2].

Name: CID5721353, CAS: 301356-95-6, stock 24.8g, assay 98.3%, MWt: 457.28, Formula: C15H9BrN2O6S2, Solubility: DMSO : ≥ 83.33 mg/mL (182.23 mM), Clinical_Informat: No Development Reported, Pathway: Apoptosis, Target: Apoptosis, Biological_Activity: CID5721353 is an inhibitor of BCL6 with an IC50 value of 212 μM, which corresponds to a Ki of 147 μM.
IC50 & Target: IC50: 212 μM (BCL6)[1] 
Ki: 147 μM(BCL6)[1]
In Vitro: BCL6 is a member of the BTB/POZ family of transcription factors. CID5721353 (Compound 79-6) specifically inhibits BCL6 repressor activity. CID5721353 disrupts BCL6 transcriptional complexes and reactivates BCL6 target genes. CID5721353 can specifically kill primary human DLBCL cells. Fifteen of 19 BCL6-positive cases (79%) display greater than 25% loss of viability in response to CID5721353 at 125 or 250 μM[1].
In Vivo: In order to test whether CID5721353 (Compound 79-6) can perform as an anti-lymphoma therapeutic agent in vivo, whether it can penetrate tumors after parenteral administration through a distal site is determined. For this purpose 107OCI-Ly7 cells are injected into the right flank of 10 SCID mice and allowed to form tumors. Once tumors reach ~1.5 grams, animals are injected IP with a single dose of 50 mg/kg of CID5721353 in 10% DMSO or vehicle (10% DMSO) and sacrificed at 0.5, 1, 1.5, 3, 6, 12 and 24 hours after CID5721353 administration. Blood and tumors are harvested. Quantitative HPLC/MS analysis of the serum shows that CID5721353 levels peak (to 55 μg/mL, which is equivalent to a 122 μM concentration) one hour after the IP injection. CID5721353 also reaches its highest peak (24.5 ng/mg) at the 1-hour time point in the tumors, and after a sharp decline in levels, decreases gradually over 24 hours[1].

Name: NPS-1034, CAS: 1221713-92-3, stock 12.6g, assay 99%, MWt: 551.54, Formula: C31H23F2N5O3, Solubility: DMSO : 34 mg/mL (61.65 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Protein Tyrosine Kinase/RTK;Apoptosis;Protein Tyrosine Kinase/RTK, Target: c-Met/HGFR;Apoptosis;TAM Receptor, Biological_Activity: NPS-1034 is a dual inhibitor of AXL and MET with IC50s of 10.3 and 48 nM, respectively.
IC50 & Target: IC50: 10.3 nM (AXL), 48 nM (MET)[1]
In Vitro: NPS-1034 is a dual inhibitor of AXL and MET with IC50s of 10.3 and 48 nM, respectively.The expression and activity of AXL is significantly increased in HCC827/ER cells, and NPS-1034 treatment effectively inhibits its tyrosine phosphorylation[1]. NPS-1034 inhibits the viability of the MKN45 and SNU638 cell lines, which highly express the MET gene and p-MET (phosphorylated MET), with IC50 values of 112.7 and 190.3 nmol, respectively. In contrast, NPS-1034 inhibits AGS, KATOIII, NCI-N87, MKN1, MKN28, and MKN74 cell viability with IC50 values ranging from 1 μmol to more than 10 μmol. MET phosphorylation is dramatically decreased after treatment with NPS-1034 in the MKN45 cells, but not in the MKN28 cells. NPS-1034 inhibits hepatocyte growth factor (HGF)-stimulated MET autophosphorylation (Y1234/1235) in the AGS and MKN1 cell lines with IC50 values of <10 and <50 nmol, respectively. HGF-induced MET phosphorylation is completely inhibited by 50 nmol NPS-1034[2].
In Vivo: NPS-1034 inhibits tumor proliferation, which highly expresses p-MET. NPS-1034 treatment induces a clear decrease in the vascularization of the tumors. The expression of alpha-smooth muscle actin (α-SMA) is decreased in the tumor sections of mice treated with NPS-1034. NPS-1034-treated mice show virtually no weight loss, indicating that NPS-1034 is generally well tolerated[2].

Name: GSK484 (hydrochloride) GTPL8577, CAS: 1652591-81-5, stock 1.8g, assay 98.3%, MWt: 510.03, Formula: C27H32ClN5O3, Solubility: DMSO : 62.5 mg/mL (122.54 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Epigenetics, Target: Protein Arginine Deiminase, Biological_Activity: GSK484 hydrochloride (GTPL8577) is a selective and reversible peptidylarginine deiminase 4 (PAD4) inhibitor. GSK484 hydrochloride (GTPL8577) demonstrates high affinity binding to PAD4 with IC50s of 50 nM in the absence of Calcium. In the presence of 2 mM Calcium, notably lower potency (250 nM) is observed.
IC50 & Target: IC50: 50 nM (PAD4, in the absence of Calcium), 250 nM (PAD4, in the presence of 2 mM Calcium)[1]
In Vitro: GSK484 demonstrates high affinity binding to the low-calcium form of PAD4 with IC50s of 50 nM and 250 nM in the absence of Calcium (0 mM) and Calcium (2 mM), respectively. GSK484 also inhibits PAD4 citrullination (at 0.2 mM Calcium) of benzoyl-arginine ethyl ester (BAEE) substrate in a concentration-dependent manner, as detected using an NH3 release assay[1].
In Vivo: To address whether PAD4 inhibition can suppress cancer-associated kidney injury, MMTV-PyMT mice are treated with the PAD4 inhibitor GSK484 at 4 mg/kg daily for one week. This dose suppress the elevated number of neutrophils undergoing NETosis in peripheral blood in mice with cancer. In parallel, the total protein level in urine from MMTV-PyMT mice is significantly reduced compared with untreated tumor-bearing mice, further supporting an improved functional status of the kidneys after GSK484 treatment. Administration of GSK484 at a dose of 4 mg/kg daily during one week reverts signs of kidney dysfunction in tumor-bearing mice to the same extent as DNase I treatment, without any detectable signs of toxicity[2].

Name: T-26c, CAS: 869296-13-9, stock 14.1g, assay 98.6%, MWt: 479.51, Formula: C24H21N3O6S, Solubility: H2O : < 0.1 mg/mL (insoluble); DMSO : 15.62 mg/mL (32.57 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: MMP, Biological_Activity: T-26c is highly potent and selective matrix metalloproteinase-13 (MMP-13) inhibitor with an IC50 of 6.75 pM and more than 2600-fold selectivity over the other related metalloenzymes[1].
IC50 & Target: IC50: 6.75 pM (MMP-13)[1]
In Vitro: T-26c significantly inhibits the breakdown of collagen (87.4% inhibition at 0.1 μM) in IL-1β and oncostatin M stimulated cartilage[1].
In Vivo: T-26c is well absorbed in all species at the oral dose of 10–20 mg/kg. Oral administration of the disodium salt formulations of T-26c to guinea pigs results in significant increases in AUC (8357 ng h/mL) and Cmax (1445 ng/ mL) compared with those of the free acid T-26c (AUC = 6478 ng h/ mL and Cmax= 911 ng/mL)[1].

Name: AN2718, CAS: 174672-06-1, stock 20g, assay 98.2%, MWt: 168.39, Formula: C7H6BClO2, Solubility: 10 mM in DMSO, Clinical_Informat: Phase 1, Pathway: Anti-infection, Target: Fungal, Biological_Activity: AN2718 inhibits fungal growth by blocking protein synthesis using the oxaborole tRNA trapping (OBORT) mechanism.
IC50 & Target: Fungal[1].
In Vitro: AN2718 inhibits cytoplasmic LeuRS from molds, A. fumigatus, and from yeasts, C. albicans, with an IC50 of 2 μM and 4.2 μM, respectively. AN2718 has good MIC90 activity against the dermatophytes, T. rubrum and T.mentagrophytes[1].

Name: Rp-cAMPS (triethylammonium salt), CAS: 151837-09-1, stock 30.7g, assay 98.1%, MWt: 446.46, Formula: C16H27N6O5PS, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Stem Cell/Wnt;Protein Tyrosine Kinase/RTK, Target: PKA;PKA, Biological_Activity: Rp-cAMPS triethylammonium salt is an analog of cAMP which acts as a potent, competitive and cell-permeable antagonist of cAMP-induced activation of cAMP-dependent PKA I and II (Kis of 6.05 µM and 9.75 µM, respectively). Rp-cAMPS triethylammonium salt is resistant to hydrolysis by phosphodiesterases[1][2][3][4][5].
IC50 & Target: Ki: 6.05 µM (PKA I) and 9.75 µM (PKA II)[1]
In Vitro: A membrane-permeable competitive cAMP antagonist (Rp-cAMPS) that blocks PKA activation by binding to the regulatory subunits without dissociating the kinase holoenzyme also inhibits synaptic plasticity but has no effect on normal synaptic transmission[1].
In Vivo: Rp-cAMPS (10 μM, 15 min) decreases the monosynaptic EPSCs evoked at the PB-CeLC and BLA-CeLC synapses in slices from arthritic rats but not in control neurons from normal animals. The inhibitory effect of Rp-cAMPS is significant compared to predrug (ACSF) control values obtained in the same neurons[1].

Name: CD437 AHPN, CAS: 125316-60-1, stock 18.3g, assay 98.7%, MWt: 398.49, Formula: C27H26O3, Solubility: DMSO : 150 mg/mL (376.42 mM; Need ultrasonic and warming); H2O : < 0.1 mg/mL (insoluble), Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease;Autophagy, Target: RAR/RXR;Autophagy, Biological_Activity: CD437 is a selective Retinoic Acid Receptor γ (RARγ) agonist.
IC50 & Target: Retinoic Acid Receptor γ (RARγ)[1]
In Vitro: CD437 is a selective RARγ agonist. Growth inhibition by CD437 in these lung cancer cell lines is apparent after 2 days of treatment with 10 μM CD437. Dose-response experiments demonstrate that CD437 reduces the numbers of H460, SK-MES-1, A549, and H292 cells with 50% inhibitory values of approximately 0.5, 0.4, 3, and 0.85 μM, respectively[1]. Treatment for 72 h with CD437 causes a strong dose-dependent growth inhibition in all melanoma cell lines. At a concentration of 5 μM CD437, only about 5 to 25% of the cells remain viable after 3 d. The concentrations of CD437 required for 50% growth inhibition (IC50) range from 10 μM for MeWo to 0.1 μM for SK-Mel-23 showing the highest sensitivity[2].
In Vivo: Tumors in CD437-treated mice stop growing, an effect that becomes already statistically significant (P<0.01) at day 13, 3 d after first administration of CD437, and is maintained for more than 3 wk after discontinuation of treatment. Further histologic analysis demonstrates marked c-fos mRNA levels at the tumor-stroma edge in CD437-treated tumors[2].

Name: WAY-100635 Maleate, CAS: 1092679-51-0, stock 28.2g, assay 98.7%, MWt: 538.64, Formula: C29H38N4O6, Solubility: H2O : 25 mg/mL (46.41 mM; Need ultrasonic); DMSO : ≥ 250 mg/mL (464.13 mM), Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein;Neuronal Signaling;Neuronal Signaling;GPCR/G Protein, Target: Dopamine Receptor;Dopamine Receptor;5-HT Receptor;5-HT Receptor, Biological_Activity: WAY-100635 maleate is a potent and selective 5-hydroxytryptamine 1A (5-HT1A) receptor antagonist with an IC50 value of 0.91 nM and Ki value of 0.39 nM. WAY-100635 maleate has pIC50 values for 5-HT1A and α1-adrenergic receptors of 8.9 and 6.6, respectively. WAY-100635 maleate is also a potent dopamine D4 receptor agonist[1][2][3].
IC50 & Target: pIC50 Value: 8.87 (5-HT1A Receptor)[1].
In Vitro: The functional properties and binding affinities of WAY-100635 are evaluated in HEK 293 cells stably expressing dopamine D2L or D4.4 receptors[1]. 
WAY-100635 displays 940, 370, and 16 nM binding affinities at D2L, D3, and D4.2 receptors, respectively. Saturation analyses demonstrat that the Kd of [3H] WAY-100635 at D4.2 receptors is 2.4 nM. WAY-100635 is potent agonist in HEK-D4.4 cells with EC50 of 9.7 nM. WAY-100635 possesses high affinity for D4.4 receptor (3.3 nM) [1].
In Vivo: WAY-100635 (1 mg/kg; subcutaneous injection; male Sprague-Dawley rats) treatment abolishes the reduction of the severity of abstinence signs induced by Rhodiola rosea administration in nicotine-dependent rat[2].

Name: Golgicide A, CAS: 1139889-93-2, stock 34.5g, assay 98.5%, MWt: 284.30, Formula: C17H14F2N2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Golgicide A is a potent, highly specific, and reversible inhibitor of the cis-Golgi ADP-ribosylation factor guanine nucleotide exchange factors (ArfGEF), GBF1[1].
IC50 & Target: GBF1[1]
In Vitro: Golgicide A (GCA) is a potent and highly effective inhibitor of shiga toxin activity. Golgicide A (GCA) inhibits the effect of shiga toxin on protein synthesis with an IC50 of 3.3 μM[1].

Name: FLLL32, CAS: 1226895-15-3, stock 23.9g, assay 98.5%, MWt: 464.55, Formula: C28H32O6, Solubility: DMSO : 125 mg/mL (269.08 mM; Need ultrasonic); H2O : < 0.1 mg/mL (insoluble), Clinical_Informat: No Development Reported, Pathway: Apoptosis;Epigenetics;Stem Cell/Wnt;JAK/STAT Signaling;JAK/STAT Signaling;Stem Cell/Wnt, Target: Apoptosis;JAK;JAK;JAK;STAT;STAT, Biological_Activity: FLLL32, a synthetic analog of curcumina, is a JAK2/STAT3 dual inhibitor with anti-tumor activity[1][2].
IC50 & Target: JAK2/STAT3[1]
In Vitro: FLLL32 specifically reduces STAT3 phosphorylation at Tyr705 (pSTAT3) and induces apoptosis at micromolar amounts in human melanoma cell lines and primary melanoma cultures[1].

Name: (S)-Crizotinib, CAS: 1374356-45-2, stock 35.2g, assay 98.1%, MWt: 450.34, Formula: C21H22Cl2FN5O, Solubility: DMSO : 12.5 mg/mL (27.76 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Apoptosis;Cell Cycle/DNA Damage, Target: Apoptosis;DNA/RNA Synthesis, Biological_Activity: (S)-Crizotinib is a potent and selective MTH1 (mutT homologue) inhibitor with an IC50 of 330 nM. (S)-Crizotinib disrupts nucleotide pool homeostasis via MTH1 inhibition, induces an increase in DNA single strand breaks, activates DNA repair in human colon carcinoma cells, and effectively suppresses tumour growth in animal models[1].
IC50 & Target: IC50: 330 nM (MTH1)[1]
In Vitro: (S)-crizotinib (0.625-80 μM; 24 hours) decreases the viability of NCI-H460, H1975 and A549 cells with IC50 values of 14.29, 16.54 and 11.25 μM, respectively[2]. 
(S)-crizotinib (10-30 μM; 24 hours) induces NCI-H460, H1975 and A549 cells apoptosis[2]. 
(S)-crizotinib (10-30 μM; 24 hours) decreases Bcl-2: Bax ratio. (S)-crizotinib decreases B cell lymphoma 2 (Bcl-2), and Bcl-2 associated protein x (Bax) is either unaltered (H460 cells) or shows an increase (H1975 cells)[2]. 
(S)-Crizotinib induces apoptosis in human non-small cell lung cancer (NSCLC) cells by activating ROS-dependent ER stress apoptotic pathway independent of mutT homologue (MTH1)[2]. 
In Vivo: (S)-crizotinib (7.5 or 15 mg/kg; intraperitoneal injections; once daily for 10 days) results in significant reductions in both tumor volume and tumor weight[2].

Name: meso-Erythritol, CAS: 149-32-6, stock 34.4g, assay 98.9%, MWt: 122.12, Formula: C4H10O4, Solubility: 10 mM in H2O, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: meso-Erythritol is a sugar alcohol that occurs naturally in a variety of foods (e.g., pear, watermelon), is 60-80% as sweet as sucrose, and is an approved low-calorie sweetener food additive[1].

Name: BTZ043 Racemate BTZ10526038; Benzothiazinone 10526038, CAS: 957217-65-1, stock 4.7g, assay 98.4%, MWt: 431.39, Formula: C17H16F3N3O5S, Solubility: DMSO : ≥ 30 mg/mL (69.54 mM), Clinical_Informat: Phase 1, Pathway: Anti-infection, Target: Bacterial, Biological_Activity: BTZ043 Racemate is the racemate of BTZ043. BTZ043 is an inhibitor of decaprenyl-phosphoribose-epimerase (DprE1), and the antimicrobial activity of BTZ043 is more potent than BTZ043 Racemate.
IC50 & Target: DprE1[1].

Name: Cyclo(RGDyK) trifluoroacetate, CAS: 250612-42-1, stock 7.4g, assay 98.2%, MWt: 847.72, Formula: C31H43F6N9O12, Solubility: DMSO : ≥ 130 mg/mL (153.35 mM), Clinical_Informat: No Development Reported, Pathway: Cytoskeleton, Target: Integrin, Biological_Activity: Cyclo(RGDyK) trifluoroacetate is a potent and selective αVβ3 integrin inhibitor with an IC50 of 20 nM.
IC50 & Target: IC50: 20 nM (αVβ3 Integrin), 3000 nM (αIIbβ3 Integrin), 4000 nM (αVβ5 Integrin)[1]
In Vitro: Cyclo(RGDyK) (c(RGDyK(SAA)) shows high affinity and selectivity for αVβ3 over αVβ5 (IC50=4000 nM) and αIIbβ3 (IC50=3000 nM)[1].

Name: Cl-amidine (hydrochloride), CAS: 1373232-26-8, stock 26.3g, assay 99%, MWt: 347.24, Formula: C14H20Cl2N4O2, Solubility: DMSO : 19.23 mg/mL (55.38 mM; Need ultrasonic); H2O : 50 mg/mL (143.99 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Epigenetics, Target: Protein Arginine Deiminase, Biological_Activity: Cl-amidine (hydrochloride) is a peptidylarginine deminase (PAD) inhibitor, with an IC50 5.9 μM for PAD4.
IC50 & Target: IC50: 5.9 μM (PAD4)[1].
In Vitro: Cl-amidine is a peptidylarginine deminase (PAD) inhibitor, with an IC50 of 5.9±0.3 μM for PAD4 and Cl-amidine is a bioavailable haloacetamidine-based compound that inhibits all the active PAD isozymes with near equal potency (kinact/KI=13,000 M-1.min-1 for PAD4)[1]. Cl-amidine induces apoptosis (identified as annexin V-positive/propidium iodide-negative cells) in such cells in a dose-dependent manner, indicating that Cl-amidine induces apoptosis of WBCs in vitro. Interestingly, the colon cancer cell line (HT29) is relatively resistant to apoptosis caused by Cl-amidine[2].
In Vivo: Significantly higher levels of colon inflammation in the 2% DSS than the 2% DSS+Cl-amidine mice are showed. The mean histology scores are 24.2±1.7 (SE) and 13.9±1.6, respectively. Most of the damage in the DSS-only group is in the distal colon, and this damage is suppressed with DSS+Cl-amidine. For the DSS-treated group, the mean colon length is 7.2±0.2 cm. In contrast, the average colon length of the DSS+Cl-amidine group is 8.4±0.2 cm, which is comparable to the mean colon lengths obtained for the wateralone and water+Cl-amidine groups (8.4±0.3 and 7.9±0.2 cm, respectively). The total distance and average speed of mice over a 96-h period are also measured. The results of these analyses demonstrate that the total distance is 5,072±381 and 3,190±401 m for the water-treated and DSS+Cl-amidine mice, but only 800±163 m for the DSS-only group. Similarly, the average speed on the wheel over the 4-day period is 6.2±0.63 and 5.3±0.58 m/min for the water-treated and DSS+Cl-amidine groups, but only 1.8±0.51 m/min for the DSS group[2].

Name: NH125, CAS: 278603-08-0, stock 8.5g, assay 98.2%, MWt: 524.56, Formula: C27H45IN2, Solubility: DMSO : 160 mg/mL (ultrasonic), Clinical_Informat: No Development Reported, Pathway: Anti-infection;Neuronal Signaling;Anti-infection;Autophagy;Anti-infection, Target: Fungal;CaMK;Bacterial;Autophagy;Virus Protease, Biological_Activity: NH125 is a potent and selective inhibitor of eukaryotic elongation factor 2 kinase (eEF-2K/CaMKIII), also could induce eEF2 phosphorylation, with an IC50 of 60 nM for eEF-2K.
IC50 & Target: IC50: 60 nM (eEF-2K/CaMKIII)[1].
In Vitro: NH125 inhibits eEF-2 kinase activity (IC50 = 60 nM) in vitro, blocks the phosphorylation of eEF-2 in intact cells, and shows relative selectivity over other protein kinases: protein kinase C (IC50 = 7.5 μM), protein kinase A (IC50 = 80 μM), and calmodulin-dependent kinase II (IC50 > 100 μM). NH125 decreases the viability of 10 cancer cell lines with IC50s ranging from 0.7 to 4.7 μM. Forced overexpression of eEF-2 kinase in a glioma cell line produces 10-fold resistance to NH125. In conclusion, these results suggest that identification of potent inhibitors of eEF-2 kinase may lead to the development of new types of anticancer drugs[1]. Anticancer effect of NH125 is not mediated through inhibition of eEF2K. Inhibition of cell growth correlates with induction of peEF2[2].

Name: Ferrostatin-1, CAS: 347174-05-4, stock 30.7g, assay 98.1%, MWt: 262.35, Formula: C15H22N2O2, Solubility: DMSO : ≥ 150 mg/mL (571.76 mM), Clinical_Informat: No Development Reported, Pathway: Apoptosis, Target: Ferroptosis, Biological_Activity: Ferrostatin-1 is a potent inhibitor of ferroptosis with an EC50 of 60 nM.
IC50 & Target: EC50: 60 nM (Ferroptosis)[1]
In Vitro: Ferrostatin-1 is the most potent inhibitor of erastin-induced ferroptosis in HT-1080 cells (EC50=60 nM). Ferrostatin-1 does not inhibit ERK phosphorylation or arrest the proliferation of HT-1080 cells. Ferrostatin-1 does, however, prevent erastin-induced accumulation of cytosolic and lipid ROS[1]. Cells pretreated with 0.4 μM Ferrostatin-1 displays significantly reduce intracellular reactive oxygen species (ROS) and nitrogen species (RNS) below basal levels. Additionally, increased intracellular ROS levels are also significantly lowered below basal levels by a 0.4 µM Ferrostatin-1 pretreatment. Ferrostatin-1 treatment for 24 h does not change the expression level of i-NOS in SHSY-5Y cell when compare with vehicle (0.02 % DMSO) treated cells[2].

Name: CORM-3, CAS: 475473-26-8, stock 18.7g, assay 98.6%, MWt: 294.61, Formula: C5H4ClNO5Ru, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: NF-κB, Target: NF-κB, Biological_Activity: CORM-3, a water-soluble carbon monoxide-releasing molecule, attenuates NF-κB p65 nuclear translocation, reduces ROS generation and enhances intracellular glutathione and superoxide dismutase levels[1][2][3].

Name: Splitomicin Splitomycin, CAS: 5690-03-9, stock 12.8g, assay 98.6%, MWt: 198.22, Formula: C13H10O2, Solubility: DMSO : 250 mg/mL (1261.22 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Epigenetics;Cell Cycle/DNA Damage, Target: HDAC;HDAC, Biological_Activity: Splitomicin (Splitomycin) is a selective Sir2p inhibitor. Splitomicin inhibits NAD+-dependent HDAC activity of Sir2 protein. Splitomicin induces dose-dependent inhibition of HDAC in the yeast extract with an IC50 of 60 μM[1].
In Vitro: Splitomicin (10-333 μM; 24 hours) elicits antiproliferative effects in MCF-7 and H1299 cells in a dose-dependent manner in colony formation assay. Splitomicin (33 μM) fails to decrease the number of colonies, but Splitomicin (100 and 333 μM) effectively inhibits colony formation in MCF-7 and H1299 cells[2].
In Vivo: Splitomicin (80 mg/kg with an intraperitoneal injection every 24 h for 5 days, in mice) enhances tissue factor (TF) activity in the arterial vessel wall and accelerates carotid artery thrombus formation in a photochemical injury model[3].

Name: Alizapride hydrochloride, CAS: 59338-87-3, stock 29g, assay 98.4%, MWt: 351.83, Formula: C16H22ClN5O2, Solubility: DMSO : 60 mg/mL (170.54 mM; Need ultrasonic and warming), Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein;Neuronal Signaling, Target: Dopamine Receptor;Dopamine Receptor, Biological_Activity: Alizapride hydrochloride is a dopamine receptor antagonist with prokinetic and antiemetic effects which can also be used in the treatment of nausea and vomiting, including postoperative nausea and vomiting.
IC50 & Target: Dopamine receptor[1]

Name: SirReal2, CAS: 709002-46-0, stock 15.8g, assay 98.1%, MWt: 420.55, Formula: C22H20N4OS2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Epigenetics;Cell Cycle/DNA Damage, Target: Sirtuin;Sirtuin, Biological_Activity: SirReal2 is a potent, isotype-selective Sirt2 inhibitor with an IC50 value of 140 nM and has very little effect on the activities of Sirt3-5. SirReal2 leads to tubulin hyperacetylation in HeLa cells and induces destabilization of the checkpoint protein BubR1[1].
IC50 & Target: IC50: 140 nM (Sirt2)[1]

Name: Saponins Saponin, CAS: 8047-15-2, stock 11.8g, assay 98.6%, MWt: 1000, Formula: N/A, Solubility: H2O : 33.33 mg/mL (Need ultrasonic), Clinical_Informat: Phase 4, Pathway: Others, Target: Others, Biological_Activity: Saponins are a class of chemical compounds of glycosides found in particular abundance in various plant species. In plants, saponins may serve as anti-feedants, and to protect the plant against microbes and fungi[1].
In Vitro: Saponins are glycosides with a distinctive foaming characteristic. Saponins consist of a polycyclic aglycone that is either a choline steroid or triterpenoid attached via C3 and an ether bond to a sugar side chain. The ability of a saponin to foam is caused by the combination of the nonpolar sapogenin and the water soluble side chain. Saponins are bitter and reduce the palatability of livestock feeds. Some saponins reduce the feed intake and growth rate of nonruminant animals while others are not very harmful. For example, the saponins found in oats and spinach increase and accelerate the body's ability to absorb calcium and silicon, thus assisting in digestion. Certain pasture weeds contain substantial quantities of dangerous saponins and result in life threatening toxicities for certain animal species[1].

Name: Grape seed extract, CAS: 84929-27-1, stock 30.9g, assay 98.9%, MWt: 1000, Formula: N/A, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Grape seed extract is a natural product with various health benefits, including anti-inflammatory effect. Grape seed extract shows inhibitory activity on the fat-metabolizing enzymes pancreatic lipase and lipoprotein lipase[1][2].

Name: Ipragliflozin (L-Proline), CAS: 951382-34-6, stock 35.7g, assay 98.5%, MWt: 519.58, Formula: C26H30FNO7S, Solubility: 10 mM in DMSO, Clinical_Informat: Phase 4, Pathway: Membrane Transporter/Ion Channel, Target: SGLT, Biological_Activity: Ipragliflozin (L-Proline) is a highly potent and selective SGLT2 inhibitor with an IC50 of 2.8 nM; little and NO potency for SGLT1/3/4/5/6.
IC50 & Target: IC50 value: 2.8 nM (SGLT2)[1][2].
In Vitro: Ipragliflozin (L-Proline) potently and selectively inhibits human, rat, and mouse SGLT2 at nanomolar ranges and exhibits stability against intestinal glucosidases[3].
In Vivo: Ipragliflozin (L-Proline) shows good pharmacokinetic properties following oral dosing, and dose-dependently increases urinary glucose excretion, which lasts for over 12 h in normal mice [3]. Oral administration of ipragliflozin increases urinary glucose excretion in a dose-dependent manner, an effect which is significant at doses of 0.3 mg/kg or higher and lasts over 12 h[4]. Single administration of ipragliflozin dose-dependently increases urinary glucose excretion, reduces blood glucose and plasma insulin levels, and improves glucose intolerance [5].

Name: BGG463 K03859, CAS: 890129-26-7, stock 4.8g, assay 98.5%, MWt: 578.58, Formula: C30H29F3N6O3, Solubility: DMSO : ≥ 125 mg/mL (216.05 mM), Clinical_Informat: No Development Reported, Pathway: Cell Cycle/DNA Damage, Target: CDK, Biological_Activity: BGG463 (K03859) is an orally active type II CDK2 inhibitor[1].
In Vitro: BGG463 potently inhibits T315I BCR–ABL autophosphorylation and shows good oral efficacy in mouse models of CML[2].

Name: Landiolol (hydrochloride) ONO1101 (hydrochloride), CAS: 144481-98-1, stock 19.1g, assay 98.1%, MWt: 546.05, Formula: C25H40ClN3O8, Solubility: 10 mM in DMSO, Clinical_Informat: Launched, Pathway: GPCR/G Protein;Neuronal Signaling, Target: Adrenergic Receptor;Adrenergic Receptor, Biological_Activity: Landiolol hydrochloride (ONO1101 hydrochloride) is a highly beta1 selective ultra-short acting beta-blocker (β1/β2 selectivity = 255:1, a half-life of 4 min)， acts as an adrenoceptor antagonist[1].
IC50 & Target: beta-adrenergic receptor[1]

Name: 4-P-PDOT, CAS: 134865-74-0, stock 37.7g, assay 98.6%, MWt: 279.38, Formula: C19H21NO, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein;Neuronal Signaling, Target: Melatonin Receptor;Melatonin Receptor, Biological_Activity: 4-P-PDOT is a potent, selective and affinity Melatonin receptor (MT2) antagonist. 4-P-PDOT is >300-fold more selective for MT2 than MT1. 4-P-PDOT significantly counteracts Melatonin-mediated antioxidant effects (GSH/GSSG ratio, phospho-ERK, Nrf2 nuclear translocation, Nrf2 DNA-binding activity)[1][2][3][4].
IC50 & Target: MT2 receptor[1]
In Vitro: In CHO-mt1 cells the amidotetraline 4-P-PDOT (10 mM) has no e€ect on forskolin-stimulated cyclic AMP levels, either alone, or in the presence of Melatonin. In contrast, in CHO-MT2 cells, 4-P-PDOT is an agonist, producing a concentration-dependent inhibition of forskolin stimulated cyclic AMP, with a pEC50 value of 8.72 and intrinsic activity of 0.86[1].
In Vivo: 4-P-PDOT (0.5-1.0 mg/kg; intravenous injection; klotho mutant mice) treatment significantly reverses antioxidant effects mediated by Melatonin. And significantly reverses the changes in the levels of these GSH-related parameters. 4-P-PDOT treatment significantly reverses the memory function of Melatonin-treated klotho mutant mice. 4-P-PDOT also counteracts Melatonin-mediated attenuation in response to the decreases in phospho-ERK expression, Nrf2 nuclear translocation, Nrf2 DNA-binding activity, and GCL mRNA expression in the hippocampi of klotho mutant mice[2].

Name: T16Ainh-A01, CAS: 552309-42-9, stock 3.1g, assay 98.3%, MWt: 416.52, Formula: C19H20N4O3S2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Membrane Transporter/Ion Channel, Target: Chloride Channel, Biological_Activity: T16Ainh-A01, an aminophenylthiazole, is a potent transmembrane protein 16A (TMEM16A) inhibitor, inhibiting TMEM16A-mediated chloride currents with an IC50 value of ~1 µM. TMEM16A (ANO1) functions as a calcium-activated chloride channel (CaCC)[1][2].
IC50 & Target: TMEM16A[1].

Name: BVT948, CAS: 39674-97-0, stock 21.5g, assay 98.7%, MWt: 241.24, Formula: C14H11NO3, Solubility: DMSO : 100 mg/mL (414.52 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Epigenetics;Metabolic Enzyme/Protease;Metabolic Enzyme/Protease, Target: Histone Methyltransferase;Cytochrome P450;Phosphatase, Biological_Activity: BVT948 is a protein tyrosine phosphatase (PTP) inhibitor which can also inhibit several cytochrome P450 (P450) isoforms and lysine methyltransferase SETD8 (KMT5A).
IC50 & Target: PTP[1], P450[1], SETD8[2]
In Vitro: Results show that the effect of BVT948 (BVT.948) is to strengthen the insulin signal and has no effects on the duration of the signal. BVT948 appears to be an effective inhibitor of both protein tyrosine phosphatases (PTP activity and P450 activity)[1]. BVT948 efficiently and selectively suppresses cellular H4 lysine 20 (H4K20me1) at doses lower than 5 μM within 24 h. The cells treated with BVT948 recapitulate cell-cycle-arrest phenotypes similar to what are reported for knocking down SETD8 by RNAi[2]. Treatment of MCF-7 cells with 0.5, 1 or 5 μM of BVT948 for 24 h does not cause any significant changes in cell viability. BVT948 inhibits TPA-induced MMP-9 up-regulation in a dose-dependent manner. Treatment with BVT948 inhibits TPA-stimulated NF-κB binding activity, but not AP-1 binding activity. BVT948 does not affect the MAPK phosphorylation by TPA. Treatment with BVT948 diminishes the TPA-induced cell invasion by 50%[3].
In Vivo: Results show that 3 μmol/kg BVT948 (BVT.948) significantly enhances glucose clearance from the blood stream in response to insulin compare with vehicle-treated controls[1].

Name: Lurasidone Metabolite 14283 hydrochloride, CAS: 186204-32-0, stock 1.1g, assay 98.2%, MWt: 545.14, Formula: C28H37ClN4O3S, Solubility: Ethanol : 100 mg/mL (183.44 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Drug Metabolite, Biological_Activity: Lurasidone Metabolite 14283 hydrochloride is a major active metabolite of Lurasidone. Lurasidone is a FDA approved drug for the treatment of schizophrenia.

Name: L002, CAS: 321695-57-2, stock 6.2g, assay 98.1%, MWt: 321.35, Formula: C15H15NO5S, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Epigenetics;JAK/STAT Signaling;Stem Cell/Wnt, Target: Histone Acetyltransferase;STAT;STAT, Biological_Activity: L002 is a novel potent, specific acetyltransferase p300 (KAT3B) inhibitor with an IC50 of 1.98 uM. L002 has weak inhibitory effects against PCAF and GCN5 (IC50s =35 and 34 µM, respectively) and is specific for p300 over a panel of additional acetyltransferases, deacetylases, and methyltransferases[1]. L002 blocks histone acetylation and p53 acetylation, and inhibits STAT3 activation[2].
IC50 & Target: IC50: 1.98 uM (KAT3B); 35 µM (PCAF); 34 µM (GCN5)[1] ;STAT3; p53[2]

Name: JTE-013, CAS: 383150-41-2, stock 30.6g, assay 98.2%, MWt: 408.29, Formula: C17H19Cl2N7O, Solubility: DMSO : 100 mg/mL (244.92 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein;Apoptosis, Target: LPL Receptor;Apoptosis, Biological_Activity: JTE-013 is a potent and specific S1P2 (Sphingosine-1-Phosphate 2; EDG-5) antagonist. JTE-013 inhibits the specific binding of radiolabeled S1P to human and rat S1P2 with IC50s of 17 nM and 22 nM, respectively[1].
IC50 & Target: IC50: 17 nM (S1P2 for human) and 22 nM (S1P2 for rat)[1]
In Vitro: JTE-013 (50-200 μM; 1-3 days) reduced cell viability[1]. 
JTE-013 (10-1000 nM; 30 mins) reverses S1P-induced Akt inhibition and inhibits S1P-induced ERK activation[1]. 
JTE-013 displays 4.2% inhibition of S1P3 and does not antagonize S1P1 at concentrations up to 10 μM[1].
In Vivo: JTE-013 (gavage; 30 mg/kg daily for 14 consecutive days) reduces tumor size and tumor weight[1].

Name: CGS 15943, CAS: 104615-18-1, stock 30.4g, assay 98.8%, MWt: 285.69, Formula: C13H8ClN5O, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: PI3K/Akt/mTOR;GPCR/G Protein, Target: PI3K;Adenosine Receptor, Biological_Activity: CGS 15943 is an orally bioavailable non-xanthine Adenosine Receptor antagonist. Its Ki for human A1, A2A, A2B, and A3 Adenosine Receptors are 3.5, 4.2, 16, and 50 nM in transfected CHO cells, respectively. [1][2].
In Vitro: CGS 15943 inhibits the kinase activity of the class IB PI3K isoform p110γ with an IC50 of 1.1 μM and shows slight inhibition on p110δ with an IC50 of 8.47 μM[3].
CGS 15943 (0-20 μM; 72 hours) inhibits growth of HLF and SK-Hep-1 cells, as well as HepG2 and PLC-PRF-5 cells[3].
CGS 15943 (0-20 μM; 24 hours) reduces the phosphorylation of Akt at its residues Ser473 and Thr308 in HLF and Sk-Hep-1 cells[3].

Name: Glucagon (19-29), human, CAS: 64790-15-4, stock 39.2g, assay 98.6%, MWt: 1352.53, Formula: C61H89N15O18S, Solubility: H2O, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Glucagon (19-29), human is a potent and efficient inhibitor of insulin secretion.
IC50 & Target: Insulin secretion[1]
In Vitro: Glucagon (19-29), from 0.1 pM to 1 nM, exerts a potent negative inotropic action. The most striking observation is a 45% increase in the amplitude of cell contractility elicited by the combination of 30 nM glucagon with 1 nM Glucagon (19-29)[3].
In Vivo: Glucagon (19-29), also named Miniglucagon, is the COOH-terminal (19-29) fragment processed from glucagon. Glucagon (19-29) dose-dependently inhibits insulin secretion stimulated by 8.3 M glucose, with no change in the perfusion flow rate. A concentration of 1 nM Glucagon (19-29) has a significant inhibitory effect on a 1 nM glucagon-like peptide 1 (7-36) amide–potentiated insulin secretion[1]. Glucagon (19-29) is a highly potent and efficient inhibitor of insulin release by closing, via hyperpolarization, voltage-dependent Ca2+ channels linked to a pathway involving a pertussis toxin-sensitive G protein[2].

Name: D-Glucuronic acid lactone D-Glucurono-6,3-lactone; D-Glucurono-γ-lactone; D-Glucuronolactone; Dicurone; Glucoxy; Glucurolactone; Glucurone, CAS: 32449-92-6, stock 19.9g, assay 98.1%, MWt: 176.12, Formula: C6H8O6, Solubility: , Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity:

Name: Propyl pyrazole triol PPT, CAS: 263717-53-9, stock 3g, assay 98.3%, MWt: 386.44, Formula: C24H22N2O3, Solubility: DMSO : ≥ 100 mg/mL (258.77 mM), Clinical_Informat: No Development Reported, Pathway: Others, Target: Estrogen Receptor/ERR, Biological_Activity: Propyl pyrazole triol (PPT) is an estrogen receptor alpha (ERα) agonist. The relative binding affinity of Propyl pyrazole triol for ERα (ERα: 49%) around 410 times higher compared with estrogen receptor beta (ERβ: 0.12%)[1].
IC50 & Target: Estrogen receptor alpha[1]
In Vitro: The EC50 of Propyl pyrazole triol for the ERα-dependent response is 140 pM in ERα-U2OS-Luc cells[1].

Name: NSC16168, CAS: 6837-93-0, stock 4.6g, assay 98.1%, MWt: 473.50, Formula: C17H15NO9S3, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: NSC16168 is a specific inhibitor of ERCC1-XPF, with an IC50 value of 0.42 μM. NSC16168 inhibits DNA repair and potentiates CDDP efficacy in cancer[1].
IC50 & Target: IC50: 0.42 μM (ERCC1-XPF)[1].

Name: PHA-793887, CAS: 718630-59-2, stock 34.7g, assay 98.3%, MWt: 361.48, Formula: C19H31N5O2, Solubility: DMSO : ≥ 50 mg/mL (138.32 mM), Clinical_Informat: Phase 1, Pathway: Apoptosis;Cell Cycle/DNA Damage, Target: Apoptosis;CDK, Biological_Activity: PHA-793887 is a potent, ATP-competitive CDK inhibitor, can inhibit Cdk2, Cdk1, Cdk4, and Cdk9 with IC50s of 8 nM, 60 nM, 62 nM and 138 nM, respectively, and also inhibits glycogen synthase kinase 3β with an IC50 of 79 nM.
IC50 & Target: IC50: 8 nM (Cdk2), 60 nM (Cdk1), 62 nM (Cdk4) 138 nM (Cdk9), 79 nM (GSK-3β)[1][4], 5 nM (CDK5/p25), 10 nM (CDK7/cyclin H)[4] 
Ki: 8 nM (CDK2/Cyclin A)[2]
In Vitro: PHA-793887 partially inhibits Rb phosphorylation at 1 μM and almost completely at 3 μM, in A2780 tumor cell line. PHA-793887 (1 μM) partially inhibits phosphorylation of the Cdk2 substrates Rb and NPM in A2780 tumor cell line. PHA-793887 (6 μM) significantly inhibits Rb and NPM phosphorylation in MCF7 cell line[1]. PHA-793887 shows cytotoxic activities against leukemic cell lines in vitro, with IC50 ranging from 0.3 to 7 μM. In colony assays, PHA-793887 is highly cytotoxic for leukemia cell lines, with an IC50 <0.1 μM. PHA-793887 induces cell-cycle arrest, inhibits Rb and nucleophosmin phosphorylation, and modulates cyclin E and cdc6 expression at low doses of 0.2 to 1 μM and induces apoptosis at the highest dose of 5 μM. PHA-793887 is a novel inhibitor of several cdk, including cdk1, cdk2, cdk4, cdk5, cdk7, and cdk9 with IC50 in the 5 to 140 nM range[3].
In Vivo: PHA-793887 induces tumor growth inhibition in the range of 50% at dose of 15 mg/kg to 75% at dose of 30 mg/kg in CD-1 nude mice. PHA-793887 (30 mg/kg, i.v.) also induces significant downregulation of the 58-gene panel in the skin of CD-1 mice[1]. PHA-793887 (20 mg/kg, i.v.) induces tumor regression in the HL60 model. In the K562 model, PHA-793887 significantly reduces tumor growth. Moreover, PHA-793887 (20 mg/kg, i.v.) inhibits human primary leukemia growth in engraftment setting in vivo[3].

Name: Pipamperone Floropipamide; McN-JR 3345; R 3345, CAS: 1893-33-0, stock 3g, assay 98.8%, MWt: 375.48, Formula: C21H30FN3O2, Solubility: 0.1 M HCL : 25 mg/mL (66.58 mM; Need ultrasonic), Clinical_Informat: Phase 3, Pathway: GPCR/G Protein;Neuronal Signaling;Neuronal Signaling;GPCR/G Protein, Target: Dopamine Receptor;Dopamine Receptor;5-HT Receptor;5-HT Receptor, Biological_Activity: Pipamperone (Floropipamide; McN-JR 3345; R 3345) is a high-affinity antagonist of 5-HT2A receptor (pKi=8.2) and D4 receptor (pKi=8.0) and a low-affinity antagonist of D2 receptor (pKi=6.7)[1].
IC50 & Target: pKi : 8.2 (5-HT2A receptor), 8.0 (D4 receptor), 6.7 (D2 receptor), 7.2 (α1 receptor), 6.9 (5-HT2C receptor), 5.7 (H1 receptor)[1]

Name: Prodigiosin Prodigiosine, CAS: 82-89-3, stock 32.7g, assay 98.9%, MWt: 323.43, Formula: C20H25N3O, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Anti-infection, Target: Fungal, Biological_Activity: Prodigiosin (Prodigiosine) is a secondary metabolite of Symbiotic bacteria, with anti-fungal and anti-cancer activity[1][2].
IC50 & Target: Fungal[1]

Name: (R)-Ornithine hydrochloride, CAS: 16682-12-5, stock 37g, assay 98.3%, MWt: 168.62, Formula: C5H13ClN2O2, Solubility: , Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity:

Name: BRD-6929, CAS: 849234-64-6, stock 25.8g, assay 98.3%, MWt: 351.42, Formula: C19H17N3O2S, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Epigenetics;Cell Cycle/DNA Damage;Anti-infection, Target: HDAC;HDAC;HIV, Biological_Activity: BRD-6929 (Cpd-60) is a brain-penetrant, selective inhibitor of HDAC1 and HDAC2 (IC50= 1 and 8 nM), extracted from patent US2018360927[1]. BRD-6929 (Cpd-60) shows high-affinity to HDAC1 and HDAC2 with Ki of 0.2 and 1.5 nM, respectively[2]. BRD-6929 (TPB) potentiates the efficacy of gnidimacrin (a PKC Agonist) against latent HIV-1[3].

Name: PF-06651600, CAS: 1792180-81-4, stock 6g, assay 98.1%, MWt: 285.34, Formula: C15H19N5O, Solubility: DMSO : 125 mg/mL (438.07 mM; Need ultrasonic), Clinical_Informat: Phase 3, Pathway: Epigenetics;Stem Cell/Wnt;JAK/STAT Signaling, Target: JAK;JAK;JAK, Biological_Activity: PF-06651600 is an orally active and selective JAK3 inhibitor with an IC50 of 33.1 nM.
IC50 & Target: IC50: 33.1 nM (JAK3)[1]
In Vitro: PF-06651600 is a potent JAK3-selective inhibitor which can inhibit the JAK3 kinase activity with an IC50 of 33.1 nM but without activity (IC50>10 000 nM) against JAK1, JAK2, and TYK2. PF-06651600 inhibits the phosphorylation of STAT5 elicited by IL-2, IL-4, IL-7, and IL-15 with IC50 values of 244, 340, 407, and 266 nM, respectively. PF-06651600 also inhibits the phosphorylation of STAT3 elicited by IL-21 with an IC50 of 355 nM. Functional assessment in T-cell differentiation assays demonstrate that PF-06651600 suppresses Th1 and Th17 differentiation as measured by IFNγ, after 5 days under Th1 conditions, and IL-17 production, after 6 days under Th17 conditions, with IC50 values of 30 nM and 167 nM, respectively. PF-06651600 also suppresses Th1 and Th17 function as measured by the inhibition of IFNγ production (IC50=48 nM) and IL-17 production (IC50=269 nM) in cells that have been previously differentiated and rested before being treated with PF-06651600[1].
In Vivo: In the rat adjuvant-induced arthritis (AIA) model, PF-06651600 reduces paw swelling with an unbound EC50 of 169 nM. Similarly, PF-06651600 significantly reduces disease severity in the experimental autoimmune encephalomyelitis (EAE) mouse model when dosed either therapeutically at 30 or 100 mg/kg or prophylactically at 20 and 60 mg/kg. The efficacy of PF-06651600 in these two rodent models of inflammatory and autoimmune diseases illustrates that JAK3-selective inhibition can be sufficient to have disease modifying effects in human diseases[1].

Name: FUBP1–IN-1, CAS: 883003-62-1, stock 6.3g, assay 98.2%, MWt: 405.39, Formula: C19H14F3N3O2S, Solubility: DMSO : 16.67 mg/mL (41.12 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: FUBP1–IN-1 is a potent FUSE binding protein 1 (FUBP1) inhibitor which interferes with the binding of FUBP1 to its single stranded target DNA FUSE sequence , with an IC50 value of 11.0 μM[1].
IC50 & Target: IC50: 11.0 μM (FUBP1)[1]

Name: (R)-(+)-Atenolol, CAS: 56715-13-0, stock 35.9g, assay 98%, MWt: 266.34, Formula: C14H22N2O3, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: (R)-(+)-Atenolol is the less active enantiomer of the (R,S)-atenolol. (R,S)-atenolol is a β-adrenergic receptor antagonist[1][2].

Name: Escin, CAS: 6805-41-0, stock 5.4g, assay 98.3%, MWt: 1131.26, Formula: C55H86O24, Solubility: 10 mM in DMSO, Clinical_Informat: Launched, Pathway: Apoptosis, Target: Apoptosis, Biological_Activity: Escin, a natural mixture of triterpenoid saponins isolated from horse chestnut (Aesculus hippocastanum) seeds, can be used as a vasoprotective anti-inflammatory, anti-edematous and anti-nociceptive agent[1].

Name: Setogepram (sodium salt) PBI-4050 (sodium salt), CAS: 1254472-97-3, stock 33.6g, assay 98.3%, MWt: 228.26, Formula: C13H17NaO2, Solubility: DMSO : ≥ 64 mg/mL (280.38 mM); H2O : ≥ 100 mg/mL (438.10 mM), Clinical_Informat: Phase 3, Pathway: GPCR/G Protein;GPCR/G Protein, Target: GPR84;GPR40, Biological_Activity: Setogepram sodium salt (PBI-4050 sodium salt) acts as an orally active agonist for GPR40 and as an antagonist or inverse agonist for GPR84[1]. Setogepram sodium salt decreases renal, liver and pancreatic fibrosis[1][2]. Setogepram sodium salt exerts anti-fibrotic, anti-inflammatory and anti-proliferative actions[2].
IC50 & Target: GPR40, GPR84[1]
In Vitro: Setogepram (PBI-4050; 500 µM; 24 hours) inhibits TGF-β (10 ng/mL)-activated human hepatic stellate cells (HSCs) proliferation[2]. 
Setogepram (PBI-4050; 250 or 500 µM; 24hours) dose-dependently arrests HSCs at the G0/G1 phase without inducing apoptosis[2].
In Vivo: Setogepram (PBI-4050; 100 mg/kg/day; gavage from 8-20 weeks of age) markedly decreases hyperglycemia and markedly improvea glucose tolerance in type 2 diabetes eNOS-/-db/db mice[1].

Name: Pancreatin, CAS: 8049-47-6, stock 31.6g, assay 98.1%, MWt: 1000, Formula: N/A, Solubility: DMSO : 5 mg/mL (Need ultrasonic); H2O : < 0.1 mg/mL (insoluble), Clinical_Informat: Phase 4, Pathway: Others, Target: Others, Biological_Activity: Pancreatin is the porcine pancreas extract (PPE) which contains the main pancreatic digestive enzymes.
In Vitro: Pancreatin is the porcine pancreas extract (PPE) which contains the main pancreatic digestive enzymes. The amount of free fatty acids (FFAs) titrated at pH 6.5 does increase by 120 and 28% for II-LC and IIIA-LC, respectively, when Pancreatin is increased from 150 to 900 USP U/mL, and the total extent of lipolysis increases by 79 and 28% II-LC and IIIA-LC, respectively. By elevating Pancreatin activity from 150 to 900 USPU/mL, the total extent of digestion on average for LC-LBFs increases by 51%, whereas the amount of FFAs detected at pH 6.5 increases by 55% on average. An increase in extent of digestion is also observed with increasing Pancreatin levels[1].

Name: 6-Methoxy-2-naphthoic acid Naproxen impurity O, CAS: 2471-70-7, stock 5.1g, assay 98.2%, MWt: 202.21, Formula: C12H10O3, Solubility: DMSO : 60 mg/mL (296.72 mM; Need ultrasonic and warming), Clinical_Informat: No Development Reported, Pathway: Membrane Transporter/Ion Channel;Neuronal Signaling, Target: iGluR;iGluR, Biological_Activity: 6-Methoxy-2-naphthoic acid is an NMDA receptor modulator extracted from patent WO 2012019106 A2.
IC50 & Target: NMDA receptor[1]

Name: Maltose monohydrate, CAS: 6363-53-7, stock 11.1g, assay 98.7%, MWt: 360.31, Formula: C12H24O12, Solubility: H2O : 100 mg/mL (277.54 mM; Need ultrasonic and warming), Clinical_Informat: Phase 3, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: Maltose monohydrate is the energy source for bacteria.

Name: Maltitol, CAS: 585-88-6, stock 19.2g, assay 98.3%, MWt: 344.31, Formula: C12H24O11, Solubility: DMSO : 33.33 mg/mL (96.80 mM; Need ultrasonic), Clinical_Informat: Launched, Pathway: Others, Target: Others, Biological_Activity: Maltitol is a sugar alcohol used as a sugar substitute. It has 75-90% of the sweetness of sucrose (table sugar) and nearly identical properties. Maltitol may also be used as a plasticizer in gelatin capsules, as an emollient, and as a humectant[1].

Name: Lactose, CAS: 63-42-3, stock 24.1g, assay 98.9%, MWt: 342.30, Formula: C12H22O11, Solubility: 10 mM in DMSO, Clinical_Informat: Phase 4, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: Lactose, a major sugar in the milk of most species, could regulate human’s intestinal microflora.

Name: Uric acid, CAS: 69-93-2, stock 31.6g, assay 98.7%, MWt: 168.11, Formula: C5H4N4O3, Solubility: H2O : < 0.1 mg/mL (insoluble); 1M NaOH : 7.14 mg/mL (42.47 mM; Need ultrasonic); DMSO : < 1 mg/mL (insoluble or slightly soluble), Clinical_Informat: Phase 3, Pathway: Metabolic Enzyme/Protease;Metabolic Enzyme/Protease;NF-κB;Immunology/Inflammation, Target: Endogenous Metabolite;Reactive Oxygen Species;Reactive Oxygen Species;Reactive Oxygen Species, Biological_Activity: Uric acid is an endogenous antioxidant that scavenges reactive oxygen species (ROS) including singlet oxygen, oxygen radicals, and peroxynitrite.
In Vitro: Uric acid is an endogenous antioxidant that scavenges reactive oxygen species (ROS) including singlet oxygen, oxygen radicals, and peroxynitrite. Incubation with indomethacin significantly increases malondialdehyde (MDA) levels in Caco-2 cells compare to those not treated indomethacin. Incubation with both indomethacin and Uric acid significantly decreases MDA levels compare to those grown in the presence of indomethacin alone. Co-treatment of cells with indomethacin and Uric acid significantly decreases ROS levels compare to those in cells incubated with indomethacin alone. Cell viability in Caco-2 cells treated with both indomethacin and Uric acid is higher than that in cells treated with indomethacin alone. Uric acid has a protective effect on indomethacin-induced intestinal cell changes through its antioxidant activity[1].
In Vivo: When mice treated with indomethacin are concurrently administered Uric acid orally, ulcer areas are significantly reduced, in a Uric acid dose-dependent manner. Indomethacin increases the ratio of crypt depth to villous height in the ileum, while the ratio is significantly lower when mice are concurrently administered Uric acid orally. Administration of indomethacin also increases the histopathological score of tissue damage in the small intestine, while mice concurrently administered Uric acid orally has a significantly lower histopathological score. The ileal levels of malondialdehyde (MDA) in indomethacin-induced enteropathy model mice orally administered Uric acid are also significantly lower than the levels in mice administered indomethacin alone[1].

Name: Casanthranol, CAS: 8024-48-4, stock 3.8g, assay 98.5%, MWt: 1000, Formula: N/A, Solubility: DMSO : ≥ 50 mg/mL, Clinical_Informat: Launched, Pathway: Others, Target: Others, Biological_Activity: Casanthranol is a concentrated mixture of anthranol glycosides from cascara sagrada (dried bark of Rhamnus p.) and used as a laxative in constipation and various medical conditions, stimulant laxative Casanthranol encourages bowel movements by acting on the intestinal wall to increase muscle contractions[1].

Name: Multifungin Bromosalicylchloranilide;Salifungin, CAS: 3679-64-9, stock 20.4g, assay 98.8%, MWt: 326.57, Formula: C13H9BrClNO2, Solubility: DMSO : 250 mg/mL (765.53 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Anti-infection, Target: Fungal, Biological_Activity: Multifungin (Bromochlorosalicylanilide) is an antifungal that treats oral candidiasis[1]. Multifungin prevents the formation and accumulation of Zearalenone and reduces the fungal population in stored-crushed corn[2].
IC50 & Target: candidiasis[1]

Name: Gramicidin, CAS: 1405-97-6, stock 33.2g, assay 98.1%, MWt: 1882.30, Formula: C99H140N20O17, Solubility: DMSO : ≥ 100 mg/mL (53.13 mM); H2O : < 0.1 mg/mL (insoluble), Clinical_Informat: Launched, Pathway: Anti-infection, Target: Bacterial, Biological_Activity: Gramicidin is an antimicrobial peptide assembling as channels in membranes and increasing their permeability towards cations.
IC50 & Target: Bacterial[1]
In Vitro: Gramicidin is an antimicrobial peptide assembling as channels in membranes and increasing their permeability towards cations. There is poor Gramicidin activity against E. coli and S. cerevisae as shown from the survival of microbes (%) over a range of Gramicidin concentrations, in contrast with the action of Gramicidin on S. aureus. The microbicidal activity occurs over a range of low Gramicidin and DODAB concentrations which are not toxic to S. cerevisae[1].

Name: Scopolamine N-oxide hydrobromide Hyoscine N-oxide hydrobromide, CAS: 6106-81-6, stock 30.3g, assay 98.3%, MWt: 400.26, Formula: C17H22BrNO5, Solubility: DMSO : 300 mg/mL (749.51 mM; Need ultrasonic and warming), Clinical_Informat: No Development Reported, Pathway: Neuronal Signaling;GPCR/G Protein, Target: mAChR;mAChR, Biological_Activity: Scopolamine N-oxide hydrobromide is an antagonist of the muscarinic acetylcholine.
IC50 & Target: muscarinic acetylcholine[1]

Name: Quadrol N,N,N′,N′-Tetrakis(2-hydroxypropyl)ethylenediamine;EDTP, CAS: 102-60-3, stock 22.4g, assay 98.7%, MWt: 292.41, Formula: C14H32N2O4, Solubility: DMSO : ≥ 83.3 mg/mL (284.87 mM), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Quadrol is an immunostimulant and has been implicated as a potentially useful agent in accelerated wound healing.
In Vitro: Results show that viability of macrophages incubated with Quadrol at concentrations of 0.5 mM, 1 mM and 4mM are identical to that for controls. Viability, however, is reduced to 50% of control at concentrations of 16 mM to 32 mM. After four hours, at concentrations of 1 mM and 4 mM, Quadrol produces enhanced spreading of 88% and 80%, respectively, as compared to the control of 28%. Quadrol, at a concentration of 16 mM, shows reduced percentage of spreading of macrophages after four hours. Exposure of macrophages to 1.0 mM or 4.0 mM Quadrol concentrations enhances phagocytic activity, 41% and 57%, respectively, over that of the cells exposed to media alone (34%)[1].

In Vivo: On day eight after the implantation, the amount of collagen in the implants of normal mice injected with Quadrol exceeds controls by more than 200% (p<0.025). By day 11, the collagen content increases to over 300% higher than controls (p<0.01) and by the end of two weeks after wounding, the time interval typically required for normal and complete wound healing, the collagen accumulated in the implants of the Quadrol-treated mice is about 50% above control (p<0.1). The accumulation of collagen in the implants of Quadrol treated STZ-diabetic mice about 100% above the untreated diabetic control on days 8 to 11. By day 14, the collagen deposition has increased to 200% above the controls (p<0.0 5)[2].

Name: Acotiamide (monohydrochloride trihydrate), CAS: 773092-05-0, stock 39.9g, assay 98%, MWt: 541.06, Formula: C21H37ClN4O8S, Solubility: DMSO : 125 mg/mL (231.03 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Neuronal Signaling, Target: AChE, Biological_Activity: Acotiamide monohydrochloride trihydrate is an orally active and first-in-class gastroprokinetic agent for the treatment of functional dyspepsia. Acotiamide monohydrochloride trihydrate enhances acetylcholine released by enteric neurons through muscarinic receptor antagonism and acetylcholinesterase (AChE) inhibition, thereby enhancing gastric emptying and gastric accommodation[1][2].
In Vitro: In in vitro studies, Acotiamide inhibits acetylcholine-induced activation of muscarinic M1 and M2 receptors in transformed Xenopus oocytes, with IC50 values of 1.8 and 10.1 μM, respectively. Acotiamide shows no/limited affinity for serotonin 5HT2, 5HT3 or 5HT4 receptors and dopamine D2 receptors[1]. 
Acotiamide inhibits AChE activity, inhibits both the slow (competitively) and fast (noncompetitively) inward currents induced by acetylcholine, enhances electrically stimulated contraction of gastric fundus and gastric body, facilitates acetylcholine release from enteric neurons and, using patch-clamp techniques, potentiates L-type voltagedependent Ca2+ current and inhibits GABA-induced current in area postrema neurons[1].
In Vivo: In in vivo animal models, Acotiamide stimulates postprandial gastroduodenal and/or colonic motor activity, and improves delayed but not normal gastric emptying. For example, Acotiamide significantly improves delayed gastric emptying and feeding inhibition in a restraintstress-induced rat model, but does not affect normal gastric emptying or feeding in intact rats[1].

Name: Menaquinone-4 Vitamin K2(MK-4);Menaquinone K4, CAS: 863-61-6, stock 19.4g, assay 98.9%, MWt: 444.65, Formula: C31H40O2, Solubility: H2O : < 0.1 mg/mL (insoluble); DMSO : 20.83 mg/mL (46.85 mM; Need ultrasonic), Clinical_Informat: Launched, Pathway: Others, Target: Others, Biological_Activity: Menaquinone-4 is a vitamin K, used as a hemostatic agent, and also a adjunctive therapy for the pain of osteoporosis.
In Vitro: Menaquinone-4 (MK-4, 0, 1, 5, 10 μM) increases the ALP activity in Caco-2 cells. Menaquinone-4 (1 μM) significantly increases intensities of hSI expression[1].
In Vivo: Menaquinone-4 (K2, 0.2 g/kg diet) in HF-K2 group produces epididymal fat in C57BL/6J mice, and also increases the bone density of mice[2].

Name: Ecabet (sodium) TA-2711, CAS: 86408-72-2, stock 8.9g, assay 99%, MWt: 402.48, Formula: C20H27NaO5S, Solubility: 10 mM in DMSO, Clinical_Informat: Launched, Pathway: Apoptosis;Anti-infection;Metabolic Enzyme/Protease;NF-κB;Immunology/Inflammation, Target: Apoptosis;Bacterial;Reactive Oxygen Species;Reactive Oxygen Species;Reactive Oxygen Species, Biological_Activity: Ecabet sodium (TA-2711) is currently applied to some clinical gastrointestinal disease by inhibiting the ROS production and improving Helicobacter pylori eradication[1]. Ecabet sodium reduces apoptosis[2].
IC50 & Target: ROS production; Bacterial[1]; Apoptosis[2]

Name: Astaxanthin, CAS: 472-61-7, stock 15g, assay 98.1%, MWt: 596.84, Formula: C40H52O4, Solubility: DMSO : < 1 mg/mL (insoluble or slightly soluble), Clinical_Informat: Launched, Pathway: Cell Cycle/DNA Damage;Metabolic Enzyme/Protease;NF-κB;Immunology/Inflammation, Target: PPAR;Reactive Oxygen Species;Reactive Oxygen Species;Reactive Oxygen Species, Biological_Activity: Astaxanthin, a red dietary carotenoid isolated from Haematococcus pluvialis, is a modulator of PPARγ and a potent antioxidant with antiproliferative, neuroprotective and anti-inflammatory activity[1]. Astaxanthin has potential in the treatment of various diseases, such as cancers and Parkinson’s disease, cardiovascular disease[2]. Due to its bright red colour, Astaxanthin could be used as a food colorant in animal feeds[3].
IC50 & Target: PPARγ[1].

Name: Rimacalib SMP 114, CAS: 215174-50-8, stock 36g, assay 98.8%, MWt: 394.44, Formula: C22H23FN4O2, Solubility: DMSO : 125 mg/mL (316.90 mM; Need ultrasonic), Clinical_Informat: Phase 2, Pathway: Neuronal Signaling;Autophagy, Target: CaMK;Autophagy, Biological_Activity: Rimacalib is a Ca2+/calmodulin-dependent protein kinase II (CaMKII) inhibitor, with IC50s of ~1 μM for CaMKIIα to ~30 μM for CaMKIIγ.
IC50 & Target: IC50: ~1 μM (CaMKIIα), ~30 μM (CaMKIIγ)[1].
In Vitro: Rimacalib (SMP-114) improves (by ~40%) Ca2+-transient potentiation during the 30 s stimulation pause, higher Fura-2 transient amplitude after the pause upon Rimacalib vs. 37.2±4.3% in control, n=60/17 cells/mice vs. n=65/17, p<0.05) and in parallel cardiomyocyte contractility (135.0±15.4% vs. 97.2±16% increase of twitch amplitude, p=0.098)[1].

Name: L-APB L-AP 4, CAS: 23052-81-5, stock 6g, assay 98.8%, MWt: 183.10, Formula: C4H10NO5P, Solubility: H2O : 50 mg/mL (273.07 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein;Neuronal Signaling, Target: mGluR;mGluR, Biological_Activity: L-APB is a potent and specific agonist for the group III mGluRs, with EC50s of 0.13, 0.29, 1.0, 249 μM for mGlu4, mGlu8, mGlu6 and mGlu7 receptors, respectively.
IC50 & Target: EC50: 0.13 μM (mGlu4), 0.29 μM (mGlu8), 1.0 μM (mGlu6), 249 μM (mGlu7)[1].
In Vivo: Paw withdrawal threshold in response to application of von Frey filaments before spinal nerve ligation is 22.6±2.4 g. The mechanical threshold decreases significantly (2.3±0.5 g, P<0.05) within 10 days after nerve ligation and remains stable for at least 8 weeks. Intrathecal injection of 5 to 30 μg of L-APB significantly increases the paw withdrawal threshold in response to application of von Frey filaments in eight nerve-ligated rats in a dose-dependent manner. The maximal effect of L-APB appears within 45 min and gradually subsided in 120 min following intrathecal administration[2].

Name: D-AP5 D-APV;D-2-Amino-5-phosphonovaleric acid, CAS: 79055-68-8, stock 1.2g, assay 98.9%, MWt: 197.13, Formula: C5H12NO5P, Solubility: H2O : 50 mg/mL (253.64 mM; Need ultrasonic); H2O : 250 mg/mL (1268.20 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Membrane Transporter/Ion Channel;Neuronal Signaling, Target: iGluR;iGluR, Biological_Activity: D-AP5 is a NMDA receptor antagonist.
IC50 & Target: NMDA[1]
In Vivo: D-AP5 is a NMDA receptor antagonist. Chronic intraventricular infusion of D-AP5 causes a parallel dose-dependent impairment of spatial learning and long-term potentiation (LTP) in vivo. Intracerebral concentrations of D-AP5 fail to induce any measurable sensorimotor disturbance when spatial learning is prevented[1]. D-AP5 infusion is associated with a progressive reduction in swim speed over trials. D-AP5 causes sensorimotor disturbances in the spatial task, but these gradually worsened as the animals fail to learn. Rats treated with D-AP5 show a delay-dependent deficit in spatial memory in the delayed matching-to-place protocol for the water maze[2].

Name: (-)-Aspartic acid (R)-Aspartic acid; D-(-)-Aspartic acid, CAS: 1783-96-6, stock 1.2g, assay 98.8%, MWt: 133.10, Formula: C4H7NO4, Solubility: DMSO : < 1 mg/mL (insoluble or slightly soluble); H2O : 7.69 mg/mL (57.78 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Membrane Transporter/Ion Channel;Neuronal Signaling;Metabolic Enzyme/Protease, Target: iGluR;iGluR;Endogenous Metabolite, Biological_Activity: (-)-Aspartic acid is an endogenous NMDA receptor agonist.
IC50 & Target: NMDA receptor

Name: Kainic acid, CAS: 487-79-6, stock 22.5g, assay 98.6%, MWt: 213.23, Formula: C10H15NO4, Solubility: H2O : ≥ 50 mg/mL (234.49 mM), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Kainic acid is a potent agonist at excitatory amino acid receptor subtypes in the CNS.
In Vivo: Kainic acid is a potent agonist at excitatory amino acid receptor subtypes in the CNS. HO-I levels are significantly enhanced one, three and seven days after i.c.v, injection of Kainic acid. One day after i.c.v, injection of Kainic acid, the HO-I protein level reaches a maximum and then decreases, but is still significantly enhanced versus the vehicle-injected group. After i.c.v. injection of Kainic acid, HO-I-immunoreactivity is strongly induced not only in the CA3 but also widely in the whole hippocampus[1].

Name: Guvacine hydrochloride, CAS: 6027-91-4, stock 31.2g, assay 98.8%, MWt: 163.60, Formula: C6H10ClNO2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Neuronal Signaling;Membrane Transporter/Ion Channel, Target: GABA Receptor;GABA Receptor, Biological_Activity: Guvacine hydrochloride is an alkaloid from the nut of Areca catechu, acts as an inhibitor of GABA transporter, and dispalys modest selectivity for cloned GABA transporters with IC50s of 14 μM (human GAT-1), 39 μM (rat GAT-1), 58 μM (rat GAT-2), 119 μM (human GAT-3), 378 μM (rat GAT-3), and 1870 μM (human BGT-3).
IC50 & Target: IC50: 14 μM (human GAT-1), 39 μM (rat GAT-1), 58 μM (rat GAT-2), 119 μM (human GAT-3), 378 μM (rat GAT-3), 1870 μM (human BGT-3)[1]
In Vitro: Guvacine hydrochloride is a potent inhibitor of GABA transporter, dispalys modest selectivity for
cloned GABA transporters with IC50s of 14 μM (human GAT-1), 39 μM (rat GAT-1), 58 μM (rat GAT-2), 119 μM (human GAT-3), 378 μM (rat GAT-3), and 1870 μM (human BGT-3). Guvacine has low affinity at hBGT-1 (IC50 >1 mM)[1]. Guvacine hydrochloride is a potent inhibitor of GABA uptake, but does not inhibit sodium-independent GABA binding, and is weak or inactive as a GABA receptor agonist[2]. Guvacine inhibits the uptake GABA and β-alanine with IC50s of 23 ± 2 μM, 66 ± 11 μM in the Cat spinal cord, and 8 ± 1 μM, 123 ± 28 μM in the rat cerebral cortex, respectively[3].

Name: 7-Chloro-4-hydroxyquinoline-2-carboxylic acid 7-Chlorokynurenic acid, CAS: 18000-24-3, stock 19.1g, assay 98.7%, MWt: 223.61, Formula: C10H6ClNO3, Solubility: DMSO : 30 mg/mL (134.16 mM; Need ultrasonic and warming), Clinical_Informat: No Development Reported, Pathway: Membrane Transporter/Ion Channel;Neuronal Signaling, Target: iGluR;iGluR, Biological_Activity: 7-Chloro-4-hydroxyquinoline-2-carboxylic acid (7-Chlorokynurenic acid) is a potent and selective antagonist of the glycine B coagonist site of the N-methyl-D-aspartate (NMDA) receptor (IC50=0.56 μM). 7-Chloro-4-hydroxyquinoline-2-carboxylic acid is also a potent inhibitor of the reuptake of glutamate into synaptic vesicles with a Ki of 0.59 μM. 7-Chloro-4-hydroxyquinoline-2-carboxylic acid has potent antinociceptive actions after neuraxial delivery[1][2].
IC50 & Target: Ki: 0.59 μM (reuptake of glutamate)[1] 
IC50: 0.56 μM (Glycine B coagonist site of NMDA receptor)[2]
In Vivo: Male Sprague-Dawley rats pretreated with 7-Chloro-4-hydroxyquinoline-2-carboxylic acid (10 nM) shows a significant retardation of development of both the electroencephalographic and motor (17.7±2.9 daily stimulations) components of the seizure response[3].

Name: Ibotenic acid (RS)-Ibotenic acid;DL-Ibotenic acid, CAS: 2552-55-8, stock 10.1g, assay 98.2%, MWt: 158.11, Formula: C5H6N2O4, Solubility: H2O : 6 mg/mL (37.95 mM; Need ultrasonic and warming), Clinical_Informat: No Development Reported, Pathway: Membrane Transporter/Ion Channel;Neuronal Signaling, Target: iGluR;iGluR, Biological_Activity: Ibotenic acid has agonist activity at both the N-methyl-D-aspartate (NMDA) and trans-ACPD or metabolotropic quisqualate (Qm) receptor sites.
IC50 & Target: NMDA receptor[1]
In Vitro: Ibotenic acid (Ibo) is capable of acting at both NMDA and trans-ACPD receptors in the CNS, although only activation of NMDA receptors is involved in Ibo neurotoxicity. Ibotenic acid is toxic to cortical neurons exposes for 5 min with an EC50=77.3±8 μM (n=5) as measured by release of lactate dehydrogenase to the culture media[1].

Name: TX1-85-1, CAS: 1603845-32-4, stock 36.9g, assay 98.9%, MWt: 580.68, Formula: C32H36N8O3, Solubility: DMSO : 3.85 mg/mL (6.63 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: JAK/STAT Signaling;Protein Tyrosine Kinase/RTK, Target: EGFR;EGFR, Biological_Activity: TX1-85-1 is an irreversible Her3 (ErbB3) inhibitor with an IC50 of 23 nM and is also the first selective Her3 ligand, which forms a covalent bond with Cys721 located in the ATP-binding site of Her3. TX1-85-1 induces partial degradation of Her3 protein and attenuates Her3-dependent signaling[1].
IC50 & Target: IC50：23 nM (ErbB3)[1]
In Vitro: TX1-85-1 possesses an anti-proliferation EC50s of 9.9, 11.5, and 16.9 μM for Ovcar8, HCC827 GR6, and PC9 GR4 cells, respectively[1].

Name: IWP-O1, CAS: 2074607-48-8, stock 25.9g, assay 98.6%, MWt: 432.48, Formula: C26H20N6O, Solubility: H2O : < 0.1 mg/mL (insoluble); DMSO : 125 mg/mL (289.03 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Stem Cell/Wnt;Stem Cell/Wnt, Target: Porcupine;Wnt, Biological_Activity: IWP-O1 is a highly potent Porcupine (Porcn) inhibitor, with an EC50 of 80 pM in L-Wnt-STF cells, suppressing the phosphorylation of Dvl2/3 and LRP6 in HeLa cells. IWP-O1 functions by preventing the secretion of Wnt proteins[1].
IC50 & Target: EC50: 80 pM (Porcn)[1].
In Vitro: IWP-O1 (17) suppresses Wnt signaling in L-Wnt-STF cells with an EC50 value of 80 pM, 2.5 times more active than the investigational drug LGK974[1].

Name: TAK-659, CAS: 1312691-33-0, stock 27g, assay 98.8%, MWt: 344.39, Formula: C17H21FN6O, Solubility: 10 mM in DMSO, Clinical_Informat: Phase 2, Pathway: Protein Tyrosine Kinase/RTK;Protein Tyrosine Kinase/RTK, Target: FLT3;Syk, Biological_Activity: TAK-659 is a highly potent, selective, reversible and orally available dual inhibitor of spleen tyrosine kinase (SYK) and fms related tyrosine kinase 3 (FLT3), with an IC50 of 3.2 nM and 4.6 nM for SYK and FLT3, respectively. TAK-659 induces cell death in tumor cells but not in nontumor cells, and with potential for the treatment of chronic lymphocytic leukemia (CLL)[1][2][3][4].
IC50 & Target: IC50: 3.2 nM (Syk), 4.6 nM (FLT3)[1]
In Vitro: TAK-659 inhibits cellular proliferation in SYK-dependent DLBCL and FLT3-dependent AML cell lines[1][3]. 
TAK-659 (5 µM; 1-24 hours) induces Casp3 activation in the LMP2A/MYC cells which was readily apparent at 4 h and reached maximum levels at 8 h of treatment[4]. 
TAK-659 (0.01-10 μM; 1 hour) stimulates expression of phospho-Syk at Tyr525 and Tyr352 and phospho-ERK1/2 increased in Ramos cells[2]. 
In Vivo: TAK-659 (100 mg/kg/day; p.o.; for 10 days) treatment totally abrogates splenomegaly and tumor development in LMP2A/MYC mice in both pretumor and tumor cell transfer experiments[4]. 
TAK-659 treatment kills tumor cells, but not host cells within the spleen and tumors[4]. 
TAK-659 treatment abrogates metastasis of tumor cells into bone marrow[4].

Name: ABX464, CAS: 1258453-75-6, stock 38.7g, assay 98.1%, MWt: 338.71, Formula: C16H10ClF3N2O, Solubility: DMSO : ≥ 100 mg/mL (295.24 mM), Clinical_Informat: Phase 2, Pathway: Anti-infection, Target: HIV, Biological_Activity: ABX464 is a potent anti-HIV agent. ABX464 inhibits HIV-1 replication in stimulated peripheral blood mononuclear cells (PBMCs) with an IC50 ranging between 0.1 μM and 0.5 μM.
IC50 & Target: IC50: 0.1-0.5 μM (HIV-1, in PBMCs)[1]
In Vitro: ABX464 inhibits HIV-1 production in PBMC- and macrophages-infected cells. ABX464 has a strong inhibitory effect for all HIV-1 subtypes tested including subtype B, C and recombinant viruses. ABX464 also very efficiently inhibits the replication of viral strains harbouring mutations that confer resistance to different therapeutic agents in vitro. While the antiviral drug 3TC is not highly active on K65R and M184V mutant strains, both strains are inhibited by ABX464. To generalize the effect of ABX464 on HIV-1 replication in other primary cells, cells are treated with between 0.01 μM up to 30 μM concentrations of ABX464 and p24 antigen levels are monitored in culture supernatants over a 12 days period. ABX464 efficiently blocks virus replication in a dose-dependent manner with an IC50 ranging between 0.1 μM and 1 μM[1].
In Vivo: Humanized mice reconstituted with human lymphoid cells provide rapid, reliable, reproducible experimental systems for testing the efficacy of ABX464 in vivo. In the initial setting, SCID mice are reconstituted with PBMCs and then infected with the HIV-1 strain JR-CSF. Mice are treated twice a day (b.i.d) for 15 days by oral gavage with 20 mg/kg of ABX464. Measures of viral RNA show that the oral treatment with ABX464 is able to significantly reduce the viral load over a period of 15 days of treatment. FACS analysis of blood samples show that treatment with ABX464 prevents depletion of CD4+ cells following infection of reconstituted mice and thereby restores the CD8+/CD4+ ratio back to that of non-infected mice[1].

Name: GCN2-IN-1 A-92, CAS: 1448693-69-3, stock 22.9g, assay 98.4%, MWt: 402.41, Formula: C19H18N10O, Solubility: DMSO : 60 mg/mL (149.10 mM; Need ultrasonic and warming), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: GCN2-IN-1 (A-92) is a potent general control nonderepressible 2 kinase (GCN2) inhibitor with an IC50 of <0.3 μM in the enzyme assay and an IC50 of 0.3-3 μM in the cell assay[1].
IC50 & Target: IC50: <0.3 μM (GCN2)[1]
In Vitro: GCN2-IN-1 (Compound A-92) is a GCN2 inhibitor, which may be useful as a chemotherapeutic drug for the treatment of cancer[1].

Name: Simurosertib TAK-931, CAS: 1330782-76-7, stock 1.4g, assay 98.4%, MWt: 341.43, Formula: C17H19N5OS, Solubility: DMSO : 75 mg/mL (219.66 mM; Need ultrasonic), Clinical_Informat: Phase 2, Pathway: Cell Cycle/DNA Damage, Target: CDK, Biological_Activity: Simurosertib (TAK-931) is a selective cycle 7 (CDC7) kinase inhibitor, with an IC50<0.3 nM.
IC50 & Target: IC50: <0.3 nM (CDC7 kinase)[1].
In Vitro: Simurosertib (TAK-931) potently inhibits CDC7 kinase activity (IC50 <0.3 nM) with a time-dependent ATP-competitive kinetics to its ATP-binding pocket. The selectivity studies using the 308 kinases reveals >120-fold selectivity of Simurosertib (TAK-931) for CDC7 kinase inhibition compared to other kinase inhibitions. Treatment with Simurosertib (TAK-931) suppresses the cellular MCM2 phosphorylation at Ser40 (pMCM2) in a dose-dependent manner, resulting in a delayed S phase progression, DNA-damage checkpoint activation, and caspase-3/7 activation[1].
In Vivo: In the COLO205-xenograft mouse model, oral administration of Simurosertib (TAK-931) inhibits pMCM2 of the xenografted COLO205 in dose- and time-dependent manners. Furthermore, Simurosertib (TAK-931) exhibits a significant antitumor activity in multiple xenograft models[1].

Name: DHPG (RS)-3,5-DHPG, CAS: 146255-66-5, stock 11.3g, assay 98.8%, MWt: 183.16, Formula: C8H9NO4, Solubility: DMSO : 1 mg/mL (5.46 mM; Need ultrasonic); H2O : 1 mg/mL (5.46 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein;Neuronal Signaling, Target: mGluR;mGluR, Biological_Activity: DHPG ((RS)-3,5-DHPG) is an amino acid, which acts as a selective and potent agonist of group I mGluR (mGluR 1 and mGluR 5), shows no effect on Group II or Group III mGluRs[1]. DHPG ((RS)-3,5-DHPG) is also an effective antagonist of mGluRs linked to phospholipase D[2].

Name: Spaglumic Acid NAAG;N-Acetylaspartylglutamic acid, CAS: 3106-85-2, stock 15.9g, assay 98.5%, MWt: 304.25, Formula: C11H16N2O8, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: Spaglumic Acid is a neuropeptide found in millimolar concentrations in brain.
In Vitro: Spaglumic Acid (N-Acetylaspartylglutamate; NAAG) is released upon depolarization by a Ca2+-dependent process and is an agonist at mGluR3 receptors and an antagonist at NMDA receptors. Spaglumic Acid is catabolized to N-acetylaspartate and glutamate primarily by glutamate carboxypeptidase II, which is expressed on the extracellular surface of astrocytes. The levels of Spaglumic Acid and the activity of carboxypeptidase II are altered in a regionally specific fashion in several neuropsychiatric disorders[1].

Name: MY-5445, CAS: 78351-75-4, stock 22.6g, assay 98.8%, MWt: 331.80, Formula: C20H14ClN3, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Phosphodiesterase (PDE), Biological_Activity: MY-5445 is a specific phosphodiesterase type 5 (PDE5) inhibitor[1].
IC50 & Target: PDE5[1]

Name: ATM-3507, CAS: 1861449-70-8, stock 6g, assay 98.9%, MWt: 611.79, Formula: C37H46FN5O2, Solubility: DMSO : 250 mg/mL (408.64 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Cytoskeleton, Target: Myosin, Biological_Activity: ATM-3507 is a potent tropomyosin inhibitor with IC50s from 3.83-6.84 μM in human melanoma cell lines.
IC50 & Target: IC50: 3.83-6.84 μM (tropomyosin, in human melanoma celllines)[1].
In Vitro: The cell lines differ in their relative expression of Tpm3.1 as well as in the expression of other isoforms. After determing the IC50 concentrations for TR100 and ATM-3507 (CHLA-20: 4.99±0.45 μM, CHP-134: 3.83±0.67 μM, CHLA-90: 6.84±2.37 μM, SK-N-BE(2): 5.00±0.42 μM) in each of the neuroblastoma cell lines, combinations of tropomyosin inhibitors plus Vincristine are tested at levels of each drug alone that kill less than 50% of the neuroblastoma cells. The combinations of both tropomyosin inhibitors plus Vincristine are completely cytotoxic in CHLA-20 cells. All 4 cell lines show some degree of synergy as determined by the Chou–Talalay method. The effect is not limited to the vinca alkaloids as a similar combination efficacy using paclitaxel plus TR100 or ATM-3507[1].
In Vivo: The maximal tolerance dose (MTD) for TR100 and ATM-3507 is 60 and 150 mg/kg, respectively. It is found that a significant inhibition of tumor growth and prolongation of animal survival using either combination compared with each monotherapy. The median survival of mice increased from 18 days for mice treated with ATM-3507 to more than 49 days for mice treated with the combination. It is also found that twice weekly intravenous administration of ATM-3507 also show combination efficacy. The impact of each treatment or the combination on body weight is minimal. Drug levels are measured following the intravenous administration of ATM-3507 at 30 mg/kg in Balb/c mice (n=3 per time point). The mean half-life of ATM-3507 is 5.01 hrs for the terminal elimination phase. The mean AUC0-t in the plasma is 14,548 ng/h/mL. The Cmax of ATM-3507 is 5,758 ng/mL and the the t1/2 is 5.01 h. The observed plasma clearance and volume of distribution at steady state of ATM-3507 is 33.8 mL/min/kg and 7.23 L/kg, respectively[1].

Name: (R)-Sulforaphane, CAS: 142825-10-3, stock 6.9g, assay 98.3%, MWt: 177.29, Formula: C6H11NOS2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: (R)-Sulforaphane is a highly potent inducer of the Keap1/Nrf2/ARE pathway. (R)-Sulforaphane is a far more potent inducer of the carcinogen-detoxifying enzyme systems in rat liver and lung than the S-isomer[1][2].

Name: Dihydroergocristine (mesylate) DHEC (mesylate), CAS: 24730-10-7, stock 4.1g, assay 98.6%, MWt: 707.84, Formula: C36H45N5O8S, Solubility: H2O : < 0.1 mg/mL (insoluble); DMSO : 50 mg/mL (70.64 mM; Need ultrasonic), Clinical_Informat: Launched, Pathway: Neuronal Signaling, Target: Amyloid-β, Biological_Activity: Dihydroergocristine mesylate (DHEC mesylate) is a inhibitor of γ-secretase (GSI), reduces the production of the Alzheimer's disease amyloid-β peptides, binds directly to γ-secretase and Nicastrin with equilibrium dissociation constants (Kd) of 25.7 nM and 9.8 μM, respectively[1].
In Vitro: Dihydroergocristine (DHEC) (2-20 μM; 24 hours) has an IC50 value of 25 μM for inhibiting the activity of γ-secretase in T100 cells without affecting cell viability[1].
Dihydroergocristine (2-20 μM; 24 hours) inhibits cellular Aβ production and causes a dose-dependent accumulation of carboxy-terminal fragments of APP (APP-CTFs) in HEK293 and decreases γ-secretase activity in fibroblast cells[1].

Name: 2,4-Diamino-6-hydroxypyrimidine, CAS: 56-06-4, stock 4.5g, assay 98.1%, MWt: 126.12, Formula: C4H6N4O, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: 2,4-Diamino-6-hydroxypyrimidine is a specific GTP cyclohydrolase I inhibitor (the rate-limiting enzyme in de novo pterin synthesis), blocks BH4 synthesis and suppresses NO production[1].
IC50 & Target: GTP cyclohydrolase I[1]

Name: Flurofamide, CAS: 70788-28-2, stock 18.8g, assay 98.5%, MWt: 217.14, Formula: C7H9FN3O2P, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Anti-infection, Target: Bacterial, Biological_Activity: Flurofamide is a potent bacterial urease inhibitor with potential clinical utility in the treatment of infection induced urinary stones[1].

Name: Dilazep (dihydrochloride), CAS: 20153-98-4, stock 37.3g, assay 98%, MWt: 677.61, Formula: C31H46Cl2N2O10, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Dilazep dihydrochloride is an inhibitor of adenosine uptake. Dilazep dihydrochloride has cerebral and coronary vasodilating action through enhancement of effect of adenosine. Dilazep dihydrochloride also inhibits the ischemic damage, platelet aggregation, and membrane transport of nucleosides[1][2].
IC50 & Target: Adenosine uptake
In Vitro: The uptake mechanism has been studied extensively in vitro and Dilazep, NBI and Dipyridamole have been reported to inhibit the uptake of adenosine into different cells. Of these compounds, Dilazep and NBI are almost 10 times more potent than Dipyridamole. In addition, only Dilazep is water soluble and no solubility aiding organic solvent is needed for preparing an aqueous solution[1].
In Vivo: After administration of Dilazep, even low doses (0.04-0.1 mg/kg/min) of exogenous adenosine significantly increases superior mesenteric arterial conductance (SMAC) and elevates arterial plasma adenosine concentration. The increased adenosine levels were highly correlated with the increased percentage of change of SMAC and values for Rmax and EC50 were 193.4% change of SMAC and 2.8 μM, respectively. Administration of bolus doses of 8-phenyltheophylline abolishes the ability of Dilazep to potentiate vasodilation, but did not affect isoproterenol-induced relaxation[1]. 
Dilazep inhibits the phospholipase activation in reperfused heart mitochondria and also inhibits the lipid peroxidation caused by cerebral ischemia and reperfusion. Dilazep may prevent ischemic cerebral injury due to an increase in cerebral blood flow and/or its protective effects on vascular endothelial cell membrane[1].

Name: (E)-AG 99 (E)-Tyrphostin 46; (E)-Tyrphostin AG 99, CAS: 122520-85-8, stock 16.5g, assay 98.3%, MWt: 204.18, Formula: C10H8N2O3, Solubility: DMSO : 165 mg/mL (808.11 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: JAK/STAT Signaling;Protein Tyrosine Kinase/RTK, Target: EGFR;EGFR, Biological_Activity: (E)-AG 99 ((E)-Tyrphostin 46; (E)-Tyrphostin AG 99) is a potent EGFR inhibitor[1].
IC50 & Target: EGFR[1]
In Vitro: (E)-AG 99 effectively blocks tyrosine phosphorylation of p145met and promotes cell death accompanied by activation of caspase-like proteases[1].

Name: Diphenyleneiodonium chloride DPI, CAS: 4673-26-1, stock 35.5g, assay 98.2%, MWt: 314.55, Formula: C12H8ClI, Solubility: DMSO : 6 mg/mL (19.07 mM; Need ultrasonic and warming), Clinical_Informat: No Development Reported, Pathway: Membrane Transporter/Ion Channel;Metabolic Enzyme/Protease;Metabolic Enzyme/Protease;NF-κB;Immunology/Inflammation;Neuronal Signaling, Target: TRP Channel;NADPH Oxidase;Reactive Oxygen Species;Reactive Oxygen Species;Reactive Oxygen Species;TRP Channel, Biological_Activity: Diphenyleneiodonium chloride is a NADPH oxidase (NOX) inhibitor and also functions as a TRPA1 activator with an EC50 of 1 to 3 μM. Diphenyleneiodonium chloride selectively inhibits intracellular reactive oxygen species.
IC50 & Target: NOX[1]
EC50: 1 to 3 μM (TRPA1)[1]
In Vitro: Diphenyleneiodonium chloride is a NADPH oxidase (NOX) inhibitor and also functions as a TRPA1 activator with an EC50 of 1 to 3 μM. Application of Diphenyleneiodonium chloride to HEK-TRPA1 cells at a concentration ranges of 0.03 to 10 μM effectively induces a Ca2+ response. However, Diphenyleneiodonium chloride fails to evoke a Ca2+ response in control HEK cells, even at a relatively high dose of 10 μM[1]. When Diphenyleneiodonium chloride is included in the co-cultures, lipopolysaccharide (LPS)-induced preOL apoptosis is significantly inhibited. Treatment with Diphenyleneiodonium chloride is found to significantly attenuate the LPS-induced O2- production by 2.0-fold, reducing it to within 27% of the controls[2].
In Vivo: Intraplantar injection of 2 mM Diphenyleneiodonium chloride to the hindpaw causes licking or biting behavior[1]. Diphenyleneiodonium chloride treatment immediately or 24 h after lipopolysaccharide (LPS) injection significantly attenuates the LPS-induced loss of O4 positive cells. Treatment with Diphenyleneiodonium chloride either immediately or 24 h after LPS injection significantly ameliorates the LPS-induced disorganization of the white matter nerve fibers. However, treatment with DPI 48 h after LPS injection does not appear to correct the LPS-induced white matter damage. DPI treatment either immediately or 24 h after LPS injection significantly reduces the accumulation of both gp91phox and p67phox in the membrane fraction[2].

Name: GBR 12783 (dihydrochloride), CAS: 67469-75-4, stock 29g, assay 98.3%, MWt: 485.49, Formula: C28H34Cl2N2O, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein;Neuronal Signaling, Target: Dopamine Receptor;Dopamine Receptor, Biological_Activity: GBR 12783 dihydrochloride is a specific, potent and selective dopamine uptake inhibitor that inhibits the [3H]dopamine uptake by rat and mice striatal synaptosomes with IC50s of 1.8 nM and 1.2 nM, respectively. GBR 12783 dihydrochloride can improve memory performance and increase hippocampal acetylcholine release in rats[1][2].
In Vivo: GBR 12783 (10 mg/kg; intraperitoneal injection; for 100 minutes; male Sprague-Dawley rats) treatment reinforces specifically dopamine transmission only at synapses instantaneously active, increases hippocampal ACh release and improves memory performance in a passive avoidance task[1].

Name: HA-100, CAS: 84468-24-6, stock 37.2g, assay 98.7%, MWt: 277.34, Formula: C13H15N3O2S, Solubility: DMSO : 150 mg/mL (540.85 mM; Need ultrasonic and warming), Clinical_Informat: No Development Reported, Pathway: Stem Cell/Wnt;Protein Tyrosine Kinase/RTK;TGF-beta/Smad;Epigenetics;Cytoskeleton, Target: PKA;PKA;PKC;PKC;Myosin, Biological_Activity: HA-100 is an inhibitor of cGMP-dependent protein kinase (PKG), cAMP-dependent protein kinase (PKA), protein kinase C (PKC) and MLC-kinase with IC50s of 4, 8, 12 and 240 μM, respectively[1].
IC50 & Target: IC50: 4 μM (PKG), 8 μM (PKA), 12 μM (PKC), 240 μM (MLC-kinase)[1]
In Vitro: HA-100 inhibits MLC-kinase and PKC competitively with respect to ATP, and the Ki values are 61 and 6.5 μM, respectively[1].

Name: L-NIO (dihydrochloride), CAS: 159190-44-0, stock 10g, assay 99%, MWt: 246.13, Formula: C7H17Cl2N3O2, Solubility: DMSO : 33.33 mg/mL (135.42 mM; Need ultrasonic); H2O : 50 mg/mL (203.14 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Immunology/Inflammation, Target: NO Synthase, Biological_Activity: L-NIO dihydrochloride is a potent, non-selective and NADPH-dependent nitric oxide synthase (NOS) inhibitor, with Kis of 1.7, 3.9, 3.9 μM for neuronal (nNOS), endothelial (eNOS), and inducible (iNOS), respectively[1][2]. L-NIO dihydrochloride induces a consistentfocal ischemic infarctin rats[2].
IC50 & Target: Ki: 1.7 μM (nNOS), 3.9 μM (eNOS), 3.9 μM (iNOS)[1]
In Vitro: L-NIO is a potent, non-selective and NADPH-dependent nitric oxide synthase (NOS) inhibitor, with Kis of 1.7, 3.9, 3.9 μM for neuronal (nNOS), endothelial (eNOS), and inducible (iNOS), respectively[1].
In Vivo: L-NIO (2.0 μmol, 3 days post-ischemia) causes focal cerebral ischemia in the adult rat brain[2].

Name: FG 7142 ZK 39106;LSU-65, CAS: 78538-74-6, stock 7.9g, assay 98.7%, MWt: 225.25, Formula: C13H11N3O, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Neuronal Signaling;Membrane Transporter/Ion Channel, Target: GABA Receptor;GABA Receptor, Biological_Activity: FG 7142 (ZK 39106; LSU-65), a non-selectively benzodiazepine inverse agonist, has high affinity for the α1 subunit-containing GABAA receptor (Ki=91 nM). FG 7142 (ZK 39106; LSU-65) also modulates GABA-induced chloride flux at GABAA receptors expressing the α1 subunit (EC50= 137 nM). FG 7142 (ZK 39106; LSU-65) can increase tyrosine hydroxylation and cause upregulation of β-adrenoceptors in mouse cerebral cortex[1].
In Vitro: FG-7142 has affinity for those expressing the α subunit, the Ki values are 91 nM; 330 nM; 492 nM and 2.150 μM for α1, α2,α3 and α5 subunits, respectively[1].
FG-7142 has a high efficacy in modulating GABA-induced chloride flux at GABAA receptors expressing the α1 subunit (EC50 = 137 nM) as compared to the other α subunits (EC50: α2= 507 nM,α3=1.021μM , α5=1.439 μM)[1].
In Vivo: FG-7142 (intraperitoneal injection; 15-30 mg/kg) activates mesolimbocortical dopaminergic projections, leading to increases in dopamine in the prefrontal cortex and the nucleus accumbens in rats[1].
FG-7142 (intraperitoneal injection; 15 mg/kg) increases tyrosine hydroxylase activity and dopamine turnover in the medial prefrontal cortex and ventral tegmentum in vivo, but effects are not detected in mesolimbic or nigrostriatal areas[1].

Name: MK-8617, CAS: 1187990-87-9, stock 10.1g, assay 98.8%, MWt: 443.45, Formula: C24H21N5O4, Solubility: DMSO : 6 mg/mL (13.53 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: HIF/HIF Prolyl-Hydroxylase, Biological_Activity: MK-8617 is an orally active pan-inhibitor of hypoxia-inducible factor prolyl hydroxylase 1-3 (HIF PHD1-3) with an IC50 of 1 nM for PHD2.
IC50 & Target: IC50: 1 nM (PHD2)[1]
In Vitro: MK-8617 is an orally active pan-inhibitor of hypoxia-inducible factor prolyl hydroxylase 1-3 (HIF PHD1-3) with an IC50 of 1 nM for PHD2. MK-8617 is not a significant inhibitor of the cytochrome p450 enzymes in vitro (IC50), CYP1A2, 3A4, 2B6, 2C9, 2C19, or 2D6, >60 μM, and is a moderate reversible inhibitor of CYP2C8 at 1.6 μM in vitro. The IC50 of MK-8617 is determined for factor inhibiting HIF (FIH) to be 18 μM[1].
In Vivo: Tritiated MK-8617 exhibits minimal metabolic turnover in liver microsomes from rat, dog, and monkey (<10% turover) but significant turnover in human liver microsomes (34% turnover) after 60 min (10 μM MK-8617, 1 mg/mL microsomal protein). In terms of its pharmacokinetic profile, MK-8617 shows good oral bioavailability across species (36 to 71%), with low clearance and volume of distribution. After 48 h treatment of MK-8617, postdose recovery of the radioactivity is about 26% bile, 12% urine, and 38% in feces, indicating that ~38% of the MK-8617 is absorbed and eliminated into bile and urine which is consistent with the oral bioavailability (~36%) observed in the rat study. MK-8617 also elicits an increase in erythropoietin (EPO) levels with a mouse MED of 1.5 mpk when dosed iv[1].

Name: PF-06263276, CAS: 1421502-62-6, stock 12.4g, assay 99%, MWt: 566.63, Formula: C31H31FN8O2, Solubility: 10 mM in DMSO, Clinical_Informat: Phase 1, Pathway: Epigenetics;Stem Cell/Wnt;JAK/STAT Signaling, Target: JAK;JAK;JAK, Biological_Activity: PF-06263276 (PF 6263276) is a potent and selective pan-JAK inhibitor, with IC50s of 2.2 nM, 23.1 nM, 59.9 nM and 29.7 nM for JAK1, JAK2, JAK3 and TYK2, respectively[1].
IC50 & Target: IC50：2.2 nM (JAK1), 23.1 nM (JAK2), 59.9 nM (JAK3), 29.7 nM (TYK2)[1]

Name: Nrf2-IN-1, CAS: 1610022-76-8, stock 9.9g, assay 98.9%, MWt: 383.87, Formula: C21H22ClN3O2, Solubility: DMSO : 260 mg/mL (677.31 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: NF-κB, Target: Keap1-Nrf2, Biological_Activity: Nrf2-IN-1 (Compound 4f) is an inhibitor of nuclear factor-erythroid 2-related factor 2 (Nrf2), acts as a promising agent in acute myeloid leukemia (AML) therapy[1].
IC50 & Target: Nrf2[1]

Name: GSK 4027, CAS: 2079896-25-4, stock 32.6g, assay 98.1%, MWt: 377.28, Formula: C17H21BrN4O, Solubility: DMSO : 50 mg/mL (132.53 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Epigenetics;Epigenetics, Target: Epigenetic Reader Domain;Histone Acetyltransferase, Biological_Activity: GSK 4027 is a chemical probe for the PCAF/GCN5 bromodomain with an pIC50 of 7.4±0.11 for PCAF in a time-resolved fluorescence resonance energy transfer (TR-FRET) assay.
IC50 & Target: pIC50: 7.4±0.11 (PCAF)[1]
In Vitro: GSK 4027 is a PCAF/GCN5 bromodomain chemical probe. p300/CREB binding protein associated factor (PCAF/KAT2B) and general control nonderepressible 5 (GCN5/KAT2A) are multidomain proteins that have been implicated in retroviral infection, inflammation pathways, and cancer development. GSK 4027 also demonstrates potency toward BRD4 BD1 and BRD9 inTR-FRET assay with pIC50s of <4.3 and 5.1±0.08, respectively. The selectivity of GSK 4027 against the wider bromodomain family is assessed in the BROMOscan panel with pKi of 8.9 and 8.9 for PCAF and GCN5, respectively. GSK 4027 shows equipotent activity against PCAF and GCN5 with Ki of 1.4 nM for both bromodomains. As expected due to the encouraging measured artificial membrane permeability (500 nm/s), treatment of HEK293 cells with GSK 4027 displace full length PCAF from histone H3.3 with little drop-off from the biochemical assay and a pIC50 7.2 (IC50 60 nM)[1].

Name: LOM612, CAS: 2173232-79-4, stock 36.2g, assay 98.2%, MWt: 258.30, Formula: C13H10N2O2S, Solubility: DMSO : 6 mg/mL (23.23 mM; Need ultrasonic); H2O : < 0.1 mg/mL (insoluble), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: LOM612 is a potent FOXO relocator, with an EC50 value of 1.5 μM in cells.
IC50 & Target: EC50: 1.5 μM (FOXO)[1]
In Vitro: LOM612 potently activates nuclear translocation of FOXO with an EC50 value of 1.5 μM, and this effect is independent of CRM-1. LOM612 effectively induces translocation of endogenous FOXO3a and FOXO1, and increases the expression of the FOXO target genes p27 and FasL. LOM612 shows no effect on the nuclear export of endogenous NFKB2 transcription factor in U2OS cells. LOM612 is cytotoxic to HepG2 cells, with an IC50 value of 0.64 μM, and does not sensitize non-cancer THLE2 cells (IC50, 2.76 μM)[1].

Name: Choline (bitartrate), CAS: 87-67-2, stock 6.5g, assay 98.1%, MWt: 253.25, Formula: C9H19NO7, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Neuronal Signaling;GPCR/G Protein, Target: mAChR;mAChR, Biological_Activity: Choline (bitartrate) is an essential nutrient, often associated with the B vitamins but not yet officially defined as a B vitamin[1]. Choline (bitartrate) plays an important role in synthesis of the neurotransmitter acetylcholine[2].
IC50 & Target: Acetylcholine[2]

Name: AR-M 1000390 (hydrochloride), CAS: 209808-47-9, stock 7.6g, assay 98.6%, MWt: 384.94, Formula: C23H29ClN2O, Solubility: DMSO : ≥ 150 mg/mL (389.67 mM), Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein;Neuronal Signaling, Target: Opioid Receptor;Opioid Receptor, Biological_Activity: AR-M 1000390 hydrochloride is an exceptionally selective, potent δ opioid receptor agonist with an EC50 of 7.2±0.9 nM for δ agonist potency.
IC50 & Target: EC50: 7.2±0.9 nM (δ opioid receptor)[1]
In Vitro: AR-M 1000390 (Compound 6a) exhibits the binding affinities (IC50) of 0.87±0.23 nM for the δ opioid receptor and extremely high selectivity over the µ receptor (IC50=3800±172 nM) and the κ receptor (IC50=7470±606 nM)[1]. RINm5F cells are treated with AR-M 1000390 (AR-M100390) and Cyclizine for 16-24 h before measurement of intracellular and secreted insulin levels. AR-M 1000390 mediates a dose-dependent decrease in insulin content with a maximal inhibition of ~90% at the highest concentration tested (10 μM)[2].
In Vivo: Rats are treated with 5, 100, and 600 μmol/kg of AR-M 1000390 (AR-M100390) for 3 and/or 7 days; another group of rats treated with 600 μmol/kg of compound are allowed to recover for 14 days. AR-M 1000390 (600 μmol/kg) causes vacuolation in the β-cell of the rat pancreas that is associated with depletion of insulin and hyperglycemia after 7 days of dosing. Treatment of rats with 600 μmol/kg of AR-M 1000390 results in vacuolation of the β-cell of the rat pancreas that is similar to that reported for cyclizine and cyproheptadine[2].

Name: D-erythro-Sphingosine Erythrosphingosine; erythro-C18-Sphingosine; trans-4-Sphingenine, CAS: 123-78-4, stock 3.8g, assay 98.7%, MWt: 299.49, Formula: C18H37NO2, Solubility: DMSO : 41.67 mg/mL (139.14 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: TGF-beta/Smad;Epigenetics;Metabolic Enzyme/Protease;Metabolic Enzyme/Protease, Target: PKC;PKC;Phosphatase;Endogenous Metabolite, Biological_Activity: D-erythro-Sphingosine (Erythrosphingosine) is a very potent activator of p32-kinase with an EC50 of 8 μM, and inhibits protein kinase C (PKC). D-erythro-Sphingosine (Erythrosphingosine) is also a PP2A activator[1][2][3][4].
IC50 & Target: EC50: 8 μM (p32-kinase)[1] 
PKC[2][3]
In Vitro: A p32-sphingosine-activated protein kinase responds to low concentrations of D-erythro-Sphingosine with an initial activation observed at 2.5 μM and a peak activity at 10-20 μM. This kinase shows a modest specificity for D-erythro-Sphingosine over other sphingosine tereoisomers, and a preference for sphingosines over ihydrosphingosines[1]. D-erythro-Sphingosine inhibits protein kinase C in vitro[2]. D-erythro-Sphingosine has been shown to inhibit protein kinase C, which affects cell regulation and several signal transduction pathways, and exhibits antitumor promoter activities in various mammalian cells[3].

Name: AZD7986 INS 1007, CAS: 1802148-05-5, stock 32.5g, assay 98.3%, MWt: 420.46, Formula: C23H24N4O4, Solubility: H2O : < 0.1 mg/mL (insoluble); DMSO : ≥ 100 mg/mL (237.83 mM), Clinical_Informat: Phase 2, Pathway: Metabolic Enzyme/Protease, Target: Dipeptidyl Peptidase, Biological_Activity: AZD7986 is a Dipeptidyl peptidase 1 (DPP1) inhibitor with pIC50s of 6.85, 7.6, 7.7, 7.8, and 7.8 in human, mouse, rat, dog and rabbit, respectively.
IC50 & Target: pIC50: 6.85 (human DPP1), 7.6 (mouse DPP1), 7.7 (rat DPP1), 7.8 (dog DPP1), 7.8 (rabbit DPP1)[1]
In Vitro: Results from cell assay show that AZD7986 is a Dipeptidyl peptidase 1 (DPP1) inhibitor with pIC50s of 6.85, 7.6, 7.7, 7.8, and 7.8 in human, mouse, rat, dog and rabbit, respectively. AZD7986 is stable in the propionaldehyde reactivity assay, with a half-life over 50 h. After differentiation in the presence of AZD7986 (38 pM to 10 μM), concentration-dependent decreases in cell lysate enzyme activity are observed for DPP1, as well as for all of the three NSPs, NE, Pr3, and CatG. AZD7986 inhibits activation of all three NSPs in a concentration dependent manner, with pIC50 values of around 7 for all three NSPs. The reduction of the activities is almost complete, with NE, Pr3, and CatG activities reduced to 4 to 10% of control at 10 μM AZD7986[1].
In Vivo: AZD7986 shows good stability in plasma, with a half life of >10 h. AZD7986 inhibits activation of NE and Pr3, but not CatG, in bone marrow cell lysates in a dose dependent manner in vivo[1].

Name: 4'-Demethylpodophyllotoxin, CAS: 40505-27-9, stock 5.3g, assay 99%, MWt: 400.38, Formula: C21H20O8, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: 4'-Demethylpodophyllotoxin is an aryltetralin lignin contained in the root of Podophyllum hexandrum and P. peltatum. 4'-Demethylpodophyllotoxin exhibits cytotoxic potential in diverse cancer cell lines[1][2].

Name: Y-26763, CAS: 127408-31-5, stock 25g, assay 98.5%, MWt: 276.29, Formula: C14H16N2O4, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Membrane Transporter/Ion Channel, Target: Potassium Channel, Biological_Activity: Y-26763 is a K+ channel opener and active metabolite of Y-27152[1]. Y-26763 is an ATP-sensitive K+ (KATP) channel activator[2].

Name: L-690330, CAS: 142523-38-4, stock 35g, assay 99%, MWt: 298.12, Formula: C8H12O8P2, Solubility: H2O : 33.33 mg/mL (111.80 mM; Need ultrasonic); DMSO : 25 mg/mL (83.86 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Phosphatase, Biological_Activity: L-690330 is a competitive inhibitor of inositol monophosphatase (IMPase) with Kis of 0.27 and 0.19 μM for recombinant human and bovine IMPase, 0.30 and 0.42 μM for human and bovine frontal cortex IMPase, respectively. L-690330 exhibits 10-fold more sensitive than mouse and rat IMPase[1].
IC50 & Target: Ki: 0.27 μM (Recombinant human IMPase), 0.19 μM (Recombinant bovine IMPase), 0.30 μM (Human frontal cortex IMPase), 0.42 μM (Bovine frontal cortex IMPase)[1]

Name: D-(+)-Cellobiose, CAS: 528-50-7, stock 19.7g, assay 98.7%, MWt: 342.30, Formula: C12H22O11, Solubility: , Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity:

Name: NSC 228155, CAS: 113104-25-9, stock 19.2g, assay 98.4%, MWt: 290.25, Formula: C11H6N4O4S, Solubility: H2O : < 0.1 mg/mL (insoluble); DMSO : 16 mg/mL (55.12 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Epigenetics;JAK/STAT Signaling;Protein Tyrosine Kinase/RTK;Epigenetics, Target: Epigenetic Reader Domain;EGFR;EGFR;Histone Acetyltransferase, Biological_Activity: NSC 228155 is an activator of EGFR, binds to the extracellular region of EGFR and enhance tyrosine phosphorylation of EGFR[1]. NSC 228155 is also a potent inhibitor of KIX-KID interaction, inhibits kinase-inducible domain (KID) from CREB and KID-interacting domain (KIX) from CBP, with an IC50 of 0.36 μM[2].
IC50 & Target: IC50: 0.36 μM (KIX-KID)[1]
In Vitro: NSC 228155 (100 μM) enhances EGFR tyrosine phosphorylation via action of SOD1[1]. 
NSC 228155 (Compound 1) inhibits CREB- and VP16-CREB-mediated gene transcription in living HEK 293T cells with IC50s of 2.09 and 6.14 μM, respectively[2]. 
NSC 228155 is not selective against CREB-mediated gene transcription in living HEK 293T cells[2].

Name: SKL2001, CAS: 909089-13-0, stock 26.7g, assay 98.8%, MWt: 286.29, Formula: C14H14N4O3, Solubility: DMSO : ≥ 96.66 mg/mL (337.63 mM), Clinical_Informat: No Development Reported, Pathway: Stem Cell/Wnt;Stem Cell/Wnt, Target: β-catenin;Wnt, Biological_Activity: SKL2001 is an agonist of the Wnt/β-catenin pathway, with anti-cancer activity. SKL2001 stabilizes intracellular β-catenin via disruption of the Axin/β-catenin interaction[1].
IC50 & Target: Wnt/β-catenin[1]
In Vitro: SKL2001 is an agonist of the Wnt/β-catenin pathway, and also upregulates the expression of Axin2, a downstream target of the Wnt/β-catenin pathway, but shows no effect on NF-κB, p53 reporter activity and GSK-3β activity. SKL2001 causes osteoblast differentiation (20 and 40 μM) and suppresses preadipocyte differentiation (5, 10, and 30 μM) via the activation of the Wnt/β-catenin pathway. SKL2001 (5, 10, and 30 μM) stabilizes intracellular β-catenin in 3T3-L1 cells[1]. SKL2001 (40 μM) significantly inhibits the proliferation of HCT116 spheroids independently of cytotoxicity and the inhibition is reversible; SKL2001 cuases cell cycle arrest in HCT116 spheroids. SKL2001 (40 μM) enhances round-shape spheroid formation and E-cadherin expression[2].

Name: Acetylcholine (iodide) ACh (iodide), CAS: 2260-50-6, stock 12.9g, assay 98.7%, MWt: 273.11, Formula: C7H16INO2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Acetylcholine iodide (ACh iodide) is a common neurotransmitter found in the central and peripheral nerve system[1].

Name: CeMMEC13, CAS: 1790895-25-8, stock 2.4g, assay 98.7%, MWt: 336.34, Formula: C19H16N2O4, Solubility: DMSO : ≥ 30 mg/mL (89.20 mM), Clinical_Informat: No Development Reported, Pathway: Cell Cycle/DNA Damage, Target: DNA/RNA Synthesis, Biological_Activity: CeMMEC13 is a potent inhibitor of TAF1 (2) bromodomain, with an IC50 of 2.1 μM.
IC50 & Target: IC50: 2.1 μM (TAF1 (2))[1]
In Vitro: CeMMEC13 is a potent inhibitor of TAF1 (2) bromodomain, with an IC50 of 2.1 μM. CeMMEC13 shows little or no effects on REDNESS, BRD4, CREBBP. CeMMEC13 (0-20 μM) in combination with (S)-JQ1 increases RFP expression in REDS3 cells and is effective reducing the viability of H23 and THP1 cells, better than that of single treatment[1].

Name: ATI-2341, CAS: 1337878-62-2, stock 22.3g, assay 98.3%, MWt: 2256.82, Formula: C104H178N26O25S2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein;Immunology/Inflammation, Target: CXCR;CXCR, Biological_Activity: ATI-2341 is a potent and functionally selective allosteric agonist of C-X-C chemokine receptor type 4 (CXCR4), which functions as a biased ligand, favoring Gαi activation over Gα13. ATI-2341 activates the inhibitory heterotrimeric G protein (Gi) to promote inhibition of cAMP production and induce calcium mobilization. ATI-2341 is a potent and efficacious mobilizer of bone marrow polymorphonuclear neutrophils (PMNs) and hematopoietic stem and progenitor cells (HSPCs)[1][2].
IC50 & Target: CXCR4[1]
In Vitro: ATI-2341 induces CXCR4- and G protein-dependent signaling, receptor internalization, and chemotaxis in CXCR4-expressing cells. ATI-2341 has an EC50 value of 194 ± 16 nM and an intrinsic activity of 81 ± 4% in CCRF-CEM cells[2].

Name: Ocaperidone R79598, CAS: 129029-23-8, stock 16.7g, assay 98.2%, MWt: 420.48, Formula: C24H25FN4O2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein;Neuronal Signaling;Neuronal Signaling;GPCR/G Protein, Target: Dopamine Receptor;Dopamine Receptor;5-HT Receptor;5-HT Receptor, Biological_Activity: Ocaperidone is an effective antipsychotic agent, acting as a potent 5-HT2 and dopamine D2 antagonist, and a 5-HT1A agonist, with Kis of 0.14 nM, 0.46 nM, 0.75 nM, 1.6 nM and 5.4 nM for 5-HT2, a1-adrenergic receptor, dopamine D2, histamine H1 and a2-adrenergic receptor, respectively, and a pEC50 and pKi of 7.60 and 8.08 for h5-HT1A.
IC50 & Target: Ki: 0.14 nM (5HT2), 0.46 nM (a1-adrenergic receptor), 0.75 nM (Dopamine D2), 1.6 nM (Histamine H1), 5.4 nM (a2-adrenergic receptor)[1] 
pEC50: 7.60 (h5-HT1A)[2] 
pKi: 8.08 (h5-HT1A)[2]
In Vitro: Ocaperidone has high affinify at 5-HT2 and dopamine D2, with Kis of 0.14 nM, 0.46 nM, 0.75 nM, 1.6 nM and 5.4 nM for 5HT2, a1-adrenergic, dopamine D2, histamine H1 and a2-adrenergic, respectively[1]. Ocaperidone shows 5-HT1A receptor agonist activity, with a pEC50 and pKi of 7.60 and 8.08[2].
In Vivo: Ocaperidone shows a potent occupation of 5HT2 receptor via in vivo binding in the frontal cortex of rats with an ED50 of 0.04 mg/kg, and 0.1 4-0.1 6 mg/kg for D2 receptor in the striatum and the nucleus accumbens[1]. Ocaperidone (R 79598) antagonizes dopamine D2 and 5-HT2, and shows a a partial generalization to buspirone with an ED50 of 0.163 mg/kg[3].

Name: PX20606 trans racemate PX-102 trans racemate, CAS: 1268244-85-4, stock 5g, assay 98.7%, MWt: 554.85, Formula: C29H22Cl3NO4, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease;Autophagy, Target: FXR;Autophagy, Biological_Activity: PX20606 trans racemate is a FXR agonist with EC50s of 32 and 34 nM for FXR in FRET and M1H assay, respectively.
IC50 & Target: EC50: 32 nM (FXR in FRET assay), 34 nM (FXR in M1H assay)[1]

Name: PD-1-IN-17, CAS: 1673560-66-1, stock 24.9g, assay 98.8%, MWt: 374.35, Formula: C13H22N6O7, Solubility: DMSO : 125 mg/mL (333.91 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Immunology/Inflammation, Target: PD-1/PD-L1, Biological_Activity: PD-1-IN-17 is a programmed cell death-1 (PD-1) inhibitor extracted from patent WO2015033301A1, Compound 12, inhibits 92% splenocyte proliferation at 100 nM[1].
IC50 & Target: PD-1[1]

Name: 1,3-Diaminopropane, CAS: 109-76-2, stock 30.9g, assay 98.9%, MWt: 74.12, Formula: C3H10N2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: 1,3-Diaminopropane, a three carbon diamine, is an ornithine decarboxylase inhibitor.

Name: L-45 L-Moses, CAS: 2079885-05-3, stock 6g, assay 98.7%, MWt: 360.46, Formula: C21H24N6, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Epigenetics, Target: Epigenetic Reader Domain, Biological_Activity: L-45 is the first potent, selective, and cell-active p300/CBP-associated factor (PCAF) bromodomain (Brd) inhibitor with a Kd of 126±15 nM.
IC50 & Target: Kd:126±15nM (PCAF Brd-binding)[1]
In Vitro: L-45 disrupts PCAF-Brd histone H3.3 interaction in cells using a nanoBRET assay, and a co-crystal structure of L-45 with the homologous Brd PfGCN5 from Plasmodium falciparum rationalizes the high selectivity for PCAF and GCN5 bromodomains. A structure using highly homologous (64 % identity) Brd from Plasmodium falciparum, PfGCN5, of which L-45 is also a potent ligand (isothermal titration calorimetry (ITC) KD 280 nM), is successfully obtained (PDB: 5TPX). L-45 binds in the acetylated lysines (KAc) -binding pocket of PfGCN (blue ribbon and sticks) and makes H-bonds (dotted lines) through the triazole to N1436 and the first of a network of four water molecules (red spheres)[1].
In Vivo: L-45 shows no observable cytotoxicity in peripheral blood mononuclear cells (PBMC), good cell-permeability, and metabolic stability in human and mouse liver microsomes, supporting its potential for in vivo use[1].

Name: KI696, CAS: 1799974-70-1, stock 22.6g, assay 98.6%, MWt: 550.63, Formula: C28H30N4O6S, Solubility: DMSO : 125 mg/mL (227.01 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: NF-κB, Target: Keap1-Nrf2, Biological_Activity: KI696 is a high affinity probe that disrupts the Keap1/NRF2 interaction. KI696 is a potent and selective inhibitor of the KEAP1/NRF2 interaction.
IC50 & Target: Target: Keap1-NRF2[1]
In Vitro: KI696 (compound 7) exhibits very high affinity for the KEAP1 Kelch domain (ITC Kd=1.3 nM with the exception of the organic anion transporting polypeptide 1B1 (OATP1B1) (IC50=2.5 µM), the bile salt export pump BSEP (IC50=4.0 µM), and the phosphodiesterase PDE3A (IC50=10 µM), no significant cross-reactivity is observed. No cytotoxicity is observed towards BEAS-2B cells with KI696 at concentrations up to 10 µM. KI696 increases NRF2 Nuclear Translocation in Normal Human Bronchial Epithelial cells. KI696 increases mRNA expression of the NRF2-dependent genes NQO1 and GCLM in NHBE cells transfected with the non-targeting siRNA, while NRF2 gene silencing significantly decreases compound activity. KI696 increases NQO1 Activity in an NRF2-Dependent Manner. Treatment with tBHP clearly has a detrimental effect on cell health and appearance while pre-treatment of cells with 1 µM KI696 before the exposure to tBHP maintained cell morphology consistent with the DMSO control. KI696 Induces the Expression of NRF2-Regulated Genes in COPD patient-derived bronchial epithelial cells[1].
In Vivo: KI696 induces the expression of each of the Nqo1, Ho-1, Txnrd1, Srxn1, Gsta3, Gclc genes in a dose-dependent manner, with maximum increases over vehicle controls of 37-(Nqo1), 17-(Ho-1), 9-(Txnrd1), 28-(Srxn1), 15-(Gsta3) and 13-fold (Gclc) occurring at the 50 µmol/kg dose. EC50 values are 44.0, 25.7, 42.6, 33.8, 28.4, and 44.1 µmol/kg, respectively, giving an average EC50 value of 36.4±3.4 µmol/kg. KI696 attenuates ozone-Induced pulmonary inflammation. KI696 restores ozone-induced depletion of lung GSH levels. KI696 is administered to rats at 10, 35 and 50 µmol/kg by IV infusion, resulting in steady state compound concentrations in the blood of 407±44 nM, 946±50 nM and 1437±186 nM, respectively, over the 6 hour infusion period. Exposure to ozone 24 hours post-dose produces a significant depletion in lung levels of the anti-oxidant molecule, GSH, which is restored by KI696 in a dose-dependent manner[1].

Name: (-)-PX20606 trans isomer (-)-PX-102 trans isomer;(-)-PX-104, CAS: 1268244-88-7, stock 0.7g, assay 98.3%, MWt: 554.85, Formula: C29H22Cl3NO4, Solubility: Ethanol : ≥ 50 mg/mL (90.11 mM), Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease;Autophagy, Target: FXR;Autophagy, Biological_Activity: (-)-PX20606 trans isomer is a FXR agonist with EC50s of 18 and 29 nM for FXR in FRET and M1H assay, respectively.
IC50 & Target: EC50: 18 nM (FXR in FRET assay), 29 nM (FXR in M1H assay)[1]

Name: JTV-519 (free base) K201 (free base), CAS: 145903-06-6, stock 28.1g, assay 98.4%, MWt: 424.60, Formula: C25H32N2O2S, Solubility: 10 mM in DMSO, Clinical_Informat: Phase 2, Pathway: Membrane Transporter/Ion Channel;Neuronal Signaling, Target: Calcium Channel;Calcium Channel, Biological_Activity: JTV-519 free base (K201 free base) is a Ca2+-dependent blocker of sarcoplasmic reticulum Ca2+-stimulated ATPase (SERCA) and a partial agonist of ryanodine receptors in striated muscle. Antiarrhythmic and cardioprotective properties[1][2].
In Vitro: JTV-519 (K201) inhibits inward Ca2+ movement into large unilamellar vesicles (LUV) caused by annexin V in a dose-dependent manner. In the presence of 50 nM annexin V and 400 μM Ca2+, 3 μM JTV-519 shows significant inhibition of Ca2+ movement due to annexin V, and 50% inhibition is achieved at 25 μM K201[2].
In Vivo: JTV-519 (0.5mg/kg/h, i.v., 2 h before the surgery) improves cardiac function in CLP mice, where the fractional shortening (FS) and ejection fraction (EF) are significantly increased as compared with CLP mice without JTV-519 treatment[3].

Name: PGMI-004A, CAS: 1313738-90-7, stock 29.1g, assay 99%, MWt: 463.38, Formula: C21H12F3NO6S, Solubility: H2O : < 0.1 mg/mL (insoluble); DMSO : ≥ 125 mg/mL (269.76 mM), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: PGMI-004A is a potent phosphoglycerate mutase 1 (PGAM1) inhibitor with an IC50 of 13.1 μM.
IC50 & Target: IC50: 13.1 μM (PGAM1)[1]
In Vitro: PGMI-004A inhibits PGAM1 with an IC50 of approximately 13.1 μM and the Kd value of the PGMI-004A-PGAM1 interaction is determined to be 7.2±0.7 μM from fluorescence-based binding assay. PGMI-004A may allosterically modulate the enzyme activity of PGAM1. The Ki value is determined to be 3.91±2.50 μM using Dixon plot analysis. The Kd value for protein-ligand interaction is calculated to be 9.4±2.0 μM. Inhibition of PGAM1 activity by PGMI-004A (20 μM) treatment results in decreased 2-PG and increased 3-PG levels in H1299 cells, which could be rescued by treatment with methyl-2-PG. Treatment with PGMI-004A (20 μM) results in significantly reduced lactate production that is rescued by methyl-2-PG treatment, but has no significant effect on intracellular ATP levels. PGMI-004A (20 μM) treatment results in decreased oxidative PPP flux and NADPH/NADP+ratio, as well as reduced biosynthesis of lipids and RNA, and cell proliferation in H1299 cells. PGMI-004A treatment results in decreased cell proliferation of diverse human cancer and leukemia cells, but not control human dermal fibroblasts (HDF), human foreskin fibroblasts (HFF), human HaCaT keratinocyte cells and human melanocyte PIG1 cells, suggesting minimal non-specific toxicity of PGMI-004A in normal, proliferating human cells[1].
In Vivo: The xenograft experiment is performed by injecting H1299 cells to nude mice. Six days post-injection, mice are divided into two groups (n=8/group) and treated with either PGMI-004A (100mg/kg/day) or vehicle for 21 days. PGMI-004A treatment results in significantly decreased tumor growth and tumor size in treated mice compared with mice receiving vehicle control. Moreover, treatment with PGMI-004A effectively inhibits PGAM1 enzyme activity in tumors in vivo in resected tumors from xenograft nude mice[1].

Name: Melperone, CAS: 3575-80-2, stock 7.4g, assay 99%, MWt: 263.35, Formula: C16H22FNO, Solubility: DMSO : 41.67 mg/mL (158.23 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Melperone, a butyrophenone, is an antipsychotic drug used for sleep induction which is frequently prescribed in psychiatric setting[1]. Melperone has been used for a variety of indications, including the treatment of schizophrenia, but also for agitation in the elderly[2].

Name: Mal-amido-PEG8-C2-acid, CAS: 1334177-86-4, stock 5.5g, assay 98.1%, MWt: 592.63, Formula: C26H44N2O13, Solubility: DMSO : 250 mg/mL (421.85 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Antibody-drug Conjugate/ADC Related, Target: ADC Linker, Biological_Activity: Mal-amido-PEG8-C2-acid (example 142) is a nonclaevable ADC linker, extracted from patent US2018339985[1].

Name: 2-Iodomelatonin, CAS: 93515-00-5, stock 36.4g, assay 98.9%, MWt: 358.17, Formula: C13H15IN2O2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein;Neuronal Signaling, Target: Melatonin Receptor;Melatonin Receptor, Biological_Activity: 2-Iodomelatonin is a potent agonist of melatonin receptor 1 (MT1) with a Ki value of 28 pM, it is more 5-fold selective for MT1 over MT2[1]. 2-iodomelatonin can be used to identify, characterize and localize melatonin binding sites in the brain and peripheral tissues[1].
In Vitro: 2-iodomelatonin (0-7.5 μM; 18 hours) shares the protective properties of melatonin, it inhibits cell death of mutant htt ST14A and inhibits the increase in Rip2 expression in stressed mutant htt ST14A cells[2].

Name: MK-6240, CAS: 1841078-87-2, stock 1g, assay 98.3%, MWt: 278.28, Formula: C16H11FN4, Solubility: DMSO : 12.5 mg/mL (44.92 mM; Need ultrasonic), Clinical_Informat: Phase 3, Pathway: Others, Target: Others, Biological_Activity: MK-6240 is a positron emission tomography (PET) tracer for neurofibrillary tangles (NFTs), exhibiting high specificity and selectivity for binding to NFTs.
IC50 & Target: Ki: NFT[1].

Name: JNJ-39758979, CAS: 1046447-90-8, stock 36.7g, assay 98.7%, MWt: 221.30, Formula: C11H19N5, Solubility: DMSO : 33.33 mg/mL (150.61 mM; Need ultrasonic), Clinical_Informat: Phase 2, Pathway: Immunology/Inflammation;GPCR/G Protein;Neuronal Signaling, Target: Histamine Receptor;Histamine Receptor;Histamine Receptor, Biological_Activity: JNJ-39758979 is a selective, high-affinity histamine H4 receptor antagonist with a Ki of 12.5 nM.
IC50 & Target: Ki: 12.5 nM (histamine H4 receptor)[1]
In Vitro: JNJ-39758979 is a selective, high-affinity histamine H4 receptor antagonist with a Ki of 12.5 nM.
The affinity of JNJ-39758979 for the rat (Ki=188 nM) and guinea pig H4R (Ki=306 nM) is moderate, and JNJ-39758979 has little if any affinity for the dog H4R (Ki≥10 μM). JNJ-39758979 is metabolically stable (t1/2 >120 min) when incubated in vitro with human, rat, dog, or monkey liver microsomes[1].
In Vivo: JNJ-39758979 shows dose-proportional pharmacokinetic (PK) in rat in the range of 2 to 500 mpK. JNJ-39758979 rapidly reaches the kidneys and liver (mean tmax=2.0 h). The elimination of JNJ-39758979 is slow from the brain, liver, and kidneys, with mean t1/2 values of 42.5, 22.3, and 20.5 h, respectively. The highest exposure (based on Cmax and AUC0-inf values) is observed in the liver followed by the kidney and brain. Tissue-to-plasma ratios for liver and kidney range from 23.2 to 95.8; the tissue-to-plasma ratios in brain increases with time from 0.256 to 22.7 up to 48 h after dosing. JNJ-39758979 is able to inhibit histamine-induced itch at doses of 5 and 20 mg/kg in mice. JNJ-39758979 exhibits dose-dependent inhibition of the clinical score in a mouse collagen-induced arthritis model[1].

Name: Zinc Protoporphyrin Zn(II)-protoporphyrin IX;ZnPP;Zinc Protoporphyrin-9, CAS: 15442-64-5, stock 5.6g, assay 98.1%, MWt: 626.02, Formula: C34H32N4O4Zn, Solubility: DMSO : 50 mg/mL (79.87 mM; Need ultrasonic); H2O : < 0.1 mg/mL (insoluble), Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease;Metabolic Enzyme/Protease;NF-κB;Immunology/Inflammation, Target: Endogenous Metabolite;Reactive Oxygen Species;Reactive Oxygen Species;Reactive Oxygen Species, Biological_Activity: Zinc Protoporphyrin (Zn(II)-protoporphyrin IX) is a competitive heme oxygenase-1 (HO-1) inhibitor, markedly attenuates the protective effects of Phloroglucinol (PG) against H2O2[1]. Zinc Protoporphyrin is a normal metabolite formed in trace amounts during heme biosynthesis and used as a screening marker of iron deficiency in individual pregnant women and children, but also to assess population iron status in combination with haemoglobin concentration[2].

Name: Riluzole hydrochloride PK 26124 hydrochloride, CAS: 850608-87-6, stock 32.3g, assay 98.9%, MWt: 270.66, Formula: C8H6ClF3N2OS, Solubility: H2O : 131 mg/mL (484.00 mM; Need ultrasonic and warming), Clinical_Informat: Launched, Pathway: Neuronal Signaling;Membrane Transporter/Ion Channel;Membrane Transporter/Ion Channel, Target: GABA Receptor;GABA Receptor;Sodium Channel, Biological_Activity: Riluzole hydrochloride is an anticonvulsant drug and belongs to the family of use-dependent Na+ channel blocker which can also inhibit GABA uptake with an IC50 of 43 μM.
IC50 & Target: Sodium channel[1]
IC50: 43 μM (GABA receptor)[1]
In Vitro: Riluzole hydrochloride is an anticonvulsant drug and belongs to the family of use-dependent Na+ channel blocker which can also inhibit GABA uptake with an IC50 of 43 μM. At 20 μM, Riluzole hydrochloride inhibits peak autaptic IPSCs only slightly but prolongs IPSCs reliably. It is also found that Riluzole hydrochloride causes a strong, concentration-dependent, readily reversible enhancement of responses to 2 μM GABA. At higher concentrations of Riluzole hydrochloride, especially 300 μM, GABA currents exhibit apparent desensitization during prolonged co-exposure to 2 μM GABA and Riluzole hydrochloride. The EC50 of Riluzole hydrochloride potentiation of GABA responses is about 60 μM[1].
In Vivo: In normal naïve rats, systemic injection of Riluzole hydrochloride (8 mg/kg, i.p.; n=6 rats) decreases the duration of ultrasonic but not audible vocalizations evoked by noxious stimulation of the knee joint compare to vehicle tested in the same rats (P<0.05). Systemic application of Riluzole hydrochloride (8 mg/kg, i.p.; n=19 rats) decreases the vocalizations of arthritic rats compare to predrug and vehicle significantly (P<0.05 to 0.001). Riluzole hydrochloride administered into the CeA significantly decreases the duration of audible and ultrasonic vocalizations evoked by noxious stimulation of the knee compare to predrug values (n=8 rats; P<0.05 to 0.01)[2].

Name: SNS-032 BMS-387032, CAS: 345627-80-7, stock 9.8g, assay 98.8%, MWt: 380.53, Formula: C17H24N4O2S2, Solubility: DMSO : 33.33 mg/mL (87.59 mM; Need ultrasonic), Clinical_Informat: Phase 1, Pathway: Apoptosis;Cell Cycle/DNA Damage, Target: Apoptosis;CDK, Biological_Activity: SNS-032 is a selective inhibitor of cyclin-dependent kinase (CDK), inhibiting CDK2/7/9 with IC50s of 38 nM/62 nM/4 nM.
IC50 & Target: IC50: 38 nM (CDK2), 62 nM (CDK7), 4 nM (CDK9)[1]
In Vitro: SNS-032 has low sensitivity to CDK1 and CDK4 with IC50 of 480 nM and 925 nM, respectively. SNS-032 effectively kills chronic lymphocytic leukemia cells in vitro regardless of prognostic indicators and treatment history. Compared with flavopiridol and roscovitine, SNS-032 is more potent, both in inhibition of RNA synthesis and at induction of apoptosis. SNS-032 activity is readily reversible; removal of SNS-032 reactivates RNA polymerase II, which led to resynthesis of Mcl-1 and cell survival[1]. SNS-032 inhibits three dimensional capillary network formations of endothelial cells. SNS-032 completely prevents U87MG cell–mediated capillary formation of HUVECs. In addition, SNS-032 significantly prevents the production of VEGF in both cell lines, SNS-032 prevents in vitro angiogenesis, and this action is attributable to blocking of VEGF. Preclinical studies have shown that SNS-032 induces cell cycle arrest and apoptosis across multiple cell lines[2]. SNS-032 blocks the cell cycle via inhibition of CDKs 2 and 7, and transcription via inhibition of CDKs 7 and 9. SNS-032 activity is unaffected by human serum[3]. SNS-032 induces a dose-dependent increase in annexin V staining and caspase-3 activation. At the molecular level, SNS-032 induces a marked dephosphorylation of serine 2 and 5 of RNA polymerase (RNA Pol) II and inhibits the expression of CDK2 and CDK9 and dephosphorylated CDK7[5].
In Vivo: SNS-032 (15 mg/kg, i.p.) inhibits both xenografted BaF3-T674I cells and KBM5-T315I cells in vivo. SNS-032 abrogates the growth of tumors transplanted in nude mice with downregulation of T674I PDGFRα and T315I-Bcr-Abl[4].

Name: MSOP, CAS: 66515-29-5, stock 7.3g, assay 98.5%, MWt: 199.10, Formula: C4H10NO6P, Solubility: 10 mM in H2O, Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein;Neuronal Signaling, Target: mGluR;mGluR, Biological_Activity: MSOP is a selective group III metabotropic glutamate receptor antagonist with apparent KD of 51 μM for the L-AP4-sensitive presynaptic mGluR.
IC50 & Target: KD: 51 μM (L-AP4-sensitive presynaptic mGluR)[1].
In Vitro: In the presence of 200 μM MSOP, a rightward parallel shift of the dose-response curve to L-AP4 is observed, with an apparent KD calculated as 51±6 μM (n=3). MSOP is shown to be selective for the L-APC sensitive presynaptic mGluR, the apparent KD for the interaction of MSOP with the (1S, 3S)-ACPD sensitive receptor calculated as greater than 700 μM (n=3)[1].
In Vivo: It is found that TBOA-induced antinociceptive effects are significantly blocked by intrathecal co-administration of MSOP (second phase of formalin model: F3,16=30.96, P<0.001; CFA model: F3,16=30.77, P<0.001). As expected, intrathecal TBOA (10 μg) reduces the number of formalin-induced flinches and shakes by 47% of the value in the saline-treated group in the second phase (P<0.001) and blocked the CFA-induced decrease in ipsilateral paw withdrawal latency by 60% of the value in the saline-treated group (P=0.01). The number of formalin-induced flinches in the second phase in the group treated with MSOP and TBOA is increased by 56% (P=0.04) of the value in the TBOA-treated group. CFA-induced paw withdrawal latency in the group treated with MSOP and TBOA is decreased by 86% (P=0.03) of the value in the TBOA-treated group[2].

Name: Tiotidine ICI 125211, CAS: 69014-14-8, stock 31g, assay 98.3%, MWt: 312.42, Formula: C10H16N8S2, 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: Tiotidine (ICI 125211) is a potent and selective antagonist of histamine H2-receptor (pA2=7.3-7.8 for guinea-pig right atrium). Tiotidine has low affinity for both the H1 and the H3 receptors[1][2].
In Vitro: Tiotidine competitively antagonizes the positive chronotropic action of histamine with an apparent dissociation constant of 30 μM (23-38 μM). Tiotidine abolishes H2-mediated increases in contractile force leaving H2-mediated negative inotropic responses unopposed. The actions of histamine at the A-V node, manifested by lengthening of the P-R interval and A-V block, are attenuated by 2.5 x 10(-7) M Tiotidine[2]. 
Tiotidine actually behaves as an inverse agonist in U-937 cells, diminishing basal cAMP levels[3].

Name: L-732138, CAS: 148451-96-1, stock 36.1g, assay 98.2%, MWt: 472.38, Formula: C22H18F6N2O3, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Neuronal Signaling;GPCR/G Protein, Target: Neurokinin Receptor;Neurokinin Receptor, Biological_Activity: L-732138 is a selective, potent and competitive neurokinin-1 (NK-1) receptor antagonist with an IC50 of 2.3 nM. L-732138 has 200-fold more potent in cloned human NK-1 receptors than cloned rat NK-1 receptors, and has > 1000-fold more potent than human NK-2 and NK-3 receptors. L-732138 can reduce hyperalgesia and has antitumor action[1][2].
In Vitro: L-732138 (0 -100 µM; first doubling time; COLO 858, MEL HO and COLO 679 cells) treatment results in a concentration-dependent cytotoxicity. L-732138 inhibits cell growth with IC50 of 44.6 μM for COLO 858 cells, 76.3 μM for MEL HO cells and 64.2 μM for COLO 679 cells. L-732138 blocks substance P (SP) mitogen stimulation[1]. 
L-732,138 treatment results in a large number of apoptotic cells were found in COLO 858, MEL HO and COLO 679 melanoma cell lines. In DAPI-stained cultures, at IC50 concentration of 43.6% apoptotic cells for the three melanoma cell lines, whereas at IC100 concentration of 51.4 % apoptotic cells[1].
In Vivo: L-732138 (10-4-10-2 mol/kg; intravenous injection; for 15 minutes; male Dunkin-Hartley guinea-pigs) treatment abolishes vagally-induced plasma exudation and significantly inhibits the enhancement by LPS. The LPS-enhanced vagally-induced plasma exudation is not completely inhibited by either L-732138 or SOD pretreatment alone, but is blocked by the combination of both pretreatments[3].

Name: AM-92016 (hydrochloride), CAS: 133229-11-5, stock 8.6g, assay 98.5%, MWt: 483.84, Formula: C19H25Cl3N2O4S, Solubility: DMSO : 260 mg/mL (537.37 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: AM-92016 hydrochloride is a specific blocker of rectifier potassium current (IK). AM-92016 hydrochloride delays rectifier potassium channel (IK), repolarizes the membrane thereby restricting the duration of the nerve impulse thereby restricting the duration of the nerve impulse[1].

Name: Luzindole N-0774, CAS: 117946-91-5, stock 16.2g, assay 98.1%, MWt: 292.37, Formula: C19H20N2O, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein;Neuronal Signaling, Target: Melatonin Receptor;Melatonin Receptor, Biological_Activity: Luzindole (N-0774) is a selective melatonin receptor antagonist. Luzindole preferentially targets MT2 (Mel1b) over MT1 (Mel1a) with Ki values of 10.2 and 158 nM for human MT2 and MT1, respectively. Luzindole suppresses experimental autoimmune encephalomyelitis (EAE), and exerts antidepressant-like activity[1][2][3].
IC50 & Target: Ki :10.2 nM (human MT2), 158 nM (human MT1)[1]
In Vitro: Luzindole (N-0774) (5-10 μg/ml) inhibits antigen-specific proliferation of the MBP-reactive LV-4 T cell line[1].
In Vivo: Luzindole (N-0774) (30 mg/kg; i.p.; days 0-5) suppresses experimental autoimmune encephalomyelitis[2]. 
Luzindole (N-0774) (30 mg/kg i.p.) reduces the time of immobility in a dose-dependent manner, the effect being more pronounced at midnight (60% reduction) than at noon (39% reduction). The effect of luzindole is time-dependent, showing a maximal effect at 60 min. The anti-immobility effect of luzindole (10 mg/kg i.p.) is prevented by the administration of melatonin (30 mg/kg i.p.). Luzindole (30 mg/kg i.p.) did not modify the time of immobility either at noon or midnight in the albino ND/4 mouse, or in the C57BL/6J mouse, which does not produce melatonin[3].

Name: Oleamide, CAS: 301-02-0, stock 1.6g, assay 98.8%, MWt: 281.48, Formula: C18H35NO, Solubility: DMSO : 9 mg/mL (31.97 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: Oleamide is an endogenous fatty acid amide which can be synthesized de novo in the mammalian nervous system, and has been detected in human plasma.
In Vitro: Oleamide accumulates in the cerebrospinal fluid (CSF) of rats after six hours of sleep deprivation and induces sleep in naive rats and mice. Inhibition of the primary catabolic enzyme of oleamide (fatty acid amide hydrolase) by trifluoromethyl-octadecenone reduces sleep latency and increases total sleep time when given centrally to rats and peripherally to mice[1]

Name: Chlormethiazole hydrochloride Clomethiazole hydrochloride, CAS: 6001-74-7, stock 6.9g, assay 98.7%, MWt: 198.11, Formula: C6H9Cl2NS, Solubility: DMSO : 125 mg/mL (630.96 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Clomethiazole hydrochloride is a sedative and anticonvulsant. Clomethiazole hydrochloride is neuroprotective and prevents the degeneration of serotonergic nerve terminals induced by 3,4-methylenedioxymethamphetamine (MDMA)[1][2].

Name: PACAP (1-27), human, ovine, rat PACAP 1-27, CAS: 127317-03-7, stock 9.6g, assay 98.2%, MWt: 3147.66, Formula: C142H224N40O39S, Solubility: H2O, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: PACAP (1-27), human, ovine, rat (PACAP 1-27) is the N-terminal fragment of PACAP-38, and is a potent PACAP receptor antagonist with IC50s of 3 nM, 2 nM and 5 nM for rat PAC1, rat VPAC1 and human VPAC2, respectively[1].
IC50 & Target: IC50: 3 nM (rat PAC1), 2 nM (rat VPAC1), 5 nM (human VPAC2)[1]
In Vitro: Radioligand receptor binding assays with I-monoiodinated PACAP (1-27), human, ovine, rat confirms the presence of PAC -receptors on AR4-2J cells, since PACAP (1-27), human, ovine, rat and PACAP(1–38) equipotently displaces radioligand binding with a Kd of 1-2 nM, whereas vasoactive intestinal peptide (VIP) is 1000-fold less potent. PACAP (1-27), human, ovine, rat exhibits a distinct and much higher susceptibility to VIP-amino acid substitutions. PACAP (1-27), human, ovine, rat has potency and binding affinity to stimulate IP3 and cAMP formation in AR4-2J cells[2].
In Vivo: The inhibitory effect of pituitary adenylate cyclase activating polypeptide (PACAP (1-27), human, ovine, rat) on the increase in total pulmonary resistance (RL) causes either by allergen or histamine in anaesthetized, ventilated guinea-pigs is studied. PACAP (1-27), human, ovine, rat given via i.v. infusion (0.045-4.5 nmol/kg/min) dose-dependently reduces the increase in RL caused by inhaled ovalbumin and histamine. At the highest dose, PACAP (1-27), human, ovine, rat prevented the increase in RL caused by ovalbumin and histamine completely. Infusion of PACAP (1-27), human, ovine, rat and the β2-adrenoceptor agonist, salbutamol (0.045-4.5 nmol/kg/min) inhibit the increase in RL similarly, but salbutamol increases the heart rate more than PACAP (1-27), human, ovine, rat[3].

Name: ATPA, CAS: 140158-50-5, stock 31.7g, assay 98.1%, MWt: 228.25, Formula: C10H16N2O4, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Membrane Transporter/Ion Channel;Neuronal Signaling, Target: iGluR;iGluR, Biological_Activity: ATPA is a selective glutamate receptor GluR5 activator with EC50s of 0.66, 9.5, 1.4, 23, 32, 18, and 14 μM for GluR5wt, GluR5(S741M), GluR5(S721T), GluR5(S721T, S741M), GluR5(S741A), GluR5(S741L), and GluR5(S741V), respectively[1].
In Vitro: ATPA also activates GluR1wt, GluR1(M722S), GluR1(T700S), GluR1(T700S, M722S), GluR1(M722A) with EC50s of 62, 4.6, 97, 14, 97 μM, respectively[1].

Name: Milademetan DS-3032, CAS: 1398568-47-2, stock 36.8g, assay 98%, MWt: 618.53, Formula: C30H34Cl2FN5O4, Solubility: 10 mM in DMSO, Clinical_Informat: Phase 1, Pathway: Metabolic Enzyme/Protease;Apoptosis, Target: E1/E2/E3 Enzyme;MDM-2/p53, Biological_Activity: Mliademetan is a specific MDM2 inhibitor, a pharmaceutical composition for use in treating acute myeloid leukemia (AML).
IC50 & Target: MDM2[1].

Name: EMT inhibitor-1, CAS: 1638526-21-2, stock 29g, assay 98.9%, MWt: 319.21, Formula: C12H12Cl2N2O2S, Solubility: DMSO : ≥ 100 mg/mL (313.27 mM), Clinical_Informat: No Development Reported, Pathway: Stem Cell/Wnt;Stem Cell/Wnt;TGF-beta/Smad;Stem Cell/Wnt, Target: Hippo (MST);TGF-beta/Smad;TGF-beta/Smad;Wnt, Biological_Activity: EMT inhibitor-1 is an inhibitor of of Hippo, TGF-β, and Wnt signaling pathways with antitumor activities.
IC50 & Target: Hippo, TGF-β, Wnt[1].
In Vitro: EMT inhibitor-1 (C19) (0-10μM; 24 hours) is an inhibitor of of Hippo, TGF-β, and Wnt signaling pathways with antitumor activities, inhibiting cancer cell migration, proliferation, and resistance to doxorubicin in vitro[1].
In Vivo: EMT inhibitor-1 (C19) (intraperitoneal injection; 5-20 mg/kg) exerts strong antitumor activity in a mouse tumor model. Mechanistically, EMT inhibitor-1 induces GSK3-β–mediated degradation of the Hippo transducer TAZ, through activation of the Hippo kinases Mst/Lats and the tumor suppressor kinase AMPK upstream of the degradation complex[1].C19 is dissolved in the vehicle solution (100 μL of DMEM containing 5% dimethyl sulfoxide).

Name: VU 6008667, CAS: 2092923-21-0, stock 6g, assay 98%, MWt: 438.85, Formula: C24H17ClF2N2O2, Solubility: DMSO : 100 mg/mL (227.87 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Neuronal Signaling;GPCR/G Protein, Target: mAChR;mAChR, Biological_Activity: VU 6008667 is a selective negative allosteric modulator of M5 NAM with IC50s of 1.2 μM and 1.6 μM for human M5 and rat M5, respectively. High CNS penetration[1].
IC50 & Target: IC50: 1.2 μM (Human M5); 1.6 μM (Rat M5)[1]
In Vivo: VU 6008667 (1 mg/kg)/PO (3 mg/kg, solution dose) displays a diminished elimination half-life (t1/2=2.3 hr) driven by a smaller volume (Vss=7.4 L/kg) and higher clearance (CLp=82 mL/min/kg), with moderate oral bioavailability (17% F)[1].

Name: DMU2105, CAS: 1821143-79-6, stock 26.4g, assay 98.6%, MWt: 259.30, Formula: C18H13NO, Solubility: DMSO : 53.33 mg/mL (205.67 mM; Need ultrasonic); H2O : < 0.1 mg/mL (insoluble), Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Cytochrome P450, Biological_Activity: DMU2105 is a potent and specific CYP1B1 inhibitor, with IC50s of 10 nM and 742 nM for CYP1B1 and CYP1A1, respectively.
IC50 & Target: IC50: 10 nM (CYP1B1), 742 nM (CYP1A1)[1].
In Vitro: DMU2105 (Compound 7k) shows 74 and 120-fold selectivity for CYP1B1 over CYP1A1 and CYP1A2. In the presence of DMU2105 however, the EC50 goes down to 1 μM indicating that the cells have suffered from toxicity which may have been mediated by CYP1B1 inhibition. Un-transfected cells (HEK293: pcDNA3.1), when treated with cisplatin and DMU2105 (10×IC50) do not show any perceptible decrease of cisplatin EC50 (8.5 μM ± 0.9)[1].

Name: DMU2139, CAS: 1821143-80-9, stock 5.4g, assay 98.2%, MWt: 289.33, Formula: C19H15NO2, Solubility: H2O : < 0.1 mg/mL (insoluble); Ethanol : 5 mg/mL (17.28 mM; Need ultrasonic); DMSO : 77.5 mg/mL (267.86 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Cytochrome P450, Biological_Activity: DMU2139 is a potent and specific CYP1B1 inhibitor, with IC50s of 9 nM and 795 nM for CYP1B1 and CYP1A1, respectively.
IC50 & Target: IC50: 9 nM (CYP1B1), 795 nM (CYP1A1)[1].
In Vitro: DMU2139 (6j) shows 88 and 133-fold selectivity for CYP1B1 over CYP1A1 and CYP1A2. In the presence of DMU2139, the EC50 is reversed back to 8.3 μM from 61 μM (seen in CYP1B1-expressing cells without any inhibitor). The EC50 value, in the presence of DMU2139, resembles the EC50 of cisplatin, 8.7μM, in cells transfected with the empty plasmid which has no CYP1B1 gene and therefore cannot express CYP1B1 protein[1].

Name: Piperlongumine Piplartine, CAS: 20069-09-4, stock 4.2g, assay 98.8%, MWt: 317.34, Formula: C17H19NO5, Solubility: DMSO : ≥ 100 mg/mL (315.12 mM), Clinical_Informat: No Development Reported, Pathway: Apoptosis;Stem Cell/Wnt;MAPK/ERK Pathway;Anti-infection;Autophagy;Apoptosis;Metabolic Enzyme/Protease;NF-κB;Immunology/Inflammation, Target: Apoptosis;ERK;ERK;Bacterial;Autophagy;Ferroptosis;Reactive Oxygen Species;Reactive Oxygen Species;Reactive Oxygen Species, Biological_Activity: Piperlongumine is a natural alkaloid isolated from Piper longum Linn[1], possesses ant-inflammatory, antibacterial, antiangiogenic, antioxidant, antitumor, and antidiabetic activities[2]. Piperlongumine induces ROS, and induces apoptosis in cancer cell lines[1]. Piperlongumine shows anti-cardiac fibrosis activity, suppresses myofibroblast transformation via suppression of the ERK1/2 signaling pathway[2].
IC50 & Target: ERK[2]
In Vitro: Piplartine (5, 10, and 15 μM) significantly decreases cell proliferation of 786-O, SKBR3, Panc1, A549, and L3.6pL cancer cells after treatment for 24 and 48 hours, induces apoptosis and ROS in these cell lines at 5 and 10 μM after 3 or 9 h of treatment[1]. 
Piplartine (5 or 10 μM) induces cleaved PARP and downregulates Sp1, Sp3, Sp4, and Sp-regulated genes[1]. 
Piplartine (20 μM) decreases the viability of cardiac fibroblasts (CFs). Piplartine (0-10 μM) suppresses myofibroblast transformation via suppression of the ERK1/2 signaling pathway[2].
In Vivo: Piperlongumine (30 mg/kg/day, i.p. for 3 weeks) exhibits potent anti-tumor effect in athymic nude mice bearing L3.6pL cells without body weight loss[1].

Name: SYM 2081, CAS: 31137-74-3, stock 12.9g, assay 98.5%, MWt: 161.16, Formula: C6H11NO4, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Membrane Transporter/Ion Channel;Neuronal Signaling, Target: iGluR;iGluR, Biological_Activity: SYM 2081 is a high-affinity ligand and potent, selective agonist of kainate receptors, inhibits [3H]-kainate binding with an IC50 of 35 nM, almost 3000- and 200-fold selectivity for kainate receptors over AMPA and NMDA receptors respectively[1].
IC50 & Target: IC50: 35 nM (kainate receptors)[1]

Name: Cilostamide OPC3689, CAS: 68550-75-4, stock 1.1g, assay 98.8%, MWt: 342.43, Formula: C20H26N2O3, Solubility: DMSO : 31 mg/mL (90.53 mM; Need ultrasonic and warming), Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Phosphodiesterase (PDE), Biological_Activity: Cilostamide is a selective and potent PDE3 inhibitor, with IC50s of 27 nM and 50 nM for PDE3A and PDE3B, respectively, and has antithrombotic and anti-intimal hyperplastic activity.
IC50 & Target: IC50: 27 nM (PDE3A), 50 nM (PDE3B)[1]
In Vitro: Cilostamide is a selective and potent PDE3 inhibitor, with IC50s of 27 nM and 50 nM for PDE3A and PDE3B, respectively, and has antithrombotic and anti-intimal hyperplastic activity. Cilostamide weakly inhibits PDE2, PDE4, PDE5, PDE7, and PDE1, with IC50s of 12.5, 88.8, 15.2, 22.0 and > 300 μM, respectively. Cilostamide potently inhibits thrombin-induced platelet aggregation (IC50, 1.1 μM)[1].

Name: BRL 37344 (sodium) BRL 37344A, CAS: 127299-93-8, stock 13.1g, assay 98.7%, MWt: 385.82, Formula: C19H21ClNNaO4, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein;Neuronal Signaling, Target: Adrenergic Receptor;Adrenergic Receptor, Biological_Activity: BRL 37344 sodium (BRL 37344A) is a specific β3-adrenergic receptor agonist. BRL 37344 sodium treatment significantly lowers the body weight of obese mice[1].
IC50 & Target: β3-adrenergic receptor[1]
In Vivo: BRL37344 sodium (BRL 37344A) treatment significantly lowers the body weight of obese mice[1].

Name: Phenylbiguanide N-Phenylbiguanide;PBG; 1-Phenylbiguanide, CAS: 102-02-3, stock 3.1g, assay 98.6%, MWt: 177.21, Formula: C8H11N5, Solubility: DMSO : 150 mg/mL (846.45 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Neuronal Signaling;GPCR/G Protein, Target: 5-HT Receptor;5-HT Receptor, Biological_Activity: Phenylbiguanide is a 5-HT3 receptor selective agonist with an EC50 of 3.0±0.1 μM.
IC50 & Target: EC50: 3.0±0.1 μM (5-HT3 Receptor)[1]
In Vitro: Phenylbiguanide (1-Phenylbiguanide) is a 5-HT3 receptor selective agonist with pEC50s of 5.57, 4.07, and 4.47 for r5-HT3A(b), h5-HT3A, m5-HT3A(b) , respectively[1]. The effect of Phenylbiguanide (1-Phenylbiguanide hydrochloride) in promoting the growth of the HT29 cell line is investigated. Phenylbiguanide causes a dose dependent proliferation of HT29 cells after 48 hours incubation. The maximum proliferation is at a 5HT concentration of 12.5 μM (P≤0.01). Phenylbiguanide significantly stimulates the growth of cells at concentrations of 3.125 μM (P≤0.05) and 6.25 μM (P≤0.01)[2].
In Vivo: In anaesthetised mice, Phenylbiguanide (PBG), a drug that is known to stimulate cardiopulmonary afferent C-fibres,is injected into the right atrium of the heart and mapped c-Fos expression within specific regions of the central nervous system. Intraatrial injection of PBG produces a reflex cardiorespiratory response including a pronounced bradycardia and a respiratory depression[3].

Name: MPDC, CAS: 159262-32-5, stock 10.1g, assay 98.4%, MWt: 171.15, Formula: C7H9NO4, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Neuronal Signaling;Membrane Transporter/Ion Channel, Target: GlyT;GlyT, Biological_Activity: MPDC is a potent and competitive inhibitor of the Na+-dependent high-affinity glutamate transporter in forebrain synaptosomes[1].
IC50 & Target: Glutamate transporter[1].

Name: RS 17053 hydrochloride RS-17053, CAS: 169505-93-5, stock 1.9g, assay 98.2%, MWt: 449.41, Formula: C24H30Cl2N2O2, Solubility: DMSO : ≥ 125 mg/mL (278.14 mM), Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein;Neuronal Signaling, Target: Adrenergic Receptor;Adrenergic Receptor, Biological_Activity: RS 17053 hydrochloride is a potent and selective α1A adrenoceptor antagonist, with a pKi value of 9.1 in native cell membrane and a pA2 value of 9.8 in functional assays.
IC50 & Target: pKi: 9.1 (α1A adrenoceptor in native cell membrane) 
pA2: 9.8 (α1A adrenoceptor)[1].
In Vitro: In several tissues from rat and cloned adrenoceptors, RS 17053 hydrochloride displays high affinity for the α1A-adrenoceptor (pKi and pA2 estimates of 9.1-9.9) and a 30-100-fold selectivity over the α1 B and the α1 D-adrenoceptor subtypes (pKi and pA2 estimates of 7.7-7.8). However, in isolated smooth muscle preparations from human LUT tissues, RS 17053 hydrochloride antagonizes responses to NE only at high concentrations. Estimates of affinity (pA2) at α1-adrenoceptors mediating NE-induced contractions are 7.5 in prostatic periurethral longitudinal smooth muscle (compared with 8.6 for prazosin), 6.9 in anterior fibromuscular stroma (prazosin, 8.9), and 7.1 in bladder neck (prazosin, 8.5)[1].
In Vivo: RS 17053 hydrochloride has a rapid onset of action, and a duration of action exceeding 60 min. RS 17053 hydrochloride pretreatment significantly alteres food intake [F(4, 132) 5 6.28, p , 0.0001]. 10 mg/kg RS-17053 significantly suppresses food intake[2].

Name: ZD7288 ICI D7288, CAS: 133059-99-1, stock 0.6g, assay 98.2%, MWt: 292.81, Formula: C15H21ClN4, Solubility: DMSO : 50 mg/mL (170.76 mM; Need ultrasonic); H2O : ≥ 50 mg/mL (170.76 mM), Clinical_Informat: No Development Reported, Pathway: Membrane Transporter/Ion Channel, Target: HCN Channel, Biological_Activity: ZD7288 is a selective hyperpolarization-activated cyclic nucleotide-gated (HCN) channel blocker.
IC50 & Target: HCN channel[1]
In Vitro: ZD7288 is a selective hyperpolarization-activated cyclic nucleotide-gated (HCN) channel blocker. ZD7288 inhibits glutamate release in a concentration-dependent manner. After incubation with 1, 5 and 50 µM ZD7288 for 24 hours, glutamate content in extracellular fluid is decreased to 69.0±2.8%, 31.4±2.0% and 4.4±0.3%, respectively (P<0.01, vs. DMEM/F12 group [100.2±4.2%]). After incubation with ZD7288 (25, 50, or 100 µM) for 20 minutes, 50 µM glutamate-induced [Ca2+]i rises are attenuated to 59.2±2.7%, 41.4±2.3% and 21.0±1.4%, respectively glutamate (P<0.01, vs. 50 µM glutamate group)[1].
In Vivo: Application of ZD7288 0.1 µM at 5 minutes before high-frequency stimulation significantly decreases the amplitude of field excitatory postsynaptic potentials (fEPSPs), and this inhibitory effect is maintained throughout the recording period. Application of 0.1 µM ZD7288 30 minutes after high-frequency stimulation almost completely reverses the established long-term potentiation (LTP). Following application of ZD7288 (0.1 µM) 5 minutes before high-frequency stimulation, glutamate content is reduced to 74.9±8.0% (P<0.05, vs. normal saline group). Furthermore, application of 0.1 µM ZD7288 30 minutes after high-frequency stimulation markedly decreases the glutamate content to 77.0%±9.4% (P<0.05, vs. normal saline group)[1].

Name: L-741626, CAS: 81226-60-0, stock 13.2g, assay 98.1%, MWt: 340.85, Formula: C20H21ClN2O, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein;Neuronal Signaling, Target: Dopamine Receptor;Dopamine Receptor, Biological_Activity: L-741626 is a selective D2 dopamine receptor antagonist, with the Ki values of 2.4, 100 and 220 nM for human D2, D3 and D4 receptors respectively[1].
IC50 & Target: Ki: 2.4 nM (human D2 receptor), 100 nM (human D3 receptor), 220 nM (human D4 receptor)[1]
In Vitro: Intrinsic activities in a functional assay using inhibition of quinpirole stimulation of mitogenesis in human dopamine D2 or D3 receptors transfected into Chinese hamster ovary (CHO) cells, L-741626 is prepared by literature methods (Ki (D2)=11.2 nM) and displays a D3/D2 and D4/D2 selectivity ratio of 15-fold and 136-fold, respectively. In the functional assay L-741626 is a potent antagonist (EC50 (D2)=4.46 nM) with some D2 selectivity (EC50 (D3)=90.4 nM)[2].
In Vivo: L-741626 (1.0 mg/kg; i.h.) is effective at shifting to the right the pramipexole dose-response curve in pramipexole-trained male Sprague Dawley rats[3]. 
Coadministrating Cocaine with the D2 antagonist L-741626 (3 mg/kg; i.p.; 15 min before Cocaine) for 5 days reduces the Cocaine-induced increase in microglial TNF-α production in adult mice[4].

Name: Methyllycaconitine citrate MLA, CAS: 351344-10-0, stock 3.3g, assay 98.4%, MWt: 874.92, Formula: C43H58N2O17, Solubility: DMSO : 250 mg/mL (285.74 mM; Need ultrasonic and warming); H2O : 2.18 mg/mL (2.49 mM; Need ultrasonic and warming), Clinical_Informat: No Development Reported, Pathway: Neuronal Signaling;Membrane Transporter/Ion Channel, Target: nAChR;nAChR, Biological_Activity: Methyllycaconitine citrate is a specific antagonist of α7 neuronal nicotinic acetylcholine receptor (α7nAChR).
IC50 & Target: α7nAChR[1]
In Vitro: Pretreatment with 5 and 10 µM Methyllycaconitine citrate (MLA) inhibits the decreased cell viability induced by Aβ25-35. Cell viability does not decrease after exposure to Methyllycaconitine citrate (2.5, 5, 10, 20 µM). Aβ25-35 treatment increases LC3-II levels, which is inhibited by administration of Methyllycaconitine citrate. Methyllycaconitine citrate also inhibits Aβ-induced autophagosome accumulation in SH-SY5Y cells. Flow cytometry also demonstrates decreased MDC-labeled vacuoles with Methyllycaconitine citrate treatment[1].
In Vivo: Methyllycaconitine citrate (MLA) (6 mg/kg) given alone intraperitoneally does not cause climbing behavior when compare with the saline group. Pretreatment with Methyllycaconitine citrate significantly inhibits methamphetamine (METH)-induced climbing behavior, by about 50%. Methyllycaconitine citrate does not modify either basal locomotor activity or METH-induced hyperlocomotion. The METH-induced depletion of dopamine neuron terminals is attenuated in mice pretreated with Methyllycaconitine citrate (250±43 fmol/mg, n=7). A direct effect of Methyllycaconitine citrate on body temperature is ruled out because Methyllycaconitine citrate does not affect basal body temperature (37.0±0.5°C, n=5) or reduce the METH-induced hyperthermia (38.2±0.4°C, n=6, MLA+METH group, n.s. versus METH group)[1].

Name: 8-M-PDOT AH-002, CAS: 134865-70-6, stock 22.5g, assay 98.6%, MWt: 233.31, Formula: C14H19NO2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein;Neuronal Signaling, Target: Melatonin Receptor;Melatonin Receptor, Biological_Activity: 8-M-PDOT (AH-002) is a selective melatonin MT2 receptor agonist. 8-M-PDOT is 5.2-fold selective for MT2 over MT1 receptors. 8-M-PDOT binds human recombinant MT2 and MT2 receptors with pKi values of 8.23 and 8.95 respectively. 8-M-PDOT has anxiolytic-like activity[1][2].
IC50 & Target: pKi: 8.23 (Melatonin MT2 receptor) and 8.95 (Melatonin MT1 receptor)[2]
In Vivo: 8-M-PDOT (10 µg/µL; administrated into the dorsal striatum by bilateral cannulas; for 30 minutes; male Wistar rats) treatment shows anxiolytic-like effect[2].

Name: 1-BCP Piperonylic acid piperidide, CAS: 34023-62-6, stock 24.4g, assay 98.9%, MWt: 233.26, Formula: C13H15NO3, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Membrane Transporter/Ion Channel;Neuronal Signaling, Target: iGluR;iGluR, Biological_Activity: 1-BCP is a centrally active drug that modulates AMPA receptor gated currents. 1-BCP is a memory-enhancing agent[1][2].
IC50 & Target: AMPA receptor[1].

Name: PD-168077 maleate, CAS: 630117-19-0, stock 26.3g, assay 98.9%, MWt: 450.49, Formula: C24H26N4O5, Solubility: DMSO : 150 mg/mL (332.97 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein;Neuronal Signaling, Target: Dopamine Receptor;Dopamine Receptor, Biological_Activity: PD-168077 maleate is a selective dopamine D4 receptor agonist, with a Ki of 9 nM.
IC50 & Target: Ki: 9 nM (Dopamine D4 receptor)[1].
In Vitro: PD-168077 is one of the first agents to be identified as putative selective D4 agonists. It shows >100-fold selectivity over other members of the D2-like receptor family and over their D1-like counterparts; PD-168077 shows a 20-fold selectivity over α1, and α2, a 45-fold selectivity over 5-HT1A, and a 460-fold selectivity over 5-HT2A receptors; PD-168077 evidences intrinsic activity at the D4 receptor in terms of quinpirole-like inhibition of forskolin-stimulated cAMP accumulation or stimulation of [3H]thymidine uptake in CHO cells expressing the human D4 receptor[1]. In the PD-168077-treated cell, p-CaMKII exhibits a significantly increased clustering at synaptic sites, as indicated by the enhanced colocalization with PSD-95[2].
In Vivo: PD-168077 (0.2-25.0 mg/kg) dose-dependently induces locomotion, which takes an unusual and characteristic ”shuffling” form with uncoordinated movements together with yawning, and episodes of myoclonic jerking; grooming, and rearing are reduced[1].

Name: Hesperin, CAS: 4430-35-7, stock 5.5g, assay 98%, MWt: 205.34, Formula: C8H15NOS2, Solubility: DMSO : 50 mg/mL (243.50 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: NF-κB, Target: Keap1-Nrf2, Biological_Activity: Hesperin is a bioactive ingredient present in Japanese horseradish (wasabi) and has been shown to be an Nrf2 activator.
IC50 & Target: Nrf2[1]
In Vitro: Hesperin (6-Methylsulfinylhexyl isothiocyanate, 6-MSITC) is an active compound in wasabi (Wasabia japonica Matsum.). Whether Hesperin induces cytotoxicity of HUVECs is determined. More than 1 μg/mL of Hesperin markedly induces cytotoxicity and morphological alterations. In subsequent experiments we used Hesperin is used at concentrations of 0-1 μg/mL, to study the anti-coagulant and anti-inflammatory properties of Hesperin in HUVECs[2].
In Vivo: Hesperin (6-Methylsulfinylhexyl isothiocyanate, 6-MSITC) activates Nrf2 and induces phase II enzyme genes but this induction is absent in Nrf2-null mice, suggesting that Hesperin is a potential activator of the Nrf2/ARE-dependent detoxification pathway. To determine whether Hesperin ameliorates hepatic steatosis and iron accumulation, wild-type and Nrf2-null mice are fed the following diets for 12 weeks: 1) control diet, 2) high-fat diet (HFD), 3) HFD plus Hesperin (10 mg/kg/day ip), 4) HFD for 6 weeks followed by an iron-supplemented HFD for 6 weeks (HFD/Iron), 5) HFD/Iron plus Hesperin. The HFD increased hepatic triglycerides in both genotypes and Hesperin suppress increased hepatic triglycerides in wild-type mice but do not reduce these
triglycerides in Nrf2-null mice[1].

Name: Oxotremorine M (iodide), CAS: 3854-04-4, stock 3.9g, assay 98.7%, MWt: 322.19, Formula: C11H19IN2O, Solubility: DMSO : 125 mg/mL (387.97 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Neuronal Signaling;GPCR/G Protein, Target: mAChR;mAChR, Biological_Activity: Oxotremorine M iodide is a potent and selective muscarinic acetylcholine receptor (mAChR) agonist. Oxotremorine M iodide potentiates NMDA receptors by muscarinic receptor dependent and independent mechanisms[1].

Name: 8-Bromo-cGMP (sodium), CAS: 51116-01-9, stock 26.2g, assay 98.5%, MWt: 446.08, Formula: C10H10BrN5NaO7P, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Membrane Transporter/Ion Channel;Neuronal Signaling, Target: Calcium Channel;Calcium Channel, Biological_Activity: 8-Bromo-cGMP sodium, a membrane-permeable analogue of cGMP, is a PKG (protein kinase G) activator and significantly inhibits Ca2+ macroscopic currents and impairs insulin release stimulated with high K+[1]. 8-Bromo-cGMP sodium has antinociceptive effects[2].
IC50 & Target: PKG, Ca2+[1]

Name: Otenzepad AF-DX 116, CAS: 102394-31-0, stock 1.8g, assay 98.3%, MWt: 421.54, Formula: C24H31N5O2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Neuronal Signaling;GPCR/G Protein, Target: mAChR;mAChR, Biological_Activity: Otenzepad (AF-DX 116) is a selective and competitive M2 muscarinic acetylcholine receptor antagonist, with IC50 values of 640 nM and 386 nM for rabbit peripheral lung and rat heart, respectively[1].
IC50 & Target: 640 nM (M2 muscarinic acetylcholine receptor in rabbit peripheral lung), 386 nM (M2 muscarinic acetylcholine receptor in rat heart)[1].
In Vivo: Otenzepad (0.5, 1 mg/kg, s.c., in rats) significantly improved win-stay acquisition relative to vehicle-injected controls[2]. 
Otenzepad (2 mg/kg, s.c., in rats) significantly improved retention relative to vehicle controls[2]. 
Otenzepad (0.3, 1.0, or 3.0 mg/kg, ip, in mice) potentiates the effects of glucose and reverses the effects of insulin on memory[3].

Name: GR 103691, CAS: 162408-66-4, stock 28.3g, assay 98.5%, MWt: 485.62, Formula: C30H35N3O3, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein;Neuronal Signaling, Target: Dopamine Receptor;Dopamine Receptor, Biological_Activity: GR 103691 is a potent, selective dopamine D3 receptor antagonist with a Ki value of 0.4 nM. GR 103691 shows more than 100-fold selectivity for human dopamine human (h)D3 over hD4 and hD1 sites[1].
IC50 & Target: Ki: 0.4 nM (Human dopamine D3 receptor)[1]
In Vitro: GR 103691 shows marked affinity for serotonin1A (5-HT1A) receptors (Ki of 5.8 nM) and α-1 adrenoceptors (Ki of 12.6 nM)[1].

Name: Neuropeptide Y (29-64), amide, human Human neuropeptide Y (29-64), CAS: 90880-35-6, stock 33.1g, assay 98.9%, MWt: 4271.68, Formula: C189H285N55O57S, Solubility: 10 mM in H2O, Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein;Neuronal Signaling, Target: Neuropeptide Y Receptor;Neuropeptide Y Receptor, Biological_Activity: Neuropeptide Y (29-64), amide, human is a biologically active 36-amino acid peptide.
In Vitro: Neuropeptide Y (29-64), amide, human is a 36 amino acid neurotransmitter found in the brain and autonomic nervous system. Neuropeptide Y (29-64), amide, human has been associated with numerous physiologic processes in the brain, including the regulation of energy balance, memory and learning, and epilepsy.

Name: Pancreatic Polypeptide, human Human pancreatic polypeptide, CAS: 75976-10-2, stock 23.3g, assay 98.7%, MWt: 4181.71, Formula: C185H287N53O54S2, Solubility: 10 mM in H2O, Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein;Neuronal Signaling, Target: Neuropeptide Y Receptor;Neuropeptide Y Receptor, Biological_Activity: Pancreatic Polypeptide, human is a C-terminally amidated 36 amino acid peptide, which acts as a neuropeptide Y (NPY) Y4/Y5 receptor agonist.
IC50 & Target: Neuropeptide Y (NPY) Y4/Y5 receptor[1]
In Vitro: Human pancreatic polypeptide (hPP) is one such peptide, being released postprandially from F cells of the pancreatic islets depending on caloric load, food consumption and circadian rhythm. It is a C-terminally amidated 36 amino acid peptide with a characteristic hairpin-like pancreatic polypeptide (PP)-fold and acts at the Y4 receptor to induce satiety and delay gastric emptying and motility[1]. Addition of the human pancreatic polypeptide (hPP) (10 nM-1 μM) results in a significant, dose-dependent reduction in both basal and stimulated release. Human pancreatic polypeptide (hPP) can also inhibit basal and stimulated NPY release with a pharmacological profile suggesting a role for Y4 presynaptic receptors[2].

Name: Endothelin-3, human, mouse, rabbit, rat Endothelin 3 (Rat,Human), CAS: 117399-93-6, stock 18.3g, assay 98.9%, MWt: 2643.04, Formula: C121H168N26O33S4, Solubility: H2O, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Endothelin-3, human, mouse, rabbit, rat is a 21-amino acid vasoactive peptide that binds to G-protein-linked transmembrane receptors, ET-RA and ET-RB.
IC50 & Target: ET-RA, ET-RB[1]
In Vitro: The endothelins (ETs) are a family of 21-amino-acid vasoconstrictor peptides comprising three distinct isoforms: ET-1, ET2 and Endothelin-3. Endothelin-3 is detected in plasma, heart, brain and vascular smooth muscle cells (VSMCs). The surface enzymes of VSMCs break down big Endothelin-3 to the corresponding mature peptide, Endothelin-3. Endothelin-3 down-regulate endothelin ETA receptor expression in coronary artery VSMCs without affecting receptor density or functional ETA receptor responses. By contrast, high concentrations of Endothelin-3 (100 nM) increase the expression of ETB receptors but abolish the vasoconstrictor response of the receptors, possibly due to the desensitizing effect of Endothelin-3[1]. Endothelin-3 stimulates ENCC adhesion to various ECM components. Endothelin-3 induces rapid changes in ENCC shape and protrusion dynamics favouring sustained growth and stabilization of lamellipodia, a process coincident with the increase in the number of focal adhesions and activated β1-integrins[2].
In Vivo: Endothelin-3 at low concentrations may attenuate inflammatory responses via ETB2 activation and NO production. Endothelin-3, which acts mainly on ETB, at low concentrations specifically inhibited platelet-activating factor (PAF)-induced paw oedema, whereas neither ET-1 nor Endothelin-2, both of which act on ETA and ETB, showed inhibitory activity. The inhibition by ET-1 and Endothelin-3 (each 0.5 pmol/paw) in the presence of BQ-123 (66.4 ± 6.7 % and 65.4 ± 22.6 %, respectively), is comparable to that by Endothelin-3 (0.5 pmol/paw) alone (65.4 ± 10.9 %), whereas neither ET-1 nor Endothelin-3 in the presence of BQ-788 showed inhibitory activity[3].

Name: DL-Homocysteine thiolactone (hydrochloride), CAS: 6038-19-3, stock 39.2g, assay 98.6%, MWt: 153.63, Formula: C4H8ClNOS, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: DL-Homocysteine thiolactone hydrochloride is a cyclic amino acid derivative that exhibits root-growth inhibitory activity.
In Vitro: DL-Homocysteine thiolactone hydrochloride shows growth inhibition toward the roots of Brassica campestris and Echinochloa utilis even at the low concentration of 50 μM[1].

Name: Procyanidin C1, CAS: 37064-30-5, stock 1.1g, assay 98.5%, MWt: 866.77, Formula: C45H38O18, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Apoptosis, Target: Apoptosis, Biological_Activity: Procyanidin C1 is a natural polyphenol, causes DNA damage, cell cycle arrest, and induces apoptosis. Procyanidin C1 decreases the level of Bcl-2, but enhances BAX, caspase 3 and 9 expression in cancer cells[1].
IC50 & Target: Apoptosis[1]

Name: Procyanidin A2, CAS: 41743-41-3, stock 13.1g, assay 98.9%, MWt: 576.50, Formula: C30H24O12, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Anti-infection, Target: Bacterial, Biological_Activity: Procyanidin A2 is a flavonoid found in cranberries and lingonberries, with anti-cancer, antioxidant, antimicrobial and anti-inflammation activity[1][2].
IC50 & Target: Bacterial[1]
In Vitro: Procyanidin A2 shows DPPH radical scavenging activity, with an IC50 of 5.08 ± 0.37 μM[1].

Name: Procyanidin A1 Proanthocyanidin A1, CAS: 103883-03-0, stock 25.8g, assay 98.1%, MWt: 576.50, Formula: C30H24O12, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: TGF-beta/Smad;Epigenetics, Target: PKC;PKC, Biological_Activity: Procyanidin A1 (Proanthocyanidin A1) is a procyanidin dimer, which inhibits degranulation downstream of protein kinase C activation or Ca2+ influx from an internal store in RBL-213 cells. Procyanidin A1 has antiallergic effects[1].
In Vivo: Procyanidin A1 suppress serum IgE and IgG1 levels in mice-immunized with ovalbumin[2].

Name: Procyanidin B3, CAS: 23567-23-9, stock 6.6g, assay 98.6%, MWt: 578.52, Formula: C30H26O12, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Epigenetics, Target: Histone Acetyltransferase, Biological_Activity: Procyanidin B3 is a natural product, acts as a specific HAT inhibitor, binds to the other site of p300 instead of the active site, selectively inhibits p300-mediated androgen receptor acetylation. Procyanidin B3 has no effect on HDAC or HMT (histone methyltransferase)[1].
IC50 & Target: p300[1]

Name: Frovatriptan (succinate hydrate), CAS: 158930-17-7, stock 1.1g, assay 98.8%, MWt: 379.41, Formula: C18H25N3O6, 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: Frovatriptan succinate hydrate is a potent, high affinity, selective and orally active 5-HT1B, HT1D receptor agonist and a moderately potent 5-HT7 receptor agonist, with pKi values of 8.6, 8.4, and 6.7, respectively. Frovatriptan succinate hydrate is effective in treating the full spectrum of migraine including the associated symptoms of nausea, vomiting, photophobia, and phonophobia. Frovatriptan succinate hydrate can also be used as in mini-prophylaxis in menstrual migraine[1][2].
In Vitro: Cerebral vasodilatation and neurogenic inflammation are considered to be prime movers in the pathogenesis of migraine. Activation of 5-HT1B reverses cerebral vasodilatation and activation of 5-HT1D prevents neurogenic inflammation. Frovatriptan has a high affinity for 5-HT1B and 5-HT1D receptors and a moderate affinity for the 5-HT1A and 5-HT1F receptors subtypes. Frovatriptan has a moderate affinity for the 5-HT7 receptors, an action associated with coronary artery relaxation in the dog[1].
In Vivo: Oral bioavailability of Frovatriptan is 22%-30% and is not affected by food. Although the maximum concentration in the plasma is achieved in 2-3 hours, 60%-70% of this is achieved in 1 hour. A steady state is achieved in 4-5 days. Plasma protein binding is low at 15%. The most unique feature is the relative terminal long half-life of about 26 hours. Frovatriptan is chiefly metabolized by CYP1A2 and is cleared by the kidney and liver making moderate failure of either organ not a limiting factor in treatment. Frovatriptan has a low risk of interactions with other drugs[1].

Name: Endothelin-2, human Endothelin-2 (human, canine);Human endothelin-2, CAS: 123562-20-9, stock 37.4g, assay 98.9%, MWt: 2546.92, Formula: C115H160N26O32S4, Solubility: H2O, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Endothelin-2, human is a 21-amino acid vasoactive peptide that binds to G-protein-linked transmembrane receptors, ET-RA and ET-RB.
IC50 & Target: ET-RA, ET-RB[1]
In Vitro: At nanomolar concentrations, Endothelin-2 exhibits a strong and long-lasting vasoconstrictor activity characteristic of endothelin (EC50=0.52 nM)[1]. Endothelin-2 is a chemoattractant for macrophages and THP-1 monocytic cells, but not for freshly isolated monocytes. The chemotactic response to Endothelin-2 shows a typical bell-shaped response curve. Experiments with endothelin receptor antagonists shows that migration to Endothelin-2 is mediated via the ET-RB receptor. Endothelin-2 expression by tumors may modulate the behavior of macrophages such that activated cells accumulate in areas of hypoxia[2].
In Vivo: Two distinct phases of pressor effects are typically seen in response to Endothelin-2: the early phase immediately follows the depressor response and dominates during the next 3-10 min, whereas the late pressor effect develops 10-20 min after the injection and lasts >1 hr[1].

Name: DAMGO, CAS: 78123-71-4, stock 39.7g, assay 98.3%, MWt: 513.59, Formula: C26H35N5O6, Solubility: DMSO : 33.33 mg/mL (64.90 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein;Neuronal Signaling, Target: Opioid Receptor;Opioid Receptor, Biological_Activity: DAMGO is a μ-opioid receptor (μ-OPR ) selective agonist with a Kd of 3.46 nM for native μ-OPR[1].
IC50 & Target: Kd: 3.46±0.84 nM (native μ-OPR)[1]
In Vitro: DAMGO, a μ-opioid receptor selective agonist, distinguishes between μ- and δ-opioid receptors around their first extracellular loops. In native μ-OPR, the Kd value for DAMGO is 3.46± 0.84 nM (n=3). The chimeric receptor MMDD, in which the carboxy-terminal half of μ-OPR is replaced with the corresponding region of δ-OPR, exhibits an equivalent affinity (Kd=2.13±0.40 nM; n=3) to DAMGO compared with the native μ-OPR[1]. DAMGO is a selective μ-opioid peptide. DAMGO abolishes the neuroprotective effect of CXCL12 in N-methyl-d-aspartate (NMDA) neurotoxicity studies. Regulation of neuronal response to CXCL12 is essential for shaping of developing and mature central nervous system (CNS). To establish whether DAMGO alter the effect of CXCL12 on neuronal survival, the ability of CXCL12 to protect neurons from N-methyl-d-aspartate (NMDA)-induced death is examined in the presence and absence of DAMGO. Cortical cultures are treated with DAMGO (1 and 10 μM). Neurons are subsequently exposed to NMDA (20 min) and/or CXCL12 (added 10 min before NMDA) in the absence of glia and then returned to the original culture dishes with the glial feeder layer. Neuronal death is evaluated after 24 h. DAMGO inhibits neuronal survival promoted by CXCL12[2].

Name: Ralfinamide FCE-26742A, CAS: 133865-88-0, stock 20.5g, assay 98.1%, MWt: 302.34, Formula: C17H19FN2O2, Solubility: DMSO : ≥ 125 mg/mL (413.44 mM), Clinical_Informat: Phase 3, Pathway: Membrane Transporter/Ion Channel, Target: Sodium Channel, Biological_Activity: Ralfinamide (FCE-26742A) is an orally available Na+ blocker derived from α-aminoamide, with function of suppressing pain[1][2].
IC50 & Target: Na+channel[1]
In Vivo: Ralfinamide (30 mg/kg, 60 mg/kg; p.o.; twice daily; 42 days) treated with Ralfinamide (80 mg/kg; p.o.; twice daily; 7 days) preoperatively suppresses neuropathic pain[1].

Name: Darbufelone CI-1004, CAS: 139226-28-1, stock 38.4g, assay 98.6%, MWt: 332.46, Formula: C18H24N2O2S, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein;GPCR/G Protein, Target: Leukotriene Receptor;Prostaglandin Receptor, Biological_Activity: Darbufelone is a dual inhibitor of cellular PGF2α and LTB4 production. Darbufelone potently inhibits PGHS-2 (IC50= 0.19 μM) but is much less potent with PGHS-1 (IC50=20 μM).
IC50 & Target: IC50: 0.19 μM (PGHS-2), 20 μM (PGHS-1)[1]
In Vitro: Darbufelone is a noncompetitive inhibitor of PGHS-2 (Ki=10±5 μM). Darbufelone quenches the fluorescence of PGHS-2 at 325 nm (lambda(ex)=280 nm) with Kd=0.98±0.03 μM[1].To test the putative anti-proliferative effect of Darbufelone, A549, H520 and H460 cell lines are used, which are established from three distinct pathological subtypes of NSCLC (adenocarcinoma, squamous and large cell lung cancer respectively). Increasing concentrations of Darbufelone, ranging from 5 to 60 μM, are tested for 72 h. The cell growth inhibition of these three cell lines gradually increases with higher drug concentration. The IC50 of A549 and H520 are 20±3.6 and 21±1.8 μM, respectively, while the H460 has much lower IC50 (15±2.7 μM)[2].
In Vivo: Darbufelone is a dual inhibitor of cellular PGF2R and LTB4 production. Darbufelone is orally active and nonulcerogenic in animal models of inflammation and arthritis[1]. When mice are treated with Darbufelone at dosage of 80 mg/kg/day, the tumor volumes decrease in a time-dependent manner. In contrast, lower dose of Darbufelone (20 or 40 mg/kg/day) dos not show any significant inhibition of tumor weight. At necropsy, the tumor weight in mice treated with Darbufelone (80 mg/kg/day) is reduced by 30.2% in comparison with control group[2].

Name: SR9238, CAS: 1416153-62-2, stock 19.8g, assay 98.8%, MWt: 595.73, Formula: C31H33NO7S2, Solubility: DMSO : 50 mg/mL (83.93 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: LXR, Biological_Activity: SR9238 is a synthetic liver X receptor (LXR) inverse agonist with IC50s of 214 nM and 43 nM for LXRα and LXRβ, respectively.
IC50 & Target: IC50: 43 nM (LXRβ), 214 nM (LXRα)[1]
In Vitro: Results from the cell-based cotransfection assays demonstrate that SR9238 is a synthetic LXR inverse agonist with IC50s of 214 nM and 43 nM for LXRα and LXRβ, respectively. SR9238 also effectively suppresses transcription from a fatty acid synthase (Fasn) promoter driven luciferase reporter. It is found that SR9238 induces increased interaction of CoRNR box peptides derived from NCoR (NCoR ID1 and NCoR ID2) with both LXRα and LXRβ, while causing decreased interaction with a coactivator NR box peptide derived from TRAP220. SR9238-induced recruitment of CoRNR box peptides is dose-dependent for both LXRα and LXRβ. HepG2 cells treated with SR9238 result in a significant decrease in Fasn and Srebp1c mRNA expression[1].
In Vivo: Approximately 6 μM SR9238 is detected in the liver 2h after the injection of SR9238, but no compound is detected in the plasma. SR9238 is also detected in the intestine with either ip or oral administration. SR9238-treated mice display greatly reduced lipid content in the liver. Results demonstrate that both Tnfa and Il1b expression are substantially reduced (~80% and >95%, respectively) in the SR9238-treated mice when compare to the vehicle-treated mice. SR9238-treated DIO mice display considerably lower intensity of F4/80 staining versus vehicle-treated DIO mice consistent with a beneficial effect of SR9238 on non-alcoholic steatohepatitis (NASH). SR9238 treatment does not alter body weight or percent body fat composition relative to vehicle treated animals during the experiment. Treatment with SR9238 suppresses diet-induced hepatosteatosis, hepatic inflammation, and hepatocellular injury[1].

Name: PBIT, CAS: 2514-30-9, stock 28.5g, assay 98.4%, MWt: 241.31, Formula: C14H11NOS, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Epigenetics, Target: Histone Demethylase, Biological_Activity: PBIT is a specific inhibitor of the Jumonji AT-rich Interactive Domain 1 (JARID1) enzymes. PBIT inhibits JARID1B (KDM5B or PLU1) histone demethylase with an IC50 of about 3 μM . PBIT also inhibits JARID1A and JARID1C with IC50 s of 6 and 4.9 μM, respectively[1].
IC50 & Target: IC50: 3 μM (JARID1B)[1]
In Vitro: PBIT inhibits proliferation of cells expressing higher levels of JARID1B. PBIT (1-10 μM for UACC-812 cells, 2.5-10μM for MCF7 and MCF10A cells; 72 hours) inhibits cell proliferation in a JARID1B level-dependent manner[1].

Name: SR0987, CAS: 303126-97-8, stock 35.5g, assay 98.8%, MWt: 397.70, Formula: C16H10ClF6NO2, Solubility: DMSO : ≥ 150 mg/mL (377.17 mM), Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: ROR, Biological_Activity: SR0987, a SR1078 analog, is a RORγt agonist, with an EC50 of 800 nM. SR0987 increases IL17 expression while repressing the expression of PD-1[1].
IC50 & Target: EC50: 800 nM (RORγt)[1].
In Vitro: SR0987 clearly shows a concentration dependent induction of reporter gene expression with an EC50 of ~800nM. SR0987 treatment results in a statistically significant reduction of the surface expression of PD-1 whereas desmostrol treatment shows no effect. Treatment with SR0987 and or desmosterol results in a trend towards increased IL17 production[1].

Name: JZP-430, CAS: 1672691-74-5, stock 0g, assay 98.4%, MWt: 354.47, Formula: C16H26N4O3S, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: MAGL, Biological_Activity: JZP-430 is a potent, highly selective, irreversible inhibitor of α/β-hydrolase domain 6 (ABHD6) with an IC50 of 44 nM, exhibits ~230-fold selectivity over fatty acid amide hydrolase (FAAH) and lysosomal acid lipase (LAL)[1].
IC50 & Target: IC50: 44 nM (ABHD6, human)[1]

Name: MMAF (sodium) Monomethylauristatin F (sodium), CAS: 1799706-65-2, stock 35.5g, assay 98.8%, MWt: 753.94, Formula: C39H64N5NaO8, Solubility: DMSO : ≥ 200 mg/mL (265.27 mM), Clinical_Informat: No Development Reported, Pathway: Cell Cycle/DNA Damage;Cytoskeleton;Antibody-drug Conjugate/ADC Related, Target: Microtubule/Tubulin;Microtubule/Tubulin;ADC Cytotoxin, Biological_Activity: MMAF sodium (Monomethylauristatin F sodium) is a potent tubulin polymerization inhibitor and is used as a antitumor agent. MMAF sodium (Monomethylauristatin F sodium) is widely used as a cytotoxic component of antibody-drug conjugates (ADCs) such as Vorsetuzumab mafodotin and SGN-CD19A[1][2][3].
In Vitro: MMAF inhibits anaplastic large cell lymphoma Karpas 299, breast carcinoma H3396, renal cell carcinoma 786-O and Caki-1 cells with IC50s of 119, 105, 257 and 200 nM in vitro cytotoxicity assay[4].

Name: Trilaciclib G1T28, CAS: 1374743-00-6, stock 38.9g, assay 98.3%, MWt: 446.55, Formula: C24H30N8O, Solubility: 10 mM in DMSO, Clinical_Informat: Phase 2, Pathway: Cell Cycle/DNA Damage, Target: CDK, Biological_Activity: Trilaciclib is a CDK4/6 inhibitor with IC50s of 1 nM and 4 nM for CDK4 and CDK6, respectively.
IC50 & Target: IC50: 1 nM (CDK4), 4 nM (CDK6)[1]
In Vitro: Incubation with Trilaciclib (G1T28) for 24 hours induces a robust G1 cell-cycle arrest (time=0). By 16 hours after Trilaciclib hydrochloride washout, cells have reentered the cell cycle and demonstrate cell-cycle kinetics similar to untreated control cells. These results demonstrate that Trilaciclib causes a transient, and reversible G1 arrest. A transient Trilaciclib-mediated G1 cell-cycle arrest in CDK4/6-sensitive cells decreases the in vitro toxicity of a variety of commonly used cytotoxic chemotherapy agents associated with myelosuppression[1].
In Vivo: Trilaciclib (G1T28) treatment results in a robust and dose-dependent suppression of proliferation in HSPCs at 12 hours, with EdU incorporation returning near baseline levels in a dose-dependent manner by 24 hours after administration. These data demonstrate that a single oral dose of Trilaciclib can produce reversible cell-cycle arrest in HSPCs in a dose-dependent manner in vivo. Mice given 100 mg/kg Trilaciclib 30 minutes prior to etoposide treatment, exhibits only background levels of caspase-3/7 activity. These data demonstrate that Trilaciclib can protect the bone marrow from chemotherapy-induced apoptosis in vivo. The data demonstrate that treatment with Trilaciclib prior to 5-FU likely decreases 5-FU-induced damage by chemotherapy in HSPCs, thus accelerating blood count recovery after chemotherapy[1].

Name: Fenobam, CAS: 57653-26-6, stock 16.6g, assay 98.4%, MWt: 266.68, Formula: C11H11ClN4O2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein;Neuronal Signaling, Target: mGluR;mGluR, Biological_Activity: Fenobam is a selective, orally active, and non-competitive mGluR5 antagonist acting at an allosteric modulatory site (Kd values are 54 and 31 nM for rat and human recombinant mGlu5 receptors, respectively). Fenobam displays inverse agonist activity which blocks the mGlu5 receptor basal activity with an IC50 of 84 nM. Fenobam exerts anxiolytic activity[1][2].
IC50 & Target: Kd: 54 nM (Rat recombinant mGlu5 receptor), 31 nM (Human recombinant mGlu5 receptor)[1] 
IC50: 84 nM (mGlu5 receptor)[1]

Name: Ralfinamide (mesylate) FCE-26742A (mesylate), CAS: 202825-45-4, stock 39.6g, assay 98.4%, MWt: 398.45, Formula: C18H23FN2O5S, Solubility: 10 mM in DMSO, Clinical_Informat: Phase 3, Pathway: Membrane Transporter/Ion Channel, Target: Sodium Channel, Biological_Activity: Ralfinamide mesylate (FCE-26742A mesylate) is an orally available Na+ channel blocker derived from α-aminoamide, with function of suppressing pain[1][2].
IC50 & Target: Na+channel[1]
In Vivo: Ralfinamide (30 mg/kg, 60 mg/kg; p.o.; twice daily; 42 days) treated with Ralfinamide (80 mg/kg; p.o.; twice daily; 7 days) preoperatively suppresses neuropathic pain[1].

Name: CC-885, CAS: 1010100-07-8, stock 39.9g, assay 98%, MWt: 440.88, Formula: C22H21ClN4O4, Solubility: DMSO : 67.5 mg/mL (153.10 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: PROTAC, Target: Ligand for E3 Ligase, Biological_Activity: CC-885 is a cereblon (CRBN) modulator with potent anti-tumour activity.
IC50 & Target: CRBN[1].
In Vitro: Acute myeloblatlic leukemia (AML) cell lines, human liver epithelial cell line (THLE-2) and human peripheral blood mononuclear cells (PBMC) are treated with varying concentrations of CC-885, with IC50s of 10×-6-1 μM. The effect of CC-885 on cell proliferation in AML cell lines, THLE-2 and human PBMC is more powerful than Lenalidomide and Pomalidomide with IC50s>10 μM. To address whether the cereblon-dependent degradation of GSPT1 is responsible for the cytotoxic effects of CC-885, a GSPT1 mutant that retains its normal function, but loses CC-885-dependent cereblon binding, is used to distinguish the role of GSPT1 from that of other substrates. CC-885 is tested in 293T HEK cells stably expressing the CC-885-sensitive or -resistant GSPT1 variants. Overexpression of a resistant variant GSPT1Δ(1–138)/(G575N) completely abrogate the CC-885-induced anti-proliferation, whereas overexpression of a CC-885-sensitive variant GSPT1Δ(1-138) only confer partial protection. Similar results are obtained in AML cell lines[1].

Name: SR-18292, CAS: 2095432-55-4, stock 24g, assay 98.7%, MWt: 366.50, Formula: C23H30N2O2, Solubility: DMSO : ≥ 100 mg/mL (272.85 mM); H2O : < 0.1 mg/mL (insoluble), Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease;Autophagy, Target: PGC-1α;Autophagy, Biological_Activity: SR-18292 is a PPAR gamma coactivator-1α (PGC-1α) inhibitor, which increases PGC-1α acetylation, suppresses gluconeogenic gene expression and reduces glucose production in hepatocytes.
IC50 & Target: PGC-1α[1]
In Vitro: The transcriptional coactivator PGC-1α plays a pivotal role in energy homeostasis by co-activating transcription factors that regulate fat and glucose metabolism. SR-18292 increases the interaction of PGC-1α with the acetyl transferase GCN5 and reduces co-activation of nuclear hormone receptor HNF4α by PGC-1α. SR-18292 suppresses HNF4α/PGC-1α gluconeogenic transcriptional function. By increasing the interaction of GCN5 with PGC-1α, SR-18292 increases the acetylation of specific PGC-1α lysine residues that might subsequently decrease its gluconeogenic activity[1].
In Vivo: SR-18292 reduces fasting blood glucose, increases hepatic insulin sensitivity and improves glucose homeostasis in diabetic mice. The high fat diet (HFD) fed mice, a dietary model of obesity and T2D, are treated with SR-18292 (45mg/kg) via I.P. injection for 3 consecutive days and again on day 4 before measuring fasting blood glucose. Strikingly, mice that are treated with SR-18292 have significantly lower levels of fasting blood glucose concentrations compared to matched vehicle-treated control mice. The induction of gluconeogenic gene expression is a regulatory component of the response to fasting. Importantly, gluconeogenic gene expression, specifically that of Pck1, is inhibited in livers isolated from mice treated with SR-18292[1].

Name: Guaiazulene, CAS: 489-84-9, stock 7.8g, assay 98.3%, MWt: 198.30, Formula: C15H18, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Guaiazulene is present in several essential oils of medicinal and aromatic plants, with antioxidant activity. Guaiazulene has in vitro cytotoxic activity against neuron and N2a neuroblastom (N2a-NB) cells[1][2].

Name: Stearic acid, CAS: 57-11-4, stock 33.9g, assay 98.5%, MWt: 284.48, Formula: C18H36O2, Solubility: DMSO : 125 mg/mL (439.40 mM; Need ultrasonic); H2O : < 0.1 mg/mL (insoluble), Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: Stearic acid is a long chain dietary saturated fatty acid which exists in many animal and vegetable fats and oils.

Name: Pico145 HC-608, CAS: 1628287-16-0, stock 2.3g, assay 98.8%, MWt: 524.88, Formula: C23H20ClF3N4O5, Solubility: DMSO : ≥ 100 mg/mL (190.52 mM), Clinical_Informat: No Development Reported, Pathway: Membrane Transporter/Ion Channel;Neuronal Signaling, Target: TRP Channel;TRP Channel, Biological_Activity: Pico145 is a remarkable inhibitor of TRPC1/4/5 channels, inhibits (−)-englerin A-activated TRPC4/TRPC5 channels, with IC50s of 0.349 and 1.3 nM in cells, and shows no effect on TRPC3, TRPC6, TRPV1, TRPV4, TRPA1, TRPM2, TRPM8.
IC50 & Target: IC50: 0.349 nM (TRPC4, cell assay), 1.3 nM (TRPC5, cell assay), 0.03 nM (TRPC4-TRPC1, cell assay), 0.2 nM (TRPC5-TRPC1, cell assay)[1]
In Vitro: Pico145 (Compound 31, C31) is a remarkable small-molecule inhibitor of TRPC1/4/5 channels, inhibits (−)-englerin A-activated TRPC4/TRPC5 channels, with IC50s of 0.349 and 1.3 nM in cells; Pico145 shows no effect on TRPC3, TRPC6, TRPV1, TRPV4, TRPA1, TRPM2, TRPM8. Pico145 also inhibits human TRPC4-TRPC1 and TRPC5-TRPC1 concatemers expressed in HEK 293 Tet+ cells (IC50, 0.03 nM and 0.2 nM, respectively). The potency of Pico145 can be reduced by increased (−)-englerin A concentration. Furthermore, Pico145 potently inhibits RPC4-TRPC1 channels activated by sphingosine 1-phosphate (S1P), and suppresses S1P-evoked Ca2+ entry through TRPC4-TRPC1 channels with an IC50 of 0.011 nM. Pico145 also sensitizes EA-sensitive cancer cell line (Hs578T cells) (IC50, 0.11 nM). Pico145 (100 nM) lacks effect on store-operated Ca2+ entry and histamine-evoked Ca2+ entry into endothelial cells[1].

Name: F1063-0967, CAS: 613225-56-2, stock 22.8g, assay 98.2%, MWt: 484.59, Formula: C24H24N2O5S2, Solubility: DMSO : 125 mg/mL (257.95 mM; Need ultrasonic and warming), Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Phosphatase, Biological_Activity: F1063-0967 is a Dual-specificity phosphatase 26 (DUSP26) inhibitor with an IC50 of 11.62 μM.
IC50 & Target: IC50: 11.62 μM (DUSP26)[1]
In Vitro: F1063-0967 is a Dual-specificity phosphatase 26 (DUSP26) inhibitor with an IC50 of 11.62 μM. At concentration above 0.1 μM, F1063-0967 remarkably induces IMR32 cell apoptosis. F1063-0967 induces apoptosis in IMR-32 cell line with an IC50 value of 4.13 μM. F1063-0967 has no effect on HL7702 cell line, and little inhibition effect on SH-SY5Y cell line[1].

Name: A-395, CAS: 2089148-72-9, stock 26g, assay 98.3%, MWt: 486.65, Formula: C26H35FN4O2S, Solubility: DMSO : 100 mg/mL (205.49 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Epigenetics, Target: Histone Methyltransferase, Biological_Activity: A-395 is an antagonist of polycomb repressive complex 2 (PRC2) protein-protein interactions that potently inhibits the trimeric PRC2 complex (EZH2-EED-SUZ12) with an IC50 of 18 nM.
IC50 & Target: IC50: 18 nM (Trimeric PRC2 complex)[1]
In Vitro: The embryonic ectoderm development (EED) protein is an essential subunit of Polycomb repressive complex 2 (PRC2). A-395 antagonizes of the H3K27me3 binding functions of EED. A-395 binds to EED in the H3K27me3-binding pocket, thereby preventing allosteric activation of the catalytic activity of PRC2. A-395 is capable of competing for H3K27me3 peptide binding to EED, with an IC50 of 7 nM. A-395, but not the close chemical analog A-395N, modulates activity of PRC2 in cells by potently reducing the H3K27 methyl mark in a highly selective manner. A-395 treatment inhibits both H3K27me2 and H3K27me3, with IC50 values of 390 nM and 90 nM, respectively. Furthermore, A-395 treatment results in growth inhibition of human tumor cell lines sensitive to SAM-competitive EZH2 inhibitors[1].
In Vivo: The embryonic ectoderm development (EED) protein is an essential subunit of Polycomb repressive complex 2 (PRC2). A-395 antagonizes of the H3K27me3 binding functions of EED. A-395 binds to EED in the H3K27me3-binding pocket, thereby preventing allosteric activation of the catalytic activity of PRC2. A-395 is capable of competing for H3K27me3 peptide binding to EED, with an IC50 of 7 nM. A-395, but not the close chemical analog A-395N, modulates activity of PRC2 in cells by potently reducing the H3K27 methyl mark in a highly selective manner. A-395 treatment inhibits both H3K27me2 and H3K27me3, with IC50 values of 390 nM and 90 nM, respectively. Furthermore, A-395 treatment results in growth inhibition of human tumor cell lines sensitive to SAM-competitive EZH2 inhibitors[1].

Name: BETd-260 ZBC 260, CAS: 2093388-62-4, stock 24.5g, assay 98.6%, MWt: 798.89, Formula: C43H46N10O6, Solubility: H2O : < 0.1 mg/mL (insoluble); DMSO : 25 mg/mL (31.29 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Epigenetics;PROTAC, Target: Epigenetic Reader Domain;PROTAC, Biological_Activity: BETd-260 is a potent BET degrader based on PROTAC technology, with as low as 30 pM against BRD4 protein in RS4;11 leukemia cell line.
IC50 & Target: BRD4[1] 
PROTAC
In Vitro: BETd-260 (ZBC260; Compound 23) shows inhibitory activity against the growth of RS4;11 leukemia cells and MOLM-13 cells with IC50s of 51 pM and 2.2 nM, respectively, and induces apoptosis in both RS4;11 and MOLM-13 cell lines at 3-10 nM[1].
In Vivo: BETd-260 (5 mg/kg, i.v., every other day, thrice a week for 3 weeks) causes rapid tumor regression with a maximum of >90% regression in mice bearing RS4;11 xenograft tumors, and with no body weight loss or other signs of toxicity in mice. BETd-260 (5 mg/kg, i.v.) degrades the BRD2, BRD3, and BRD4 proteins for more than 24 h, with robust cleavage of PARP and caspase-3, and strong down-regulation of c-Myc protein in RS4;11 xenograft mice model[1].

Name: Cdc7-IN-1, CAS: 1402055-25-7, stock 11.5g, assay 98.5%, MWt: 409.82, Formula: C21H16ClN3O4, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Cell Cycle/DNA Damage, Target: CDK, Biological_Activity: Cdc7-IN-1 (Compound 13) is a highly potent, selective and ATP competitive inhibitor of Cdc7 kinase, with an IC50 value of 0.6 nM at 1 mM ATP and with slow off-rate characteristics. Cdc7-IN-1 potently inhibits Cdc7 activity in cancer cells, and effectively induces cell death[1].
IC50 & Target: IC50: 0.6 nM (Cdc7, at 1 mM ATP)[1]

Name: TC13172, CAS: 2093393-05-4, stock 5.5g, assay 98.4%, MWt: 388.40, Formula: C17H16N4O5S, Solubility: H2O : < 0.1 mg/mL (insoluble); DMSO : 25 mg/mL (64.37 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: MAPK/ERK Pathway, Target: Mixed Lineage Kinase, Biological_Activity: TC13172 is a mixed lineage kinase domain-like protein (MLKL) inhibitor with an EC50 value of 2 nM for HT-29 cells.
IC50 & Target: EC50: 2±0.6 nM (MLKL, in HT-29 cells)[1].
In Vitro: The anti-necroptosis potency of TC13172 is evaluated in the HT-29 cell line, the EC50 value is 2±0.6 nM. TC13172 has an inhibition potency of 2 nM against cell necroptosis. TC13172 inhibits MLKL by directly binding to Cys-86. TC13172 does not disrupt the phosphorylation of MLKL, but do decrease the level of MLKL in the membrane phase, demonstrating that these MLKL inhibitors block the translocation of MLKL to the cell membrane, thereby protecting cells from necroptosis[1].

Name: GENZ-882706 RA03546849, CAS: 2070864-35-4, stock 19.6g, assay 98%, MWt: 455.51, Formula: C26H25N5O3, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Protein Tyrosine Kinase/RTK, Target: c-Fms, Biological_Activity: GENZ-882706 is a potent colony stimulating factor-1 receptor (CSF-1R) Inhibitor extracted from patent WO 2017015267A1.
IC50 & Target: Target: CSF-1R[1]
In Vitro: Genz-882706 induces an increased level of proliferative activity on unstimulated cells 48 hours post treatment and the reason for this effect is unclear[1].
In Vivo: Daily treatment with Genz-882706 significantly reduces experimental autoimmune encephalomyelitis. Treatment with Genz-882706 in experimental autoimmune encephalomyelitis (EAE) mice results in significant decreases in MCP-1, IL-6, IL-Ιβ and IP-10 levels in spinal cord homogenates when compared to Vehicle treated animals. Treatment with Genz-882706 shows a significant increase in TNF-a levels in the spinal cord when compared to the vehicle treated group. Genz-882706 at both the 30 mg/kg and the 100 mg/kg dose significantly reduces the number of microglia and monocytes/macrophages in the brain and spinal cord compared to the vehicle and LPS controls. Treatment with Genz-882706 modestly reduces CD80 expression on monocytes/macrophages in the brain[1].

Name: AZD-5991, CAS: 2143061-81-6, stock 24.7g, assay 98.3%, MWt: 672.26, Formula: C35H34ClN5O3S2, Solubility: H2O : < 0.1 mg/mL (insoluble); DMSO : 41.67 mg/mL (61.98 mM; Need ultrasonic), Clinical_Informat: Phase 1, Pathway: Apoptosis, Target: Bcl-2 Family, Biological_Activity: AZD-5991 is a potent and selective Mcl-1 inhibitor with an IC50 of 0.7 nM in FRET assay and a Kd of 0.17 nM in surface plasmon resonance (SPR) assay.
In Vitro: The selectivity of AZD-5991 is evaluated against pro-survival Bcl-2 family members using FRET assays. AZD-5991 is selective for Mcl-1 (IC50 0.72 nM, Ki=200 pM) vs. Bcl-2 (IC50=20 µM, Ki=6.8 µM), Bcl-xL (IC50=36 µM, Ki=18 µM), Bcl-w (IC50=49 µM, Ki=25 µM), and Bfl-1 (IC50=24 µM, Ki=12 µM). MOLP-8, MV4-11, and NCI-H23 cells are treated with AZD5991 (EC50=0.033, 0.024, 0.19 µM, respectively).AZD5991 binds directly to Mcl-1 and induces rapid apoptosis in cancer cells, most notably myeloma and acute myeloid leukemia, by activating the Bak-dependent mitochondrial apoptotic pathway. AZD5991 reduces the levels of Mcl-1 protein in AZD5991-sensitive but not in AZD5991-resistant MM cell lines further supporting the notion that activation of caspases by AZD5991 reduces Mcl-1 protein levels in AZD5991-sensitive cell lines[1].
In Vivo: A single intravenous (i.v.) dose of AZD5991 leads to a dose-dependent antitumor effect ranging from tumor growth inhibition (TGI) to tumor regression (TR). Ten days after treatment, AZD5991 shows 52% and 93% TGI (p<0.0001) at 10 and 30 mg/kg, respectively. At the same time point, AZD5991 at 60 mg/kg leads to 99% TR with no detectable tumors in 6 out of 7 mice, while complete TR is seen in 7 out of 7 mice in the 100 mg/kg dose group. AZD5991 also shows a dose-dependent duration of response with tumors in the 100 mg/kg group growing back later than those in the 60 mg/kg group. The magnitude of in vivo tumor efficacy is correlated with activation of caspase-3 in the tumor and concentration of AZD5991 in plasma. Treatment with AZD5991 was well tolerated at all dose levels with no significant body weight loss. A single dose of AZD5991 36 days after the first dose causes tumor regression in 4 out of 4 mice. In mice dosed with AZD5991 at 100 mg/kg on day 0 and day 1, tumors grow back later than those dosed with a single dose of AZD5991 at the same dose level[1].

Name: NMI 8739, CAS: 129024-87-9, stock 16.9g, assay 98.2%, MWt: 463.65, Formula: C30H41NO3, Solubility: DMSO : ≥ 100 mg/mL (215.68 mM), Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein;Neuronal Signaling, Target: Dopamine Receptor;Dopamine Receptor, Biological_Activity: NMI 8739 is a dopamine D2 autoreceptor agonist, which is an amine conjugate of the DHA carrier and the neurotransmitter dopamine.
In Vitro: NMI 8739 is a dopamine D2 autoreceptor agonist[1], which is an amine conjugate of the DHA carrier and the neurotransmitter dopamine[2]. NMI 8739 reduces nitric oxide (NO) production in LPS-stimulated RAW264.7 Macrophages. NMI 8739 elicits concentration-dependent suppression of CCL-20, MCP-1 and IL-6 Release in RAW264.7 macrophages after LPS-stimulation. Production of PGE2 is concentration-dependently suppressed with a reduction of 25.3% at 100 nM NMI 8739 and a 75% reduction for 1 μM NMI 8739. 2 μM NMI 8739 significantly inhibits IL-6 and CCL-20 release up to 49% and 37%, respectively[3].

Name: Docosahexaenoic Acid methyl ester Methyl docosahexaenoate; all cis-DHA methyl ester, CAS: 2566-90-7, stock 6.2g, assay 98.7%, MWt: 342.51, Formula: C23H34O2, Solubility: DMSO : 25 mg/mL (72.99 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Docosahexaenoic Acid methyl ester is a methylated docosahexaenoic acid analog which can be intercalated into membrane phospholipids without being oxidized or hydrolyzed.
In Vitro: Sharp wave (SPW) incidence relative to baseline appears to decrease following Docosahexaenoic Acid methyl ester (DHA-Me) application[1]. There is no generation of a new protein band when bovine serum albumin (BSA) is exposed to the Fe2+ and ascorbic acid (AsA) mixed-function oxidation system in the absence of Docosahexaenoic Acid methyl ester (DHA). However, the high-molecular-weight protein band is observed after only 24 h when BSA is incubated with DHA. Incubation of BSA with 1.0 mM DHA leads to a substantial increase in protein carbonyl content and the addition of oxygen radical scavengers leads to a substantial decrease in protein carbonyl content[2].

Name: Guancydine Guancidine, CAS: 1113-10-6, stock 38.2g, assay 98.6%, MWt: 154.21, Formula: C7H14N4, Solubility: DMSO : ≥ 125 mg/mL (810.58 mM), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Guancydine (Guancidine) is an antihypertensive agent[1].

Name: L,L-Dityrosine o,o'-Dityrosine, CAS: 63442-81-9, stock 3.8g, assay 98.4%, MWt: 360.36, Formula: C18H20N2O6, Solubility: H2O : 5.56 mg/mL (15.43 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: L,L-Dityrosine is a constituent of acid hydrolysates of a number of biological materials, including the insect cuticular resilin[1].

Name: Linrodostat BMS-986205;ONO-7701, CAS: 1923833-60-6, stock 16.2g, assay 98.1%, MWt: 410.91, Formula: C24H24ClFN2O, Solubility: DMSO : 50 mg/mL (121.68 mM; Need ultrasonic); H2O : < 0.1 mg/mL (insoluble), Clinical_Informat: Phase 3, Pathway: Metabolic Enzyme/Protease, Target: Indoleamine 2,3-Dioxygenase (IDO), Biological_Activity: Linrodostat (BMS-986205) is a selective and irreversible indoleamine 2,3-dioxygenase 1 (IDO1) inhibitor with an IC50 value of 1.1 nM in IDO1-HEK293 cells. Linrodostat is well tolerated with potent pharmacodynamic activity in advanced cancers[1][2].
IC50 & Target: IDO1[1]
In Vitro: Linrodostat (0.01-100 μM; 72 hours; SKOV-3 and Jurkat clone E6-1 cells) treatment reduces the number of viable cells compared with the non-treated control. Linrodostat also induces cell death at much lower concentrations and its IC50 is 6.3 μM[1].

Name: JNJ-64619178, CAS: 2086772-26-9, stock 24.6g, assay 98.3%, MWt: 483.36, Formula: C22H23BrN6O2, Solubility: DMSO : 125 mg/mL (258.61 mM; Need ultrasonic), Clinical_Informat: Phase 1, Pathway: Epigenetics, Target: Histone Methyltransferase, Biological_Activity: JNJ-64619178 is a selective, orally active and pseudo-irreversible PRMT5 inhibitor with an IC50 of 0.14 nM. JNJ-64619178 has potent activity In lung cancer[1][2].
IC50 & Target: IC50: 0.14 nM (PRMT5)[2]
In Vitro: JNJ-64619178 binds simultaneously to the S-adenosylmethionine (SAM)- and protein substrate- binding pockets of the PRMT5/MEP50 complex with a pseudo-irreversible mode-of-action. JNJ-64619178 shows potent and broad inhibition of cellular growth[1].
In Vivo: Oral administration of JNJ-64619178 results in efficient inhibition of dimethylation of SMD1/3 proteins, components of the splicing machinery and direct substrates of the methylosome, in several non-small cell lung cancer and small cell lung cancer cancer mouse xenograft models[1].

Name: AMG-176, CAS: 1883727-34-1, stock 29.7g, assay 98%, MWt: 613.21, Formula: C33H41ClN2O5S, Solubility: DMSO : 62.5 mg/mL (101.92 mM; Need ultrasonic), Clinical_Informat: Phase 1, Pathway: Apoptosis, Target: Bcl-2 Family, Biological_Activity: AMG-176 is a potent, selective and orally bioavailable MCL-1 inhibitor, with a Ki of 0.13 nM.
IC50 & Target: Ki: 0.13 nM (MCL1)[1][2].
In Vitro: AMG-176 is an inhibitor of induced myeloid leukemia cell differentiation protein MCL-1 (Ki=0.13 nM), with potential pro-apoptotic and antineoplastic activities. Upon administration, AMG 176 binds to and inhibits the activity of MCL-1. This disrupts the formation of MCL-1/Bcl-2-like protein 11 (BCL2L11; BIM) complexes and induces apoptosis in tumor cells[1][2].

Name: BAY-1895344, CAS: 1876467-74-1, stock 36g, assay 99%, MWt: 375.43, Formula: C20H21N7O, Solubility: DMSO : 5.4 mg/mL (14.38 mM; Need ultrasonic), Clinical_Informat: Phase 1, Pathway: Cell Cycle/DNA Damage;PI3K/Akt/mTOR, Target: ATM/ATR;ATM/ATR, Biological_Activity: BAY-1895344 is a potent, orally available and selective ATR inhibitor, with IC50 of 7 nM. Anti-tumor activity[1].
IC50 & Target: IC50: 7 nM (ATR)[1]
In Vitro: BAY-1895344 potently inhibits the proliferation of a broad spectrum of human tumor cell lines with a median IC50 of 78 nM[1]. 
BAY-1895344 potently suppresses hydroxyurea-induced H2AX phosphorylation (IC50, 36 nM)[1].
In Vivo: BAY-1895344 shows potent anti-tumor efficacy in monotherapy in a variety of xenograft models of ovarian and colorectal cancer, and causes complete tumor remission in mantle cell lymphoma models[2].

Name: Nedisertib M3814, CAS: 1637542-33-6, stock 26.7g, assay 99%, MWt: 481.91, Formula: C24H21ClFN5O3, Solubility: DMSO : 100 mg/mL (207.51 mM; Need ultrasonic); H2O : < 0.1 mg/mL (insoluble), Clinical_Informat: Phase 2, Pathway: PI3K/Akt/mTOR;Cell Cycle/DNA Damage, Target: DNA-PK;DNA-PK, Biological_Activity: Nedisertib (M3814) is a potent and selective inhibitor of DNA-dependent Protein Kinase (DNA-PK), with an IC50 of <3 nM.
IC50 & Target: IC50: <3 nM (DNA-PK)[3]
In Vitro: Nedisertib (Compound 136) is a potent and selective inhibitor of DNA-PK, with an IC50 of <3 nM for DNA-PK and <0.5 μΜ for cellular pDNA-PK[3].
In Vivo: In combination with IR, Nedisertib shows efficacy in all of the 6 mouse models of human cancer. In all models, a dose of 2 Gy administered daily for 1 week in combination with Nedisertib induces statically significant tumor growth inhibition compare to IR alone. Nedisertib, alone or in combination with IR, does not induce significant weight loss or visual signs of toxicity in the mice in any study[1].

Name: Gefapixant AF219;MK-7264, CAS: 1015787-98-0, stock 22.1g, assay 98.5%, MWt: 353.40, Formula: C14H19N5O4S, Solubility: DMSO : 5 mg/mL (14.15 mM; ultrasonic and adjust pH to 5-6 with HCl), Clinical_Informat: Phase 3, Pathway: Membrane Transporter/Ion Channel, Target: P2X Receptor, Biological_Activity: Gefapixant is an orally active P2X3 receptor (P2X3R) antagonist with IC 50s of ~30 nM versus recombinant hP2X3 homotrimers and 100-250 nM at hP2X2/3 heterotrimeric receptors.
IC50 & Target: IC50: ~30 nM (recombinant hP2X3 homotrimers), 100-250 nM (hP2X2/3 heterotrimeric receptors)[1].
In Vitro: The aryloxy-pyrimidinediamine, Gefapixant (AF-219) is an orally active small molecule antagonist at human P2X3-containing receptors. The IC50 of Gefapixant has been reported as ~30 nM versus recombinant hP2X3 homotrimers and 100-250 nM at hP2X2/3 heterotrimeric receptors, potencies very similar to those reported for recombinant rat receptors, and it displays no inhibitory impact on any non-P2X3 subunit containing receptors (IC50 values>>10,000 nM at recombinant homotrimeric hP2X1, hP2X2, hP2X4, rP2X5 and hP2X7 channels)[1].
In Vivo: In an adjuvant-induced rthritis model in rat (7d following intraplantar administration of complete Freund's adjuvant), AF-353 produces dose-dependent antihyperalgesia in weight-bearing asymmetry and von Frey filament mechanical tests; magnitude of effect is compared with that of the NSAID naproxen. In a rat model of knee osteoarthritis (14d following intra-articular administration of monoiodoacetate), Gefapixant (7d bid, orally; right) attenuates the weight bearing laterality with complete reversal of apparent hyperalgesia at the two higher doses[2].

Name: (9Z,11E)-Prodlure (9Z,11E)-Tetradecadien-1-yl acetate;Ferodin SL;Litlure A, CAS: 50767-79-8, stock 30.3g, assay 98.1%, MWt: 252.39, Formula: C16H28O2, Solubility: H2O : < 0.1 mg/mL (insoluble); DMSO : ≥ 150 mg/mL (594.32 mM), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: (9Z,11E)-Prodlure is the main component of the sex pheromone of female Spodoptera littoralis.

Name: SQ-31765, CAS: 138383-07-0, stock 8.2g, assay 98.1%, MWt: 464.48, Formula: C24H27F3N2O4, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Membrane Transporter/Ion Channel;Neuronal Signaling, Target: Calcium Channel;Calcium Channel, Biological_Activity: SQ-31765 is a benzazepine calcium channel blocker.
IC50 & Target: Calcium channel[1]
In Vivo: SQ-31765 (SQ 31,765) can reduce the severity of ischemia in a manner which is independent of changes in myocardial blood flow or hemodynamic alterations. Anesthetized dogs are given saline (n=6), SQ-31765 (n=6; 0.2 mg/kg) or SQ 32,189 (n=6; 0.2 mg/kg) i.v. 10 min before ischemia. The effect on pacing-induced ST-segment elevation (pacing+left anterior descending coronary artery stenosis) and myocardial blood flow are determined. SQ-31765 reduces ST-elevation (P<0.05) compared to saline at 10, 40 and 70 min after infusion (5.9±1.4 and 12.0±1.4 mV, respectively, at 70 min). Left anterior descending coronary artery stenosis during atrial pacing resulted in a significant reduction in subendocardial flow in all groups before drug infusion (41±7, 44±7 and 35±9 mL/min/100 g for saline, SQ-31765 and SQ 32,189, respectively)[1].

Name: (R)-MG-132, CAS: 1211877-36-9, stock 32.6g, assay 98.9%, MWt: 475.62, Formula: C26H41N3O5, Solubility: DMSO : ≥ 100 mg/mL (210.25 mM); H2O : < 0.1 mg/mL (insoluble), Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Proteasome, Biological_Activity: (R)-MG-132 is the enantiomer of MG-132. (R)-MG-132 is a proteasome inhibitor with weaker cell cytotoxicity than MG-132. (S,R,S)-(-)-MG-132 stereoisomer is a more potent proteasome inhibitor than MG-132[1].
IC50 & Target: Proteasome[1]
In Vitro: (R)-MG-132, the stereoisomer of MG-132, is studied as a potential inhibitor of chymotrypsin-like, trypsin-like, and peptidylglutamyl peptide hydrolyzing activities of proteasome[1]. 
MG-132 and (S,R,S)-(-)-MG-132 are investigated for inhibition of ChTL, trypsin-like (TL) and peptidylglutamyl peptide hydrolyzing (PGPH) activities of purified 20S proteasomes isolated from human erythrocytes. For MG-132, the IC50s of 0.89 μM, 104.43 μM, and 5.7 μM for ChTL, TL, and PGPH, respectively. For (S,R,S)-(-)-MG-132, the IC50s of 0.22 μM, 34.4 μM, and 2.95 μM for ChTL, TL, and PGPH, respectively[1].

Name: Lintitript SR 27897, CAS: 136381-85-6, stock 32.6g, assay 98.5%, MWt: 411.86, Formula: C20H14ClN3O3S, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein;Neuronal Signaling, Target: Cholecystokinin Receptor;Cholecystokinin Receptor, Biological_Activity: Lintitript (SR 27897) is a highly potent, selective, orally active, competitive and non-peptide cholecystokinin (CCK1) receptor antagonist with an EC50 of 6 nM and a Ki of 0.2 nM. Lintitript displays > 33-fold selectivity more selective for CCK1 than CCK2 receptors (EC50 value of 200 nM). Lintitript increases plasma concentration of leptin and food intake as well as plasma concentration of insulin[1][2][3].
IC50 & Target: EC50: 6 nM (cholecystokinin (CCK1) receptor)[2]; Ki: 0.2 nM (cholecystokinin (CCK1) receptor)[1]
In Vitro: In vitro, Lintitript (SR 27897) is a competitive antagonist of cholecystokinin (CCK)-stimulated amylase release in isolated rat pancreatic acini (pA2 = 7.50) and of CCK-induced guinea pig gall bladder contractions (pA2 = 9.57)[1]. 
Lintitript produces concentration dependent inhibition of [125I]CCK binding to CCK1 receptor sites in the rat pancreas (IC50 value of 0.58 nM) and also to CCK 2 sites in the guinea pig cortex (IC2 value of 479 nM). Lintitript inhibits [125I]gastrin binding to gastrin receptors. Lintitript (0.5 nM) increases the dissociation constant of CCK for the CCK A receptor (Kd = 1.8 to 7.2 nM) without modifying the maximum number of receptors (Bmax = 1800 to 1770 fmol/mg)[1].
In Vivo: Lintitript (SR 27897; 1 mg/kg, i.v.) completely reverses the CCK-induced amylase secretion. Lintitript also inhibits CCK-induced gastric and gallbladder emptying in mice (ED50s = 3 and 72 μg/kg, respectively). Lintitript is also very active (ED50 = 27 μg/kg p.o.) in the gall bladder emptying protocol with egg yolk as an inducer of endogenous CCK release[1].

Name: Btk inhibitor 2 BGB-3111 analog, CAS: 1558036-85-3, stock 33.1g, assay 98.2%, MWt: 431.49, Formula: C24H25N5O3, Solubility: DMSO : 75 mg/mL (173.82 mM; Need ultrasonic and warming), Clinical_Informat: No Development Reported, Pathway: Protein Tyrosine Kinase/RTK, Target: Btk, Biological_Activity: Btk inhibitor 2 (BGB-3111 analog) is a Bruton's tyrosine kinase (BTK) inhibitor extracted from patent US 20170224688 A1.
IC50 & Target: BTK[1]

Name: Zanubrutinib BGB-3111, CAS: 1691249-45-2, stock 19g, assay 98.5%, MWt: 471.55, Formula: C27H29N5O3, Solubility: DMSO : ≥ 56.75 mg/mL (120.35 mM); Ethanol : < 1 mg/mL (insoluble), Clinical_Informat: Launched, Pathway: Protein Tyrosine Kinase/RTK, Target: Btk, Biological_Activity: Zanubrutinib (BGB-3111) is a selective Bruton tyrosine kinase (BTK) inhibitor.
IC50 & Target: BTK[1]
In Vitro: Zanubrutinib (BGB-3111) is a selective Bruton tyrosine kinase (BTK) inhibitor. In both biochemical and cellular assays, Zanubrutinib demonstrates nanomolar BTK inhibition activity. In several MCL and DLBCL cell lines, Zanubrutinib inhibits BCR aggregation-triggered BTK autophosphorylation, blocks downstream PLC-γ2 signaling, and potently inhibits cell proliferation. In comparison with PCI-32765, Zanubrutinib shows much more restricted off-target activities against a panel of kinases, including ITK[1].
In Vivo: Zanubrutinib (BGB-3111) induces dose-dependent anti-tumor effects against REC-1 MCL xenografts engrafted either subcutaneously or systemically via tail vein injection in mice. In the subcutaneous xenografts, Zanubrutinib at 2.5 mg/kg BID shows similar activity as PCI-32765 at 50 mg/kg QD. In the systemic model, the median survival of Zanubrutinib 25 mg/kg BID group is significantly longer than those of both PCI-32765 50 mg/kg QD and BID groups. In an ABC-subtype DLBCL (TMD-8) subcutaneous xenograft model, Zanubrutinib also demonstrates better anti-tumor activity than PCI-32765. Preliminary 14-day toxicity study in rats shows that Zanubrutinib is very well tolerated and maximal tolerate dose (MTD) is not reached when it is dosed up to 250 mg/kg/day[1].

Name: (R)-Zanubrutinib (R)-BGB-3111, CAS: 1691249-44-1, stock 39g, assay 98.7%, MWt: 471.55, Formula: C27H29N5O3, Solubility: DMSO : ≥ 64.25 mg/mL (136.25 mM); Ethanol : < 1 mg/mL (insoluble), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: (R)-Zanubrutinib is the R enantiomer of Zanubrutinib. Zanubrutinib is a selective Bruton tyrosine kinase (BTK) inhibitor.

Name: PACAP (6-38), human, ovine, rat, CAS: 143748-18-9, stock 1.1g, assay 98.2%, MWt: 4024.74, Formula: C182H300N56O45S, Solubility: H2O, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: PACAP (6-38), human, ovine, rat is a potent PACAP receptor antagonist with IC50s of 30, 600, and 40 nM for PACAP type I receptor, PACAP type II receptor VIP1, and PACAP type II receptor VIP2, respectively.
IC50 & Target: IC50: 30 nM (PACAP type I receptor), 600 nM (PACAP type II receptor VIP1), 40 nM (PACAP type II receptor VIP2)[1]
In Vitro: An increase of dopamine (DA) content by HPLC analysis and/or cell proliferation identified by MTT assay by Dexamethasone (DEX) is also observed which can be inhibited by PACAP (6-38) at concentration sufficient to block PACAP type 1 (PAC1) receptor. Pretreatment with PAC1 receptor antagonist PACAP (6-38) at 0.1 or 1 μM for 2 h significantly blocks this increase of DA content by 1 μM DEX. The MTT assay shows that DEX increases cell proliferation. Moreover, this action is also inhibited by the pre-incubation of PACAP (6-38). PACAP (6-38) at 1μM shows no effect on DA content and cell proliferation for 24 h. However, PACAP (6-38) at 0.3 μM has been mentioned to reduce the spontaneous tyrosine hydroxylase (TH) accumulation in differentiated retinal cultured cells for 5 days[2].
In Vivo: Intravesical administration of the PAC1 receptor antagonist, PACAP (6-38) (300 nM), significantly (p≤0.01) increases intercontraction interval (2.0-fold) and void volume (2.5-fold) in NGF-OE mice. Intravesical instillation of PACAP (6-38) also decreases baseline bladder pressure in NGF-OE mice. Intravesical administration of PACAP (6-38) (300 nM) significantly (p≤0.01) reduces pelvic sensitivity in NGF-OE mice but is without effect in WT mice[3].

Name: PACAP (1-38), human, ovine, rat Pituitary Adenylate Cyclase Activating Polypeptide 38, CAS: 137061-48-4, stock 3g, assay 98.1%, MWt: 4534.26, Formula: C203H331N63O53S, Solubility: H2O, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: PACAP (1-38), human, ovine, rat is a neuropeptide with 38 amino acid residues. PACAP (1-38) binds to PACAP type I receptor, PACAP type II receptor VIP1, and PACAP type II receptor VIP2 with IC50s of 4 nM, 2 nM, and 1 nM, respectively.
IC50 & Target: IC50: 4 nM (PACAP type I receptor), 2 nM (PACAP type II receptor VIP1), and 1 nM (PACAP type II receptor VIP2)[1]
In Vitro: PACAP (1-38), human, ovine, rat is a fragment of pituitary adenylate cyclase activating polypeptide[1]. PACAP (1-38) shows high affinity for PACAP specific (PAC1) receptor in membranes from various tissues including the endocrine pancreas[2]. In vitro, PACAP (1-38) relaxes guinea-pig and rabbit tracheal smooth muscle precontracted by histamine and by acetylcholine. PACAP (1-38) also increases adenosine 3':5'-cyclic monophosphate (cyclic AMP) in tracheal smooth muscle, providing a possible mechanism for the relaxant effect of PACAP (1-38)[3].
In Vivo: PACAP (1-38) alone in sham animals does not result in changes in any of the retinal layers. PACAP (1-38) dissolved in solutio ophthalmica cum benzalkonio leads to significant protection in the retina in bilateral common carotid artery occlusion (BCCAO)-lesioned retinas; retinas treated with PACAP (1-38) eye drops have preserved structure compared to control retinas. OLM-ILM (outer limiting membrane-inner limiting membrane) distance is reduced by 49.7% (p<0.001) in BCCAO retinas compared to sham controls, but it is only 40.6% (p<0.001) in the eyes treated with PACAP (1-38) eye drops. A protection to a similar degree is found in the inner nuclear layer (INL) (BCCAO: 38.5%, PACAP (1-38): 30.5%; p<0.001), and inner plexiform layer (IPL) (BCCAO: 64.8%, PACAP (1-38): 38.2%; p<0.05), while no statistically significant attenuation of the damage is observed in the outer nuclear layer (ONL) (BCCAO: 36.5%, PACAP (1-38): 37.7%) or outer plexiform layer (OPL) (BCCAO: 53.0%, PACAP (1-38): 48.2%). The number of cells in the ganglion cell layer (GCL) is significantly decreased after BCCAO by 52.4% (p<0.05) and is significantly ameliorated by PACAP (1-38) eye drops (decreased by 25.9%; p<0.05)[4].

Name: TC-O 9311, CAS: 444932-31-4, stock 35.4g, assay 98.4%, MWt: 365.38, Formula: C20H19N3O4, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein;Neuronal Signaling, Target: GPR139;GPR139, Biological_Activity: TC-O 9311 is a potent orphan G protein-coupled receptor 139 (GPR139) agonist with an EC50 of 39 nM[1].
IC50 & Target: EC50: 39 nM (Orphan G protein-coupled receptor 139)[1]

Name: ML311, CAS: 315698-17-0, stock 33.7g, assay 98.6%, MWt: 415.45, Formula: C23H24F3N3O, Solubility: DMSO : 67.5 mg/mL (162.47 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Apoptosis, Target: Bcl-2 Family, Biological_Activity: ML311 is a potent and selective inhibitor of the Mcl-1/Bim interaction.
IC50 & Target: Mcl-1/Bim[1].
In Vitro: ML311 potently halts viability of several types of Mcl-1 primed cells, including MCL-1-1780 (EC50=0.31 μM), DHL-6 (EC50=3.3 μM), and NCI-H929 (EC50=1.6 μM), with generally high maximal effect (>80%). ML311 also displays activity in a leukemia-derived cell line particularly reliant upon Bcl-2 function (Bcl2-1863, EC50=1.1 μM). ML311 has strong growth inhibitory effects in many cell lines, with GI50<900 nM for nine cell types (RPMI-8226, SR, NCI-H322M, NCI-H60, HCC-2998, KM12, SF-295, U251, PC-3 cell lines), and <2 μM for 14 additional types[1].

Name: NE 52-QQ57, CAS: 1401728-56-0, stock 31.7g, assay 98.8%, MWt: 416.52, Formula: C24H28N6O, Solubility: DMSO : 25 mg/mL (60.02 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: NE 52-QQ57 is a selective, and orally available GPR4 antagonist with an IC50 of 70 nM[1]. Anti-inflammatory activities[1].
IC50 & Target: IC50: 70 nM (GPR4)[1].
In Vitro: NE 52-QQ57 effectively blocks GPR4-mediated cAMP accumulation (IC50 26.8 nM in HEK293 cells)[2].
In Vivo: NE 52-QQ57 (Compound 13) shows a significant anti-inflammatory effect in the rat antigen induced arthritis model after oral administration at 30 mg/kg bid for 20 days[1].
NE 52-QQ57 (30 mg/kg bid po for 4 days) also prevents angiogenesis in the mouse chamber model as well as pain as demonstrated in the rat complete Freund’s adjuvant model[1].

Name: eIF4A3-IN-2, CAS: 2095677-20-4, stock 5.4g, assay 98%, MWt: 602.70, Formula: C25H19Br2ClN4O2, Solubility: DMSO : 100 mg/mL (165.92 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Cell Cycle/DNA Damage;Autophagy, Target: Eukaryotic Initiation Factor (eIF);Autophagy, Biological_Activity: eIF4A3-IN-2 is a highly selective and noncompetitive eukaryotic initiation factor 4A-3 (eIF4A3) inhibitor with an IC50 of 110 nM.
IC50 & Target: IC50: 110 nM (eIF4A3)[1]
In Vitro: eIF4A3-IN-2 (compound 2) binds to the allosteric region in eIF4A3 and inhibits in vitro ATPase, helicase, and cellular nonsense-mediated RNA decay (NMD) activities[1].

Name: FTBMT, CAS: 1358575-02-6, stock 25.9g, assay 98.4%, MWt: 392.35, Formula: C19H16F4N4O, Solubility: H2O : < 0.1 mg/mL (insoluble); DMSO : 125 mg/mL (318.59 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: FTBMT is a selective GPR52 agonist with an EC50 of 75 nM[1]. Antipsychotic and procognitive properties[2].
IC50 & Target: IC50: 75 nM (GPR52)[1]
In Vitro: FTBMT (0.1-10 μM) increases intracellular cAMP levels in CHO cells expressing human, mouse, or rat GPR52, with pEC50s of 7.03, 6.85, and 6.87, respectively[2].
In Vivo: FTBMT (30 mg/kg, 90 minutes) exhibits antipsychotic-like activity without causing catalepsy in mice[2].
FTBMT (3 or 10 mg/kg, 48 hours) improves recognition and spatial working memory in rats[2].
FTBMT (3, 10, 30 mg/kg, 2 hours) stimulates neuronal activity in brain regions related to cognition[2].

Name: ZM223, CAS: 2031177-48-5, stock 31.8g, assay 98.7%, MWt: 502.53, Formula: C23H17F3N4O2S2, Solubility: H2O : < 0.1 mg/mL (insoluble); DMSO : 83.33 mg/mL (165.82 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: NEDD8-activating Enzyme, Biological_Activity: ZM223 is a potent non-covalent NEDD8 activating enzyme (NAE) inhibitor, orally active[1].
IC50 & Target: NEDD8 activating enzyme (NAE)[1]
In Vitro: ZM223 (0.1-1 μM; 4 hours) inhibits both HCT-116 and U-2OS cancer cells with IC50s of 100 and 122 nM, respectively[1].
ZM223 (0.1-1 μM; 4 hours) causes a dose-response decrease in the level of NEDD8 and accumulation of the UBC12 protein, indicating the decrease of the subsequent NEDD8-UBC12 complex[1].

Name: BMS-935177, CAS: 1231889-53-4, stock 13.7g, assay 98.6%, MWt: 502.56, Formula: C31H26N4O3, Solubility: DMSO : ≥ 130 mg/mL (258.68 mM), Clinical_Informat: No Development Reported, Pathway: Protein Tyrosine Kinase/RTK, Target: Btk, Biological_Activity: BMS-935177 is a potent and selective reversible inhibitor of Bruton’s tyrosine kinase (Btk) with an IC50 of 3 nM.
IC50 & Target: IC50: 3 nM (BTK)[1]
In Vitro: In B cells stimulated through the BCR, BMS-935177 selectively inhibits several different readouts. BMS-935177 inhibits calcium flux in human Ramos B cells (IC50=27 nM) and inhibits CD69 surface expression in peripheral B cells stimulated with antiIgM and anti-IgG. However, BMS-935177 has no effect on CD69 surface expression in B cells stimulated through the CD40 receptor with CD40 ligand. Against IgG-containing immune complexdriven low affinity activating Fcγ receptor (FcγRIIa and FcγRIII) end points in peripheral blood mononuclear cells (PBMCs), BMS-935177 effectively inhibits TNFα production with an IC50 value of 14 nM. BMS-935177 shows mean IC50 values of 550±100 (n=11) and 2060±240 nM (n=3) in human and mouse whole blood, respectively[1].
In Vivo: When dosed orally once daily at 5, 20, and 45 mg/kg to mice, BMS-935177 inhibits anti-KLH antibodies of the IgG isotype at day 14, with statistically significant reductions at all doses. In satellite mice from this study dosed with 6 at 5 mg/kg, the plasma concentration is maintained above the mouse whole blood BCR-stimulated CD69 IC50 value of 2 μM for only approximately 5 h. At once daily oral doses of 10, 20, and 30 mg/kg beginning on the day of primary immunization, BMS-935177 provides a clear dose-dependent reduction in both the severity and incidence of clinically evident disease in this rodent model of RA. At 10 mg/kg of BMS-935177, disease severity is reduced about 40% compared to vehicle treatment, and the percentage of animals showing any signs of disease is reduced by a third[1].

Name: SOS1-IN-1, CAS: 4551-00-2, stock 20.8g, assay 98.6%, MWt: 325.36, Formula: C22H15NO2, Solubility: DMSO : 12.5 mg/mL (38.42 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: SOS1-IN-1 is a SOS1 inhibitor.
IC50 & Target: SOS1[1].
In Vitro: The growth inhibitory rate (IR)=(average OD value in the control group-average OD value in the treatment group)/average OD value in the control group×100% are compared. Treatments with SOS1-IN-1 at 40 μM and NSC-658497 at 30 μM result in growth inhibitory rate of 29% and 8% respectively. The combination treatment results in growth inhibitory rate of 54%, showing the synergistic effect of SOS1-IN-1 and NSC-658497 on cell growth inhibition. It is showed that the treatment with NSC-658497 at 40 μM for 2 hours alone or in combìnation with the treatment with 40 μM of SOS1-IN-1 overnight resulted in lower expression levels of P-AKT and P-ERK. The treatment wlth 40 μM of SOS1-IN-1 overnight resulted in lower expression levels of P-ERK[1].

Name: Decoyinine Angustmycin A, CAS: 2004-04-8, stock 10.2g, assay 98.4%, MWt: 279.25, Formula: C11H13N5O4, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Decoyinine is a selective inhibitor of GMP synthetase (GMPS).
IC50 & Target: GMPS[1].
In Vitro: Decoyinine is an analog of adenosine which causes a decrease in intracellular GTP levels by inhibition of GMP synthetase. Decoyinine exerts a stimulatory effect on oaamylase synthesis only in the strain in which the catabolite repression component of a-amylase regulation has been rendered inoperable by the gra-10 mutation. The apparent stimnulation of a-amylase activity in WLN-11 by Decoyinine is not an artifactual effect exerted at the level of enzyme activity itself. It is observed that purine nucleotides, most notably GMP, exhibits a dramatic inhibitory effect on the activity of Bacillus circulans F-2 amylase and a less-pronounced inhibitory effect on B. subtilis aamylase. At the concentration used in the experiments (1.07 mM), Decoyinine has no effect in vitro on B. subtilis WLN-11 oaamylase activity. At the same concentration, GMP exerts a slight inhibitory effect on aamylase activity[2].
In Vivo: It is showed that Decoyinine (Angustmycin A) treatment hinders tumor growth in xenograft mouse model. Moreover, like GMPS activity, the effect of Decoyinine does not appear to be subtype specific as it impairs growth of xenografts from cells harboring NRASQ61R (SK-Mel-103) or BRAFV600E (SK-Mel-28) mutations[1].

Name: dBET1, CAS: 1799711-21-9, stock 20.8g, assay 98.9%, MWt: 785.27, Formula: C38H37ClN8O7S, Solubility: DMSO : ≥ 50 mg/mL (63.67 mM); H2O : < 0.1 mg/mL (insoluble), Clinical_Informat: No Development Reported, Pathway: Epigenetics;PROTAC, Target: Epigenetic Reader Domain;PROTAC, Biological_Activity: dBET1 is a potent BRD4 protein degrader based on PROTAC technology with an EC50 of 430 nM. dBET1 is a PROTAC that composes of (+)-JQ1 (HY-13030) linked to Thalidomide (HY-14658) with a linker[1].
IC50 & Target: EC50: 430 nM (BRD4)[1]
In Vitro: Treatment with dBET1 down regulates MYC and PIM1 transcription. Degradation of BRD4 by dBET1 is associated with a more potent apoptotic consequence in MV4;11 cell line. Significantly increased apoptosis after only 4 h of dBET1 treatment is enhanced at 8 h. dBET1 also induces a potent and superior inhibitory effect on MV4;11 cell proliferation at 24 hours (measured by ATP content, IC50= 0.14 μM, compare to IC50= 1.1 μM with JQ1)[1].
In Vivo: Administration of dBET1 attenuates tumor progression as determined by serial volumetric measurement, and decreases tumor weight assessed post-mortem. Acute pharmacodynamic degradation of BRD4 is observed four hours after a first or second daily treatment with dBET1 (50 mg/kg IP). A statistically significant destabilization of BRD4, down regulation of MYC and inhibition of proliferation is observed with dBET1 compare to vehicle control in excised tumors. Two weeks of dBET1 is well tolerated by mice without a meaningful effect on weight, white blood count, hematocrit or platelet count[1].

Name: R547, CAS: 741713-40-6, stock 29.9g, assay 98.8%, MWt: 441.45, Formula: C18H21F2N5O4S, Solubility: H2O : < 0.1 mg/mL (insoluble); DMSO : ≥ 50 mg/mL (113.26 mM), Clinical_Informat: No Development Reported, Pathway: Cell Cycle/DNA Damage, Target: CDK, Biological_Activity: R547 is a potent ATP-competitive inhibitor of CDK1/2/4 with Ki of 2 nM/3 nM/1 nM.
IC50 Value: 2 nM(Ki for CDK1); 3 nM(Ki for CDK2); 1 nM(Ki for CDK4)
Target: CDK
in vitro: R547 effectively inhibits CDK1/cyclinB, CDK2/cyclinE, and CDK4/cyclinD1(Ki=1-3nM) and is inactive(Ki>5,000nM) against a panel of >120 unrelated kinases. R547 effectively inhibits the proliferation of tumor cell lines independent of multidrug resistant status, histologic type, retinoblastoma protein, or p53 status, with IC50s <0.60 μM. R547 reduces phosphorylation of the cellular retinoblastoma protein at specific CDK phosphorylation sites at the same concentrations that induced cell cycle arrest, suggesting a potential pharmaco dynamics marker for clinical use. R547 inhibits the proliferation of tumor cell lines and is active in all 19 cell lines tested irrespective of tissue of origin, multidrug resistance (MDR), p53, or retinoblastoma status. R547 possessing both 5-and 6-fluoro substitution culminated in an Inhibitor with low, single-digit nanomolar potency against the CDKs(Ki=0.001,0.003,and 0.001 μM for CDK1,CDK2, and CDK4,respectively) and excellent cellular potency (IC50=0.08 μM,HCT116 cell line).
in vivo: R547 administered with oral and i.v. dosing in multiple established human tumor significantly inhibits tumor activity(P < 0.01). R547 administered orally at dose of 40 mg/kg daily in colon, lung, breast, prostate, and melanoma human tumor xenograft models shows significant TGI (79-99%). R547 is equally efficacious (TGI, 61-95%) when dosed with 40 mg/kg i.v. once weekly. These doses of R547 are not toxic and did not result in body weight loss. R547 does not show signs of overt toxicity during the course of the 3-week study and any gross pathology at necropsies done at the end of the studies. R547 inhibits tumor growth up to 95% in the HCT116 human colorectal tumor xenograft model in nude mice . R547 causes significant TGI in all of the models tested when dosed orally and i.v. at or below the maximum tolerated dose. R547 inhibits phosphorylation of retinoblastoma protein in tumors at the efficacious exposures in tumor xenograft models, providing a pharmacodynamic biomarker for clinical use. R547 reported here suggests that this is a promising molecule for evaluation in the treatment of solid tumors.

Name: 42-(2-Tetrazolyl)rapamycin, CAS: 221877-56-1, stock 30.3g, assay 98.5%, MWt: 966.21, Formula: C52H79N5O12, Solubility: DMSO : ≥ 130 mg/mL (134.55 mM), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: 42-(2-Tetrazolyl)rapamycin is a prodrug compound of a rapamycin analog extracted from patent US 20080171763 A1, Example 1. Rapamycin is a specific mTOR inhibitor.

Name: AG 1295, CAS: 71897-07-9, stock 29.3g, assay 98.7%, MWt: 234.30, Formula: C16H14N2, Solubility: DMSO : 62.5 mg/mL (266.75 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Protein Tyrosine Kinase/RTK, Target: PDGFR, Biological_Activity: AG 1295 is a selective platelet-derived growth factor receptor (PDGFR) tyrosine-kinase inhibitor. AG 1295 reduces neointimal formation in aortic allograft vasculopathy by inhibition of PDGFR-beta-triggered tyrosine phosphorylation[1][2].
IC50 & Target: PDGFR[1]

Name: L-Kynurenine, CAS: 2922-83-0, stock 32.1g, assay 98.5%, MWt: 208.21, Formula: C10H12N2O3, Solubility: DMSO : 50 mg/mL (240.14 mM; Need ultrasonic), Clinical_Informat: Phase 1, Pathway: Immunology/Inflammation;Metabolic Enzyme/Protease, Target: Aryl Hydrocarbon Receptor;Endogenous Metabolite, Biological_Activity: L-Kynurenine is a metabolite of the amino acid L-tryptophan. L-Kynurenine is an aryl hydrocarbon receptor agonist.
IC50 & Target: Target: Aryl Hydrocarbon Receptor[1]
In Vitro: Kynurenine and its further breakdown products carry out diverse biological functions, including dilating blood vessels during inflammation and regulating the immune response. Some cancers increase kynurenine production, which increases tumor growth. L-kynurenine (Kyn) is an aryl hydrocarbon receptor (AHR) agonist that activates AHR-directed, naive T cell polarization to the anti-inflammatory Treg phenotype. Kynurenine activates AHR signaling at physiological concentrations in H1L7.5c3 cells and acts as an AHR agonist after a 24-hr exposure by inducing the AHR-regulated luciferase gene in H1L7.5c3 mouse hepatocyte cells[1].
In Vivo: Kynurenine dilates arteries from rats as well as humans via Kv7 channels in the vascular smooth muscle. In rats, this tryptophan metabolite causes hypotension, which is partly counteracted by Kv7 channel inhibition[2]. L-kynurenine administered 1 h before the hypoxia-ischemia shows a dose-dependent significant neuroprotective effect, with complete protection at a dose of 300 mg/kg. The induction of c-fos immunoreactivity in cerebral cortex is also blocked by this dose of L-kynurenine[3].

Name: L-Carnitine (hydrochloride) (R)-Carnitine (hydrochloride), CAS: 6645-46-1, stock 6.7g, assay 98.8%, MWt: 197.66, Formula: C7H16ClNO3, Solubility: 10 mM in DMSO, Clinical_Informat: Launched, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: L-Carnitine hydrochloride ((R)-Carnitine hydrochloride), a highly polar, small zwitterion, is an essential co-factor for the mitochondrial β-oxidation pathway. L-Carnitine hydrochloride functions to transport long chain fatty acyl-CoAs into the mitochondria for degradation by β-oxidation. L-Carnitine hydrochloride is an antioxidant. L-Carnitine hydrochloride can ameliorate metabolic imbalances in many inborn errors of metabolism[1][2][3].
In Vivo: L-Carnitine hydrochloride ((R)-Carnitine hydrochloride) (125, 250 mg/kg; i.p.) has a more pronounced bronchodilator effect in this chronic murine asthma model, and decreases urinary LTE4 excretion[4].

Name: BMS-986142, CAS: 1643368-58-4, stock 15.3g, assay 98.8%, MWt: 572.60, Formula: C32H30F2N4O4, Solubility: DMSO : 125 mg/mL (218.30 mM; Need ultrasonic); H2O : < 0.1 mg/mL (insoluble), Clinical_Informat: Phase 2, Pathway: Protein Tyrosine Kinase/RTK, Target: Btk, Biological_Activity: BMS-986142 is a potent and highly selective reversible inhibitor of Bruton's tyrosine kinase (BTK) with an IC50 of 0.5 nM.
IC50 & Target: IC50: 0.5 nM (BTK), 10 nM (TEC), 15 nM (ITK), 23 nM (BLK), 28 nM (TXK), 32 nM (BMX), 71 nM (LCK), 1100 nM (SRC) [1].
In Vitro: BMS-986142 potently inhibits human recombinant BTK with an IC50 of 0.5 nM in enzymatic assays. Against a panel of 384 kinases, BMS-986142 is highly selective, with only five other kinases (Tec, ITK, BLK, Txk, BMX) inhibited with <100-fold selectivity for BTK. Four of these kinases are Tec family kinases, of which BTK is a member, and only Tec (IC50=10 nM) is inhibited with <30-fold selectivity compared with BTK. BMS-986142 does not inhibit CD40L-induced expression of CD86 or CD69 on peripheral blood B cells (IC50>10,000 nM for both). When Ramos B cells are treated with anti-IgM to activate BCR, BMS-986142 inhibits BTK-dependent calcium flux with an IC50 of 9 nM[2].
In Vivo: BMS-986142 at 4, 10, and 30 mg/kg results in dose-dependent reductions of 26%, 43%, and 79% in clinically evident disease, respectively, at the end of the study. Interestingly, 4 mg/kg BMS-986142 provides an additive benefit in clinical scores (54% inhibition) when co-administered with MTX versus 19% inhibition with MTX alone. Co-administration of BMS-986142 at 4 mg/kg with MTX result in a 53% reduction in inflammation and bone resorption compared with 24% and 10%, respectively, with either drug alone. Furthermore, serum anti-collagen II IgG titers are significantly inhibited with 10 and 30 mg/kg BMS-986142. BMS-986142 also produces dose-dependent reductions in clinical scores when administration is delayed until the collagen booster on day 21. BMS-986142 doses of 2, 4, and 25 mg/kg in this therapeutic dosing regimen result in clinical score reductions of 17%, 37%, and 67%, respectively, at the end of the study[2].

Name: Miridesap CPHPC;Ro63-8695;GSK2315698, CAS: 224624-80-0, stock 27.5g, assay 98.5%, MWt: 340.37, Formula: C16H24N2O6, Solubility: DMSO : 75 mg/mL (220.35 mM; Need ultrasonic), Clinical_Informat: Phase 2, Pathway: Others, Target: Others, Biological_Activity: Miridesap is a ligand for serum amyloid P component (SAP) and intends to inhibit and dissociate SAP binding to amyloid fibrils and tangles.
IC50 & Target: SAP[1]
In Vitro: Miridesap is a ligand for serum amyloid P component (SAP) and intends to inhibit and dissociate SAP binding to amyloid fibrils and tangles[1]. Miridesap depletes circulating SAP almost completely but leaves some SAP in amyloid deposits for specific recognition by subsequently administered therapeutic anti-SAP antibodies[2].

Name: MK-0343 MRK-409, CAS: 233275-76-8, stock 5.7g, assay 98.9%, MWt: 397.38, Formula: C19H17F2N7O, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Neuronal Signaling;Membrane Transporter/Ion Channel, Target: GABA Receptor;GABA Receptor, Biological_Activity: MK0343 (MRK-409) is an orally bioavailable GABAA receptor subtype-selective partial agonist. MK0343 is a non-sedating anxiolytic[1].
IC50 & Target: Ki: 0.22 nM (rGABAA α1), 0.4 nM (rGABAAα2) , 0.21 nM (rGABAAα3), 78 nM (rGABAAα4), 0.23 nM (rGABAAα5), 980 nM (rGABAAα6)[1]
In Vivo: MK0343 readily penetrates the brain in rats and occupies the benzodiazepine site of GABAA receptors, measured using an in vivo [3H]flumazenil binding assay, with an Occ50 of 2.2 mg/kg p.o. and a corresponding plasma EC50 of 115 ng/mL[1].

Name: CNDAC (hydrochloride), CAS: 134665-72-8, stock 24.9g, assay 98.4%, MWt: 288.69, Formula: C10H13ClN4O4, Solubility: DMSO : 125 mg/mL (432.99 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Cell Cycle/DNA Damage;Metabolic Enzyme/Protease, Target: Nucleoside Antimetabolite/Analog;Drug Metabolite, Biological_Activity: CNDAC hydrochloride is a metabolite of the orally active agent sapacitabine, and a nucleoside analog[1].

Name: Thionin (acetate) Thionine acetate, CAS: 78338-22-4, stock 11.1g, assay 98.5%, MWt: 287.34, Formula: C14H13N3O2S, Solubility: DMSO : 41.67 mg/mL (145.02 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Thionin acetate (Thionine acetate) is a metachromic cationic histology dye used in biological staining widely.

Name: PSI-7409 tetrasodium, CAS: 1621884-22-7, stock 23.8g, assay 98.2%, MWt: 592.12, Formula: C10H16FN2Na4O14P3, Solubility: H2O : ≥ 125 mg/mL (211.11 mM), Clinical_Informat: No Development Reported, Pathway: Anti-infection, Target: HCV, Biological_Activity: PSI-7409 tetrasodium is an active 5'-triphosphate metabolite of sofosbuvir (PSI-7977), inhibiting HCV NS5B polymerases, with IC50s of 1.6, 2.8, 0.7 and 2.6 μM for GT 1b_Con1, GT 2a_JFH1, GT 3a, and GT 4a NS5B polymerases, respectively.
IC50 & Target: IC50: 1.6 μM (GT 1b_Con1), 2.8 μM (GT 2a_JFH1), 0.7 μM (GT 3a), 2.6 μM (GT 4a)[1]
In Vitro: PSI-7409 tetrasodium is an active 5'-triphosphate metabolite, inhibiting HCV NS5B polymerases, with IC50s of 1.6, 2.8, 0.7 and 2.6 μM for GT 1b_Con1, GT 2a_JFH1, GT 3a, and GT 4a NS5B polymerases, respectively. PSI-7409 also weakly inhibits human DNA polymerase α, with an IC50 of 550 μM, but shows no inhibition on DNA Pol β and γ[1]. In clone A cells, the levels of PSI-7409 gradually increases to a maximum concentration of about 25 μM over a period of 48 h. PSI-7409 forms at a much faster rate in primary human hepatocytes, achieving a maximum intracellular concentration of ∼100 μM at 4 h and remains at that concentration for 48 h[2].

Name: BMS CCR2 22, CAS: 445479-97-0, stock 11.7g, assay 98.3%, MWt: 593.66, Formula: C28H34F3N5O4S, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Immunology/Inflammation;GPCR/G Protein, Target: CCR;CCR, Biological_Activity: BMS CCR2 22 is a potent, specific and high affinity CC-type chemokine receptor 2 (CCR2) antagonist with excellent binding affinity (binding IC50 of 5.1 nM) and potent functional antagonism (calcium flux IC50 of 18 nM and chemotaxis IC50 of 1 nM)[1][2].
In Vitro: BMS CCR2 22 (Compound 22) has binding affinity for wild-type and E291A mutants with IC50 values of 7.5 nM and 3.7 nM, respectively[1].
BMS CCR2 22 prevents both the binding and the internalization of fluorescently labeled hMCP-1_AF647 internalization in human monocytes. BMS CCR2 22 inhibits the internalization of hMCP1_AF647 with an IC50 value of approximately 2 nM[2]. 
The addition of BMS CCR2 22 (0.1-10 μM; 24 h), cenicriviroc (CVC) or a combination of both BMS CCR2 22 and MVC to human aortic endothelial cells (HAoECs) prior to MCP-1 stimulation do not alter E-selectin, ICAM-1, or CD99 cell surface expression. Incubation of HAoECs with BMS CCR2 22 before MCP-1 significantly increases VCAM-1 and PECAM1 cell surface levels (from 72.8 to 160% and from 97.2 and 127%, respectively)[3].

Name: LYN-1604, CAS: 2088939-99-3, stock 4.9g, assay 98.7%, MWt: 584.62, Formula: C33H43Cl2N3O2, Solubility: DMSO : 100 mg/mL (171.05 mM; Need ultrasonic and warming), Clinical_Informat: No Development Reported, Pathway: Autophagy;Autophagy, Target: ULK;Autophagy, Biological_Activity: LYN-1604 is a potent UNC-51-like kinase 1 (ULK1) agonist with an EC50 of 18.94 nM.
IC50 & Target: EC50: 18.94 nM (ULK1)[1]
In Vitro: LYN-1604 is a potent UNC-51-like kinase 1 (ULK1) agonist with an EC50 of 18.94 nM in ADP-Glo™ kinase assay. The in vitro kinase assay reveals that the LYN-1604 increases the phosphorylation of mATG13 at ser318 in wild-type ULK1 transfected HEK-293T cells. It is found that LYN-1604-treated cells display a remarkable green fluorescence with MDC staining and the autophagy ratio is increased in a dose-dependent manne. It is also found that LYN-1604 induces remarkable up-regulation of Beclin-1 and degradation of p62, as well as transformation of LC3-I to LC3-II[1].
In Vivo: Based on the results of tumor volume and weight, it is found that LYN-1604 can significantly inhibit the growth of xenograft MDA-MB-231 cells. The body weights of mice are stable, with no obvious distinctions between LYN-1604-treated and control mice. It also reveals that LYN-1604 induces remarkable autophagy in vivo[1].

Name: CU-CPT17e, CAS: 2109805-75-4, stock 4.7g, assay 98.6%, MWt: 504.49, Formula: C27H24N2O8, Solubility: DMSO : 5 mg/mL (9.91 mM; Need ultrasonic and warming), Clinical_Informat: No Development Reported, Pathway: Immunology/Inflammation, Target: Toll-like Receptor (TLR), Biological_Activity: CU-CPT17e is a potent multi-Toll-like receptor (TLR) agonist that activates TLR3, TLR8, and TLR9.
IC50 & Target: TLR3, TLR8, and TLR9[1]
In Vitro: CU-CPT17e shows strong NF-κB activation in TLR3, TLR8 and TLR9 HEK293 cells with EC50 values of 4.80±0.73, 13.5±0.58 and 5.66±0.17 μM, respectively. CU-CPT17e significantly improves the activity with 13.9±0.9 fold of NF-κB activation and an EC50 value of 4.8±0.7 μM. CU-CPT17e inhibits the proliferation of HeLa cancer cells by triggering apoptosis and arresting the cell cycle at the S phase. The induction of apoptosis by CU-CPT17e in HeLa cells is investigated. HeLa cells are cultured with increasing concentrations of CU-CPT17e or poly I:C or blank control (DMSO) for 24 h. Treatment with CU-CPT17e for 24 h at different concentrations (10 to 40 μM) results in an elevation of apoptotic cell population ranging from 10% to 17%, which is more effective than poly I:C at 5 μg/mL. These results suggest that the antiproliferative activity of CU-CPT17e against HeLa cells might result from its ability to directly induce apoptosis[1].

Name: CM-4620, CAS: 1713240-67-5, stock 3.4g, assay 98.7%, MWt: 421.76, Formula: C19H11ClF3N3O3, Solubility: DMSO : ≥ 100 mg/mL (237.10 mM); H2O : < 0.1 mg/mL (insoluble), Clinical_Informat: Phase 2, Pathway: Membrane Transporter/Ion Channel, Target: CRAC Channel, Biological_Activity: CM-4620 is a calcium-release activated calcium-channel (CRAC channel) inhibitor, with IC50s of 119 nM, 895 nM for Orai1/STIM1 and Orai2/STIM1 channels, respectively.
IC50 & Target: IC50: 119 nM (Orai 1/STIM1), 895 nM (Orai 1/STIM1)[1].
In Vitro: It is determined that CM-4620 (compound 1) inhibits Orai 1/STIM1 channels with an IC50 of 119 nM, and Orai2/STIM1 channels with an IC50 of 895 nM. It is more potent on Orai1 than Orai2-type CRAC channels. In human PBMCs, CM-4620 potently inhibits release of multiple cytokines which play important roles in T cells (IC50s, IFN γ: 138 nM, IL-4: 879 nM, IL-6: 135 nM, IL-1β: 240 nM, IL-10: 303 nM, TNFα: 225 nM, IL-2: 59 nM, IL-17 120 nM)[1].
In Vivo: Mouse PACs are treated with CRAC inhibitors CM-4620 or GSK-7975A and monitored for their rate of Calcium uptake. Both CRAC inhibitors reduce the rate of store-operated Calcium entry into the ER to 50% of controllevels upon treatment with 700 nM of inhibitor. CM-4620 blocks 100% of reuptake at 10 mM[1].

Name: LY 345899, CAS: 10538-99-5, stock 30.5g, assay 98.1%, MWt: 471.42, Formula: C20H21N7O7, Solubility: DMSO : 125 mg/mL (265.16 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: LY 345899 is a methylene tetrahydrofolate dehydrogenase (MTHFD1; DC301) and MTHFD2 ibhibitor with IC50 values of 96 nM and 663 nM, respectively and a Ki of 0.018 μM[1][2][3].
IC50 & Target: Ki: 0.018 μM (MTHFD1)[1]; IC50: 96 nM (MTHFD1) and 663 nM (MTHFD2)[3]

Name: Inarigivir ORI-9020;SB-9000, CAS: 475650-36-3, stock 19.4g, assay 98.5%, MWt: 587.50, Formula: C20H26N7O10PS, Solubility: 10 mM in DMSO, Clinical_Informat: Phase 2, Pathway: Anti-infection, Target: HBV, Biological_Activity: Inarigivir (ORI-9020;SB-9000) is a dinucleotide which can significantly reduce liver HBV DNA in transgenic mice expressing hepatitis B virus.
IC50 & Target: Target: HBV[1]
In Vivo: I.p. injection of Inarigivir at 100 mg/kg/day significantly reduces viral DNA in the liver and shows anti-HBV activity similar ADV positive control. Serum HBV DNA is not reduced in response to treatment. Inarigivir does not affect levels of HBV RNA in liver, levels of HBeAg in serum, or mean titers of HBsAg. The minimal effective dose is identified to be between 1.6 and 0.5 mg/kg/day using liver HBV DNA values[1].

Name: (+)-Gallocatechin, CAS: 970-73-0, stock 30g, assay 98%, MWt: 306.27, Formula: C15H14O7, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: (+)-Gallocatechin is a polyphenol compound from green tea, possesses anticancer activity[1].

Name: Cy 3 (Non-Sulfonated) Cyanine3, CAS: 146397-20-8, stock 21.7g, assay 98.2%, MWt: 911.01, Formula: C43H50N4O14S2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Cy 3 Non-Sulfonated (Cyanine3) is a fluorescent label for protein and nucleic acid.

Name: AZ PFKFB3 26, CAS: 1704740-52-2, stock 38.1g, assay 98.8%, MWt: 402.49, Formula: C24H26N4O2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: AZ PFKFB3 26 is a potent and selective inhibitor of the metabolic kinase PFKFB3 with an IC50 of 23 nM. AZ PFKFB3 26 inhibits PFKFB1 and PFKFB2 with IC50s of 2.06 and 0.384 μM, respectively[1].
IC50 & Target: IC50: 23 nM (PFKFB3), 2.06 μM (PFKFB1), 0.384 μM (PFKFB2)[1]

Name: JAK3-IN-6, CAS: 1443235-95-7, stock 16.2g, assay 98.9%, MWt: 350.37, Formula: C19H18N4O3, Solubility: DMSO : 260 mg/mL (742.07 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Epigenetics;Stem Cell/Wnt;JAK/STAT Signaling, Target: JAK;JAK;JAK, Biological_Activity: JAK3-IN-6 is a potent, selective irreversible Janus Associated Kinase 3 (JAK3) inhibitor, with an IC50 of 0.15 nM.
IC50 & Target: IC50: 0.15 nM (JAK3)[1].
In Vitro: JAK3-IN-6 (compound 2), a potent inhibitor of JAK3 (0.15 nM) is 4300-fold selective for JAK3 over JAK1 in enzyme assays, 67-fold (IL-2 vs. IL-6) or 140-fold (IL-2 vs. EPO or GMCSF) selective in cellular reporter assays and >35-fold selective in human PBMC assays (IL-7 vs. IL-6 or GMCSF). Irreversible JAK3-IN-6 with a JAK1 selective inhibitor 3 (JAK1: 0.96 nM, JAK2: 14 nM, JAK3: >1500 nM, TYK2: 10 nM) are cross titrated to determine if there is an additive or synergistic effect of co-inhibiting JAK1 and JAK3 enzymes on IL-7 signaling in CD3+, CD4+ PBMCs. As shown, the predicted levels of pSTAT5 inhibition based on addition of JAK1 and JAK3 inhibition are very close to the measured effects of cross titrating each compound, demonstrating that there is an additive effect but no synergistic effect of inhibiting JAK1 and JAK3 on blocking STAT5 phosphorylation. Furthermore inhibition of either JAK1 or JAK3 alone is sufficient to fully inhibit pSTAT5[2].

Name: Ethylmalonic acid, CAS: 601-75-2, stock 35g, assay 98.5%, MWt: 132.11, Formula: C5H8O4, Solubility: 10 mM in H2O, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: Ethylmalonic acid is non-carcinogenic potentially toxic and associated with anorexia nervosa and malonyl-CoA decarboxylase deficiency.

Name: Selitrectinib LOXO-195, CAS: 2097002-61-2, stock 7.2g, assay 98.6%, MWt: 380.42, Formula: C20H21FN6O, Solubility: DMSO : 62.5 mg/mL (164.29 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Protein Tyrosine Kinase/RTK;Neuronal Signaling, Target: Trk Receptor;Trk Receptor, Biological_Activity: Selitrectinib (LOXO-195) is a next-generation TRK kinase inhibitor (TKI), with IC50s of 0.6 nM, <2.5 nM for TRKA and TRKC respectively.
IC50 & Target: 0.6 nM (TRKA), <2.5 nM (TRKC)[1].
In Vitro: Selitrectinib (LOXO-195) demonstrates strong binding to the wild-type TRKA, TRKB and TRKC kinase domains. Selitrectinib (LOXO-195) has potent (IC50<1 nM) inhibitory activity in kinase enzyme assays. Importantly, Selitrectinib (LOXO-195) achieves low nanomolar inhibitory activity against TRKA G595R, TRKC G623R, and TRKA G667C, with IC50s ranging from 2.0-9.8 nM. 228 individual kinases in vitro are profiled at a Selitrectinib (LOXO-195) concentration of 1 μM, which is ~1667-fold higher than its IC50 for TRKA (0.6 nM). Selitrectinib (LOXO-195) is more than 1000-fold selective for 98% of non-TRK kinases tested. Selitrectinib (LOXO-195) demonstrates potent inhibition of cell proliferation in TRK fusion-containing KM12, CUTO-3, and MO-91 cell lines (IC50≤5 nM)[1].
In Vivo: Stably transfected NIH-3T3 ΔTRKA and ΔTRKA-G595R cells are implanted subcutaneously into the flanks of nude mice. Both larotrectinib and Selitrectinib (LOXO-195) are effective at reducing phosphorylated TRKA in tumors driven by ΔTRKA. In contrast, only Selitrectinib (LOXO-195) strongly suppresses phospho-TRKA in ΔTRKA-G595R cells in a dose-dependent manner. Selitrectinib (LOXO-195) also causes inhibition of tumor growth relative to vehicle at all doses in four TRKA-dependent tumor models (ΔTRKA, ΔTRKA-G595R, ΔTRKAG667C, and TPM3-NTRK1 fusion-positive KM12 colorectal cancer cells. Larotrectinib inhibits KM12 and NIH 3T3-ΔTRKA tumors to a similar degree. Group mean body weight loss does not exceed 5% for any agent. Selitrectinib (LOXO-195) displays high selectivity for the TRK proteins[1]

Name: AZD4635 HTL1071, CAS: 1321514-06-0, stock 32.3g, assay 98.3%, MWt: 315.73, Formula: C15H11ClFN5, Solubility: DMSO : ≥ 83.3 mg/mL (263.83 mM); H2O : < 0.1 mg/mL (insoluble), Clinical_Informat: Phase 2, Pathway: GPCR/G Protein, Target: Adenosine Receptor, Biological_Activity: AZD4635 is a potent and selective, orally available adenosine A2A receptor (A2AR) antagonist. AZD4635 binds to human A2AR with a Ki of 1.7 nM and with > 30-fold selectivity over other adenosine receptors[1].
IC50 & Target: Ki: 1.7 nM (A2AR)
In Vitro: In the presence of 0.1, 1 and 10 μM adenosine, the IC50s of AZD4635 for inhibition of cAMP production are 0.79, 10.0 and 142.9 nM, respectively[1].

Name: Uridine 5'-monophosphate 5'-Uridylic acid, CAS: 58-97-9, stock 39.8g, assay 98.9%, MWt: 324.18, Formula: C9H13N2O9P, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: Uridine 5'-monophosphate (5'-Uridylic acid), a monophosphate form of UTP, can be acquired either from a de novo pathway or degradation products of nucleotides and nucleic acids in vivo and is a major nucleotide analogue in mammalian milk[1].

Name: Lys-SMCC-DM1 Lys-Nε-MCC-DM1, CAS: 1281816-04-3, stock 23.4g, assay 98.2%, MWt: 1103.71, Formula: C53H75ClN6O15S, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Antibody-drug Conjugate/ADC Related, Target: Drug-Linker Conjugates for ADC, Biological_Activity: Lys-SMCC-DM1 is the active metabolite of DM1. DM1 is a tubulin inhibitor.

Name: N6,N6-Dimethyladenosine, CAS: 2620-62-4, stock 15.4g, assay 98.8%, MWt: 295.29, Formula: C12H17N5O4, Solubility: DMSO : ≥ 125 mg/mL (423.31 mM), Clinical_Informat: No Development Reported, Pathway: Cell Cycle/DNA Damage, Target: Nucleoside Antimetabolite/Analog, Biological_Activity: N6,N6-Dimethyladenosine is a modified ribonucleoside previously found in rRNA, and also exhibits in mycobacterium bovis Bacille Calmette-Guérin tRNA[1].

Name: Prexasertib (Mesylate Hydrate) LY2606368 Mesylate Hydrate;LY2940930, CAS: 1234015-57-6, stock 1.5g, assay 98.4%, MWt: 479.51, Formula: C19H25N7O6S, Solubility: 10 mM in DMSO, Clinical_Informat: Phase 2, Pathway: Cell Cycle/DNA Damage, Target: Checkpoint Kinase (Chk), Biological_Activity: Prexasertib Mesylate Hydrate (LY2606368 Mesylate Hydrate) is a potent, selective, ATP competitive CHK1 and CHK2 inhibitor, with a Ki of 0.9 nM for CHK1 and IC50s of <1 nM, 8 nM for CHK1 and CHK2, respectively. Prexasertib Mesylate Hydrate inhibits HT-29 CHK1 autophosphorylation (S296) and HT-29 CHK2 autophosphorylation (S516). Prexasertib Mesylate Hydrate shows potent anti-tumor activity, significantly abrogates the G2/M checkpoint in p53 deficient HeLa cells with an EC50 of 9 nM[1].
IC50 & Target: Ki: 0.9 nM (CHK1)[1] 
IC50: <1 nM (CHK1), 8 nM (CHK2)[1]
In Vitro: Prexasertib Mesylate Hydrate (LY2606368 Mesylate Hydrate) is an ATP competitive CHK1 inhibitor, with a Ki of 0.9 nM and an IC50 of <1 nM[1]. 
Prexasertib (LY2606368) shows high anti-tumor activity against U-2 OS, Calu-6 and HeLa cells (IC50, 3, 3, 37 nM, respectively), causes DNA damage during S-phase requiring CDC25A and CDK2 at 4 μM[1]. 
Prexasertib (0-20 nM) synergizes with olaparib (0-20 μM) to decrease cell viability in HGSOC cells[2].

Name: BIIE-0246 AR-H 053591, CAS: 246146-55-4, stock 5.4g, assay 98.8%, MWt: 896.05, Formula: C49H57N11O6, Solubility: DMSO : 100 mg/mL (111.60 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein;Neuronal Signaling, Target: Neuropeptide Y Receptor;Neuropeptide Y Receptor, Biological_Activity: BIIE-0246 is a potent and highly selective non-peptide neuropeptide Y (NPY) Y2 receptor antagonist, with an IC50 of 15 nM.
IC50 & Target: IC50: 15 nM (NPYY2 receptor)[1].
In Vitro: Receptor binding assays in HEK 293 cells transfected with the rat Y2 receptor cDNA demonstrate that BIIE-0246 competes with high affinity (IC50=15±3 nM) against specific [125I]PYY3-36 binding sites. In contrast, BIIE-0246, at concentrations up to 10 μM, fails to compete for significant amounts of specific [125I]GR231118, [125I]hPP and [125I][Leu31, Pro34]PYY binding sites in HEK 293 cells transfected with the rat Y1, Y4 or Y5 receptor cDNA, respectively[1].
In Vivo: On chow diet, genetically obese NPY mice show increased gain in body weight and adiposity. Treatment with BIIE-0246 promotes body weight gain in both genotypes after 4.5 weeks, and already at 2 weeks. BIIE-0246 has no significant effect on fat mass gain. In DIO, BIIE-0246 has different effects on body weight and composition depending on the genotype (treatment×genotype interaction in body weight P<0.05, in fat mass P<0.001 and in lean mass P<0.05). In DIO-WT group, post hoc analysis reveals increased body weight and fat mass gain, and a tendency to decrease lean mass gain. In DIO-NPY, BIIE-0246 inhibits fat mass gain (P=0.05). Interestingly, increased cholesterol levels are detected also in WT mice treated with BIIE-0246 for 2 weeks, but not in the 4.5-week cohort. In DIO-NPY mice in both treatment groups, cholesterol levels correlate positively with body fat mass (DIO-NPY vehicle P<0.01; DIO-NPY BIIE-0246 P<0.001), but not in any other group, and the slope of the regression curve of cholesterol and fat mass is significantly decreased in BIIE-0246-treated DIO-NPY group when compared with vehicle-treated group[2].

Name: Rilapladib SB 659032, CAS: 412950-08-4, stock 6.3g, assay 98.3%, MWt: 735.81, Formula: C40H38F5N3O3S, Solubility: H2O : < 0.1 mg/mL (insoluble); DMSO : 86.67 mg/mL (117.79 mM; Need ultrasonic), Clinical_Informat: Phase 2, Pathway: Metabolic Enzyme/Protease, Target: Phosphatase, Biological_Activity: Rilapladib is a selective Lipoprotein-Associated Phospholipase A2 (Lp-PLA2) inhibitor with an IC50 of 230 pM.
IC50 & Target: IC50: 230 pM (Lp-PLA2)[1].

Name: Gamitrinib TPP, CAS: 1131626-46-4, stock 13.8g, assay 98.1%, MWt: 891.06, Formula: C52H65N3O8P, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Gamitrinib TPP is a GA mitochondrial matrix inhibitor. Gamitrinib TPP is offered as the hexafluorophosphate salt (Cat# HY-102007A).
IC50 & Target: GA mitochondrial matrix[1].
In Vitro: Within a 16-hour exposure, concentrations of Gamitrinib TPP of 15-20 μM indistinguishably kill patient-derived and cultured glioblastoma cell lines. This cell death response has the hallmarks of mitochondrial apoptosis, with loss of organelle inner membrane potential, release of cytochrome c in the cytosol, activation of initiator caspase-9 and effector caspase-3 and -7, and cellular reactivity for annexin V. Because Hsp90s are selectively present in mitochondria of tumor cells, but not normal tissues, Gamitrinib TPP does not kill normal fetal human astrocytes (FHAS). Under comparable conditions, nonsubcellularly targeted 17-AAG has no effect on normal or tumor cells[1].
In Vivo: Interestingly, 2 cycles of intracranial TRAIL combined with systemic G-TPP suppress the growth of established glioblastomas, with no significant animal weight loss throughout treatment. Analysis of brain sections from these mice, but not single agent-treated animals, show loss of tumor cell proliferation, internucleosomal DNA fragmentation, and caspase-3 activity, consistent with extensive activation of apoptosis in vivo[1].

Name: BMS-1166, CAS: 1818314-88-3, stock 18.6g, assay 98.7%, MWt: 641.11, Formula: C36H33ClN2O7, Solubility: DMSO : 125 mg/mL (194.97 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Immunology/Inflammation, Target: PD-1/PD-L1, Biological_Activity: BMS-1166 is a potent PD-1/PD-L1 interaction inhibitor with an IC50 of 1.4 nM. BMS-1166 antagonizes the inhibitory effect of PD-1/PD-L1 immune checkpoint on T cell activation.
IC50 & Target: IC50: 1.4 nM (PD-1/PD-L1 interaction)[1].
In Vitro: BMS-1166 is a potent PD-1/PD-L1 interaction inhibitor with an IC50 of 1.4 nM in a homogenous time-resolved fluorescence binding assay[1]. BMS-1166 antagonizes the inhibitory effect of PD-1/PD-L1 immune checkpoint on T cell activation. BMS-1166 dose dependently abolishes the inhibition of ECs stimulation by sPD-L1[2].

Name: Chelerythrine, CAS: 34316-15-9, stock 23.8g, assay 98.7%, MWt: 348.37, Formula: C21H18NO4, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Apoptosis;TGF-beta/Smad;Epigenetics;Autophagy;Apoptosis, Target: Apoptosis;PKC;PKC;Autophagy;Bcl-2 Family, Biological_Activity: Chelerythrine is a natural alkaloid, acts as a potent and selective Ca2+/phospholopid-dependent PKC antagonist, with an IC50 of 0.7 μM[1]. Chelerythrine has antitumor, antidiabetic and anti-inflammatory activity[2]. Chelerythrine inhibits the BclXL-Bak BH3 peptide binding with IC50 of 1.5 μM and displaces Bax from BclXL. Chelerythrine triggers apoptosis and autophagy[3][4].

Name: Hinokiflavone, CAS: 19202-36-9, stock 7.5g, assay 98.7%, MWt: 538.46, Formula: C30H18O10, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: E1/E2/E3 Enzyme, Biological_Activity: Hinokiflavone is a novel modulator of pre-mRNA splicing activity in vitro and in cellulo. Hinokiflavone blocks splicing of pre-mRNA substrates by inhibiting spliceosome assembly, specifically preventing B complex formation. Hinokiflavone is a SUMO protease inhibitor, inhibiting sentrin-specific protease 1 (SENP1) activity[1].

Name: N-Benzylpalmitamide N-Benzylhexadecanamide;Macamide 1, CAS: 74058-71-2, stock 6.5g, assay 98.7%, MWt: 345.56, Formula: C23H39NO, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Neuronal Signaling;Metabolic Enzyme/Protease;Autophagy, Target: FAAH;FAAH;Autophagy, Biological_Activity: N-Benzylpalmitamide is a macamide isolated from Lepidium meyenii, acts as an inhibitor of fatty acid amide hydrolase (FAAH).
IC50 & Target: FAAH[1]
In Vitro: N-Benzylpalmitamide is an inhibitor of fatty acid amide hydrolase (FAAH), and shows 24.8% and 43.8% inhibition on FAAH at 10 μM and 500 μM, respectively[1].

Name: Chelidonine, CAS: 476-32-4, stock 19.5g, assay 98%, MWt: 353.37, Formula: C20H19NO5, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Apoptosis, Target: Apoptosis, Biological_Activity: Chelidonine is an isoquinoline alkaloid isolated from Chelidonium majus L., causes G2/M arrest and induces caspase-dependent and caspase-independent apoptosis, with anticancer and antiviral activity[1].

Name: Fraxinol, CAS: 486-28-2, stock 22.6g, assay 98.2%, MWt: 222.19, Formula: C11H10O5, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Cytochrome P450, Biological_Activity: Fraxinol is isolated from Lobelia chinensis[1].

Name: Eupatorin, CAS: 855-96-9, stock 29.6g, assay 98.1%, MWt: 344.32, Formula: C18H16O7, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Eupatorin, a naturally occurring flavone, arrests cells at the G2-M phase of the cell cycle and induces apoptotic cell death involving activation of multiple caspases, mitochondrial release of cytochrome c and poly(ADP-ribose) polymerase cleavage[1].

Name: L-Quebrachitol, CAS: 642-38-6, stock 9.5g, assay 98.9%, MWt: 194.18, Formula: C7H14O6, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Stem Cell/Wnt;Stem Cell/Wnt, Target: β-catenin;Wnt, Biological_Activity: L-Quebrachitol is a natural product isolated from many plants, promotes osteoblastogenesis by uppregulation of BMP-2, runt-related transcription factor-2 (Runx2), MAPK (ERK, JNK, p38α), and Wnt/β-catenin signaling pathway[1].

Name: Chrysin-7-O-glucuronide, CAS: 35775-49-6, stock 17g, assay 98.5%, MWt: 430.36, Formula: C21H18O10, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Chrysin-7-O-glucuronide is a flavonoid extracted from Scutellaria baicalensis, with antioxidant activity[1].

Name: N-Benzoyl-(2R,3S)-3-phenylisoserine, CAS: 132201-33-3, stock 27.3g, assay 98.1%, MWt: 285.29, Formula: C16H15NO4, Solubility: DMSO : ≥ 160 mg/mL (560.83 mM), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: N-Benzoyl-(2R,3S)-3-phenylisoserine is a Taxol C-13 Side Chain and crucial for the strong antitumor activity of Taxol[1].

Name: Kalii Dehydrographolidi Succinas Potassium dehydroandrographolide succinate, CAS: 76958-99-1, stock 26.6g, assay 98.9%, MWt: 571.68, Formula: C28H36KO10, Solubility: 10 mM in DMSO, Clinical_Informat: Launched, Pathway: Others, Target: Others, Biological_Activity: Kalii Dehydrographolidi Succinas (Potassium dehydroandrographolide succinate), extracted from herbal medicine Andrographis paniculata (Burm f) Nees, is widely used for the treatment of viral pneumonia and viral upper respiratory tract infections because of its immunostimulatory, anti-infective and anti-inflammatory effect[1][2].

Name: Febrifugine, CAS: 24159-07-7, stock 16.7g, assay 98.8%, MWt: 301.34, Formula: C16H19N3O3, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Febrifugine is a quinazolinone alkaloid found in the roots and leaves of Dichroa febrifuga, with antimalarial activity [1].

Name: Pinosylvin, CAS: 22139-77-1, stock 5.5g, assay 99%, MWt: 212.24, Formula: C14H12O2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Apoptosis;Anti-infection;Autophagy, Target: Apoptosis;Bacterial;Autophagy, Biological_Activity: Pinosylvin is a pre-infectious stilbenoid toxin isolated from the heartwood of Pinus spp, has anti-bacterial activities[1]. Pinosylvin is a resveratrol analogue, can induce cell apoptosis and autophapy in leukemia cells[2].
In Vitro: Pinosylvin (0-100 μM; 24 hours) is cytotoxic to THP‐1 and U937 cells, exhibits an IC50 value of 20-30 μM in leukemia cells, the maximal cytotoxic effect occurred at 100 μM following incubation for 24 hr[3].
Pinosylvin (0-100 μM; 24 hours) enhances the number of annexin V+ and PI+ cells in the U937 population at 50 μM, increases annexin V+ and PI+ cells in the THP‐1 population at 100 μM[3].
Pinosylvin (0-100 μM; 24 hours) promotes autophagy in leukemia cells by enhancing the level of LC3‐II and p62/SQSTM1 degradation in leukemia cells[3].
In Vivo: Pinosylvin (intravenous injection; 10 mg/kg) yields the plasma AUC, urine t , CL and Vd values of 5.23 ± 1.20 mgh mL-1, 13.13 ± 2.05 h, 1.84 ± 0.44 Lh-1kg-1 and 2.29 Lkg-1, respectively in male Sprague-Dawley rats, in a PK study[1].

Name: Auraptene, CAS: 495-02-3, stock 26g, assay 98.3%, MWt: 298.38, Formula: C19H22O3, Solubility: DMSO : 125 mg/mL (418.93 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: MMP, Biological_Activity: Auraptene is the most abundant naturally occurring geranyloxycoumarin. Auraptene is primarily isolated from plants in the Rutaceae family, such as citrus fruits. Auraptene decreases the secretion of matrix metalloproteinase 2 (MMP-2) as well as key inflammatory mediators, including IL-6, IL-8, and chemokine (C-C motif) ligand-5(CCL5)[1].

Name: Formosanin C, CAS: 50773-42-7, stock 21.4g, assay 98.8%, MWt: 1015.18, Formula: C51H82O20, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Apoptosis, Target: Apoptosis, Biological_Activity: Formosanin C is a diosgenin saponin isolated from Paris formosana Hayata and an immunomodulator with antitumor activity. Formosanin C induces apoptosis[1][2].

Name: Kukoamine A, CAS: 75288-96-9, stock 6.2g, assay 98.8%, MWt: 530.66, Formula: C28H42N4O6, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Kukoamine A is a natural occurring spermine derivative, acts as a potent inhibitor of trypanothione reductase (Ki, 1.8 μM), with antihypertensive activity[1].
IC50 & Target: Ki: 1.8 μM (Trypanothione reductase)[1]

Name: Kukoamine B, CAS: 164991-67-7, stock 5.5g, assay 98.5%, MWt: 530.66, Formula: C28H42N4O6, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Kukoamine B is a component of Lycii Cortex, with anti-oxidant, anti-acute inflammatory and anti-diabetic properties[1].

Name: N-(3-Methoxybenzyl-(9z,12z)-octadecadienamide, CAS: 883715-22-8, stock 33.3g, assay 98.5%, MWt: 399.61, Formula: C26H41NO2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: N-(3-Methoxybenzyl-(9z,12z)-octadecadienamide (Macamide impurity 10), the impurity of Macamide isolated from Lepidium meyenii.

Name: 9''-Methyl salvianolate B, CAS: 1167424-31-8, stock 28g, assay 98.7%, MWt: 732.64, Formula: C37H32O16, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: 9''-Methyl salvianolate B is a phenolic compound isolated from Radix Salvia miltiorrhizae[1].

Name: Dihydrolycorine, CAS: 6271-21-2, stock 11.1g, assay 98.4%, MWt: 289.33, Formula: C16H19NO4, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Dihydrolycorine is isolated from Lycoris radiate Herb with antihypertensive and neuroprotective activities[1]. Dihydrolycorine is an inhibitor of protein synthesis in eukarytic cells by inhibiting the peptide bone formation step[2].
IC50 & Target: Protein synthesis[2]
In Vivo: Dihydrolycorine reduces infarct size, cerebral edema, and myeloperoxidase activity in a rat model of focal cerebral ischemia-reperfusion injury when administered following reperfusion[1].
Dihydrolycorine inhibits methoxamine-induced contraction of isolated rabbit aortic rings and rat anococcygeus muscle with pA2 values of 5.93 and 6.35, respectively[3].

Name: β,β-Dimethylacrylshikonin, CAS: 24502-79-2, stock 9.7g, assay 98.5%, MWt: 370.40, Formula: C21H22O6, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: β,β-Dimethylacrylshikonin is a naphthoquinone derivative isolated from Arnebia nobilis, promotes angiogenesis by inducing eNOS, VEGF and HIF-1α expression through the PI3K-dependent pathway. Arnebin 1 has anti-tumor activity[1].

Name: Dihydrocaffeic acid 3,4-Dihydroxy-benzenepropanoic acid, CAS: 1078-61-1, stock 28.8g, assay 98.4%, MWt: 182.17, Formula: C9H10O4, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: MAPK/ERK Pathway, Target: p38 MAPK, Biological_Activity: Dihydrocaffeic acid is a phenolic acid found in Gynura bicolor, reduces phosphorylation of MAPK p38 and prevent UVB-induced skin damage. Antioxidant potential and anti-inflammatory activity[1].
IC50 & Target: MAPK p38 phosphorylation[1]

Name: N-trans-Feruloyltyramine N-feruloyltyramine; Moupinamide, CAS: 66648-43-9, stock 24.6g, assay 98.7%, MWt: 313.35, Formula: C18H19NO4, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Immunology/Inflammation, Target: COX, Biological_Activity: N-trans-Feruloyltyramine (N-feruloyltyramine), an alkaloid from Piper nigru, is an inhibitor of COX1 and COX2, with potential antioxidant properties. N-trans-Feruloyltyramine possesses anti-inflammatory activity[1].

Name: Geissoschizine methyl ether, CAS: 60314-89-8, stock 34.7g, assay 98%, MWt: 366.45, Formula: C22H26N2O3, 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: Geissoschizine methyl ether, a major indole alkaloid found in Uncaria hook, is a major active component of Yokukansan with psychotropic effects. Geissoschizine methyl ether is potent 5-HT1A receptor agonist[1][2].
IC50 & Target: 5-HT1A[2]

Name: Gomisin D, CAS: 60546-10-3, stock 18.8g, assay 98.7%, MWt: 530.56, Formula: C28H34O10, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Gomisin D, a lignan compound isolated from Fructus Schisandra, is a potential antidiabetic and anti-Alzheimer’s agent. Gomisin D inhibits UDP-Glucuronosyltransferases activity and scavenges ABTS(+) radicals. Gomisin D is used as a quality marker of Shengmai San and shenqi Jiangtang Granule[1].
IC50 & Target: UDP-Glucuronosyltransferases[1]

Name: Taccalonolide A, CAS: 108885-68-3, stock 35.3g, assay 98.6%, MWt: 702.74, Formula: C36H46O14, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Cell Cycle/DNA Damage;Cytoskeleton;Apoptosis, Target: Microtubule/Tubulin;Microtubule/Tubulin;Apoptosis, Biological_Activity: Taccalonolide A is a microtubule stabilizer, which is a steroid isolated from Tacca chantrieri, with cytotoxic and antimalarial activities[1][2]. Taccalonolide A causes G2-M accumulation, Bcl-2 phosphorylation and initiation of apoptosis[1]. Taccalonolide A is effective in vitro against cell lines that overexpress P-glycoprotein (Pgp) and multidrug resistance protein 7 (MRP7), with an IC50 of 622 nM for SK-OV-3 cells[3].
IC50 & Target: microtubule[1]

Name: Dipotassium glycyrrhizinate, CAS: 68797-35-3, stock 13.3g, assay 98.8%, MWt: 861.02, Formula: C42H61KO16, Solubility: 10 mM in DMSO, Clinical_Informat: Launched, Pathway: Others, Target: Others, Biological_Activity: Dipotassium glycyrrhizinate is a natural compound, inhibits atopic dermatitis-related gene expression with anti-anti-inflammatory activity[1].

Name: LY 344864 racemate, CAS: 186543-64-6, stock 7.7g, assay 98.4%, MWt: 351.42, Formula: C21H22FN3O, 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: LY 344864 racemate is a 5-HT1F receptor agonist extracted from patent US 5708187 A.
IC50 & Target: 5-HT1F receptor[1]

Name: GNF351, CAS: 1227634-69-6, stock 2.9g, assay 98.6%, MWt: 411.50, Formula: C24H25N7, Solubility: DMSO : ≥ 125 mg/mL (303.77 mM); H2O : < 0.1 mg/mL (insoluble), Clinical_Informat: No Development Reported, Pathway: Immunology/Inflammation, Target: Aryl Hydrocarbon Receptor, Biological_Activity: GNF351 is a full aryl hydrocarbon receptor (AHR) antagonist. GNF351 competes with a photoaffinity AHR ligand for binding to the AHR with an IC50 of 62 nM. GNF351 is minimal toxicity in mouse or human keratinocytes[1].
IC50 & Target: IC50: 62 nM (aryl hydrocarbon receptor)[1]
In Vitro: GNF351 (500 nM, 48 hours) significantly reduces the percentage of Ki67-positive cells and cell number after treating proliferating monolayer cultures of human keratinocytes[1].

Name: Rhodiosin, CAS: 86831-54-1, stock 38.2g, assay 98.8%, MWt: 610.52, Formula: C27H30O16, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Neuronal Signaling, Target: AChE, Biological_Activity: Rhodiosin, isolated from the root of Rhodiola crenulata, is a specific non-competitive cytochrome P450 2D6 inhibitor with an IC50 of 0.420 μM and a Ki of 0.535 μM[1]. Rhodiosin exhibits potent, dose-dependent inhibitory effects on acetylcholinesterase (AChE) with IC50 ranged from 57.50 to 2.43 μg/mL[2]. Rhodiosin exhibits potent DPPH free radical scavenging activities, with an IC50 of 27.77 μM[3].
IC50 & Target: IC50: 0.420 μM (cytochrome P450 2D6)[1]；57.50-2.43 μg/mL (AChE)[2]；27.77 μM (DPPH free radical scavenging)[3]

Name: [10]-Shogaol, CAS: 36752-54-2, stock 7.7g, assay 98%, MWt: 332.48, Formula: C21H32O3, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Immunology/Inflammation, Target: COX, Biological_Activity: [10]-Shogaol is an antioxidant from Zingiber officinale for human skin cell growth and a migration enhancer. [10]-Shogaol inhibits COX-2 with an IC50 of 7.5 μM and has antiproliferation activity[1][2][3].
IC50 & Target: IC50: 7.5 μM (COX-2)[2]

Name: [8]-Shogaol, CAS: 36700-45-5, stock 13.7g, assay 98.2%, MWt: 304.42, Formula: C19H28O3, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Apoptosis;Immunology/Inflammation, Target: Apoptosis;COX, Biological_Activity: [8]-Shogaol, one of the pungent phenolic compounds in ginger, exhibits anti-platelet activity (IC50=5 μM) and inhibits COX-2 (IC50=17.5 μM). [8]-Shogaol induces apoptosis in human leukemia cells[1][2][3][4].

Name: Methylophiopogonanone B, CAS: 74805-91-7, stock 2.1g, assay 98.7%, MWt: 328.36, Formula: C19H20O5, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein, Target: Ras, Biological_Activity: Methylophiopogonanone B, homoisoflavonoid, is extracted from the root of Ophiopogon japonicas, shows high antioxidant ability[1]. Methylophiopogonanone B increases GTP-Rho and acts via the Rho signaling pathway, inducing cell morphological change via actin cytoskeletal reorganization, including dendrite retraction and stress fiber formation[2].

Name: Gypenoside A, CAS: 157752-01-7, stock 10.7g, assay 98.6%, MWt: 899.07, Formula: C46H74O17, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Gypenoside A is a natural compound isolaated from Gynostemma pentaphyllum Makino[1].

Name: Methylophiopogonone A, CAS: 74805-90-6, stock 0.3g, assay 98.6%, MWt: 340.33, Formula: C19H16O6, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Methylophiopogonone A, a homoisoflavonoid isolated from the tuberous roots of Ophiopogon japonicas, shows anti-inflammatory activity[1].

Name: Flavokawain C, CAS: 37308-75-1, stock 3.9g, assay 98.1%, MWt: 300.31, Formula: C17H16O5, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Apoptosis, Target: Apoptosis, Biological_Activity: Flavokawain C is a natural chalcone found in Kava root. Flavokawain C exerts cytotoxicity against human cancer cell lines, with an IC50 of 12.75 μM for HCT 116 cells[1].

Name: Amarogentin, CAS: 21018-84-8, stock 18.9g, assay 98.5%, MWt: 586.54, Formula: C29H30O13, Solubility: DMSO : 130 mg/mL (221.64 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Apoptosis;Epigenetics;PI3K/Akt/mTOR, Target: Apoptosis;AMPK;AMPK, Biological_Activity: Amarogentin is a secoiridoid glycoside that is mainly extracted from Swertia and Gentiana roots. Amarogentin exhibits many biological effects, including anti-oxidative, anti-tumour, and anti-diabetic activities. Amarogentin exerts hepatoprotective and immunomodulatory effects. Amarogentin promotes apoptosis, arrests G2/M cell cycle and downregulates of PI3K/Akt/mTOR signalling pathways. Amarogentin exerts beneficial vasculo-metabolic effect by activating AMPK[1][2][3].

Name: Aloe-emodin-8-O-β-D-glucopyranoside, CAS: 33037-46-6, stock 21g, assay 98.1%, MWt: 432.38, Formula: C21H20O10, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Phosphatase, Biological_Activity: Aloe-emodin-8-O-β-D-glucopyranoside, a compound isolated from Saussrurea lappa, is a moderate inhibitor of human protein tyrosine phosphatase 1B (hPTP1B) with an IC50 of 26.6 μM[1].
IC50 & Target: IC50：26.6 μM (hPTP1B)[1]

Name: Ganoderic acid G, CAS: 98665-22-6, stock 25g, assay 98.6%, MWt: 532.67, Formula: C30H44O8, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Ganoderic acid G is a triterpene isolated from the surface part of gills of Ganoderma lucidum[1].

Name: Aloesin Aloeresin, CAS: 30861-27-9, stock 9.4g, assay 98.5%, MWt: 394.37, Formula: C19H22O9, Solubility: DMSO : 270 mg/mL (684.64 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Aloesin (Aloeresin) is an active constituent of the herb aloe vera and displays anti-inflammatory activity, ultraviolet protection, and antibacterium effects. Aloesin exerts its anticancer effect through the MAPK signaling pathway[1][2].

Name: Maltotetraose Amylotetraose; Fujioligo 450; α-1,4-Tetraglucose, CAS: 34612-38-9, stock 38.4g, assay 99%, MWt: 666.58, Formula: C24H42O21, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: Maltotetraose can be used as a substrate for the enzyme-coupled determination of amylase activity in biological fluids.

Name: Xylotriose, CAS: 47592-59-6, stock 18.6g, assay 98.9%, MWt: 414.36, Formula: C15H26O13, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Xylotriose is a natural xylooligosaccharide, acts as a bifidogenic factor[1].

Name: Medicagenic acid Castanogenin, CAS: 599-07-5, stock 12.1g, assay 98.1%, MWt: 502.68, Formula: C30H46O6, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Anti-infection, Target: Bacterial, Biological_Activity: Medicagenic acid (Castanogenin) is isolated from the roots of Herniaria glabra L, exhibits potent fungistatic effects against several plant pathogens and human dermatophytes[1]. Medicagenic acid (Castanogenin) has low enzyme inhibitory activities, the target enzymes are xanthine oxidase, collagenase, elastase, tyrosinase, ChE[2].

Name: Methylnissolin-3-O-glucoside, CAS: 94367-42-7, stock 1.6g, assay 98.2%, MWt: 462.45, Formula: C23H26O10, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Methylnissolin-3-O-glucoside (Methylnissolin-3-O-β-D-glucoside) is a flavonoid from the roots of Astragalus membranaceus with anti-inflammatory effects[1].

Name: Hydroprotopine, CAS: 128397-41-1, stock 24.8g, assay 98%, MWt: 354.38, Formula: C20H20NO5+, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Hydroprotopine is a alkaloid from Hypecoum leptocarpumand. Leptopidine can suppress growth and induce cytotoxicity in breast cancer cells and that the cytotoxicity of leptopidine may be related to its inhibitory effect on fatty acid synthase expression[1].

Name: 4'-Methoxyresveratrol 4'-O-Methylresveratrol, CAS: 33626-08-3, stock 30.8g, assay 98%, MWt: 242.27, Formula: C15H14O3, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: 4'-Methoxyresveratrol (4'-O-Methylresveratrol) is a polyphenol derived from Dipterocarpaceae, with antiandrogenic, antifungal and anti-inflammatory activities. 4'-Methoxyresveratrol alleviates AGE-induced inflammation through suppressing RAGE-mediated MAPK/NF-κB signaling pathway and NLRP3 inflammasome activation[1].

Name: Desoxyrhaponticin, CAS: 30197-14-9, stock 5.5g, assay 98%, MWt: 404.41, Formula: C21H24O8, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Apoptosis;Metabolic Enzyme/Protease, Target: Apoptosis;Fatty Acid Synthase (FAS), Biological_Activity: Desoxyrhaponticin is a stilbene glycoside from the Tibetan nutritional food Rheum tanguticum Maxim. Desoxyrhaponticin is a Fatty acid synthase (FAS) inhibitor, and has apoptotic effect on human cancer cells[1].

Name: 5-Hydroxy-7-acetoxyflavone, CAS: 6674-40-4, stock 1.4g, assay 98.8%, MWt: 296.27, Formula: C17H12O5, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: 5-Hydroxy-7-acetoxyflavone, an active natural flavone derivative found in various plant sources, modulates several biological activities[1].

Name: Demethylsuberosin 7-Demethylsuberosin, CAS: 21422-04-8, stock 19.7g, assay 98.1%, MWt: 230.26, Formula: C14H14O3, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Demethylsuberosin (7-Demethylsuberosin) is a coumarin compound isolated from Angelica gigas Nakai, and has anti-inflammatory activity[1].

Name: Dehydrotrametenolic acid, CAS: 6879-05-6, stock 23g, assay 98.5%, MWt: 468.71, Formula: C31H48O3, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Apoptosis, Target: Caspase, Biological_Activity: Dehydrotrametenolic acid is a sterol isolated from the sclerotium of Poria cocos. Dehydrotrametenolic acid induces apoptosis through caspase-3 pathway. Dehydrotrametenolic acid has anti-tumor activity, anti-inflammatory, anti-diabetic effects[1].
In Vivo: Dehydrotrametenolic acid selectively inhibits the growth of H-ras transformed cells with a GI50 value of 40 μM[1].

Name: Glomeratose A, CAS: 202471-84-9, stock 9.4g, assay 98.7%, MWt: 562.52, Formula: C24H34O15, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Glomeratose A is a lactate dehydrogenase inhibitor, isolated from Polygala tenuifolia[1].
IC50 & Target: IC50: Lactate dehydrogenase[1]

Name: Dehydrotumulosic acid, CAS: 6754-16-1, stock 29.5g, assay 98.8%, MWt: 484.71, Formula: C31H48O4, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Dehydrotumulosic acid, one of the effective constituents of Poria cocos, was isolated from the chloroform-soluble material of ethanol extract of the fungus. Poria cocos, a popular Chinese medicinal herb of fungal origin, has been included in many combinations with other CM herbs for its traditionally claimed activities of inducing diuresis, excreting dampness, invigorating the spleen and tranquilizing the mind and its modern pharmacological use of modulating the immune system of the body[1].

Name: Deoxypodophyllotoxin, CAS: 19186-35-7, stock 39.8g, assay 98.3%, MWt: 398.41, Formula: C22H22O7, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Cell Cycle/DNA Damage;Cytoskeleton;Apoptosis;Autophagy, Target: Microtubule/Tubulin;Microtubule/Tubulin;Apoptosis;Autophagy, Biological_Activity: Deoxypodophyllotoxin (DPT), a derivative of podophyllotoxin, is a lignan with potent antimitotic, anti-inflammatory and antiviral properties isolated from rhizomes of Sinopodophullumhexandrum (Berberidaceae). Deoxypodophyllotoxin, targets the microtubule, has a major impact in oncology not only as anti-mitotics but also as potent inhibitors of angiogenesis[1]. Deoxypodophyllotoxin induces cell autophagy and apoptosis[2]. Deoxypodophyllotoxin evokes increase of intracellular Ca2+ concentrations in DRG neurons[3].
In Vitro: Deoxypodophyllotoxin (25-75 nM; 6-48 hours) increases the percentage of early apoptotic cell population from 2.05 to 5.62 and 18.49% for 24 h and 48 h, respectively[1].
Deoxypodophyllotoxin (25-75 nM; 6-48 hours) treats SGC-7901 cells arrested in G2/M phase in time- and dose- dependent manners[1].
Deoxypodophyllotoxin (25-75 nM; 6-48 hours) results in a remarkably time- and dose-dependent decrease in Cdc2 and Cdc25C expression levels and increases cyclin B1 within 6h, decreases PARP, Bcl-2 and caspase-3 activity[1].
In Vivo: Deoxypodophyllotoxin (intravenously injected; 5, 10, and 20 mg/kg; 3 times a week; 28 days) suppresses the tumors in a dose-dependent manner, the growth of tumors is inhibited by 22.19%, 47.91% and 50.93% with DPT at 5, 10 and 20 mg/kg, respectively[1].

Name: Ginsenoside F4, CAS: 181225-33-2, stock 35.7g, assay 98.5%, MWt: 767.00, Formula: C42H70O12, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Apoptosis;Metabolic Enzyme/Protease, Target: Apoptosis;MMP, Biological_Activity: Ginsenoside F4 (GF4), ginseng saponinis, isolated from notoginseng or red ginseng. Ginsenoside F4 (GF4) has inhibitory effect on human lymphocytoma JK cell by inducing its apoptosis[1].
Ginsenoside F4 (GF4) inhibits matrix metalloproteinase 13 (MMP 13) expression in IL-1β-treated chondrocytes and blocks cartilage breakdown in rabbit cartilage tissue culture, shows therapeutic potential for preventing cartilage collagen matrix breakdown in diseased tissues[2].

Name: 1-Monomyristin, CAS: 589-68-4, stock 1g, assay 98.1%, MWt: 302.45, Formula: C17H34O4, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Anti-infection;Neuronal Signaling;Metabolic Enzyme/Protease;Anti-infection;Autophagy;Metabolic Enzyme/Protease, Target: Fungal;FAAH;FAAH;Bacterial;Autophagy;Endogenous Metabolite, Biological_Activity: 1-Monomyristin, extracted from Serenoa repens, inhibits the hydrolysis of 2-oleoylglycerol (IC50=32 μM) and fatty acid amide hydrolase (FAAH) activity (IC50=18 μM). 1-Monomyristin shows antibacterial activity against Staphylococcus aureus and Aggregatibacter actinomycetemcomitans and also antifungal activity against Candida albicans[1][2][3].
IC50 & Target: IC50: 18 μM (FAAH)[2]

Name: β-Boswellic acid, CAS: 631-69-6, stock 11.1g, assay 98.5%, MWt: 456.70, Formula: C30H48O3, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease;Cell Cycle/DNA Damage, Target: Lipoxygenase;DNA/RNA Synthesis, Biological_Activity: β-Boswellic acid is isolated from the gum resin of Boswellia serrate.
β-Boswellic acid is a nonreducing-type inhibitor of the 5-lipoxygenase (5-LO) product formation either interacting directly with the 5-LO or blocking its translocation[1]. β-Boswellic acid inhibits the synthesis of DNA, RNA and protein in human leukemia HL-60 cells[2].

Name: Ginsenoside Rk1, CAS: 494753-69-4, stock 21.9g, assay 98.1%, MWt: 767.00, Formula: C42H70O12, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: PI3K/Akt/mTOR;Apoptosis;Epigenetics;Stem Cell/Wnt;JAK/STAT Signaling;NF-κB, Target: PI3K;Apoptosis;JAK;JAK;JAK;NF-κB, Biological_Activity: Ginsenoside Rk1 is a unique component created by processing the ginseng plant (mainly Sung Ginseng, SG) at high temperatures[1].
Ginsenoside Rk1 has anti-inflammatory effect, suppresses the activation of Jak2/Stat3 signaling pathway and NF-κB[2].
Ginsenoside Rk1 has anti-tumor effect, antiplatelet aggregation activities, anti-insulin resistance, nephroprotective effect, antimicrobial effect, cognitive function enhancement, lipid accumulation reduction and prevents osteoporosis[1].
Ginsenoside Rk1 induces cell apoptosis by triggering intracellular reactive oxygen species (ROS) generation and blocking PI3K/Akt pathway[3].
In Vitro: Ginsenoside Rk1 (0-40 μM; 6 hours) inhibits MCP-1 and TNF-α mRNA induced by lipopolysaccharide (LPS), expression of IL-1β is inhibited at 40 μM[2].
Ginsenoside Rk1 (0-40 μM; 24 hours) inhibits phosphorylation of JAK2 and STAT3 (Tyr705 and Ser727) in LPS-induced RAW264.7 cells in a dose-dependent manner[2].
Ginsenoside Rk1 (0-160 μM; 48 hours) results in cell viability significant decrease 75.52 ± 2.51% (40 μM), 52.72 ± 2.54% (80 μM), 17.41 ± 2.94% (120 μM)and 12.63 ± 3.24% (160 μM) compared with control[3].
Ginsenoside Rk1 (0-120 μM; 24 hours) increases G0/G1 phase proportion accompanied with S and G2/M phase proportion decrease in MDA-MB-231 cells[3].
Ginsenoside Rk1 (0-120 μM; 24 hours) promotes the percentage of apoptotic cells in a dose-dependent manner, exhibits to reduction of cell number with nucleus fragmentation, condensation and apoptotic body formation[3].

Name: Agnuside Agnoside, CAS: 11027-63-7, stock 31.9g, assay 98.7%, MWt: 466.44, Formula: C22H26O11, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein, Target: Prostaglandin Receptor, Biological_Activity: Agnuside is a compound isolated from Vitex negundo, down-regulates pro-inflammatory mediators PGE2 and LTB4, and reduces the expression of cytokines, with anti-arthritic activity[1].

Name: Carboxyatractyloside (dipotassium) Gummiferin (dipotassium), CAS: 33286-30-5, stock 11.2g, assay 98.7%, MWt: 847.00, Formula: C31H44K2O18S2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Carboxyatractyloside dipotassium is a toxic natural product, acts as an inhibitor of ADP/ATP carrier, inhibits mitochondrial ADP/ATP transport[1].

Name: Gigantol, CAS: 67884-30-4, stock 14.3g, assay 98.3%, MWt: 274.31, Formula: C16H18O4, Solubility: DMSO : ≥ 160 mg/mL (583.28 mM), Clinical_Informat: No Development Reported, Pathway: Stem Cell/Wnt, Target: Wnt, Biological_Activity: Gigantol is a bibenzyl compound derived from several medicinal orchids. Giganto shows promising therapeutic potential against cancer cells. Gigantol is a novel inhibitor of the Wnt/β-catenin pathway.
IC50 & Target: Wnt[1]
In Vitro: Gigantol decreases the level of phosphorylated LRP6 and cytosolic β-catenin in HEK293 cells. In breast cancer MDA-MB-231 and MDA-MB-468 cells, treatment with gigantol reduces the level of phosphorylated LRP6[1]. Gigantol significantly inhibits the proliferation and induces apoptosis of the HepG2 cells. Gigantol at concentrations of 1, 40 and 150 µM markedly decreases the cell viability by 11.7, 30.0 and 56.4% at 24 h and 21.1, 66.8 and 85.5% at 48 h, respectively. The IC50 value is 9.30 µM[2].
In Vivo: LDD and gigantol (25–100 mg/kg, p.o.) significantly increase the hot-plate latency in comparison to vehicle-treated mice and decreased carrageenaninduced inflammation in rats[2].

Name: Camelliaside A, CAS: 135095-52-2, stock 32.1g, assay 98.7%, MWt: 756.66, Formula: C33H40O20, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Camelliaside A is a flavonoid from the methanol extract of tea (Camellia oleifera) seed pomace[1].

Name: Nervonic acid Selacholeic acid; cis-15-Tetracosenoic acid, CAS: 506-37-6, stock 30.2g, assay 98.9%, MWt: 366.62, Formula: C24H46O2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: Nervonic acid is a monounsaturated fatty acid important in the biosynthesis of myelin.

Name: Notoginsenoside Fa, CAS: 88100-04-3, stock 11g, assay 98.6%, MWt: 1241.41, Formula: C59H100O27, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Notoginsenoside Fa, a protopanaxadiol (ppd)-type saponin isolated from P. notoginseng, could possibly activate and recover the function of degenerated brain[1][2].

Name: Coniferaldehyde Ferulaldehyde, CAS: 458-36-6, stock 14.1g, assay 98.4%, MWt: 178.18, Formula: C10H10O3, Solubility: DMSO : 120 mg/mL (673.48 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Coniferaldehyde (Ferulaldehyde), isolated from the ethanol extract of Vitex rotundifolia fruits, is an effective inducer of heme oxygenase-1 (HO-1). Coniferaldehyde exerts anti-inflammatory properties in response to LPS. Coniferaldehyde inhibits LPS-induced apoptosis through the PKCα/β II/Nrf-2/HO-1 dependent pathway in RAW264.7 macrophage cells[1].

Name: Complement factor D-IN-1, CAS: 1386455-76-0, stock 9.6g, assay 98%, MWt: 483.32, Formula: C21H19BrN6O3, Solubility: DMSO : 250 mg/mL (517.26 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Complement factor D-IN-1 is a potent and selective small-molecule reversible factor d inhibitor, with IC50s of 0.006 and 0.05 μM in FD Thioesterolytic Fluorescent Assay and a MAC Deposition Assay, respectively.
IC50 & Target: IC50: 0.006 μM (FD), 0.05 μM (MAC)[1]
In Vitro: The highly specific S1 serine protease factor D (FD) plays a central role in the amplification of the complement alternative pathway (AP) of the innate immune system. Complement factor D-IN-1 (compound 2) shows similar potency against human and monkey FD (IC50s in FD thioesterolytic assays of 0.005 μM and in 50% serum MAC deposition assays of 0.011 μM for both human and monkey)[1].
In Vivo: Complement factor D-IN-1 displays an excellent oral PK profile in Sprague–Dawley rats and, following an oral dose (10 mg/kg) in Brown Norway rats, demonstrates a good distribution and sustained exposure in ocular tissues including the neural retina and the posterior eye cup (PEC), which comprises the sclera, retinal pigmented epithelium, and choroid. Mean exposure levels in plasma, the PEC, and the retina at 6 h after dosing are 0.36, 0.43, and 0.09 μM, respectively[1].

Name: SSTR5 antagonist 1, CAS: 1628741-91-2, stock 4.5g, assay 98.2%, MWt: 511.59, Formula: C28H34FN3O5, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein;Neuronal Signaling, Target: Somatostatin Receptor;Somatostatin Receptor, Biological_Activity: SSTR5 antagonist 1 is a potent, selective, and orally available somatostatin receptor subtype 5 (SSTR5) antagonist with IC50s of 9.6 and 57 nM for hSSTR5 and mSSTR5, respectively. (Compound 25a)[1]
IC50 & Target: IC50: 9.6 nM (hSSTR5), 57 nM (mSSTR5)[1]

Name: FM381, CAS: 2226521-65-7, stock 15.3g, assay 98%, MWt: 428.49, Formula: C24H24N6O2, Solubility: DMSO : 12.8 mg/mL (29.87 mM; Need ultrasonic and warming), Clinical_Informat: No Development Reported, Pathway: Epigenetics;Stem Cell/Wnt;JAK/STAT Signaling, Target: JAK;JAK;JAK, Biological_Activity: FM381 is a potent covalent reversible inhibitor of JAK3 targeting the unique Cys909 at the gatekeeper position +7 in JAK3. FM-381 has an IC50 of 127 pM for JAK3, with 410, 2700 and 3600-fold selectivity over JAK1, JAK2 and TYK2, respectively.
IC50 & Target: IC50: 127 pM (JAK3)[1]
In Vitro: FM381 is screened against a panel of 410 kinases at concentrations of 100 nM and 500 nM. FM381 has no relevant effect on the activity of any tested kinases except JAK3 at a concentration of 100 nM. At 500 nM, FM381 moderately inhibits 11 other kinases besides JAK3 with residual activities below 50%. FM-381 is found to be inactive in a selectivity panel of frequently hit BRDs (BRD4, BRPF, CECR, FALZ, TAF1, BRD9). Strongest hits is 500 nM for TAF1@2. FM381 selectively Inhibit JAK3 Signaling in Human CD4+ T Cells. FM-381 shows an apparent EC50 of 100 nM in a dose dependent BRET assay and blocks IL2 stimulated (JAK3/JAK1 dependent) STAT5 phosphorylation at 100 nM, but not JAK3 independent IL6 (JAK1/2/TYK dependent) stimulated STAT3 signalling in Human CD4+ T cells up to 1 µM[1].

Name: KDOAM-25, CAS: 2230731-99-2, stock 18.7g, assay 98.6%, MWt: 307.39, Formula: C15H25N5O2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Epigenetics, Target: Histone Demethylase, Biological_Activity: KDOAM-25 is a potent and highly selective KDM5 sub-family of histone lysine demethylases inhibitor with IC50s of 71 nM, 19 nM, 69 nM, 69 nM for KDM5A, KDM5B, KDM5C, KDM5D, respectively. KDOAM-25 increases global H3K4 methylation at transcriptional start sites and impairs proliferation in multiple myeloma MM1S cells[1].
IC50 & Target: IC50: 71 nM (KDM5A), 19 nM (KDM5B), 69 nM (KDM5C), 69 nM (KDM5D)[1]

Name: PF-05085727, CAS: 1415637-72-7, stock 37.5g, assay 98.5%, MWt: 413.40, Formula: C20H18F3N7, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Phosphodiesterase (PDE), Biological_Activity: PF-05085727 is a potent, selective and brain penetrant Phosphodiesterase 2A (PDE2A) inhibitor with an IC50 of 2 nM.
IC50 & Target: IC50: 2 nM (PDE2A)[1]

Name: Peptide YY (PYY) (3-36), human Peptide YY (3-36), CAS: 126339-09-1, stock 0.3g, assay 98.4%, MWt: 3980.42, Formula: C176H272N52O54, Solubility: H2O, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Peptide YY (PYY) (3-36), human is a gut hormone peptide that acts as a Y2 receptor agonist to reduce appetite.
IC50 & Target: Y2 receptor[1]
In Vitro: Peptide YY (PYY) (3-36), human is a Y2 receptor agonist, generated via cleaving the first two amino acids at the N terminus of PYY1-36 by enzyme dipeptidyl peptidase-IV (DPP-IV), and can reduces food intake[1].
In Vivo: In mice, actinonin significantly prolongs the anorectic effect of PYY3-36 (50 nmol/kg) and maintains higher PYY3-36 plasma levels than treatment with PYY3-36 alone[1].

Name: Apimostinel NRX-1074;AGN-241660, CAS: 1421866-48-9, stock 21.6g, assay 98.1%, MWt: 503.59, Formula: C25H37N5O6, Solubility: DMSO : 155 mg/mL (307.79 mM; Need ultrasonic), Clinical_Informat: Phase 2, Pathway: Membrane Transporter/Ion Channel;Neuronal Signaling, Target: iGluR;iGluR, Biological_Activity: Apimostinel (NRX-1074; AGN-241660) is an orally active NMDA receptor partial agonist.
In Vitro: Apimostinel (NRX-1074) modulates the NMDA receptor in a similar fashion to GLYX-13, but has a synthetic modification to one of the amino acids, conferring increased potency and oral bioavailability[1].
In Vivo: In preclinical models the two compounds both appear to be highly efficacious across a number of CNS disorders[1].

Name: HSL-IN-2, CAS: 654059-21-9, stock 25.7g, assay 98.3%, MWt: 266.34, Formula: C14H22N2O3, Solubility: DMSO : 250 mg/mL (938.65 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: HSL-IN-2 is a potent and selective inhibitor of Hormone Sensitive Lipase (HSL), with an IC50 of 0.023 μM.
IC50 & Target: IC50: 0.023 μM (HSL)[1].

Name: WM-1119, CAS: 2055397-28-7, stock 15.7g, assay 99%, MWt: 389.38, Formula: C18H13F2N3O3S, Solubility: DMSO : ≥ 150 mg/mL (385.23 mM), Clinical_Informat: No Development Reported, Pathway: Epigenetics, Target: Histone Acetyltransferase, Biological_Activity: WM-1119 is a highly potent and selective KAT6A inhibitor, with an IC50 of 0.25 μM for KAT6A in lymphoma cells, the binding KD values of WM-1119 with KAT6A, KAT5 and KAT7 are 2 nM, 2.2 μM, 0.5 μM , respectively.
IC50 & Target: IC50: 0.25 μM (KAT6A in lymphoma cells), KD: 2 nM (KAT6A), 2.2 μM (KAT5), 0.5 μM (KAT7)[1].
In Vitro: WM-1119 induces cell cycle exit and cellular senescence without causing DNA damage. WM-1119 is 1,100-fold and 250-fold more active against KAT6A than against KAT5 or KAT7, respectively, and so shows greater specificity for KAT6A than does WM-8014. Treatment of MEFs with WM-1119 results in cell cycle arrest in G1 and a senescence phenotype similar to that seen upon treatment with WM-8014. Notably, the activity of WM-1119 in this cell-based assay is an order of magnitude greater than WM-8014 and WM-1119 is able to induce cell cycle arrest at 1 μM. Treatment with WM-1119 inhibits the proliferation of the EMRK1184 lymphoma cells in vitro, WM-1119 (IC50=0.25 μM) is ninefold more active than WM-8014 (IC50=2.3 μM), as expected on the basis of reduced protein binding[1].
In Vivo: By day 14, the cohorts that are treated four times per day with WM-1119 have arrested tumour growth, with the exception of one mouse that does not respond. Spleen weights in the WM-1119-treatment group (treated four times per day) are substantially lower than spleen weights in the vehicle-treated group. Treatment with WM-1119 three times per day leads to a significant reduction in tumour burden and spleen weight, but is not as effective as treatment four times per day. WM-1119 is well-tolerated; mice show no generalized ill effects and weight loss is not observed. The proportion and overall number of tumour cells is substantially reduced by WM-1119 treatment (four times per day)[1].

Name: WM-8014, CAS: 2055397-18-5, stock 3.2g, assay 98.9%, MWt: 384.42, Formula: C20H17FN2O3S, Solubility: DMSO : ≥ 250 mg/mL (650.33 mM), Clinical_Informat: No Development Reported, Pathway: Epigenetics, Target: Histone Acetyltransferase, Biological_Activity: WM-8014 is an inhibitor of MOZ, a member of histone acetyltransferases, with an IC50 of 55 nM.
IC50 & Target: IC50: 55 nM (MOZ)[1]
In Vitro: WM-8014 (Compound 36) is an inhibitor of MOZ, with an IC50 of 55 nM. WM-8014 causes cell senescence and suppresses the proliferation with IC50s of 1.6 μM and 551 nM, respectively. WM-8014 also reduces mRNA coding for the MOZ gene Cdc6 by 65.1%[1].

Name: Euphorbia Factor L1, CAS: 76376-43-7, stock 22.4g, assay 98.3%, MWt: 552.66, Formula: C32H40O8, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Apoptosis, Target: Apoptosis, Biological_Activity: Euphorbia Factor L1 is a diterpenoid from Euphorbia lathyris L., reduces the expression of Bcl-2, PI3K, AKT and mTOR protein and mRNA, upregulates cleaved caspase-9 and caspase-3 levels, buts shows no effect on pro-caspase-9 and pro-caspase-3. Euphorbia Factor L1 induces apoptosis, has anticancer, antiadipogenesis, antiosteoclastogenesis and multidrug resistance-modulating effect[1].

Name: Maltohexaose Amylohexaose, CAS: 34620-77-4, stock 31.8g, assay 98%, MWt: 990.86, Formula: C36H62O31, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Maltohexaose is a natural saccharide, and can be produced from amylose, amylopectin and whole starch.

Name: Senecionine Senecionan-11,16-dione, 12-hydroxy-;Aureine;Senecionin, CAS: 130-01-8, stock 25.3g, assay 98.8%, MWt: 335.39, Formula: C18H25NO5, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Senecionine is a pyrrolizidine alkaloid isolated from Senecio vulgaris. Senecionine is toxic to animals and humans.
In Vitro: Pyrrolizidine alkaloids (PAs) are considered to be one of the most hepatotoxic groups of compounds of plant origin and are present in about 3% of the world's flowering plants. Most PAs represent a considerable health hazard to both livestock and humans through the consumption of plants and PA-contaminated products such as milk, honey, herbal teas, and medicines[1].
In Vivo: Upon intravenous administration and oral administration of Senecionine and Adonifoline, significant differences in pharmacokinetics were observed, with the Senecionine and Adonifoline being absorbed fast with lower bioavailability and being quickly metabolized to PA N-oxides and hydroxylation products of PAs or their N-oxides[1]. Senecionine fails to stimulate epoxide hydrase, it diminishs the activity of glutathione-s-transferase, aminopyrine demethylase and AHH[2]. Twice-weekly injections of a third constituent, senecionine, beginning on Day 12 or later, results in premature deliveries in three of seven rats, and the pups from all litters are stillborn or die shortly after birth[3].

EOS Med Chem, Medicinal Chemical is Big

搜索此博客

2020年3月13日星期五

EOS Med Chem Building block stock list 2348

举报滥用情况

2016 China CPHI meet