EOS Med Chem, Medicinal Chemical is Big: EOS Med Chem Building block stock list 2350

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: UK-370106, CAS: 230961-21-4, stock 8g, assay 98.5%, MWt: 572.73, Formula: C35H44N2O5, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: MMP, Biological_Activity: UK-370106 is a potent and highly selective MMP-3 (IC50 of 23 nM) and MMP-12 (IC50 of 42 nM) inhibitor with >1200-fold higher potency than MMP-1, MMP-2, MMP-9, and MMP-14, and about 100-fold than MMP-13 and MMP-8. UK-370106 potently inhibits cleavage of [3H]-fibronectin by MMP-3 (IC50 of 320 nM) and has little effect on keratinocyte migration in vitro[1][2].
In Vitro: The potency of UK-370106 (compound 7) for the inhibition of MMP-13 is 2.3 µM, some 100-fold less potent than its inhibition of MMP-3. UK-370106 is found to be inactive (IC50 > 100 µM) vs zinc metalloproteases PCP and TACE and possesses the following inhibitory potencies vs MMP-2 (IC50 of 34.2 µM), MMP-7 (IC50 of 5.8 µM), MMP-8 (IC50 of 1.75 µM), MMP-9 (IC50 of 30.4 µM) and MMP-14 (IC50 of 66.9 µM)[1]. 
UK-370106 potently inhibits cleavage of [3H]-fibronectin by MMP-3 (IC50 of 320 nM) but does not inhibit cleavage of [3H]-gelatin by either MMP-2 or -9 up to the highest concentration tested (100 µM)[1]. 
UK-370106 is not cytotoxic to, nor affected proliferation of, fibroblasts, keratinocytes, or endothelial cells at 50-100 µM in vitro[1].
In Vivo: Following iv (rat; 2 mg/kg) or topical administration to dermal wounds (rabbit), UK-370106 (compound 7) is cleared rapidly (t1/2 = 23 min) from plasma, but slowly (t1/2 approximately 3 days) from dermal tissue. In a model of chronic dermal ulcers, topical administration of UK-370106 for 6 days substantially inhibits MMP-3 ex vivo[1].

Name: MA-2029, CAS: 287206-61-5, stock 39.1g, assay 98.1%, MWt: 556.71, Formula: C31H45FN4O4, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein, Target: Motilin Receptor, Biological_Activity: MA-2029 is a selective, orally active, and competitive motilin receptor antagonist (IC50=4.9 nM). MA-2029 is selective for the motilin receptor over various other receptors and ion channels. MA-2029 may be useful for gastrointestinal disorders associated with disturbed gastrointestinal motility[1].
IC50 & Target: IC50: 4.9 nM (motilin receptor)[1]
In Vitro: MA-2029 (1 to 30 nM) competitively inhibits motilin-induced contractions in isolated rabbit duodenal longitudinal muscle strips, with a pA2 value of 9.17±0.01. Contractile responses to acetylcholine and substance P are unaffected even at 1 μM of MA-2029. MA-2029 concentration-dependently inhibits the binding of [125I]motilin to motilin receptors in a homogenate of rabbit colon smooth muscle tissue and membranes of HEK 293 cells expressing human motilin receptors. The pKi of MA-2029 is 8.58±0.04 in the rabbit colon homogenate and 8.39 in the HEK 293 cells[1].
In Vivo: MA-2029 (0.3-3 mg/kg; p.o.) dose-dependently inhibits the number of abdominal muscle contractions induced under the same conditions and causes significant inhibition at 3 mg/kg[1]. 
MA-2029 (10 mg/kg; p.o.) treatment shows that the t1/2 is 2 hours[1]. 
The inhibition is significant at 30 min after administration of 3 mg/kg or more and at 4 h after administration of 10 mg/kg or more (MA-2029), so administration of 10 mg/kg or more causes inhibitory effects from 30 min or less to at least 4 h after administration[1].

Name: Reversan CBLC4H10, CAS: 313397-13-6, stock 17.7g, assay 98.6%, MWt: 441.52, Formula: C26H27N5O2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Membrane Transporter/Ion Channel, Target: P-glycoprotein, Biological_Activity: Reversan (CBLC4H10) is a potent and nontoxic multidrug resistance-associated protein 1 (MRP1) and P-glycoprotein (Pgp) inhibitor[1][2].
IC50 & Target: Multidrug resistance-associated protein 1, P-glycoprotein[1]

Name: VU 0365114, CAS: 1208222-39-2, stock 36g, assay 98.6%, MWt: 397.35, Formula: C22H14F3NO3, Solubility: H2O : < 0.1 mg/mL (insoluble); DMSO : ≥ 77.5 mg/mL (195.04 mM), Clinical_Informat: No Development Reported, Pathway: Neuronal Signaling;GPCR/G Protein, Target: mAChR;mAChR, Biological_Activity: VU 0365114 is a mAChR M5 positive allosteric modulator, with an EC50 of 2.7 μM.
IC50 & Target: EC50: 2.7 μM (mAChR M5)[1].

Name: SN 6, CAS: 415697-08-4, stock 13.7g, assay 98.5%, MWt: 402.46, Formula: C20H22N2O5S, Solubility: DMSO : 62.5 mg/mL (155.29 mM; Need ultrasonic); H2O : < 0.1 mg/mL (insoluble), Clinical_Informat: No Development Reported, Pathway: Membrane Transporter/Ion Channel, Target: Na+/Ca2+ Exchanger, Biological_Activity: SN 6 is a selective Na+/Ca2+ exchanger (NCX) inhibitor, and inhibits 45Ca2+ uptake by NCX1, NCX2, and NCX3, with IC50s of 2.9, 16, and 8.6 μM, respectively.
IC50 & Target: IC50：2.9 μM (NCX1), 16 μM (NCX2), 8.6 μM (NCX3)[1]
In Vitro: SN 6 is a selective Na+/Ca2+ exchanger inhibitor, which inhibits the initial rate of 45Ca2+ uptake into NCX1, NCX2, and NCX3 transfectants with IC50 values of 2.9 ± 0.12, 16 ± 1.1, and 8.6 ± 0.27 μM. SN 6 (up to 30 μM) also less potently inhibits muscarinic acetylcholine receptor, with a higher IC50 of 18 μM. SN 6 (0.3-30 μM) completely inhibits the initial rate of Na+i-dependent 45Ca2+ uptake into Na+-loaded sarcolemmal vesicles in a dose dependent manner (IC50, 5.3 ± 0.37 μM). SN 6 (0.3-10 μM) dose-dependently protects against the hypoxia/reoxygenation-induced LDH release in parental LLC-PK1 cells and NCX1 transfectants but not in K229Q transfectants[1]. SN 6 (1-30 μM) suppresses the bidirectional outward and inward INCX in a concentration-dependent manner, with IC50 values of 2.3 μM and 1.9 μM, respectively. SN 6 also inhibits bidirectional current (INCX) in a [Na+]i concentration-dependent manner, with IC50 values of 3.4 μM, 2.3 μM, and 1.1 μM at 10 mM, 20 mM, and 30 mM [Na+]i, respectively[2]. SN 6 inhibits hypoxia/reoxygenation-induced LDH release with an IC50 value of 0.63 ± 0.15 μM in NCX1 transfectants[3].

Name: Carperitide Atrial Natriuretic Peptide (ANP) (1-28), human, porcine, CAS: 89213-87-6, stock 24.5g, assay 98.4%, MWt: 3080.44, Formula: C127H203N45O39S3, Solubility: 10 mM in H2O, Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein, Target: Endothelin Receptor, Biological_Activity: Carperitide (Atrial Natriuretic Peptide (ANP) (1-28), human, porcine) is a 28-amino acid hormone, that is normally produced and secreted by the human heart in response to cardiac injury and mechanical stretch. Carperitide (Atrial Natriuretic Peptide (ANP) (1-28), human, porcine) inhibits endothelin-1 secretion in a dose-dependent way.
IC50 & Target: Endothelin-1[1]
In Vitro: Carperitide (Atrial Natriuretic Peptide (ANP) (1-28), human, porcine) is a diuretic, natriuretic, and vasodilatory peptide hormone originally isolated from mammalian hearts. In cultured porcine endothelial cells the inhibition by porcine ANP (1-28) of immunoreactive endothelin-1 secretion after stimulation with Angiotensin II (Ang II) is paralleled by an increase in the cellular cGMP level. Porcine ANP (1-28) strongly inhibits immunoreactive endothelin-1 secretion in porcine aorta after stimulation with Ang II[1]. ANP is a cardiac hormone involved in electrolyte and fluid homeostasis. The inhibition by ANP of endothelin-1 secretion stimulated by angiotensin II (ANGII) and thrombin using cultured human umbilical-vein endothelial cells. Human ANP (1-28) inhibits immunoreactive (ir)-endothelin-1 secretion and increases cyclic GMP in the human umbilical-vein endothelial cells[2]. In glomeruli from normal rats, Human 125I-ANP (1-28) binds to a single population of high affinity receptors with a mean equilibrium dissociation constant of 0.46 nM. Human ANP (1-28) binds to the glomerular ANP receptor with high affinity stimulated cGMP accumulation. Human ANP (1-28) markedly stimulates cGMP generation, but not cAMP generation in normal rat glomeruli[3].

Name: Atrial Natriuretic Peptide (ANP) (1-28), rat Atrial natriuretic factor (1-28) (rat), CAS: 88898-17-3, stock 23.6g, assay 98.9%, MWt: 3062.41, Formula: C128H205N45O39S2, Solubility: H2O, Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein, Target: Endothelin Receptor, Biological_Activity: Atrial Natriuretic Peptide (ANP) (1-28), rat is a major circulating form of ANP in rats, potently inhibits Angiotensin II (Ang II)-stimulated endothelin-1 secretion in a concentration-dependent manner.
IC50 & Target: Endothelin-1[1]
In Vitro: Rat ANP (1-28) and rat BNP-45, which are the respective major circulating forms of ANP and BNP in rats, potently inhibited Ang II-stimulated endothelin-1 secretion in a concentration-dependent manner. Rat ANP (5-25) is less effective that Rat ANP(1-28) with respect to inhibiting immunoreactive (ir)-endothelin-1 secretion and increasing cellular cyclic GMP. Rat ANP (1-28) inhibits the secretion of ir-endothelin-1 in a concentration-dependent manner between 0.01 and 1 μM[1].

Name: PD 144418, CAS: 154130-99-1, stock 4.2g, assay 98.3%, MWt: 282.38, Formula: C18H22N2O, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Neuronal Signaling;GPCR/G Protein, Target: Sigma Receptor;Sigma Receptor, Biological_Activity: PD 144418 is a highly affinity, potent and selective sigma 1 (σ1) receptor ligand (Ki values of 0.08 nM and 1377 nM for σ1 and σ2 respectively), devoid of any significant affinity for other receptors, ion channels and enzymes. PD 144418 shows potential antipsychotic activity[1][2].
IC50 & Target: Ki: 0.08 nM (σ1receptor) and 1377 nM (σ2 receptor)[1]
In Vitro: In vitro, PD 144418 reverses the N-methyl-D-aspartate (NMDA)-induced increase in cyclic GMP (cGMP) in rat cerebellar slices without affecting the basal levels, suggesting that σ1 sites may be important in the regulation of glutamine-induced actions. PD 144418 potentiates the decrease in 5-hydroxytryptophan caused by Haloperidol in the mesolimbic region, but by itself has no effect in 5-HT and dopamine (DA) synthesis[1].
In Vivo: PD 144418 (10 mg/kg; intraperitoneal injection; male CD-1 mice) treatment antagonizes Mescaline-induced scratching at doses that did not alter spontaneous motor activity, with PD 144418 showing ED50 values of 7.0 mg/kg i.p.[1].

Name: C-Type Natriuretic Peptide (CNP) (1-22), human, CAS: 127869-51-6, stock 19.1g, assay 98.2%, MWt: 2197.60, Formula: C93H157N27O28S3, Solubility: H2O, Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein, Target: Angiotensin Receptor, Biological_Activity: C-Type Natriuretic Peptide (CNP) (1-22), human is the 1-22 fragment of C-Type Natriuretic Peptide. C-type natriuretic peptide is natriuretic peptide family peptide that is involved in the maintenance of electrolyte-fluid balance and vascular tone.
In Vitro: C-Type Natriuretic Peptide (CNP) has been shown to be present in the central nervous system of mammals and to participate in the regulation of the homeostasis of the fluid, electrolytic balance and blood pressure, learning and memory[1].
In Vivo: I.c.v. administration of C-Type Natriuretic Peptide (CNP) (1-22) in a dose of 2 nM induces an increase in the severity of picrotoxin-kindled convulsions 24 and 48 hrs after application of the peptide[1].

Name: Neuromedin U, rat Neuromedin U (rat);Rat neuromedin U-23, CAS: 117505-80-3, stock 9.8g, assay 98.9%, MWt: 2642.97, Formula: C124H180N34O31, Solubility: H2O, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Neuromedin U, rat is a 23-amino acid brain-gut peptide. Neuromedin U (NMU), through its cognate receptor NMUR2 in the central nervous system, regulates several important physiological functions, including energy balance, stress response, and nociception.
IC50 & Target: NMUR2[1]
In Vitro: To establish an electrochemiluminescent (ECL) binding assay for NMUR2 receptor, the peptide Neuromedin U (NMU-23) is labeled at the N terminus with Ru(bpy)2+3 and allowed to bind to the human NMUR2 receptor in the cell membranes immobilized on the electrode on the bottom of each assay plate. Upon application of an electric current, the receptor-bound Ru(bpy)2+3-ligand undergoes an oxidation-reduction cycle in the presence of a coreactant tripropylamine and emits light. Signal is only generated when the Ru(bpy)2+3 label is in proximity to the electrode, thus discriminating the bound label from the unbound and enabling a no wash, homogenous assay format. The ECL-based NMUR2 binding assay is used to screen our corporate compound collection. Approximately 670,000 compounds with diverse structures are tested at 10 μM for their ability to displace the binding of 0.5 nM Ru(bpy)2+3-NMU-23 to human NMUR2 receptors. From competition binding experiments, the Ki values for NMU-23 is determined to be 4.7 nM[1].

Name: Myelin Oligodendrocyte Glycoprotein Peptide (35-55), mouse, rat MOG (35-55), CAS: 149635-73-4, stock 0.8g, assay 98.4%, MWt: 2581.95, Formula: C118H177N35O29S, Solubility: H2O, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Myelin Oligodendrocyte Glycoprotein Peptide (35-55), mouse, rat is a minor component of CNS myelin. Myelin Oligodendrocyte Glycoprotein Peptide (35-55), mouse, rat produces a relapsing-remitting neurological disease with extensive plaque-like demyelination. Myelin Oligodendrocyte Glycoprotein Peptide (35-55), mouse, rat induces strong T and B cell responses and is highly encephalitogenic[1][2][3].

Name: Secretin (33-59), rat Secretin (rat), CAS: 121028-49-7, stock 26.8g, assay 98.7%, MWt: 3027.35, Formula: C129H216N42O42, Solubility: H2O, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Secretin (33-59), rat is a 27-aa peptide, acts on secretin receptor, enhances the secretion of bicarbonate, enzymes, and K+ from the pancreas.
IC50 & Target: Secretin receptor[2]
In Vitro: Secretin (33-59), rat inhibits adrenocorticotropic hormone (ACTH) release, and selectively suppresses the glucocorticoid response to ACTH of dispersed zona fasciculata-reticularis (ZF/R) cells[1]. Secretin retrograde messenger to facilitate GABA transmission in the rat cerebellum[2].

Name: Thiolutin Acetopyrrothin, CAS: 87-11-6, stock 35.5g, assay 99%, MWt: 228.29, Formula: C8H8N2O2S2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Thiolutin (Acetopyrrothin) is a disulfide-containing antibiotic and anti-angiogenic compound produced by Streptomyces. Thiolutin inhibits the JAMM metalloproteases Csn5, Associated-molecule-with-the-SH3-Domain-of-STAM (AMSH) and Brcc36[1]. Thiolutin is a potent and selective inhibitor of endothelial cell adhesion accompanied by rapid induction of Heat-shock protein beta-1 (Hsp27) phosphorylation[2].

Name: SB-772077B dihydrochloride, CAS: 607373-46-6, stock 11.5g, assay 98.9%, MWt: 415.28, Formula: C15H20Cl2N8O2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: TGF-beta/Smad;Stem Cell/Wnt;Cell Cycle/DNA Damage, Target: ROCK;ROCK;ROCK, Biological_Activity: SB-772077B dihydrochloride is an aminofurazan-based Rho kinase (ROCK) inhibitor with IC50s of 5.6 nM and 6 nM toward ROCK1 and ROCK2, respevtively[1].
IC50 & Target: IC50: 5.6 nM (ROCK1), 6 nM (ROCK2)[1]

Name: Fluorobexarotene, CAS: 1190848-23-7, stock 34g, assay 98.9%, MWt: 366.47, Formula: C24H27FO2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: RAR/RXR, Biological_Activity: Fluorobexarotene (compound 20) is a potent retinoid-X-receptor (RXR) agonist, with a Ki value of 12 nM and an EC50 value of 43 nM for RXRα receptor. Fluorobexarotene possesses an apparent RXR binding affinity that is 75% greater than Bexarotene[1].

Name: AC-55649, CAS: 59662-49-6, stock 38g, assay 98.7%, MWt: 310.43, Formula: C21H26O2, Solubility: DMSO : 100 mg/mL (322.13 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease;Autophagy, Target: RAR/RXR;Autophagy, Biological_Activity: AC-55649 is a potent, highly isoform-selective agonist of human RARβ2 receptor, with a pEC50 of 6.9.
IC50 & Target: AC-55649 is a potent, highly isoform-selective agonist of human RARβ2 receptor, with a pEC50 of 6.9.
In Vitro: AC-55649 is a potent, highly isoform-selective agonist at the human RARβ2 receptor, with a pEC50 of 6.9[1]. AC-55649 is a potent and selective activator of RARβ2 transcriptional activity[2].

Name: CE3F4, CAS: 143703-25-7, stock 8.5g, assay 98.1%, MWt: 351.01, Formula: C11H10Br2FNO, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: CE3F4 is a selective antagonist of exchange protein directly activated by cAMP (Epac1), with IC50s of 10.7 μM and 66 μM for Epac1 and Epac2(B), respectively.
IC50 & Target: IC50: 10.7 μM (Epac1), 66 μM (Epac2(B))[1]
In Vitro: CE3F4 is a selective antagonist of Epac1, with IC50s of 10.7 μM and 66 μM for Epac1 and Epac2(B), respectively. CE3F4 is more active on Epac1 than (S)-stereoisomer ((S)-CE3F4, IC50, 56 μM), but less active than (R)-CE3F4 (IC50, 5.8 μM). CE3F4 (50 μM) shows more inhibitory activities against GEF activity of Epac1, than that of Epac2(AB) or Epac2(B)[1]. CE3F4 reduces the exchange activity of Epac1 induced by 007, with IC50 of 23 ± 3 μM. CE3F4 (40 μM) specifically inhibits Epac1 guanine nucleotide exchange activity without interference with Rap1 activity or Epac1-Rap1 interaction. CE3F4 has no influence on PKA activity. CE3F4 (20 μM) inhibits Epac-induced Rap1 activation in living cultured HEK293 cells[2]. CE3F4 (20 μM) significantly inhibits the late phase of ERK activation stimulated by glucose in INS-1 cells[3].

Name: Arundic Acid ONO-2506;(R)-2-Propyloctanoic acid, CAS: 185517-21-9, stock 37.8g, assay 98.9%, MWt: 186.29, Formula: C11H22O2, Solubility: DMSO : 40 mg/mL (214.72 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Arundic acid (ONO-2506) is an astrocyte-modulating agent, which delays the expansion of cerebral infarcts by modulating the activation of astrocytes through inhibition of S-100β synthesis. Arundic acid (ONO-2506) has been developed as a therapeutic agent for stroke and Alzheimer’s disease[1][2][3].

Name: LAT1-IN-1 BCH, CAS: 20448-79-7, stock 24.7g, assay 98.1%, MWt: 155.19, Formula: C8H13NO2, Solubility: DMSO : < 1 mg/mL (insoluble or slightly soluble); H2O : 25 mg/mL (161.09 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Apoptosis, Target: Apoptosis, Biological_Activity: LAT1-IN-1 (BCH) is a selective and competitive inhibitor of large neutral amino acid transporter 1 (LAT1) significantly inhibit cellular uptake of amino acids and mTOR phosphorylation, which induces the suppression of cancer growth and apoptosis[1][2][3].
IC50 & Target: LAT1[1]
In Vitro: LAT1-IN-1 (1-100 mM; 3 days; KYSE30 and KYSE150 esophageal cancer cells) treatment suppresses cell proliferation in a dose-dependent manner[1]. 
LAT1-IN-1 (30 mM; 24 and 48 hours; KYSE30 and KYSE150 cells) treatment significantly increases cell population in the G0/G1 phase in both KYSE30 and KYSE150 cells, indicating that LAT1-IN-1 induces cell cycle arrest at G1 phase[1]. 
LAT1-IN-1 (30 mM; 0-24 hours; KYSE30 and KYSE150 cells) treatment decreases phosphorylation of 4E-BP1 and p70S6K at 30 minutes and the decrease is continued for 24 hours. The amount of mTOR, 4E-BP1, and p70S6K proteins is slightly decreased[1].
In Vivo: LAT1-IN-1 (200 mg/kg; intravenous injection; daily; for 14 days; male BALB/c nude mice) treatment significantly delays tumor growth and decreases glucose metabolism, indicating that LAT1 inhibition potentially suppresses esophageal cancer growth in vivo[1].

Name: NSC 95397, CAS: 93718-83-3, stock 36.8g, assay 98.9%, MWt: 310.39, Formula: C14H14O4S2, Solubility: DMSO : ≥ 100 mg/mL (322.18 mM), Clinical_Informat: No Development Reported, Pathway: Apoptosis;Metabolic Enzyme/Protease, Target: Apoptosis;Phosphatase, Biological_Activity: NSC 95397 is a potent, selective Cdc25 dual specificity phosphatase inhibitor (Ki=32 nM (Cdc25A), 96 nM (Cdc25B), 40 nM (Cdc25C); IC50=22.3 nM (human Cdc25A), 56.9 nM (human Cdc25C), 125 nM (Cdc25B))[1]. NSC 95397 inhibits mitogen-activated protein kinase phosphatase-1 (MKP-1) and suppresses proliferation and induces apoptosis in colon cancer cells through MKP-1 and ERK1/2 pathway[2].
IC50 & Target: Ki: 32 nM (Cdc25A), 96 nM (Cdc25B), 40 nM (Cdc25C)[1] 
IC50: 22.3 nM (human Cdc25A) , 56.9 nM (human Cdc25C), 125 nM (Cdc25B)[1]
In Vitro: NSC 95397 (0, 10, and 20 µM; 24 hour) decreases the cell viability of three colon cancer cell lines SW480, SW620, and DLD-1 in a concentration-dependent manner[2]. 
NSC 95397(10 μM; 24 hour) upregulates p21 while downregulates CDK4 and CDK6 were d in all three colon cancer cell lines SW480, SW620, and DLD-1 cells[2]. 
NSC 95397 (10 μM; 24 hour) reduces the phosphorylation of retinoblastoma protein (Rb) on Ser795 and Ser807/811[2]. 
NSC 95397 (20 μM; 24 hours) significantly increases cleaved caspase-9, -3, -7 and PARP levels[2]. 
NSC 95397 (10 μM; 6 hours) enhances the phosphorylation of its downstream ERK1/2 at Thr202/Tyr 204[2].

Name: Fumonisin B1, CAS: 116355-83-0, stock 20.2g, assay 98.9%, MWt: 721.83, Formula: C34H59NO15, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Acyltransferase, Biological_Activity: Fumonisin B1 is a mycotoxin produced from Fusarium moniliforme. Fumonisin B1 is a potent inhibitor of sphingosine N-acyltransferase (ceramide synthase) and disrupts de novo sphingolipid biosynthesis. Fumonisin B1 is the most abundant and toxic fumonisin[1][2].
IC50 & Target: Sphingosine N-acyltransferase[2]
In Vitro: Fumonisin B1 alters the gene expression and signal transduction pathways in monkey kidney cells[3]. 
Fumonisin B1 increases the initial disruption of sphingolipid metabolism and the accumulation of sphinganine in LLC-PK1 kidney cells, causes DNA damage of apoptotic type in rat astrocytes[3].

Name: Neuropeptide AF (93-110), Human Neuropeptide AF (human), CAS: 192387-38-5, stock 38.6g, assay 99%, MWt: 1978.17, Formula: C90H132N26O25, Solubility: 10 mM in H2O, Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein;Neuronal Signaling, Target: Opioid Receptor;Opioid Receptor, Biological_Activity: Neuropeptide AF (93-110), Human is an endogenous antiopioid peptide.
IC50 & Target: Opioid

Name: Kinetensin Kinetensin (human), CAS: 103131-69-7, stock 32.7g, assay 98%, MWt: 1172.38, Formula: C56H85N17O11, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein;Neuronal Signaling, Target: Neurotensin Receptor;Neurotensin Receptor, Biological_Activity: Kinetensin is a neurotensin-like peptide isolated from pepsin-treated human plasma.
IC50 & Target: Neurotensin Receptor[1]
In Vitro: The peptide kinetensin isolated from pepsin-treated human plasma induces a dose-dependent release of histamine when exposed to rat peritoneal mast cells. The threshold concentration is around 1 μM, the ED50 is 10 μM, and the optimal concentration of between 100 to 1000 μM released 80% of the total histamine. Kinetensin is 10 to 100 times less potent than neurotensin and equipotent with the opioid peptide dynorphin. The histamine release is clearly temperature-dependent, with no release occurring at 0 or 45 °C and with an optimum around 37 °C. The histamine release is significantly reduced in the absence of extracellular calcium[2].
In Vivo: Kinetensin also induces a dose-dependent increase in vascular permeability when injected intradermally into rats[2].

Name: Gliotoxin Aspergillin, CAS: 67-99-2, stock 0.1g, assay 98.9%, MWt: 326.39, Formula: C13H14N2O4S2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Stem Cell/Wnt;Protein Tyrosine Kinase/RTK;Apoptosis;NF-κB, Target: PKA;PKA;Apoptosis;NF-κB, Biological_Activity: Gliotoxin is a secondary metabolite, the most abundant mycotoxin secreted by A. fumigatus, inhibits the phagocytosis of macrophages and the immune functions of other immune cells [1]. Gliotoxin inhibits inducible NF-κB activity by preventing IκB degradation, which consequently induces host-cell apoptosis[2]. Gliotoxin activates PKA and increases intracellular cAMP concentration; modulates actin cytoskeleton rearrangement to facilitate A. fumigatus internalization into lung epithelial cells[3].

Name: Epoprostenol (sodium) Prostaglandin I2 (sodium salt); Prostacyclin (sodium salt); Flolan, CAS: 61849-14-7, stock 38.2g, assay 98.6%, MWt: 374.45, Formula: C20H31NaO5, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Epoprostenol sodium (Prostaglandin I2 (sodium salt)), the synthetic form of the natural prostaglandin derivative prostacyclin (prostaglandin I2), is registered worldwide for the treatment of Pulmonary arterial hypertension (PAH)[1]. Epoprostenol sodium is used in pulmonary hypertension and transplantation as a potent inhibitor of platelet aggregation[2].

Name: Desformylflustrabromine hydrochloride Deformylflustrabromine hydrochloride;dFBr hydrochloride, CAS: 951322-11-5, stock 2.5g, assay 99%, MWt: 357.72, Formula: C16H22BrClN2, Solubility: DMSO : ≥ 105 mg/mL (293.53 mM); H2O : 5 mg/mL (13.98 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Neuronal Signaling;Membrane Transporter/Ion Channel, Target: nAChR;nAChR, Biological_Activity: Desformylflustrabromine hydrochloride is a selective agonist of α4β2 neuronal nicotinic acetylcholine receptor (nAChR) with a pEC50 of 6.48.
IC50 & Target: α4β2 nAChR
In Vitro: Desformylflustrabromine hydrochloride is a selective agonist of α4β2 neuronal nicotinic acetylcholine receptor (nAChR) with a pEC50 of 6.48[1]. ACh-induced currents are potentiated and inhibited by Desformylflustrabromine hydrochloride in the high sensitivity (HS) and low sensitivity (LS) isoform preparations, although Desformylflustrabromine hydrochloride displays a higher potency on the LS isoform (pEC50=6.4±0.2) compare with the HS isoform (pEC50=5.6±0.2). Desformylflustrabromine hydrochloride potentiates ACh-induced responses of wild-type receptors expressed using the HS isoform preparation maximally by 350±20%, which is similar to receptors expressed via the LS isoform preparation (350±30%)[2].

Name: SIB-1553A, CAS: 191611-89-9, stock 23.1g, assay 98%, MWt: 273.82, Formula: C13H20ClNOS, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Neuronal Signaling;Membrane Transporter/Ion Channel, Target: nAChR;nAChR, Biological_Activity: SIB-1553A is an orally bioavailable nicotinic acetylcholine receptors (nAChRs) agonist, with selectivity for β4 subunit-containing nAChRs. SIB-1553A is also a selective neuronal nAChR ligand. SIB-1553A is a cognitive enhancer, and has therapeutic potential for the symptomatic treatment of Alzheimer’s disease and other cognitive disorders[1][2].
In Vitro: SIB-1553A displaces the binding of [H]nicotine (NIC) to the rat brain nAChRs with an IC50 value of 110 nM[1]. 
In calcium flux assays, SIB-1553A (0.1-5 μM), shows a greater selectivity for beta4-subunit containing recombinant hnAChRs (alpha2beta4, alpha3beta4 and alpha4beta4) vs. beta2-subunit containing nAChRs (alpha4beta2 and alpha3beta2) both in terms of efficacy and potency[2].
In Vivo: SIB-1553A (1-40 mg/kg; s.c.) produces dose-dependent increases in ACh levels[3].

Name: P-1075, CAS: 60559-98-0, stock 15.2g, assay 98.1%, MWt: 231.30, Formula: C12H17N5, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Membrane Transporter/Ion Channel, Target: Potassium Channel, Biological_Activity: P-1075 is a potent activator of sulfonylurea receptor 2-associated ATP-sensitive potassium channels (SUR2-KIR6), with an EC50 value of 45 nM for SUR2B-KIR6 channel activation[1]. P-1075 also P1075 opens mitochondrial K(ATP) channels and generates reactive oxygen species resulting in cardioprotection of rabbit hearts[2].
IC50 & Target: EC50: 45 nM (SUR2-KIR6)[1].

Name: Tertiapin-Q, CAS: 910044-56-3, stock 30.3g, assay 98.7%, MWt: 2452.00, Formula: C106H175N35O24S4, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Membrane Transporter/Ion Channel, Target: Potassium Channel, Biological_Activity: Tertiapin-Q is a highly selective blocker of GIRK1/4 heterodimer and ROMK1 (Kir1.1).
IC50 & Target: Potassium channel[1]
In Vitro: Tertiapin-Q is a highly selective blocker of G protein-coupled inwardly rectifying potassium (GIRK1/4) heterodimer and renal outer medullary potassium channel (ROMK1, Kir1.1)[1]. Tertiapin-Q is a potent and selective blocker for Kir1.1 renal outer medullary potassium, Kir3.1-Kir3.4 channels and calcium activated large conductance potassium channels (big potassium channels). The somatostatin (SS-14)-activated current is almost completely blocked (93.2±2.9%, n=5; P<0.01) by preincubation with the G protein-coupled inwardly rectifying potassium (GIRK) channel blocker Tertiapin-Q (TPN-Q)[2].
In Vivo: Tertiapin-Q is a muscarinic acetylcholine receptor-operated K+ current (IK,Ach) blocker. After the cessation of rapid atrial pacing, the atrial effective refractory period (AERP) is unchanged during the experimental period in the rapid atrial pacing (RAP) rabbits (n=6). Bepridil (1 mg/kg, n=5 for each group), Amiodarone (10 mg/kg, n=5 for each group), Vernakalant (3 mg/kg, n=5 for each group), Ranolazine (10 mg/kg, n=6 for each group) or Tertiapin-Q (0.03 mg/kg, n=5 for each group) on the AERP in the control and RAP rabbits. Tertiapin-Q significantly prolongs the AERP at each pacing cycle length both in the control and RAP rabbits. The extents of prolonging effect of Tertiapin-Q on the AERP in the RAP rabbits are greater than those in the control animals[3].

Name: Men 10376 Neurokinin-2 receptor antagonist, CAS: 135306-85-3, stock 2.1g, assay 98.2%, MWt: 1081.22, Formula: C57H68N12O10, Solubility: 10 mM in H2O, Clinical_Informat: No Development Reported, Pathway: Neuronal Signaling;GPCR/G Protein, Target: Neurokinin Receptor;Neurokinin Receptor, Biological_Activity: Men 10376 is a selective tachykinin NK-2 receptor antagonist, with a Ki of 4.4 μM for rat small intestine NK-2 receptor.
IC50 & Target: Ki: 4.4 μM (NK-2 receptor, rat small intestine)[1]
In Vitro: Men 10376 is a selective tachykinin NK-2 receptor, with a Ki of 4.4 μM, and shows low selectivity for NK-1 and NK-3 receptors (Ki, >10 μM)[1]. Men 10376 shows pA2s of 5.66 and 8.08 for NK-1 (guinea-pig ileum) and NK-2 receptors (endothelium-deprived rabbit pulmonary artery). Men 10376 shows no effect on NK-3 receptor (Ki, >10 μM)[2].
In Vivo: Men 10376 (1 and 3 μmol/kg) antagonizes increase in bladder motility produced by the NK-2 receptor agonist in rats[2].

Name: Nonactin Ammonium ionophore I, CAS: 6833-84-7, stock 2.6g, assay 98.8%, MWt: 736.93, Formula: C40H64O12, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Apoptosis;Membrane Transporter/Ion Channel;Metabolic Enzyme/Protease, Target: Apoptosis;Potassium Channel;Mitochondrial Metabolism, Biological_Activity: Nonactin is a naturally occurring macrotetrolide antibiotic from Streptomyces griseus. Nonactin acts as an ionophore for monovalent cations, including K+, and NH4+[1]. Nonactin is able to uncouple the oxidative phosphorylation of mitochondria. Nonactin selectively induces apoptosis in cell lines harboring active mutant β-catenin[2]. Nonactin inhibits the surface expression of endogenous HSP60[3].

Name: CGP 37849, CAS: 127910-31-0, stock 28.8g, assay 98.3%, MWt: 209.14, Formula: C6H12NO5P, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Membrane Transporter/Ion Channel;Neuronal Signaling, Target: iGluR;iGluR, Biological_Activity: CGP 37849 is a potent, competitive and orally active N-methyl-D-aspartate (NMDA) receptor antagonist. CGP 37849 is an anticonvulsant in rodents and has antidepressant and anxiolytic-like effects[1].
In Vitro: In the hippocampal slice in vitro, CGP 37849 selectively and reversibly antagonizes NMDA-evoked increases in CA1 pyramidal cell firing rate. In slices bathed in medium containing low Mg2+ levels, concentrations of CGP 37849 up to 10 μM suppresses burst firing evoked in CA1 neurones by stimulation of Schaffer collateral-commissural fibres without affecting the magnitude of the initial population spike[1].
In Vivo: CGP 37849 potently (Ki of 220 nM) and competitively inhibits NMDA-sensitive l-[3H]-glutamate binding to postsynaptic density (PSD) fractins from rat brain. CGP 37849 inhibits the binding of the selective NMDA receptor antagonist, [3H]-(±)-3-(2-carboxypiperazin-4-yl)propyl-1-phosphonate (CPP), with a Ki of 35 nM[1]. 
In vivo, oral administration to rats of CGP 37849 selectively blocks firing in hippocampal neurones induced by ionophoretically-applied NMDA, without affecting the responses to quisqualate or kainate[1]. 
Oral administration to mice of CGP 37849 suppresses maximal electroshock-induced seizures in mice with an ED50 of 21 mg/kg[1].

Name: Flindokalner BMS-204352, CAS: 187523-35-9, stock 30.7g, assay 98.4%, MWt: 359.70, Formula: C16H10ClF4NO2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Membrane Transporter/Ion Channel, Target: Potassium Channel, Biological_Activity: Flindokalner (BMS-204352) is a potassium channel modulator. Flindokalner is a positive modulator of all neuronal Kv7 channel subtypes expressed in HEK293 cells. Flindokalner is also a large conductance calcium-activated K channel (BKca) positive modulator. Flindokalner shows a negative modulatory activity at Kv7.1 channels (Ki=3.7 μM), and acts as a negative modulator of GABAA receptors. Flindokalner shows anxiolytic efficacy in vivo[1][2].
IC50 & Target: Ki: 3.7 μM (Kv7.1), 230 μM (Kv7.4), 605 μM (Kv7.5)[1]
In Vitro: Flindokalner (BMS-204352) (10 μM) inhibits Kv7.4and Kv7.5 with Kis of 230 and 605 μM, respectively[1]. 
Flindokalner (1-10 μM) causes inhibition of the Ca2+ current in a dose-dependent manner, with a Kd of 6 μM and a Hill coefficient of 1.33. Flindokalnerinhibits cardiac L-type Ca2+ channels in a direct manner, without affecting BKCa channels or intracellular signal transduction, in freshly isolated rat ventricular myocytes[2].
In Vivo: Flindokalner (BMS-204352) (3-30 mg/kg; i.p.) induces a dose-dependent anxiolytic effect[1]. 
In shock-based conditioned model of anxiety in male Wistar rats, Flindokalner (3-60 mg/kg; i.p.) engenderes an anxiolytic profile[1].

Name: MK-4074, CAS: 1039758-22-9, stock 19.1g, assay 98.3%, MWt: 565.62, Formula: C33H31N3O6, Solubility: DMSO : 83.3 mg/mL (147.27 mM; Need ultrasonic), Clinical_Informat: Phase 1, Pathway: Metabolic Enzyme/Protease, Target: Acetyl-CoA Carboxylase, Biological_Activity: MK-4074 is a liver-specific inhibitor of acetyl-CoA carboxylase ACC1 and ACC2 with IC50 values of approximately 3 nM.
IC50 & Target: IC50: 3 nM (Acetyl-CoA Carboxylase)[1]
In Vitro: MK-4074 strongly inhibits both ACC1 and ACC2 with IC50 values of approximately 3 nM. MK-4074 is highly liver specific because it is a substrate of organic anion transport protein (OATP) transporters that are present only in hepatocytes, and excretion of MK-4074 from hepatocytes into bile is dependent on the MRP2 efflux transporter[1].
In Vivo: In male KKAy mice, a mouse model of obesity, type 2 diabetes, and fatty liver, a single oral dose of MK-4074 (0.3-3 mg/kg) significantly decreases DNL in a dose-dependent manner with an ID50 value of 0.9 mg/kg 1 hr post-administration. In a time course study, MK-4074 orally at 30 mg/kg reduces hepatic DNL by 83%, 70%, and 51% at 4, 8, and 12 hr post-dose, respectively. Single oral doses of MK-4074 at 30 and 100 mg/kg significantly increases plasma total ketones, a surrogate biomarker for hepatic FAO, by 1.5-fold to 3-fold for up to 8 hr[1].

Name: VU591 hydrochloride, CAS: 1315380-70-1, stock 32g, assay 98.6%, MWt: 404.76, Formula: C16H13ClN6O5, Solubility: 10 mM in H2O, Clinical_Informat: No Development Reported, Pathway: Membrane Transporter/Ion Channel, Target: Potassium Channel, Biological_Activity: VU591 hydrochloride is a potent, selective renal outer medullary potassium channel (ROMK or Kir1.1) inhibitor, with an IC50 of 0.24 μM[1].
IC50 & Target: IC50: 0.24 μM (ROMK)[1].

Name: NS3623, CAS: 343630-41-1, stock 29.5g, assay 98.2%, MWt: 427.18, Formula: C15H10BrF3N6O, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Membrane Transporter/Ion Channel, Target: Potassium Channel, Biological_Activity: NS3623 is an activator of human ether-a-go-go-related gene (hERG1/KV11.1) potassium channels. NS3623 activates the IKr and Ito currents and has antiarrhythmic effect. NS3623 has a dual mode of action, being an inhibitor of hERG1 channels[1][2][3].
In Vitro: In isolated canine cardiomyocytes, application of NS3623 (5 μM) greatly increases the size of the tail current confirming previous studies demonstrating this drug increased IKr. The effect of NS3623 on IKr recorded from cells kept in culture is evaluated. After 48 h, the magnitude of IKr is greatly reduced compared to freshly isolated cells. Peak IKr tail currents are 0.47 ± 0.08 pA/pF in freshly isolated myocytes and 0.28 ± 0.06 pA/pF in 2 day cultured myocytes. Application of NS3623 increases IKr in cultured Mid cells. Analysis of the current-voltage (I-V) relation of IKr tail current showed that NS3623 increased current density in both 1 day and 2 day cultured Mid cells. On a percentage basis, NS3623 increases IKr tail currents (at +50 mV activating pulse) by 60% in normal Mid cells, and 68% in 48 h cultured cells[3].
In Vivo: NS3623 (30 mg/kg; i.v.; lasting for 3 minutes) shortens the corrected QT interval by 25 +/- 4% in anaesthetized guinea pigs[1]. 
NS3623 (50 mg/kg) shortenes the QT interval by 30 +/- 6% in conscious guinea pigs. NS3623 (50 mg/kg) immediately decreases the QTcF interval and remains significantly shortened for approximately 30 minutes[1].

Name: NS5806, CAS: 426834-69-7, stock 4.1g, assay 99%, MWt: 574.07, Formula: C16H8Br2F6N6O, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Membrane Transporter/Ion Channel, Target: Potassium Channel, Biological_Activity: NS5806, a potent potassium current activator, increases KV4.3/KChIP2 peak current amplitudes with an EC50 of 5.3 μM. NS5806 slows KV4.3 and KV4.2 current dacay in channel complexes containing KChIP2[1].
IC50 & Target: IC50: 5.3 nM (KV4.3)[1]
In Vitro: NS5806 (10 µM) induces a 65% increase of KV4.3/KChIP2/DPP6 peak current amplitudes concentration-dependently and the time course of inactivation (τ) is slowed with an EC50 value of 25.4 µM in CHO-K1 cells[1]. 
NS5806 activates canine transient outward potassium current (Ito) with an IC50 of 40.7 nM and an EC50 of 1.6 nM for inhibition and stimulation on rabbit, respectively[2]. 
NS5806 (10-100 nM) has concentration-dependent effects on ventricular and atrial Ito[2].

Name: BMS-191011 BMS-A, CAS: 202821-81-6, stock 22.1g, assay 98.8%, MWt: 370.71, Formula: C16H10ClF3N2O3, Solubility: DMSO : 125 mg/mL (337.19 mM; Need ultrasonic); H2O : < 0.1 mg/mL (insoluble), Clinical_Informat: No Development Reported, Pathway: Membrane Transporter/Ion Channel, Target: Potassium Channel, Biological_Activity: BMS-191011 (BMS-A) is an opener of the large-conductance, Ca2++-activated potassium (maxi-K) channel, effective in stroke models[1].

Name: PD-118057, CAS: 313674-97-4, stock 31.6g, assay 98.1%, MWt: 386.27, Formula: C21H17Cl2NO2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Membrane Transporter/Ion Channel, Target: Potassium Channel, Biological_Activity: PD-118057 is a human ether-a-go-go-related gene (hERG) channel activator that does not cause hERG blockade[1].
IC50 & Target: Human ether-a-go-go-related gene channel[1]

Name: BL-1249, CAS: 18200-13-0, stock 26.8g, assay 98.8%, MWt: 291.35, Formula: C17H17N5, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Membrane Transporter/Ion Channel, Target: Potassium Channel, Biological_Activity: BL-1249 is a nonsteroidal anti-inflammatory drug (NSAID) and a potassium channel activator. BL-1249 potently activates K2P2.1 (TREK-1) and K2P10.1 (TREK-2) with EC50 values of 5.5 μM and 8.0 μM, respectively. BL-1249 extracellular application activates all TREK subfamily members but has no effect on other K2P subfamilies. BL-1249 exhibits more selective for the bladder (EC50 of 1.26 μM) than vascular tissue (EC50 of 21.0 μM)[1][2].
IC50 & Target: EC50: 5.5 μM (TREK-1) and 8.0 μM (TREK-2)[1]
In Vitro: BL-1249 produces a concentration-dependent membrane hyperpolarization of cultured human bladder myocytes, assessed as either a reduction in fluorescence of the voltage-sensitive dye bis-(1,2-dibutylbarbituric acid)trimethine oxonol (EC50 of 1.26 μM) or by direct electrophysiological measurement EC50 of 1.49 μM). BL-1249 produced a concentration-dependent hyperpolarization with an EC50 of 21.0 μM in human aortic smooth muscle cells[1]. 
In in vitro organ bath experiments, BL-1249 produces a concentration-dependent relaxation of 30 mM KCl-induced contractions in rat bladder strips (EC50 of 1.12 μM), yet has no effect on aortic strips up to the highest concentration tested (10 μM). The bladder relaxation produced by BL-1249 is partially blocked by Ba2+ (1 and 10 mM)[1]. 
BL-1249 is a selective agonist of the TREK subfamily when applied extracellularly, having preferential action on K2P2.1(TREK-1) and K2P10.1(TREK-2) over K2P4.1(TRAAK) and establish that its mechanism of action relies on gating at the selectivity filter C-type gate[2].
In Vivo: BL-1249 (1 mg/kg) inhibits isovolumic bladder contractions in vivo. The short duration of the effect of BL-1249 on bladder contraction ( 30 min) is likely due to a fast elimination half-life of the compound after i.v. administration (0.69 h)[1]. 
BL-1249 (1 mg/kg) has little effect on mean arterial blood pressure, an observation again consistent with the in vitro bladder to vascular relaxant selectivity[1].

Name: Valinomycin NSC 122023, CAS: 2001-95-8, stock 1.6g, assay 98.8%, MWt: 1111.32, Formula: C54H90N6O18, Solubility: Ethanol : 50 mg/mL (44.99 mM; Need ultrasonic); DMSO : 50 mg/mL (44.99 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Apoptosis, Target: Apoptosis, Biological_Activity: Valinomycin (NSC 122023) is a cyclic depsipeptide antibiotic first isolated from Streptomyces fulvissimus, act as a potassium selective ionophore. Valinomycin (NSC 122023) inhibits lymphocyte proliferation by its effects on the cell membrane, and induces apoptosis in CHO cells[1]. Valinomycin induces activation of PINK1 leading to Parkin Ser65 phosphorylation[2].

Name: TC-S 7005, CAS: 1082739-92-1, stock 6.8g, assay 98.8%, MWt: 359.38, Formula: C21H17N3O3, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Cell Cycle/DNA Damage, Target: Polo-like Kinase (PLK), Biological_Activity: TC-S 7005 is a Polo-like kinases (Plks) inhibitor with IC50s of 4 nM, 24 nM and 214 nM for Plk2, Plk3, and Plk1, respectively[1].
IC50 & Target: IC50: 4 nM (Plk2), 24 nM (Plk3), 214 nM (Plk1)[1]
In Vitro: TC-S 7005 markedly induces myofibroblast differentiation and reduces fibroblast proliferation rates[2].

Name: DCP-LA FR236924, CAS: 28399-31-7, stock 29.2g, assay 98.7%, MWt: 308.50, Formula: C20H36O2, Solubility: H2O : < 0.1 mg/mL (insoluble); DMSO : 5 mg/mL (16.21 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: TGF-beta/Smad;Epigenetics, Target: PKC;PKC, Biological_Activity: DCP-LA (FR236924), a linoleic acid derivative, selectively and directly activates PKCε[1].
IC50 & Target: PKCε[1]

Name: PI-828, CAS: 942289-87-4, stock 8.5g, assay 98.3%, MWt: 322.36, Formula: C19H18N2O3, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: PI3K/Akt/mTOR;Stem Cell/Wnt;Cell Cycle/DNA Damage, Target: PI3K;Casein Kinase;Casein Kinase, Biological_Activity: PI-828 is a dual PI3K and casein kinase 2 (CK2) inhibitor with IC50s of 173 nM, 149 nM, and 1127 nM for p110α, CK2, and CK2α2 in lipid kinase assay, respectively[1].
In Vitro: PI-828 (0.01-100 μM) exhibits cytotoxic effect on the 4T1 breast cancer cells and 4306 ovarian cancer cells[2]. PI-828 (0.78-3.12 µM; 48 hours) decreases caspase 3 activation; higher concentrations of PI-828 (6.25-12.5 μM) alone causes apoptosis[3].

Name: Urocortin, human Urocortin (human);Human urocortin; Human urocortin 1; Human urocortin I, CAS: 176591-49-4, stock 38.4g, assay 98.7%, MWt: 4696.24, Formula: C204H337N63O64, Solubility: 10 mM in H2O, Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein, Target: CRFR, Biological_Activity: Urocortin, human, a 40-aa neuropeptide, acts as a selective agonist of endogenous CRF2 receptor, with Kis of 0.4, 0.3, and 0.5 nM for hCRF1, rCRF2α and mCRF2β, respectively.
IC50 & Target: Ki: 0.4 nM (hCRF1, cell assay), 0.3 nM (rCRF2α, cell assay), and 0.5 nM (mCRF2β, cell assay)[1]
In Vitro: Urocortin, human is a selective agonist of CRF2 receptor, with Kis of 0.4, 0.3, and 0.5 nM for human CRF1, rat CRF2α and mouse CRF2β receptors in cell assay, respectively[1].
In Vivo: Urocortin (0.01 to 10 μg) decreases food intake in both food-deprived and non-deprived rats and such a effect also observed in mice after 1 μg of Urocortin i.c.v. administration. Urocortin has the potential of inducing anxiogenic behavior[2].

Name: Urocortin, rat Urocortin (Rattus norvegicus);Rat urocortin;, CAS: 171543-83-2, stock 18.8g, assay 98.5%, MWt: 4707.26, Formula: C206H338N62O64, Solubility: 10 mM in H2O, Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein, Target: CRFR, Biological_Activity: Urocortin, rat is a selective agonist of CRF receptor, with Kis of 0.32, 2.2, and 0.62 nM for hCRF1, rCRF2α and mCRF2β, respectively.
IC50 & Target: Ki: 0.32 nM (hCRF1), 2.2 nM (rCRF2α), and 0.62 nM (mCRF2β)[1]
In Vitro: Urocortin, rat is a selective agonist of CRF receptor, with Kis of 0.32, 2.2, and 0.62 nM for human CRF1, rat CRF2α and mouse CRF2β, respectively[1].
In Vivo: Urocortin (0.01 to 10 μg) decreases food intake in both food-deprived and non-deprived rats and such a effect also observed in mice after 1 μg of Urocortin i.c.v. administration. Urocortin has the potential of inducing anxiogenic behavior[2].

Name: JJKK 048, CAS: 1515855-97-6, stock 11.2g, assay 98.5%, MWt: 434.44, Formula: C23H22N4O5, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: MAGL, Biological_Activity: JJKK 048 is an ultrapotent and highly selective inhibitor of Monoacylglycerol lipase (MAGL).
IC50 & Target: MAGL[1]

Name: SU16f, CAS: 251356-45-3, stock 18.8g, assay 98.8%, MWt: 386.44, Formula: C24H22N2O3, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Protein Tyrosine Kinase/RTK, Target: PDGFR, Biological_Activity: SU16f is a potent and selective PDGFRβ inhibitor with IC50s of 10 nM, 140 nM, 2.29 μM for PDGFRβ, PDGFR1, PDGFR2, respectively[1]. Neutralization of PDGFRβ receptor by SU16f blocks the promoting role of GC-MSCs (gastric cancer-derived mesenchymal stem cells) conditioned medium in gastric cancer cell proliferation and migration[2].
In Vitro: SU16f (20 μM; for 8 hours) pretreatment inhibits the promoting role of GC-MSC-CM in SGC-7901 cell proliferation[1]. 
SU16f (20 μM; for 8 hours) significantly abolishes PDGFRβ activation in SGC-7901 by GC-MSC-CM. SU16f pretreatment results in the upregulation of E-cadherin and downregulation of N-cadherin, Vimentin, and α-SMA. SU16f pretreatment leads to downregulation of p-AKT, Bcl-xl, and Bcl-2 levels and upregulation of Bax expression in SGC-7901 cells by GC-MSC-CM [1].

Name: U-73343, CAS: 142878-12-4, stock 22.7g, assay 98.4%, MWt: 466.66, Formula: C29H42N2O3, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Phospholipase, Biological_Activity: U-73343, an inhibitor of PLC (putative phospholipase C)-dependent processes, is an analog of U-73122 and can be used as a negative control[1].

Name: Protease-Activated Receptor-2 Activating Peptide, CAS: 171436-38-7, stock 0.7g, assay 98.8%, MWt: 656.82, Formula: C29H56N10O7, Solubility: 10 mM in H2O, Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein, Target: Protease-Activated Receptor (PAR), Biological_Activity: Protease-Activated Receptor-2 Activating Peptide is an agonist of Protease-Activated Receptor-2 (PAR-2).
IC50 & Target: PAR-2[1]
In Vitro: Protease-Activated Receptor-2 Activating Peptide (SLIGRL-NH2) is an agonist of PAR-2 and MrgprC11[1]. Protease-Activated Receptor-2 Activating Peptide (SLIGRL-NH2) causes an L-NAME-inhibited relaxation. Based on SLIGRL-NH2 causing a concentration-dependent relaxation with an EC50 of 10 µM in endothelium-free preparations in the presence of perivascular adipose tissue (PVAT) , 20 µM is used as a suitable ‘test’ concentration of peptide in subsequent experiments designed to evaluate the effects of potential inhibitors of ADRF release/action. In the endothelium-free aorta preparations, SLIGRL-NH2 causes a concentration-dependent relaxation in preparations only in the presence of PVAT [+PVAT, -ENDO (endothelium)][2].

Name: PAR-4 Agonist Peptide, amide PAR-4-AP;AY-NH2, CAS: 352017-71-1, stock 5.3g, assay 98.2%, MWt: 680.79, Formula: C34H48N8O7, Solubility: H2O, Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein, Target: Protease-Activated Receptor (PAR), Biological_Activity: PAR-4 Agonist Peptide, amide (PAR-4-AP; AY-NH2) is a proteinase-activated receptor-4 (PAR-4) agonist, which has no effect on either PAR-1 or PAR-2 and whose effects are blocked by a PAR-4 antagonist.
IC50 & Target: PAR-4[1]
In Vivo: Compared with their BALB/cBy controls, SCID mice have a significantly greater abdominal response to colorectal distension (CRD) at the distension levels of 0.04 to 0.1 mL increasing the intensity of EMG response by 384% to 132%, respectively (P<0.01; P<0.01; P<0.01; P<0.001). PAR-4 activation effectively reverses this hypersensitivity (P<0.01, P<0.05; P<0.05; P<0.05) [1].

Name: 2-Furoyl-LIGRLO-amide, CAS: 729589-58-6, stock 1.4g, assay 98.4%, MWt: 777.95, Formula: C36H63N11O8, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein, Target: Protease-Activated Receptor (PAR), Biological_Activity: 2-Furoyl-LIGRLO-amide is a potent and selective proteinase-activated receptor 2 (PAR2) agonist with a pD2 value of 7.0[1][2]..
IC50 & Target: Proteinase-activated receptor 2 (PAR2)[1]
In Vitro: 2-Furoyl-LIGRLO-amide (2-Furoyl-LIGRLO-NH2) is equally effective to and 10 to 25 times more potent than SLIGRLNH2 for increasing intracellular calcium in cultured human and rat PAR2-expressing cells, respectively[1]. 
In bioassays of tissue PAR2 activity, measured as arterial vasodilation and hyperpolarization, 2-Furoyl-LIGRLO-amide (2-Furoyl-LIGRLO-NH2) is 10 to 300 times more potent than SLIGRL-NH2. Unlike trans-cinnamoyl-LIGRLO-NH2, 2-Furoyl-LIGRLO-amide do not cause a prominent non-PAR2-mediated contraction of murine femoral arteries[1].

Name: Apafant WEB 2086, CAS: 105219-56-5, stock 28.6g, assay 98.9%, MWt: 455.96, Formula: C22H22ClN5O2S, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Apafant (WEB 2086), a potent platelet-activating factor (PAF) antagonist, inhibits PAF binding to human PAF receptors with a Ki of 9.9 nM[1].
IC50 & Target: Ki: 9.9 nM (Platelet-activating factor)[1]

Name: PhiKan 083, CAS: 880813-36-5, stock 3.2g, assay 98.3%, MWt: 238.33, Formula: C16H18N2, Solubility: H2O : < 0.1 mg/mL (insoluble); DMSO : 130 mg/mL (545.46 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Apoptosis, Target: MDM-2/p53, Biological_Activity: PhiKan 083 is a carbazole derivative, which binds to the surface cavity and stabilizes Y220C (a p53 mutant), with a Kd of 167 μM[1], and a relative binding affinity (Kd) of 150 μM in Ln229 cells[3].
IC50 & Target: Kd: 167 μM (p53-Y220C)[1], 150 μM (p53Y220C, in Ln229 cells)[3]
In Vitro: PhiKan 083 is a carbazole derivative, which binds to the surface cavity and stabilizes Y220C (a p53 mutant), with a Kd of 167 μM[1], shows a relative binding affinity (Kd) of 150 μM for p53Y220C in Ln229 cells[3]. 
PhiKan 083 slows down its thermal denaturation rate[2]. 
PhiKan 083 (125 μM, 48 hours) reduces the cell viability of engineered variants of Ln229 cells[3]. 
PhiKan 083 (100 μM) in conbination with NSC 123127 (1 μM) enhances the pro-apoptotic activity in all variants of Ln229 cells (p53wt, p53Y220C, p53G245S, p53R282W)[3].

Name: CMPD1, CAS: 41179-33-3, stock 16.2g, assay 98.7%, MWt: 349.40, Formula: C22H20FNO2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: MAPK/ERK Pathway, Target: MAPKAPK2 (MK2), Biological_Activity: CMPD1 is a selective and non-ATP-competitive p38 MAPK-mediated MK2 phosphorylation inhibitor with apparent Ki (Kiapp) of 330 nM[1][2].
IC50 & Target: Kiapp: 330 nM (MK2 phosphorylation)[2]
In Vitro: CMPD1 does not inhibit p38 MAPK-mediated phosphorylation of other two substrates, MBP and ATF2[1]. 
CMPD1 induced mitotic arrest and apoptosis in U87 cells[1]. 
CMPD1 inhibits tubulin polymerisation in glioblastoma cells[3].

Name: AL 8697, CAS: 1057394-06-5, stock 16.4g, assay 98.5%, MWt: 402.41, Formula: C21H21F3N4O, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: MAPK/ERK Pathway;Autophagy, Target: p38 MAPK;Autophagy, Biological_Activity: AL 8697, a specific and orally active p38α MAPK inhibitor with an IC50 of 6 nM, 14-fold less potent in p38β MAPK (IC50=82 nM), exhibits anti-inflammatory activity[1].
IC50 & Target: IC50: 6 nM (p38α), 82 nM (p38β)[1]
In Vivo: AL 8697 (1-30 mg/kg; p.o.; once daily for 10 days) dose-dependently decreases the oedema in right and left paws[1].

Name: CGP71683 hydrochloride CGP71683A, CAS: 192322-50-2, stock 17.3g, assay 98.5%, MWt: 512.07, Formula: C26H30ClN5O2S, Solubility: DMSO : 160 mg/mL (312.46 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein;Neuronal Signaling, Target: Neuropeptide Y Receptor;Neuropeptide Y Receptor, Biological_Activity: CGP71683 hydrochloride is a competitive neuropeptide Y5 receptor antagonist with a Ki of 1.3 nM, and shows no obvious activity at Y1 receptor (Ki, >4000 nM) and Y2 receptor (Ki, 200 nM) in cell membranes.
IC50 & Target: Ki: 1.3 nM (Y5 receptor), 200 nM (Y2 receptor), >4000 nM (Y1 receptor)[1]
In Vitro: CGP71683 hydrochloride is a competitive neuropeptide Y5 receptor antagonist with a Ki of 1.3 nM, and shows no obvious activity at Y1 receptor (Ki, >4000 nM) and Y2 receptor (Ki, 200 nM) in cell membranes[1].
In Vivo: CGP71683 (15 nmol/rat, icv, twice daily) shows anorexigenic effect, reducing food intake and bady weight of fed rats. CGP71683 causes 3-times higher serum total T4 and 37% increase in free T4 in the fasted rats than in the fasted controls rats[2].

Name: L 152804, CAS: 6508-43-6, stock 4.3g, assay 98.3%, MWt: 366.45, Formula: C23H26O4, Solubility: DMSO : ≥ 125 mg/mL (341.11 mM), Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein;Neuronal Signaling, Target: Neuropeptide Y Receptor;Neuropeptide Y Receptor, Biological_Activity: L 152804 is an orally active and selective neuropeptide Y Y5 receptor (NPY5-R) antagonist, with a Ki of 26 nM for hY5. L 152804 causes weight loss in diet-induced obese mice by modulating food intake and energy expenditure[1][2].
IC50 & Target: Ki: 26 nM (NPY5-R)[1].
In Vitro: L 152804 displays > 300-fold selectivity over hY1, hY2, and hY4 receptors[1].

Name: CYM 9484, CAS: 1383478-94-1, stock 35.9g, assay 98.6%, MWt: 509.68, Formula: C27H31N3O3S2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein;Neuronal Signaling, Target: Neuropeptide Y Receptor;Neuropeptide Y Receptor, Biological_Activity: CYM 9484 is a selective and highly potent neuropeptide Y (NPY) Y2 receptor antagonist with an IC50 value of 19 nM[1].
In Vitro: SF-11 is a selective, brain-penetrant NPY Y2 receptor antagonist with an IC50 value of 190 nM. Systematically explore the SAR of the hit molecule SF-11 that leads to the identification of selective and highly potent small molecule NPY Y2 receptor antagonist CYM 9484 (Compound 16). CYM 9484 is 10-fold more potent than the hit molecule SF-11. CYM 9484 is prepared by the coupling of α,α-diphenylpiperidino-4-methanol with a variety of aryl isothiocyanates[1].

Name: Guggulsterone Z/E-Guggulsterone, CAS: 95975-55-6, stock 23.7g, assay 98.2%, MWt: 312.45, Formula: C21H28O2, Solubility: DMSO : 20.83 mg/mL (66.67 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: MAPK/ERK Pathway;Apoptosis;Metabolic Enzyme/Protease;Apoptosis;PI3K/Akt/mTOR;Autophagy, Target: JNK;Apoptosis;FXR;Caspase;Akt;Autophagy, Biological_Activity: Guggulsterone is a plant sterol derived from the gum resin of the tree Commiphora wightii. Guggulsterone inhibits the growth of a wide variety of tumor cells and induces apoptosis through down regulation of antiapoptotic gene products (IAP1, xIAP, Bfl-1/A1, Bcl-2, cFLIP and survivin), modulation of cell cycle proteins (cyclin D1 and c-Myc), activation of caspases and JNK, inhibition of Akt[1]. Guggulsterone, a farnesoid X receptor (FXR) antagonist, decreases CDCA-induced FXR activation with IC50s of 17 and 15 μM for Z- and E-Guggulsterone, respectively[2].
IC50 & Target: IC50: 17 μM (Z-Guggulsterone for FXR) and 15 μM (E-Guggulsterone for FXR)[2]
In Vitro: Guggulsterone (0.5-20 μM; 24 hours) suppresses TREM-1, TLR4 and TNF-α expression as well as the phosphorylation of IκBα and NF-κB p65 by LPS[2].
In Vivo: Guggulsterone (orally; 100 mg/kg once per day for 8 days) significantly improved the survival rates of wild-type mice with TNBS-induced colitis[2].

Name: Naloxone benzoylhydrazone NalBzoH, CAS: 119630-94-3, stock 34.5g, assay 98.8%, MWt: 445.51, Formula: C26H27N3O4, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein;Neuronal Signaling, Target: Opioid Receptor;Opioid Receptor, Biological_Activity: Naloxone benzoylhydrazone (NalBzoH) is a mixed agonist/antagonist. Naloxone benzoylhydrazone is a prototypic κ3-opioid receptor agonist, and a partial agonist at the cloned μ and δ opioid receptors, and an antagonist at opioid-like NOP receptors. Naloxone benzoylhydrazone has potently analgesia effect[1][2][3].
IC50 & Target: κ3-opioid receptor; μ- and δ-opioid receptors; Opioid-like NOP receptors[1][2]
In Vitro: At the mu-opioid receptor (MOR), Naloxone benzoylhydrazone stimulates [35S]GTPγS binding (pEC50=8.59) and inhibits cyclic AMP accumulation (pEC50=8.74) with maximal effects (Emax) corresponding to 55 and 65% of those obtained with the MOR agonist DAMGO, respectively[1]. 
At the κ-opioid receptor (KOR), Naloxone benzoylhydrazone stimulates [35S]GTPγS binding (pEC50=9.70) and inhibits cyclic AMP formation (pEC50=9.45) [1]. 
In CHO cells expressing the δ-opioid receptor (DOR), Naloxone benzoylhydrazone increases [35S]GTPγS binding (pEC50=8.49) and inhibits cyclic AMP formation (pE50=8.61)[1].
In Vivo: Analgesic studies in mice examining increasing doses of Naloxone benzoylhydrazone with a fixed dose of morphine reveals a biphasic curve. Naloxone benzoylhydrazone at doses as low as 1 μg/kg partially antagonized morphine analgesia. Higher Naloxone benzoylhydrazone doses continued to inhibit morphine analgesia in a dose-dependent manner, with the 1-mg/kg dose antagonizing completely morphine analgesia. As the Naloxone benzoylhydrazone dose increased beyond 1 mg/kg analgesia returned. Naloxone benzoylhydrazone also prduces a similar analgesic response when administered alone in mice and also is active in rats. Naloxone benzoylhydrazone has excellent p.o. activity, with an analgesic potency in mice equivalent to s.c. administration. In addition to blocking morphine analgesia, low doses of Naloxone benzoylhydrazone also partially reverses the inhibition of gastrointestinal transit in mice produced by morphine, antagonizes completely morphine lethality and precipitates withdrawal in morphine-dependent mice[4].

Name: BAM-22P Bovine adrenal medulla-22P, CAS: 76622-26-9, stock 35.5g, assay 98.2%, MWt: 2839.22, Formula: C130H184N38O31S2, Solubility: 10 mM in H2O, Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein;Neuronal Signaling, Target: Opioid Receptor;Opioid Receptor, Biological_Activity: BAM-22P, a highly potent opioid peptide, is a potent opioid agonist.
IC50 & Target: Opioid receptor[1]
In Vivo: Bovine adrenal medulla docosapeptide (BAM-22P) is a potent opioid agonist, derived from the proenkephalin A gene, which is present in the adrenal medulla. Plasma levels of BAM-22P are determined by a sensitive radioimmunoassay, and the specificity of the assay is confirmed using high-performance liquid chromatography. Plasma BAM-22P levels s cholestatic rats are significantly higher than those in control rats. This increase in plasma BAM-22P levels is completely prevented by adrenalectomy. Adrenal steady-state levels of proenkephalin mRNA, as determined by Northern blot hybridization analyses, are also increased significantly in cholestatic rats. These increases in proenkephalin mRNA levels are not paralleled by changes in adrenal BAM-22P peptide levels, which are similar in cholestatic rats and their respective controls. Similar levels of proenkephalin mRNA expression are observed in innervated and denervated adrenal glands from cholestatic rats, suggesting that the increase in adrenal proenkephalin mRNA levels in acute cholestasis is not due to splanchnic nerve activation. Thus acute cholestasis in the rat is associated with adrenal secretion and accumulation in plasma of the highly potent opioid peptide BAM-22P and an augmentation of adrenal proenkephalin mRNA expression. The increase in plasma BAM-22P levels may contribute substantially to the increase in total circulating opioid activity documented in cholestatic rats. Adrenal gland levels of BAM-22P are similar in BDR and sham-resected rats (BDR, 1.10±0.39 ng/g; sham, 0.93±0.16 ng/g; NS). BAM-22P levels in ANIT-treated and oil-gavaged controls are also similar (ANIT, 2.88±0.29 ng/g; control, 2.75±0.30 ng/g; NS). However, adrenal BAM-22P levels are lower in BDR and sham-resected rats than in ANIT-treated and oil-gavaged controls (P<0.01). Acute cholestasis in the rat is associated with enhanced synthesis and secretion of the proen-kephalin-derived opioid peptide BAM-22P from the adrenal gland[1].

Name: Deltorphin I Deltorphin 1; Deltorphin C, CAS: 122752-15-2, stock 20.8g, assay 98.5%, MWt: 768.86, Formula: C37H52N8O10, Solubility: 10 mM in H2O, Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein;Neuronal Signaling, Target: Opioid Receptor;Opioid Receptor, Biological_Activity: Deltorphin I is a δ-opioid receptor agonist with high affinity and selectivity.
IC50 & Target: δ-opioid receptor[1]
In Vivo: Twice daily administration of Deltorphin I (20μg/mouse) for 4 days produces tolerance to Deltorphin I analgesia, as shown by the decrease in the analgesic response. The peak analgesic response to Deltorphin I (20 μg/mouse) at 10 min after injections is decreased from 8.36±0.28 s (the 1st day) to 4.53±0.14 s (the 4th day) markedly. Concurrent treatment of Melatonin (0.5, 1 and 2.5 mg/kg) and Deltorphin I (20 μg/mouse) twice daily for 4 days can attenuate the tolerance to Deltorphin I analgesia (P<0.05, <0.05 and <0.05), and this effect is dose dependent[1].

Name: Dynorphin B (1-13), CAS: 83335-41-5, stock 24.3g, assay 98.6%, MWt: 1570.84, Formula: C74H115N21O17, Solubility: H2O, Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein;Neuronal Signaling, Target: Opioid Receptor;Opioid Receptor, Biological_Activity: Dynorphin B (1-13) acts as an agonist on opioid κ-receptor.
IC50 & Target: κ-opioid receptor[1]
In Vitro: Dynorphin B (1-13), a 13 amino acid, is an extraordinarily potent opioid peptide. The neurophysiological actions of Dynorphin B (1-13) have been the subject of considerable research effort[1].

Name: L-368,899 hydrochloride, CAS: 160312-62-9, stock 5.7g, assay 98.6%, MWt: 591.23, Formula: C26H43ClN4O5S2, Solubility: DMSO : 130 mg/mL (219.88 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein, Target: Oxytocin Receptor, Biological_Activity: L-368,899 hydrochloride is a potent, selective, orally bioavailable, non-peptide oxytocin receptor antagonist, with IC50s of 8.9 nM and 26 nM for rat uterus and human uterus oxytocin receptor, respectively, used as a tocolytic agent.
IC50 & Target: IC50: 8.9 nM (rat uterus oxytocin receptor), 26 nM (human uterus oxytocin receptor)[1]
In Vitro: L-368,899 hydrochloride is a potent, orally bioavailable, non-peptide oxytocin receptor antagonist, with IC50s of 8.9 nM and 26 nM for rat uterus and human uterus oxytocin receptor, respectively. L-368,899 is less active on vasopressin receptor in human liver and kidney, rat liver and kidney (IC50, 510 nM, 960 nM, 890 nM, 2400 nM, respectively)[1].

Name: Orexin B, human Human orexin B, CAS: 205640-91-1, stock 16.5g, assay 98.3%, MWt: 2899.34, Formula: C123H212N44O35S, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein;Neuronal Signaling, Target: Orexin Receptor (OX Receptor);Orexin Receptor (OX Receptor), Biological_Activity: Orexin B, human is an endogenous agonist at Orexin receptor with Kis of 420 and 36 nM for OX1 and OX2, respectively.
IC50 & Target: Ki: 420 nM (OX1), 36 nM (OX2)[1]
In Vitro: Orexin B is derived by proteolytic amino acid precursor, prepro-orexin, which is encoded by a gene localized to chromosome 17q21 in humans. In radioligand binding studies, Orexin B has a higher affinity for the OX2 receptor[1]. Human Orexin B has two amino acid substitutions when compared with the rodent sequence. OX2 receptor is indeed a high-affinity receptor for human orexin B, with an IC50 of 36 nM in the binding assay and an EC50 of 60 nM in the [Ca2+]i transient assay. Human Orexin B has significantly lower affinity for the human OX1: the calculated IC50 in the competitive binding assay and the EC50 in the [Ca2+]i transient assay are 420 nM and 2500 nM for human orexin-B, respectively[2].
In Vivo: Human Orexin B significantly augments food intake; at the 2 hr time point, 5- and 12-fold stimulation of food consumption is observed by 3 nM and 30 nM orexin-B, respectively[2].

Name: Orexin B, rat, mouse Rat orexin B;Orexin B (mouse), CAS: 202801-92-1, stock 37.2g, assay 98.4%, MWt: 2936.40, Formula: C126H215N45O34S, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein;Neuronal Signaling, Target: Orexin Receptor (OX Receptor);Orexin Receptor (OX Receptor), Biological_Activity: Orexin B, rat, mouse is an endogenous agonist at Orexin receptor with Kis of 420 and 36 nM for OX1 and OX2, respectively.
IC50 & Target: Ki: 420 nM (OX1), 36 nM (OX2)[1]
In Vitro: Orexin B is derived by proteolytic amino acid precursor, prepro-orexin, which is encoded by a gene localized to chromosome 17q21 in humans. In radioligand binding studies, Orexin B has a higher affinity for the OX2 receptor[1]. Human Orexin B has two amino acid substitutions when compared with the rodent sequence. OX2 receptor is indeed a high-affinity receptor for human orexin B, with an IC50 of 36 nM in the binding assay and an EC50 of 60 nM in the [Ca2+]i transient assay. Human Orexin B has significantly lower affinity for the human OX1: the calculated IC50 in the competitive binding assay and the EC50 in the [Ca2+]i transient assay are 420 nM and 2500 nM for human orexin-B, respectively[2].
In Vivo: Human Orexin B significantly augments food intake; at the 2 hr time point, 5- and 12-fold stimulation of food consumption is observed by 3 nM and 30 nM orexin-B, respectively[2].

Name: EMPA, CAS: 680590-49-2, stock 19.7g, assay 98.7%, MWt: 454.54, Formula: C23H26N4O4S, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein;Neuronal Signaling, Target: Orexin Receptor (OX Receptor);Orexin Receptor (OX Receptor), Biological_Activity: EMPA is a high-affinity, reversible and selective orexin OX2 receptor antagonist. [3H]EMPA binds to human and rat OX2-HEK293 membranes with KD values of 1.1 and 1.4 nM respectively[1].
In Vitro: EMPA competitively antagonizes orexin-A-and orexin-B-evoked accumulation of [3H]inositol phosphates (IP) at hOX2 receptors with pA2 values of 8.6 and 8.8 respectively[1]. 
EMPA displaces the [3H]EMPA binding from cell membranes containing human and rat OX2 receptors, with Ki values of 1.10±0.24 nM and 1.45±0.13 nM, respectively[1]. 
EMPA shows an IC50=5.75 µM, Ki=2.63 µM, and IC50=12.8 µM, Ki=5.8 µM in the binding assay at human and mouse V1a receptors, respectively[1]. 
In CHO(dHFr-) cells stably expressing hOX2 receptors, EMPA inhibits orexin-A-or orexin-B-evoked [Ca2+]i response with IC50s of 8.8±1.7 nM and 7.9±1.7 nM, respectively[1].
In Vivo: EMPA (1-300 mg/kg; i.p.) dose-dependently reverses this [Ala11,D-Leu15]orexin-B-induced hyperlocomotion without itself significantly affecting locomotor activity (LMA) in male NMRI mice[1]. 
EMPA (3-30 mg/kg; i.p.) induces a significant and dose-dependent reduction in the baseline LMA in france and male Wistar rats. EMPA (3-30 mg/kg; i.p.) demonstrates a clear dose-dependent inhibition of spontaneous activity as compared with vehicle-treated animals[1].

Name: BI-6C9, CAS: 791835-21-7, stock 15.8g, assay 98.8%, MWt: 471.59, Formula: C23H25N3O4S2, Solubility: DMSO : 250 mg/mL (530.12 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Mitochondrial Metabolism, Biological_Activity: BI-6C9 is a BH3 interacting domain (Bid) inhibitor, which prevents mitochondrial outer membrane potential (MOMP) and mitochondrial fission, and protects the cells from cell death[1].

Name: GSK963, CAS: 2049868-46-2, stock 2.6g, assay 98.5%, MWt: 230.31, Formula: C14H18N2O, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Apoptosis, Target: RIP kinase, Biological_Activity: GSK963 is a chiral, highly potent and selective inhibitor of RIP1 kinase, with an IC50 of 29 nM. GSK963 is a selective and potent inhibitor of necroptosis in murine and human cells in vitro[1].
IC50 & Target: IC50: 29 nM (RIP1 in FP binding assay)[1].

Name: GSK2033, CAS: 1221277-90-2, stock 5.1g, assay 98.9%, MWt: 591.66, Formula: C29H28F3NO5S2, Solubility: DMSO : 30 mg/mL (50.70 mM; Need ultrasonic and warming), Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: LXR, Biological_Activity: GSK2033 is a LXR antagonist with pIC50s of 7 and 7.4 for LXRα or LXRβ, respectively.
IC50 & Target: pIC50: 7 (LXRα), 7.4 (LXRβ)[1]
In Vitro: GSK2033 is a LXR antagonist with pIC50s of 7 and 7.4 for LXRα or LXRβ, respectively. GSK2033 dose-dependently suppresses basal transcription in full-length LXRα or full-length LXRβ cotransfection assays with IC50s of 17 nM and 9 nM, respectively. GSK2033 also effectively suppresses the transcription of an ABCA1 driven luciferase reporter dose-dependently displaying IC50s of 52 nM for LXRα and 10 nM for LXRβ. GSK2033 also suppresses the expression of both of fatty acid synthase (FASN) and SREBP1[2].
In Vivo: One month treatment of GSK2033 does not have significant effects on hepatic triglyceride levels. Plasma triglyceride levels are also unaffected by treatment with GSK2033[2].

Name: Fluxametamide, CAS: 928783-29-3, stock 30.4g, assay 98.8%, MWt: 474.26, Formula: C20H16Cl2F3N3O3, Solubility: H2O : < 0.1 mg/mL (insoluble); DMSO : 125 mg/mL (263.57 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Neuronal Signaling;Membrane Transporter/Ion Channel, Target: GABA Receptor;GABA Receptor, Biological_Activity: Fluxametamide is an insecticide with wide spectrum, acts as an antagonist of GABA- and glutamate-gated chloride channels, with IC50 of 1.95 nM and 225 nM for M. domestica GABACls and GluCls.
IC50 & Target: IC50: 1.95 nM (M. domestica GABACls), 225 nM (M. domestica GluCls)[1]
In Vitro: Fluxametamide is an antagonist of GABA- and glutamate-gated chloride channels, dose-dependently inhibits currents induced by GABA and glutamate in M. domestica GABACls and GluCls, with IC50 values of 1.95 (1.18-3.21) nM and 225 (137-372) nM, respectively, and displays potent antagonistic activity against T. urticae GABACls with an IC50 of 0.219 (0.127-0.381) nM. Fluxametamide inhibits GABA responses in the wild-type L. striatellus GABACls with IC50 values of 1.40 (0.57-3.29) nM; in the A2′N mutant GABACls, the IC50 value is 3.51 (2.17-5.69) nM. Moreover, Fluxametamide scarcely inhibits GABA (EC50)-induced currents in rat GABACls at 10 μM and with no inhibition on glycine (EC50)-induced current in human α1 GlyCls at tested concentrations[1].
In Vivo: Fluxametamide shows significant insecticidal activity with an LD50 (LD95) value of 12.9 ± 4.9 ng/fly (38.7 ± 6.3 ng/fly)[1].

Name: STING agonist-3, CAS: 2138299-29-1, stock 34.8g, assay 98.3%, MWt: 750.81, Formula: C37H42N12O6, Solubility: DMSO : 250 mg/mL (332.97 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Immunology/Inflammation, Target: STING, Biological_Activity: STING agonist-3, compound 3, is a selective and non-nucleotide small-molecule STING agonist, which has durable anti-tumor effect and tremendous potential to improve treatment of cancer.
STING agonist-3 induces activation of STING and secretion of IFN-β with ECapp50 values of 130 nM, 186 nM in human PBMCs and Mouse PBMCs[1].
In Vitro: STING agonist-3 (Compound 3) induces dose-dependent activation of STING and secretion of IFN-β with ECapp50s of 130 nM,186 nM in human PBMCs and Mouse PBMCs[1].
In Vivo: STING agonist-3 (subcutaneous injection; 2.5mg/kg) activates secretion of IFN-β, IL-6, TNF-α, and KC/GROα (CXCL1) in wild-type but not Sting−/− mice, induces STING-dependent activation of type-I interferon and pro-inflammatory cytokines in vivo[1].
STING agonist-3 (subcutaneous injection; 3 mg/kg) exhibits systemic exposure with a half-life of 1.4 h and achieves systemic concentrations with EC50=200 ng /ml for mouse STING[1].
STING agonist-3 (injection intravenously; 1.5 mg/kg) results in significant tumor growth inhibition, and improves survival with 8 out of 10 mice remaining tumors free at day 43[1].

Name: Duocarmycin TM, CAS: 157922-77-5, stock 26g, assay 98.4%, MWt: 466.91, Formula: C25H23ClN2O5, Solubility: DMSO : ≥ 50 mg/mL (107.09 mM); H2O : < 0.1 mg/mL (insoluble), Clinical_Informat: No Development Reported, Pathway: Cell Cycle/DNA Damage;Antibody-drug Conjugate/ADC Related, Target: DNA Alkylator/Crosslinker;ADC Cytotoxin, Biological_Activity: Duocarmycin TM is an exceptionally potent antitumor antibiotic. Duocarmycin TM is a DNA alkylator.

Name: Duocarmycin MB, CAS: 1613286-58-0, stock 12.6g, assay 98.8%, MWt: 491.97, Formula: C27H26ClN3O4, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Cell Cycle/DNA Damage;Antibody-drug Conjugate/ADC Related, Target: DNA Alkylator/Crosslinker;ADC Cytotoxin, Biological_Activity: Duocarmycin MB is an antibody drug conjugates (ADCs) toxin. Duocarmycin is a DNA alkylating agent that binds in the minor groove. Duocarmycin MB can be used against multi-drug resistant cell lines.

Name: Tivantinib ARQ 197, CAS: 905854-02-6, stock 24.7g, assay 98.7%, MWt: 369.42, Formula: C23H19N3O2, Solubility: DMSO : ≥ 100 mg/mL (270.69 mM), Clinical_Informat: Phase 3, Pathway: Protein Tyrosine Kinase/RTK;Apoptosis, Target: c-Met/HGFR;Apoptosis, Biological_Activity: Tivantinib is a novel and highly selective c-Met tyrosine kinase inhibitor with Ki of 355 nM.

IC50 & Target: Ki: 355 nM (c-Met)[1]
In Vitro: Tivantinib (ARQ 197) selectively inhibits c-Met activity in cell-free and cell-based assays. c-Met-expressing cancer cell lines treated with Tivantinib display either a dose-dependent loss of proliferative capacity or caspase-dependent apoptosis that positively correlates with either ligand-dependent c-Met activity or constitutively active c-Met. To examine the biochemical mode of inhibition of Tivantinib, kinetic analyses are done using recombinant human c-Met in a filtermat-based assay. The Km of ATP is 50.5±2.2 μM, which is similar to the Km value of ATP. In these kinetic studies, Tivantinib inhibits human recombinant c-Met with a calculated inhibitory constant (Ki) of ~355 nM. In vitro exposure to Tivantinib inhibits constitutive c-Met phosphorylation in HT29 and MKN-45 cells, and HGF-induced c-Met phosphorylation in MDA-MB-231 and NCI-H441 cells with an IC50 of 100 to 300 nM[1]. Tivantinib is a low-molecular-weight compound, and is the first in class orally available selective inhibitor of c-Met[2].
In Vivo: Pharmacodynamically, the phosphorylation of c-Met in human colon xenograft tumors (HT29) is strongly inhibited by Tivantinib (ARQ 197), as assessed by a dramatic reduction of c-Met autophosphorylation 24 hours after a single oral dose of 200 mg/kg of Tivantinib. This same dosage in mice shows that tumor xenografts are exposed to sustained plasma levels of Tivantinib, consistent with the observed pharmacodynamic inhibition of c-Met phosphorylation and inhibition of proliferation of c-Met harboring cancer cell lines. A Cmax of 5.73 μg/mL (13 μM), an area under the concentration-time curve of 12.1 μg/mL h, and a t1/2 of 2.4 hours are measured. Plasma levels of Tivantinib 10 hours after dosing are determined to be 1.3 μM, >3-fold above the biochemical inhibitory constant of Tivantinib for c-Met[1].

Name: GNE-781, CAS: 1936422-33-1, stock 4.2g, assay 98.6%, MWt: 525.59, Formula: C27H33F2N7O2, Solubility: DMSO : 100 mg/mL (190.26 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Epigenetics;Epigenetics, Target: Epigenetic Reader Domain;Histone Acetyltransferase, Biological_Activity: GNE-781 is a highly potent and selective CBP inhibitor with an IC50 of 0.94 nM in TR-FRET assay. GNE-781 also inhibits BRET and BRD4(1) with IC50s of 6.2 nM and 5100 nM, respectively.
IC50 & Target: IC50: 0.94 nM (CBP), 6.2 nM (BRET), 5100 nM (BRD4(1))[1]
In Vitro: GNE-781 is a highly advanced potent and selective bromodomain inhibitor of cyclic adenosine monophosphate response element binding protein, binding protein (CBP). GNE-781 reduces FOXP3 (forkhead box P3) transcript levels. Examination of a subset of bromodomains reveals that GNE-781 is exquisitely selective for CBP/P300 and is remarkably selective for CBP (5425-fold) and P300 (4250-fold). GNE-781 demonstrates an appropriate balance of cell potency, selectivity (5425-fold over BRD4(1)) [1].
In Vivo: GNE-781 is a highly potent and selective CBP inhibitor that is efficacious in a MOLM-16 AML xenograft model. GNE-781 displays antitumor activity in an AML tumor model and is also shown to decrease Foxp3 transcript levels in a dose dependent manner.GNE-781 shows moderate to low clearance in vivo in all species evaluated, with acceptable oral bioavailability. The effect of GNE-781 is determined in an in vivo PK/PD experiment using a MOLM-16 (adult AML cell line) xenograft mouse model. Single doses of GNE-781 are given at dose levels between 3 and 30 mg/kg in MOLM-16 tumor-bearing animals, and samples are collected at time points covering 2-24 h. Tumor RNA is generated and used to assess MYC transcript by quantitative RT-PCR relative to vehicle-treated animals. Suppression of MYC is observed at doses as low as 3 mg/kg at 2 and 8 h, with maximal suppression observed at 10 and 30 mg/kg at 2 h (87% and 88% inhibition, respectively). To evaluate the in vivo efficacy of GNE-781, MOLM-16 AML xenografts are established in SCID beige mice. Upon tumor establishment, dosing of GNE-781 is initiated with po doses of 3-30 mg/kg, twice daily (BID). Single-agent efficacy is observed at all doses, as evidenced by inhibition of MOLM-16 tumor growth. Tumor growth inhibition (%TGI) is 73%, 71%, and 89% at 3, 10, and 30 mg/kg, respectively. All doses of GNE-781 are well tolerated over the 21-day dosing window, with a maximal body weight loss of 3.7%[1].

Name: PT2399, CAS: 1672662-14-4, stock 34.4g, assay 98.9%, MWt: 419.32, Formula: C17H10F5NO4S, Solubility: DMSO : ≥ 200 mg/mL (476.96 mM), Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: HIF/HIF Prolyl-Hydroxylase, Biological_Activity: PT2399 is a potent and selective HIF-2α antagonist, which directly binds to HIF-2α PAS B domain with an IC50 of 6 nM. PT2399 displays potent antitumor activity in vivo[1][2][3].
IC50 & Target: IC50: 6 nM (HIF-2α)[3]
In Vitro: PT2399 (compound 10f) inhibits HIF-2α with an IC50 of 6 nM[3]. 
PT2399 can bind directly to the HIF-2α PAS B domain, and cripple HIF-2α’s ability to bind to Aryl hydrocarbon receptor nuclear translocator (ARNT)[2]. 
PT2399 (20 μM) causes off-target toxicity because it inhibits the proliferation of HIF-2α −/− 786-O cells and other cancer cell lines with undetectable HIF-2α[2]. 
PT2399 (0.2–2 μM; 0-21 days) inhibits 786-O cells soft agar growth[2]. 
PT2399 represses various HIF target genes in 786-O VHL−/− ccRCC cells, does not suppress HIF-1α-specific targets such as BNIP3[2]. 
In Vivo: PT2399 inhibits tumor cell proliferation 3.5 fold in renal cell carcinoma (RCC) bearing mice[1]. 
PT2399 reduces tumor cell density and increases fibrosis in RCC bearing mice[1]. 
PT2399 (100 mg/kg; oral gavage; every 12 hours) is more active than SU 11248, and inhibits tumor growth in several SU 11248-resistant tumors in RCC bearing mice [1]. 
PT2399 directly inhibits HIF-2α causes tumor regression in preclinical models of primary and metastatic pVHL-defective ccRCC in an on-target fashion[2].

Name: TM-N1324, CAS: 1144477-35-9, stock 2.2g, assay 98.7%, MWt: 397.79, Formula: C18H13ClFN7O, Solubility: DMSO : 6 mg/mL (15.08 mM; Need ultrasonic and warming), Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein, Target: GHSR, Biological_Activity: TM-N1324 is an agonist of G-Protein-Coupled Receptor 39 (GPR39) with EC50s of 9 nM/5 nM in the presence of Zn2+, and 280 nM/180 nM in the absence of Zn2+ for human/murine GPR39.
IC50 & Target: EC50: 280 nM (human GPR39 without Zn2+), 9 nM (human GPR39 with Zn2+), 180 nM (murine GPR39 without Zn2+), 5 nM (murine GPR39 with Zn2+)[1]
In Vitro: TM-N1324 activates human GPR39 with high efficacy and potencies of 280 nM and 9 nM in the absence and presence of Zn2+, respectively. TM-N1324 has similar potencies on murine GPR39, 180 nM and 5 nM. TM-N1324 is also found to have promising in vitro ADME properties. TM-N1324 has reasonably good aqueous solubility (65 μM at pH 7.0). Measurements of somatostatin confirms that the GPR39 agonist TM-N1324 increases somatostatin release by 53%[1].

Name: ML-792, CAS: 1644342-14-2, stock 18.4g, assay 98.8%, MWt: 551.41, Formula: C21H23BrN6O5S, Solubility: DMSO : 250 mg/mL (453.38 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: E1/E2/E3 Enzyme, Biological_Activity: ML-792 is a specific small ubiquitin-like modifier (SUMO)-activating enzyme (SAE) inhibitor. ML-792 is a potent and selective inhibitor of SAE/SUMO1 and SAE/SUMO2 in enzymatic assays (IC50s of 3 and 11 nM, respectively) compared with NAE/NEDD8 and UAE/ubiquitin (IC50s of 32 μM and >100 μM, respectively)[1].

Name: BI-3802, CAS: 2166387-65-9, stock 23.8g, assay 98.5%, MWt: 484.98, Formula: C24H29ClN6O3, Solubility: H2O : < 0.1 mg/mL (insoluble); Methanol : 2 mg/mL (4.12 mM; ultrasonic and adjust pH to 5 with 1M HCl); DMSO : 5 mg/mL (10.31 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: BI-3802 is a highly potent BCL6 degrader, inhibiting the BTB domain of BCL6, with an IC50 of ≤3 nM; BI-3802 has antitumor activity.
IC50 & Target: IC50: ≤3 nM (BCL6 BTB)[1]
In Vitro: BI-3802 is a BCL6 inhibitor, with an IC50 of ≤3 nM. BI-3802 shows an IC50 of 43 nM for the cellular BCL6[1].

Name: GeA-69, CAS: 2143475-98-1, stock 25.1g, assay 98.4%, MWt: 300.35, Formula: C20H16N2O, Solubility: DMSO : ≥ 125 mg/mL (416.18 mM), Clinical_Informat: No Development Reported, Pathway: Epigenetics;Cell Cycle/DNA Damage, Target: PARP;PARP, Biological_Activity: GeA-69 is a selective, highly cell permeable allosteric inhibitor of poly-adenosine-diphosphate-ribose polymerase 14 (PARP14) targeting macrodomain 2, with a Kd of 2.1 µM[1].
IC50 & Target: Kd: 2.1 µM (PARP14)[1]

Name: GSK656, CAS: 2131798-13-3, stock 26.5g, assay 98.1%, MWt: 293.94, Formula: C10H14BCl2NO4, Solubility: DMSO : 67.5 mg/mL (229.64 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Anti-infection, Target: Bacterial, Biological_Activity: GSK656 is a potent antitubercular agent, acting as an inhibitor of Mycobacterium tuberculosis (Mtb) leucyl-tRNA synthetase (LeuRS), with an IC50 of 0.2 μM.
IC50 & Target: IC50: 0.2 μM (Mtb LeuRS)[1]
In Vitro: GSK656 is highly selective inhibitor for Mycobacterium tuberculosis (Mtb) leucyl-tRNA synthetase (LeuRS), with an IC50 of 0.2 μM, and shows IC50s of >300 μM and 132 μM for human mitochondrial LeuRS and human cytoplasmic LeuRS, respectively. GSK656 exhibits antitubercular activity with minimal inhibitory concentration (MIC) of 80 nM against Mtb H37Rv. GSK656 also exhibits EC50s of 381 μM against HepG2 cell, and 137 μM against HepG2 protein synthesis[1].
In Vivo: GSK656 shows potent antitubercular activity in mice infected with M. tuberculosis H37Rv, with ED99 of 0.4 mg/kg[1].

Name: VU0650786, CAS: 1809085-30-0, stock 29.9g, assay 98.9%, MWt: 387.80, Formula: C18H15ClFN5O2, Solubility: H2O : < 0.1 mg/mL (insoluble); DMSO : 250 mg/mL (644.66 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein;Neuronal Signaling, Target: mGluR;mGluR, Biological_Activity: VU0650786 is a potent and selective CNS penetrant negative allosteric modulator of metabotropic glutamate receptor subtype 3 (mGlu3 NAM), with an IC50 of 392 nM. VU0650786 has antidepressant and anxiolytic activity in rodents[1].
IC50 & Target: IC50: 392 nM (mGlu3)[1].

Name: LLY-283, CAS: 2040291-27-6, stock 3.8g, assay 98.5%, MWt: 342.35, Formula: C17H18N4O4, Solubility: DMSO : 250 mg/mL (730.25 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Epigenetics, Target: Histone Methyltransferase, Biological_Activity: LLY-283 is a potent, selective and oral protein arginine methyltransferase 5 (PRMT5) inhibitor, with an IC50 of 22 nM and a Kd of 6 nM for PRMT5:MEP50 complex, and shows antitumor activity.
IC50 & Target: IC50: 22 nM (PRMT5:MEP50)[1] 
Ki: 6 nM (PRMT5:MEP50)[1]
In Vitro: LLY-283 is a potent, oral and selective arginine methyltransferase 5 (PRMT5) inhibitor, with an IC50 of 22 nM in vitro and 25 nM in cells, as well as a Kd of 6 nM for PRMT5:MEP50 complex in vitro; LLY-283 inhibits the proliferation of A375 cell with an IC50 of 46 nM[1].
In Vivo: LLY-283 (20 mg/kg; p.o., QD (once a day)) causes a significant inhibition on tumor growth in mice bearing A375 cells after treatment for 28 days[1].

Name: PF-9366, CAS: 72882-78-1, stock 7.7g, assay 98.5%, MWt: 350.84, Formula: C20H19ClN4, Solubility: DMSO : 25 mg/mL (71.26 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: PF-9366 is a human methionine adenosyltransferase 2A (Mat2A) inhibitor, with an IC50 of 420 nM and a Kd of 170 nM.
IC50 & Target: IC50: 420 nM (Mat2A)[1] 
Kd: 170 nM (Mat2A)[1]
In Vitro: PF-9366 is a Mat2A inhibitor, with an IC50 of 420 nM and a Kd of 170 nM. PF-9366 displays no substantial off-target activity in GPCRs, neurotransporters, phosphodiesterases, and ion channels. PF-9366 has inhibitory activity against Mat2A in cancer cells. PF-9366 inhibits cellular S-Adenosyl-L-methionine (SAM) production with an IC50 of 1.2 μM in H520 lung carcinoma cells. PF-9366 is more potent in Huh-7 cells against SAM synthesis, with an IC50 of 255 nM, and also suppresses the proliferation of cells with an IC50 of 10 μM.

Name: AZD7624, CAS: 1095004-78-6, stock 25.2g, assay 98.2%, MWt: 491.56, Formula: C27H30FN5O3, Solubility: 10 mM in DMSO, Clinical_Informat: Phase 2, Pathway: MAPK/ERK Pathway;Autophagy, Target: p38 MAPK;Autophagy, Biological_Activity: AZD7624 is an inhaled p38 inhibitor, with potent anti-inflammatory activity.
IC50 & Target: p38[1]
In Vitro: AZD7624 is an inhaled p38 inhibitor, with potent anti-inflammatory activity. AZD7624 inhibits LPS-induced TNFα in human mononuclear cells, in whole blood as well as in alveolar macrophages in vitro, with pIC50s of 8.4, 8.1, and 9.0[1].

Name: Apararenone MT-3995, CAS: 945966-46-1, stock 13.3g, assay 98.9%, MWt: 364.39, Formula: C17H17FN2O4S, Solubility: DMSO : ≥ 125 mg/mL (343.04 mM), Clinical_Informat: Phase 2, Pathway: Metabolic Enzyme/Protease, Target: Mineralocorticoid Receptor, Biological_Activity: Apararenone (MT-3995) is a novel non-steroidal mineralocorticoid receptor antagonists under development for the treatment of diabetic nephropathies and non-alcoholic steatohepatitis.
IC50 & Target: Mineralocorticoid receptor[1]
In Vivo: Recently, a phase II clinical trial has been initiated among patients with non-alcoholic steatohepatitis (NASH) in Japan[1].

Name: Padsevonil UCB-0942, CAS: 1294000-61-5, stock 32.6g, assay 98.2%, MWt: 432.80, Formula: C14H14ClF5N4O2S, Solubility: H2O : < 0.1 mg/mL (insoluble); DMSO : 100 mg/mL (231.05 mM; Need ultrasonic), Clinical_Informat: Phase 3, Pathway: Others, Target: Others, Biological_Activity: Padsevonil is a potent antiepileptic agent.
In Vitro: Padsevonil (UCB0942) is a potent antiepileptic agent[1].

Name: Rosiptor AQX-1125, CAS: 782487-28-9, stock 2.8g, assay 98.6%, MWt: 321.50, Formula: C20H35NO2, Solubility: DMSO : 150 mg/mL (466.56 mM; Need ultrasonic and warming), Clinical_Informat: Phase 3, Pathway: Metabolic Enzyme/Protease, Target: Phosphatase, Biological_Activity: Rosiptor (AQX-1125) is a selective and orally active phosphatase SHIP1 activator with anti-inflammatory effects. Rosiptor (AQX-1125) inhibits Akt phosphorylation, inflammatory mediator production and leukocyte chemotaxis in vitro[1][2].
IC50 & Target: SHIP1[1]
In Vitro: Rosiptor (0.1-10 μM; 30 minutes) inhibits Akt activation in MOLT-4, but not in Jurkat cells[1].
In Vivo: Rosiptor (3-30 mg/kg; p.o.; daily for 3 days) significantly reduces the total number of BAL leukocytes in NSC-125066-challenged mice and reduces MPO activity[2]. 
Rosiptor (10 mg/kg; p.o.) has the Cmax value of 0.830 μM and the t1/2 value of 5.2 hours. AQX-1125 also exhibits >80% oral bioavailability[1].

Name: Seltorexant JNJ-42847922, CAS: 1293281-49-8, stock 38.4g, assay 98.4%, MWt: 407.44, Formula: C21H22FN7O, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein;Neuronal Signaling, Target: Orexin Receptor (OX Receptor);Orexin Receptor (OX Receptor), Biological_Activity: Seltorexant (JNJ-42847922) is an orally active, high-affinity, and selective OX2R antagonist (pKi values of 8.0 and 8.1 for human and rat OX2R). Seltorexant (JNJ-42847922) crosses the blood-brain barrier and quickly occupies OX2R binding sites in the rat brain[1].
IC50 & Target: pKi: 8.0 (human OX2R), 8.1 (rat OX2R)[1]

Name: Tucidinostat Chidamide;HBI-8000;CS 055, CAS: 1616493-44-7, stock 15.1g, assay 99%, MWt: 390.41, Formula: C22H19FN4O2, Solubility: DMSO : ≥ 50 mg/mL (128.07 mM), Clinical_Informat: Launched, Pathway: Epigenetics;Cell Cycle/DNA Damage, Target: HDAC;HDAC, Biological_Activity: Tucidinostat is a potent and orally bioavailable HDAC enzymes class I (HDAC1/2/3) and class IIb (HDAC10) inhibitor, with IC50s of 95, 160, 67 and 78 nM, less active on HDAC8 and HDAC11 (IC50s, 733 nM, 432 nM, respectively), and shows no effect on HDAC4/5/6/7/9.
IC50 & Target: IC50: 95 nM (HDAC1), 160 nM (HDAC2), 67 nM (HDAC3), 78 nM (HDAC10), 733 nM (HDAC8), 432 nM (HDAC11)[1]
In Vitro: Tucidinostat (Chidamide/CS055/HBI-8000) is a potent and orally bioavailable HDAC enzymes class I (HDAC1, 2, 3) and class IIb (HDAC10) inhibitor, with IC50s of 95, 160, 67 and 78 nM, less active on HDAC8 and HDAC11 (IC50s, 733 nM, 432 nM, respectively), and shows no effect on HDAC4/5/6/7/9 (IC50s, >30 μM). Tucidinostat shows potent antitumor activity, and inhibits several human derived tumor cell lines, such as HL-60, U2OS, LNCaP with GI50s of 0.4 ± 0.1, 2.0 ± 0.6, and 4.0 ± 1.2 μM, respectively. In addition, Tucidinostat shows less toxic to normal cells from human fetal kidney (CCC-HEK) and liver (CCCHEL)[1].
In Vivo: Tucidinostat (12.5-50 mg/kg, p.o.) dose-dependently reduces tumor size and tumor weight in mice bearing HCT-8 colorectal carcinoma, A549 lung carcinoma, BEL-7402 liver carcinoma, and MCF-7 breast carcinoma, and with no obvious body loss[1].

Name: Vorolanib CM082;X-82, CAS: 1013920-15-4, stock 10.2g, assay 99%, MWt: 439.48, Formula: C23H26FN5O3, Solubility: DMSO : 27 mg/mL (61.44 mM; Need ultrasonic), Clinical_Informat: Phase 3, Pathway: Protein Tyrosine Kinase/RTK;Protein Tyrosine Kinase/RTK, Target: VEGFR;PDGFR, Biological_Activity: Vorolanib (CM082; X-82) is an orally active, multikinase VEGFR/PDGFR inhibitor. Vorolanib minimizes toxicity, disrupts tumor angiogenesis and tumor cell proliferation, and induces of tumor cell death[1].
IC50 & Target: VEGFR, PDGFR[1]

Name: Acrizanib, CAS: 1229453-99-9, stock 32.3g, assay 99%, MWt: 445.40, Formula: C20H18F3N7O2, Solubility: DMSO : 41.67 mg/mL (93.56 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Protein Tyrosine Kinase/RTK, Target: VEGFR, Biological_Activity: Acrizanib is a VEGFR-2 inhibitor, with an IC50 of 17.4 nM for BaF3-KDR.
IC50 & Target: IC50: 17.4 nM (VEGFR-2)[1].
In Vitro: Acrizanib is a VEGFR-2 inhibitor, with an IC50 of 17.4 nM for BaF3-KDR. Acrizanib (compound 35) exhibits ≤10% remaining kinase activity against only 13 wild type kinases: CSF1R, Kit, PDGFRα, PDGFRβ, VEGFR1, VEGFR2, VEGFR3, Fms (soluble VEGFR1), DDR1, DDR2, TIE1, and ABL1 (nonphosphorylated)[1].
In Vivo: Rat ocular PK studies with Acrizanib shows a distinctly different profile from that observed with compound 25. While prolonged exposure is once again evident in the PEC, the AUC ratio to the level of Acrizanib in plasma is markedly increased (>21000-fold higher exposure in the PEC than plasma on day 11). Furthermore, unlike 25, Acrizanib also afford much improved retina to plasma AUC exposure ratio after 10 days of dosing (598× for Acrizanib vs 0.8× for 25)[1].

Name: NGP555, CAS: 1304630-27-0, stock 6.4g, assay 98.3%, MWt: 406.52, Formula: C23H23FN4S, Solubility: DMSO : 25 mg/mL (61.50 mM; Need ultrasonic), Clinical_Informat: Phase 1, Pathway: Stem Cell/Wnt;Neuronal Signaling, Target: γ-secretase;γ-secretase, Biological_Activity: NGP555 is a γ-secretase modulator.
IC50 & Target: γ-secretase[1]
In Vitro: NGP555 potently lowers Aβ42 in cell cultures (9 nM) while increasing shorter forms of Aβ[1].
In Vivo: NGP555 significantly lowers Aβ42 in the cerebrospinal fluid (CSF) at time points from 8 to10 hours post dose, panel B shows that reduction of Aβ cerebrospinal fluid (CSF) levels is significant at 3.75 mg/kg of NGP555 and above, and panel C shows an increase in Aβ38 levels at 15 mg/kg of NGP555 and above. When combining the reduction of Aβ42 with an increase in Aβ38, NGP555 is effective at raising CSF Aβ38/42 ratio at 1.87 mg/kg and above (panel D). NGP555-treated Tg mice show a significant protection from decline in performance with >65% less decline (P<0.005) when comparing the differential of Tg to non-Tg vehicle-treated mice. NGP555 also shows good oral bioavailability and is brain-penetrant with a brain:plasma ratio of ~0.93 in mice[1].

Name: BI-882370, CAS: 1392429-79-6, stock 15.1g, assay 98.2%, MWt: 569.67, Formula: C28H33F2N7O2S, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: MAPK/ERK Pathway, Target: Raf, Biological_Activity: BI-882370 is a potent and selective RAF kinase inhibitor that binds to the ATP binding site of the kinase positioned in the DFG-out (inactive) conformation of the BRAF kinase. BI-882370 (BI 882370) inhibits the oncogenic BRAFV600E-mutant, the WT BRAF and CRAF kinases with IC50s of 0.4, 0.8, and 0.6 nM, respectively. BI-882370 also inhibits SRC family kinases[1].
IC50 & Target: IC50: of 0.4 nM (BRAFV600E-mutant kinase), 0.8 nM (WT BRAF kinase), 0.6 nM (CRAF kinase)[1]
In Vitro: BI-882370 (0.9-6000 nM; 3 days) inhibits the BRAF-mutant human melanoma and colorectal cancer cells proliferation with a EC50 range of 1-10 nM[1].
BI 882370 (0.1-100 nM, 0.1-3000 nM; 2 hours) results in a reduction of p-MEK1/2, p-ERK1/2 and cyclin D1/D2 expression in BRAFV600E-mutant A375 cells; induces phosphorylation of MEK1/2 and enhanced phosphorylation of ERK1/2 in WT BRO cells (3-300 nM)[1].
BI 882370 (0.1-100 nM, 0.1-3000 nM; 24 hours) suppresses cyclin D1/D2 expression, induces Kip1/p27 expression at concentrations of 1 nM or higher in BRAFV600E-mutant A375 cells, expression of cyclins D1/D2 or Kip1/p27 is not affected in WT BRO cells[1].
In Vivo: BI-882370 (deliver orally; 25 mg/kg, 50 mg/kg; twice daily; 2 weeks) is efficacious in multiple mouse models of BRAF-mutant melanomas and colorectal carcinomas, shows superior efficacy compared with Vemurafenib, Dabrafenib, or Trametinib[1].
BI-882370 (deliver orally; 25 mg/kg; twice daily; 40 days) developes resistance within 3 weeks, but resistance is not observed during 5 weeks of second-line therapy in combination with trametinib[1].
BI-882370 (deliver orally; 60 mg/kg; once daily; 2 weeks) indicates lack of toxicity in terms of clinical chemistry, hematology, pathology, and toxicogenomics in rats[1].

Name: PAT-505, CAS: 1782070-22-7, stock 2.2g, assay 98.8%, MWt: 473.92, Formula: C23H18ClF2N3O2S, Solubility: DMSO : 48.33 mg/mL (101.98 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Phosphodiesterase (PDE), Biological_Activity: PAT-505 is a potent, selective, noncompetitive and orally available autotaxin inhibitor, with an IC50 of 2 nM in Hep3B cells, 9.7 nM in human blood and 62 nM in mouse plasma.
IC50 & Target: IC50: 2 nM (Autotaxin, Hep3B cell), 9.7 nM (Autotaxin, Human blood), 62 nM (Autotaxin, Mouse plasma)[1]
In Vitro: PAT-505 is a potent, selective, noncompetitive and orally available autotaxin inhibitor, with an IC50 of 2 nM in Hep3B cells, 9.7 nM in human blood and 62 nM in mouse plasma. PAT-505 is selective for ATX versus other ENPP proteins, and shows marginal inhibition of radiolabeled agonist or antagonist binding to the adenosine A3 receptor, MT1 melatonin receptor, prostaglandin E2 EP4 receptor, 5-HT5a serotonin receptor, and GABA-gated Cl- channel with 50%-70% inhibition at 10 µM[1].
In Vivo: PAT-505 suppresses ATX lysoPLD activity with an average IC50 value of 62 nM and an average IC90 value of 630 nM in mouse plasma, and the IC90 in rat plasma is ∼770 nM. PAT-505 (30 mg/kg, p.o.) significantly reduces fibrotic score, the percentage of PSR-positive area, and α-SMA immunoreactivity in mouse model of nonalcoholic steatohepatitis (NASH)[1].

Name: Balovaptan RG7314, CAS: 1228088-30-9, stock 20.5g, assay 98%, MWt: 409.91, Formula: C22H24ClN5O, Solubility: DMSO : 62.5 mg/mL (152.47 mM; Need ultrasonic), Clinical_Informat: Phase 3, Pathway: GPCR/G Protein, Target: Vasopressin Receptor, Biological_Activity: Balovaptan (RG7314) is a highly potent and selective brain-penetrant vasopressin 1a (hV1a) receptor antagonist, with Kis of 1 and 39 nM for human (hV1a) and mouse (mV1a) receptors, and is used for the research of autism.
IC50 & Target: Ki: 1 nM (hV1a), 39 nM (mV1a)[1]
In Vitro: Balovaptan (RG7314) is a highly potent and selective brain-penetrant vasopressin 1a (hV1a) receptor antagonist, with Kis of 1 and 39 nM for hV1a and mhV1a, and is used for the research of autism. Balovaptan shows >30000-fold selectivity for hV1a over hV2 receptors, 9891-fold selectivity over hOTR (human oxytocin receptor)[1].

Name: Baloxavir marboxil S-033188, CAS: 1985606-14-1, stock 26.3g, assay 98.5%, MWt: 571.55, Formula: C27H23F2N3O7S, Solubility: DMSO : 33.33 mg/mL (58.32 mM; Need ultrasonic), Clinical_Informat: Launched, Pathway: Anti-infection, Target: Influenza Virus, Biological_Activity: Baloxavir marboxil is a small molecule inhibitor of the cap-dependent endonuclease of influenza A and B viruses.

Name: Dotinurad, CAS: 1285572-51-1, stock 19.7g, assay 98.6%, MWt: 358.20, Formula: C14H9Cl2NO4S, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Dotinurad is a potent uricosuric agent, with an IC50 of 3.6 µM for uric acid[1].

Name: Picrotin, CAS: 21416-53-5, stock 38.3g, assay 98.5%, MWt: 310.30, Formula: C15H18O7, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Picrotin is an inhibitor of glycine receptors (GlyRs) which blocks α2 GlyR, α1 GlyR and α3 GlyR[1][2].
IC50 & Target: α2 GlyR, α1 GlyR, α3 GlyR[1][2]

Name: 6''-O-Acetylglycitin, CAS: 134859-96-4, stock 34.7g, assay 98.6%, MWt: 488.44, Formula: C24H24O11, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: 6''-O-Acetylglycitin, a acetyl glucoside, is one of the isoflavone isomer in soybeans, shows various extents of content reduction dependent on storage temperature, packaging condition, and its isoflavone isomer kind[1].

Name: Inarigivir soproxil SB9200, CAS: 942123-43-5, stock 2.5g, assay 98.4%, MWt: 703.62, Formula: C25H34N7O13PS, Solubility: DMSO : ≥ 102 mg/mL (144.96 mM), Clinical_Informat: Phase 2, Pathway: Anti-infection, Target: HCV, Biological_Activity: Inarigivir soproxil is an agonist of innate immunity and shows potent antiviral activity against resistant hepatitis C virus (HCV) variants, with EC50s of 2.2 and 1.0 μM for HCV 1a/1b in cells of genotype 1 HCV replicon systems.
IC50 & Target: EC50: 2.2/1.0 μM (HCV 1a/1b)[1].
In Vitro: Inarigivir soproxil (SB 9200) is an oral modulator of innate immunity that is believed to act via the activation of the RIG-I and NOD2 pathways. SB 9200 has broad-spectrum antiviral activity against RNA viruses including hepatitis C virus (HCV), norovirus, respiratory syncytial virus and influenza and has demonstrated activity against hepatitis B virus (HBV). Inarigivir soproxil is shown to inhibit HCV replication and the range of inhibition is comparable between genotypes 1a and 1b. Inarigivir soproxil demonstrates pan-genotypic antiviral activity against HCV. Inarigivir soproxil is active against DAA-resistant HCV variants[1].

Name: 5-Methoxyflavone, CAS: 42079-78-7, stock 11.3g, assay 98.7%, MWt: 252.26, Formula: C16H12O3, Solubility: DMSO : 125 mg/mL (495.52 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Cell Cycle/DNA Damage, Target: DNA/RNA Synthesis, Biological_Activity: 5-Methoxyflavone, belonged to Flavonoid family, is a DNA polymerase-beta inhibitor and neuroprotective agent against beta-amyloid toxicity. possess central nervous system (CNS) depressant effect mediated through the ionotropic GABAA receptors.
IC50 & Target: DNA polymerase-beta[1].
In Vitro: 5-Methoxyflavone (compound 1) is identified as a candidate compound endowed with the ability to inhibit DNA pol-β in multiple and to prevent cell-cycle initiation and subsequent neuronal apoptosis in Aβ-challenged primary neuronal cultures. 5-methoxyflavone (10-30 μM) is able to significantly enhance toxicity of MMS on 92TAg cells. 5-Methoxyflavone (1 or 10 μM) significantly reduces polymerase activity on a gapped substrate[1]. 
5-Methoxyflavone (5-MF, 0-100 μg/mL) results in a time dependent reduction in the levels of antiapoptotic proteins cFLIP, Mcl-1 and an increase in the proapoptotic protein BAX. 5-MF induces both TRAIL-R1(DR4) and TRAIL-R2 (DR5) in a time-dependent manner[2].
In Vivo: 5-Methoxyflavone (100, 150 mg/kg, i.p) significantly decreases the latency time to loss of righting reflex. 5-Methoxyflavone (50, 100 and 150 mg/kg, i.p) exhibits a significant and dose-dependent reduction in the spontaneous locomotor activity. 5-Methoxyflavone (50, 100 mg/kg, i.p) reduces the rearing response. 5-Methoxyflavone (100, 125 and 150 mg/kg, i.p) completely abolishesed the grooming response similar to diazepam treated animals[3].

Name: Elemicin, CAS: 487-11-6, stock 38.2g, assay 98.9%, MWt: 208.25, Formula: C12H16O3, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Stearoyl-CoA Desaturase (SCD), Biological_Activity: Elemicin is a alkenylbenzene widely distributed in many herbs and spices. Elemicin inhibits Stearoyl-CoA Desaturase 1 (SCD1) by metabolic activation. Elemicin is one of the main components in aromatic food and has antimicrobial, antioxidant, and antiviral activities. Elemicin possesses genotoxicity and carcinogenicity[1].
IC50 & Target: SCD1[1]

Name: Benorilate Salipran, CAS: 5003-48-5, stock 18.9g, assay 98.1%, MWt: 313.30, Formula: C17H15NO5, Solubility: DMSO : 125 mg/mL (398.98 mM; Need ultrasonic), Clinical_Informat: Launched, Pathway: GPCR/G Protein, Target: Prostaglandin Receptor, Biological_Activity: Benorylate (Salipran) is the esterification product of paracetamol and acetylsalicylic acid. It has anti-inflammatory, analgesic and antipyretic properties. Benorylate (Salipran) could also inhibit prostaglandin (PG) synthesis.
IC50 & Target: Prostaglandin[4].
In Vitro: Benorylate (Salipran) is an esterified aspirin preparation whose antirheumatic properties are reported to be as good as those of aspirin[1]. Benorylate (Salipran) causes a large decrease in the liver’s conversion rate of lactate into glucose, an important component of glucose homeostasis. Benorylate (Salipran) also impairs the urea synthesis rate from ammonia, another important function of the liver[2].
In Vivo: Benorylate (Salipran) is probably absorbed as the intact molecule which accounts for its good gastric tolerance[3]. Benorylate (Salipran) could inhibit PG synthesis in laboratory animals and in human tissue[4].

Name: Inosine pranobex Imunovir; Delimmun; Groprinosin;, CAS: 36703-88-5, stock 26.6g, assay 99%, MWt: 1115.23, Formula: C52H78N10O17, Solubility: DMSO : 62.5 mg/mL (56.04 mM; Need ultrasonic), Clinical_Informat: Launched, Pathway: Anti-infection, Target: HIV, Biological_Activity: Inosine pranobex is a potent, broad-spectrum antiviral compound for HIV infection. Inosine pranobex is an immunopotentiator[1].

Name: D-(+)-Trehalose dihydrate D-Trehalose dihydrate; α,α-Trehalose dihydrate, CAS: 6138-23-4, stock 13.8g, assay 98.9%, MWt: 378.33, Formula: C12H26O13, Solubility: H2O : 150 mg/mL (396.48 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: D-(+)-Trehalose dihydrate, isolated from Saccharomyces cerevisiae, can be used as a food ingredient and pharmaceutical excipient.
In Vitro: Trehalose dihydrate is a safe, naturally occurring disaccharide used as a food ingredient and pharmaceutical excipient[1].

Name: Cinnamylideneacetic acid Cinnamalacetic acid, CAS: 1552-94-9, stock 31.7g, assay 98.9%, MWt: 174.20, Formula: C11H10O2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Anti-infection, Target: Bacterial, Biological_Activity: Cinnamylideneacetic acid is a photoresponsive compound which is capable of a photoinduced [2+2] cycloaddition[1].

Name: 4-Hydroxychalcone, CAS: 20426-12-4, stock 12.6g, assay 98.5%, MWt: 224.25, Formula: C15H12O2, Solubility: DMSO : ≥ 250 mg/mL (1114.83 mM), Clinical_Informat: No Development Reported, Pathway: NF-κB, Target: NF-κB, Biological_Activity: 4-Hydroxychalcone is a chalcone metabolite with anti-angiogenic and anti-inflammatory activities. 4-Hydroxychalcone suppresses angiogenesis by suppression of growth factor pathway with no signs of cytotoxicity[1]. 4-Hydroxychalcone inhibits TNF-α induced NF-κB pathway activation and activates BMP signaling, reduces resistant hypertension (RH) by attenuating hyperaldosteronism and renal injury in mice[2].
IC50 & Target: NF-κB[2]

Name: 5α-Cholestan-3β-ol Dihydrocholesterol;5α-Cholestanol;NSC 18188, CAS: 80-97-7, stock 24.7g, assay 98.8%, MWt: 388.67, Formula: C27H48O, Solubility: DMSO : 1 mg/mL (2.57 mM; ultrasonic and warming and heat to 60°C); H2O : < 0.1 mg/mL (insoluble), Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: 5α-Cholestan-3β-ol is a derivitized steroid compound, which is isolated from the testes of White Carneau pigeons.
In Vitro: 5α-Cholestan-3β-ol is derived from cholesterol by the action of intestinal microorganisms. It is known to induce the formation of gall stones in rabbits in the presence of sodium ions. 5α-Cholestan-3β-ol is used as a standard in lipid analysis using HPLC.

Name: Ethylvanillin acetate, CAS: 72207-94-4, stock 29.1g, assay 98.9%, MWt: 208.21, Formula: C11H12O4, Solubility: DMSO : ≥ 250 mg/mL (1200.71 mM), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Ethyl vanillin acetate is acectate form of ethyl vanillin. Ethyl vanillin acetate is a flavorant used in chocolate or candy[1].

Name: 6-Hydroxyflavone, CAS: 6665-83-4, stock 30g, assay 98.5%, MWt: 238.24, Formula: C15H10O3, Solubility: DMSO : 125 mg/mL (524.68 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: 6-Hydroxyflavone is a naturally occurring flavone, with anti-inflammatory activity. 6-Hydroxyflavone exhibits inhibitory effect towards bovine hemoglobin (BHb) glycation. 6-Hydroxyflavone can activate AKT, ERK 1/2, and JNK signaling pathways to effectively promote osteoblastic differentiation. 6-Hydroxyflavone inhibits the LPS-induced NO production[1] [2].

Name: D-Melibiose, CAS: 585-99-9, stock 33.6g, assay 98.1%, MWt: 342.30, Formula: C12H22O11, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: D-Melibiose is a disaccharide which is composed of one galactose and one glucose moiety in an alpha (1-6) glycosidic linkage.

Name: Flavonol, CAS: 577-85-5, stock 2.1g, assay 98.9%, MWt: 238.24, Formula: C15H10O3, Solubility: , Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity:

Name: Spiculisporic acid, CAS: 469-77-2, stock 11g, assay 98.4%, MWt: 328.40, Formula: C17H28O6, Solubility: DMSO : 250 mg/mL (761.27 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Spiculisporic acid is a γ-butenolide isolated from the cultue of Aspergillus sp [1].

Name: 3-Aminopropionitrile fumarate (2:1) Di-β-aminopropionitrile fumarate; β-Aminopropionitrile fumarate; β-Ammoniumpropionitrile hemifumarate, CAS: 2079-89-2, stock 1.5g, assay 98.2%, MWt: 256.26, Formula: C4H4O4.2C3H6N2, Solubility: H2O : 125 mg/mL (487.79 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: 3-Aminopropionitrile fumarate (2:1) is a lathyrogen which inhibits crosslinking of collagen.
IC50 & Target: Collagen[1].
In Vivo: Twenty days after the induction of tendinitis, intralesional treatment with 3-Aminopropionitrile fumarate (2:1) (BAPN-F) is performed and the contralateral limbs receive saline. A biopsy is obtained and gross and histopathological analysis is performed on the 150 th day of the experiment. The collagen fibrillar alignment pattern in the healing area is better in the 3-Aminopropionitrile fumarate (2:1) group submitted to controlled exercise than in the other group, as observed by sonographic and histopathologic examination. The present results indicate that 3-Aminopropionitrile fumarate (2:1) in combination with controlled loading improved scar remodeling and tendon wound collagen maturation[1].

Name: 5-Acetylsalicylic acid, CAS: 13110-96-8, stock 13.2g, assay 98.1%, MWt: 180.16, Formula: C9H8O4, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: 5-Acetylsalicylic acid has anti-inflammatory and is considered to be the active agent in inflammatory bowel disease (IBD)[1].

Name: Ketoisophorone 4-Oxoisophorone, CAS: 1125-21-9, stock 5.3g, assay 98%, MWt: 152.19, Formula: C9H12O2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Ketoisophorone (4-Oxoisophorone) is a key intermediate in the synthesis of carotenoids and flavouring agents. Ketoisophorone is an industrially important cyclic endione[1].

Name: Methiothepin mesylate Metitepine mesylate;Ro 8-6837 mesylate, CAS: 74611-28-2, stock 5.3g, assay 98.9%, MWt: 452.65, Formula: C21H28N2O3S3, Solubility: DMSO : ≥ 125 mg/mL (276.15 mM), Clinical_Informat: No Development Reported, Pathway: Neuronal Signaling;GPCR/G Protein, Target: 5-HT Receptor;5-HT Receptor, Biological_Activity: Methiothepin mesylate is a potent and non-selective 5-HT2 receptor antagonist, with pKds of 7.10 (5-HT1A), 7.28 (5HT1B), 7.56 (5HT1C), 6.99 (5HT1D), 7.0 (5-HT5A), 7.8 (5-HT5B), 8.74 (5-HT6), and 8.99 (5-HT7), and pKis of 8.50 (5HT2A), 8.68 (5HT2B), and 8.35 (5HT2C).
IC50 & Target: pKd: 7.10 (5-HT1A), 7.28 (5HT1B), 7.56 (5HT1C), 6.99 (5HT1D)[1], 7.0 (5-HT5A), 7.8 (5-HT5B), 8.74 (5-HT6), 8.99 (5-HT7)[3] 
pKi: 8.50 (5-HT2A), 8.68 (5-HT2B), 8.35 (5-HT2C)[2]
In Vitro: Methiothepin mesylate is a 5-HT receptor antagonist, with pKds of 7.10, 7.28, 7.56, and 6.99 for 5-HT1A, 5HT1B, 5HT1C, 5HT1D[1]. Methiothepin mesylate also shows pKds of 7.0, 7.8, 8.74, and 8.99 for 5-HT5A, 5-HT5B, 5-HT6, and 5-HT7, respectively[2]. Methiothepin exhibits high affinity at 5-HT2A, 5HT2B, and 5HT2C with pKis of 8.50, 8.68, and 8.35, respectively[3].

Name: 2-Phospho-L-ascorbic acid trisodium salt L-Ascorbic acid 2-phosphate trisodium salt;Sodium L-ascorbyl-2-phosphate, CAS: 66170-10-3, stock 14.9g, assay 98.8%, MWt: 322.05, Formula: C6H6Na3O9P, Solubility: DMSO : < 1 mg/mL (insoluble or slightly soluble); H2O : 150 mg/mL (465.77 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Protein Tyrosine Kinase/RTK;Metabolic Enzyme/Protease;Metabolic Enzyme/Protease;NF-κB;Immunology/Inflammation, Target: c-Met/HGFR;Endogenous Metabolite;Reactive Oxygen Species;Reactive Oxygen Species;Reactive Oxygen Species, Biological_Activity: 2-Phospho-L-ascorbic acid trisodium salt acts as an antioxidant and a stimulator of hepatocyte growth factor (HGF) production.
In Vitro: 2-Phospho-L-ascorbic acid (Asc 2-P) acts as an antioxidant and a stimulator of hepatocyte growth factor (HGF) production. 2-Phospho-L-ascorbic acid is a stable derivative of L-ascorbic acid (AA) and possesses similar biological properties as AA. AA and Asc-2P regulate a number of biological processes[1]. When 2-Phospho-L-ascorbic acid is added together with DHT, DHT-induced DKK-1 mRNA expression in DPCs is significantly attenuated. It is also found that DKK-1 promoter activity is increased by DHT treatmen. When 2-Phospho-L-ascorbic acid is added together with DHT, DHT-induced activation of luciferase activity is significantly repressed[2].

Name: TAME hydrochloride, CAS: 1784-03-8, stock 12g, assay 98.2%, MWt: 378.87, Formula: C14H23ClN4O4S, Solubility: DMSO : 155 mg/mL (409.11 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Cell Cycle/DNA Damage, Target: APC, Biological_Activity: TAME hydrochloride is an inhibitor of anaphase-promoting complex/cyclosome (APC/C or APC), which binds to APC/C and prevents its activation by Cdc20 and Cdh1, produces mitotic arrest[1].
IC50 & Target: Anaphase-promoting complex (APC)[1]
In Vitro: The absence of APC substrates, TAME hydrochloride ejects Cdc20 from the APC by promoting Cdc20 auto-ubiquitination in its N-terminal region. Cyclin B1 antagonizes TAME hydrochloride's effect by promoting binding of free Cdc20 to the APC and suppressing Cdc20 auto-ubiquitination[2]. 
TAME hydrochloride stabilizes cyclin B1 in Xenopus extract by two mechanisms. First, it reduces the kcat of the APCCdc20/cyclin B1 complex without affecting the Km, slowing the initial ubiquitination of unmodified cyclin B1. Second, as cyclin B1 becomes ubiquitinated, it loses its ability to promote Cdc20 binding to the APC in the presence of TAME hydrochloride. As a result, cyclin B1 ubiquitination terminates before reaching the threshold necessary for proteolysis[2].

Name: N-Acetyl-5-hydroxytryptamine N-Acetylserotonin; Normelatonin; O-Demethylmelatonin, CAS: 1210-83-9, stock 10.5g, assay 98.9%, MWt: 218.25, Formula: C12H14N2O2, Solubility: DMSO : 250 mg/mL (1145.48 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Protein Tyrosine Kinase/RTK;Metabolic Enzyme/Protease;Neuronal Signaling, Target: Trk Receptor;Endogenous Metabolite;Trk Receptor, Biological_Activity: N-Acetyl-5-hydroxytryptamine is a Melatonin precursor, and that it can potently activate TrkB receptor.
IC50 & Target: TrkB receptor[1]
In Vitro: N-Acetyl-5-hydroxytryptamine (NAS), a precursor of Melatonin, is acetylated from serotonin by AANAT (arylalkylamine N-acetyltransferase). N-acetylserotonin activates TrkB receptor in a circadian rhythm. N-Acetyl-5-hydroxytryptamine swiftly activates TrkB in a circadian manner and exhibits antidepressant effect in a TrkB-dependent manner. N-Acetyl-5-hydroxytryptamine rapidly activates TrkB, but not TrkA or TrkC, in a neurotrophin- and MT3 receptor-independent manner[1].
In Vivo: To explore whether N-Acetyl-5-hydroxytryptamine, can trigger TrkB activation in vivo, TrkB F616A knockin mice are employed, where it has been shown that TrkB F616A activation can be selectively blocked by 1NMPP1, a derivative of kinase inhibitor PP1, leading to TrkB-null phenotypes. To assess whether N-Acetyl-5-hydroxytryptamine can mimic BDNF, cortical neurons from TrkB F616A knockin mice are prepared. In alignment with a previous report, BDNF- and NAS-mediated TrkB phosphorylation are selectively reduced by 1NMPP1 but not by K252a, whereas serotonin or Melatonin had no effect . These findings suggest that NAS strongly provokes both wild-type TrkB and TrkB F616A tyrosine phosphorylation and activation[1].

Name: 5-Fluorouridine, CAS: 316-46-1, stock 12.3g, assay 98.6%, MWt: 262.19, Formula: C9H11FN2O6, Solubility: H2O : 100 mg/mL (381.40 mM; Need ultrasonic); DMSO : ≥ 100 mg/mL (381.40 mM), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: 5-Fluorouridine is a metabolite of 5-fluorouracil with anticancer activity[1][2][3][4]. 5-fluorouridine inhibits rRNA synthesis of human colon carcinoma cells[3]. 5-Fluorouridine exhibits cytotoxic effect on growth of L1210 cells with an IC50 of 2 nM[4].

Name: Veratryl alcohol 3,4-Dimethoxybenzyl alcohol, CAS: 93-03-8, stock 39.7g, assay 98.8%, MWt: 168.19, Formula: C9H12O3, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Veratryl alcohol (3,4-Dimethoxybenzenemethanol), a secondary metabolite of some lignin degrading fungi, is commonly used nonphenolic substrate for assaying ligninolytic activity[1][2].

Name: Sodium erythorbate D-Araboascorbic acid (sodium);D-Isoascorbic acid (sodium), CAS: 6381-77-7, stock 12.7g, assay 98.1%, MWt: 199.11, Formula: C6H8NaO6+, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Sodium erythorbate (D-Isoascorbic acid sodium), produced from sugars derived from different sources, such as beets, sugar cane, and corn, is a food additive used predominantly in meats, poultry, and soft drinks.

Name: D-Arabinose, CAS: 28697-53-2, stock 15.1g, assay 98.6%, MWt: 150.13, Formula: C5H10O5, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: D-Arabinose, a monosaccharide, shows strong growth inhibition against the Caenorhabditis elegans with an IC50 of 7.5 mM[1].

Name: Dihydroferulic acid Hydroferulic acid, CAS: 1135-23-5, stock 20.1g, assay 98.4%, MWt: 196.20, Formula: C10H12O4, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Dihydroferulic acid (Hydroferulic acid) is one of the main metabolites of curcumin and antioxidant/radical-scavenging properties with an IC50 value of 19.5 μM. Dihydroferulic acid is a metabolite of human gut microflora as well as a precursor of vanillic acid[1][2].
In Vitro: Uptake of hydroxycinnamic acids by control, organic anion transporter 1 (OAT1), OAT2, OAT3, and OAT4 over expressing 293H cells. In 293H control cells, there was significant uptake of Dihydroferulic acid. The uptake of Dihydroferulic acid is also enhanced ~2-fold in the OAT1-expressing cells[3].
In Vivo: Assessing the influence of an 11 weeks intervention with a resistant starch-enriched whole grain diet (HI-RS-WG, 25% RS) compared to a WG control diet (LOW-RS-WG, 6.9% RS) on serum profile of polyphenols (PPs) in 20 Zucker Diabetic Fatty rats. Five PPs were identified and quantified in serum samples of rats belonging to both intervention groups. HI-RS-WG rats had 2.6 folds higher serum concentrations of total PPs than LOW-RS-WG rats. An explorative data reduction approach, based on the Principal Component Analysis identified two principal components related to the gut microbiota fermentation and food intake, respectively. Results showed that the abundance of hippuric acid and Dihydroferulic acid in HI-RS-WG rats was explained by the stronger gut microbiota fermentation in those rats than in LOW-RS-WG rats[4].

Name: Flavanone, CAS: 487-26-3, stock 39.4g, assay 98.4%, MWt: 224.25, Formula: C15H12O2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Flavanone is used to characterize the authenticity of lemon juice by monitoring of flavanone content.

Name: Hyaluronidase Hyaluronate 4-glycanohydrolase;Hyaluronoglucosaminidase, CAS: 37326-33-3, stock 3.7g, assay 98.6%, MWt: 1000, Formula: N/A, Solubility: H2O : 100 mg/mL (Need ultrasonic), Clinical_Informat: Launched, Pathway: Others, Target: Others, Biological_Activity: Hyaluronidase (Hyaluronate 4-glycanohydrolase; Hyaluronoglucosaminidase) is a naturally occurring enzyme that depolymerizes hyaluronic acid by cleavage of glycosidic bonds and has been used as a local anesthetic additive[1][2].

Name: Durvalumab MEDI 4736, CAS: 1428935-60-7, stock 17.9g, assay 98.2%, MWt: 1000, Formula: N/A, Solubility: H2O, Clinical_Informat: Launched, Pathway: Immunology/Inflammation, Target: PD-1/PD-L1, Biological_Activity: Durvalumab (MEDI 4736) is an humanized anti-PD-L1 monoclonal antibody[1]. Durvalumab (MEDI4736) completely blocks the binding of PD-L1 to both PD-1 and CD80, with IC50s of 0.1 and 0.04 nM, respectively[2].
IC50 & Target: IC50: 0.1 nM (PD-L1/PD-1), 0.04 nM (PD-L1/CD80)[2]
In Vivo: Durvalumab inhibits tumor growth in mouse xenograft models of human melanoma (A375) and pancreatic (HPAC) tumour cell lines, via a T-cell-mediated mechanism. Durvalumab (5-0.01 mg/kg for NOD/SCID mice with HPAC tumor; 5-0.1 mg/kg for NOD/SCID mice with A375 tumor; administration i.p.; twice per week; for 3 weeks) significantly inhibits the tumor growth of both HPAC and A375 xenografts compared with an isotype-matched control antibody. Tumor growth inhibition of the HPAC cells reaches 74%, whereas inhibition of the A375 cells reaches 77%. When administered in the absence of T cells, Durvalumab has no effect on the growth of the A375 tumor xenograft[2].

Name: Desoxycorticosterone pivalate DOCP, CAS: 808-48-0, stock 38.3g, assay 98.3%, MWt: 414.58, Formula: C26H38O4, Solubility: 10 mM in DMSO, Clinical_Informat: Launched, Pathway: Others, Target: Others, Biological_Activity: Desoxycorticosterone pivalate (DOCP) is a mineralocorticoid hormone and an analog of Desoxycorticosterone. Desoxycorticosterone pivalate is used for the management of canine hypoadrenocorticism[1][2].
In Vivo: A starting dosage of 1.5 mg/kg Desoxycorticosterone pivalate (DOCP) is effective in controlling clinical signs and serum electrolyte concentrations in the majority of dogs with PH. An additional dose reduction often is needed to maintain an injection interval of 28-30 days. Young and growing animals seem to need higher dosages[1].

Name: Avelumab Anti-Human PD-L1, Human Antibody;MSB 0010718C; MSB0010718C, CAS: 1537032-82-8, stock 9.4g, assay 98.2%, MWt: 1000, Formula: N/A, Solubility: 10 mM in DMSO, Clinical_Informat: Launched, Pathway: Immunology/Inflammation, Target: PD-1/PD-L1, Biological_Activity: Avelumab is a fully human IgG1 anti-PD-L1 monoclonal antibody with potential antibody-dependent cell-mediated cytotoxicity.
IC50 & Target: PD-1/PD-L1[1]
In Vitro: Avelumab is a fully human IgG1 anti-PD-L1 monoclonal antibody with potential antibody-dependent cell-mediated cytotoxicity property. Avelumab increases NK-cell lysis 3.1-fold (P=0.01) in JHC7 cells relative to isotype control. When the cells are treated with IFN-γ, Avelumab markedly enhances NK-cell lysis relative to isotype control in the following cell lines: JHC7 (7.56-fold; P=0.001), UM-Chor1 (7.34-fold; P<0.001), U-CH2 (2.6 fold; P=0.008), MUG-Chor1 (8.38-fold; P=0.0016). Avelumab effectively increases antibody-dependent cell-mediated cytotoxicity (ADCC) of both the non-cancer stem cell (CSC) and CSC subpopulations to the same degree[1]. Results also demonstrate that the addition of Avelumab increases the frequency of antigen-specific multifunctional CD8+ T cells by more than fivefold, relative to the isotype control in CEFT-stimulated peripheral blood mononuclear cells (PBMCs)[2].
In Vivo: Measurement of individual tumors clearly shows a slowing of tumor growth in the Avelumab-treated mice. By day 36 post-tumor implantation, there is a significant (P<0.01) reduction in the average tumor volume of the Avelumab-treated mice. Reduction in MB49 tumor growth in the mice treated with Avelumab is durable and leads to a significant (P<0.05) improvement in percent survival. Avelumab treatment of 10 mice with bladder tumors results in complete tumor regression in 8 mice, confirmed by histopathology. However, in mice depleted of either CD4 or CD8 cells, Avelumab treatment is much less effective in controlling bladder tumor burden with tumor breakthrough occurring in a higher frequency in mice depleted of CD4 T cells[3].

Name: Calcium polystyrene sulfonate Poly(styrenesulfonic acid) calcium salt, CAS: 37286-92-3, stock 28.7g, assay 98.3%, MWt: 1000, Formula: (C8H8O3S)x.xCa, Solubility: DMSO : < 1 mg/mL (insoluble or slightly soluble), Clinical_Informat: Launched, Pathway: Others, Target: Others, Biological_Activity: Calcium polystyrene sulfonate is an ion-exchange resin used for reducing blood levels of potassium. Calcium polystyrene sulfonate is used to treat hyperkalemia in patients with chronic kidney disease (CKD).

Name: Demecarium Bromide BC-48, CAS: 56-94-0, stock 27.8g, assay 98.5%, MWt: 716.59, Formula: C32H52Br2N4O4, Solubility: DMSO : 160 mg/mL (223.28 mM; Need ultrasonic), Clinical_Informat: Launched, Pathway: Neuronal Signaling, Target: AChE, Biological_Activity: Demecarium Bromide (BC-48) is a potent cholinesterase inhibitor, with an apparent affinity (Kiapp) of 0.15 μM[1]. Demecarium Bromide (BC-48) is used as a glaucoma agent[2].
IC50 & Target: Kiapp: 0.15 μM (Cholinesterase)[1]
In Vivo: Demecarium Bromide (0.125 and 0.5%) causes long-term miosis and decreases intraocular pressure (IOP) in beagles with both normotensive eyes and inherited glaucoma[1].

Name: Etelcalcetide AMG 416;KAI-4169, CAS: 1262780-97-1, stock 16g, assay 98.3%, MWt: 1048.25, Formula: C38H73N21O10S2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein, Target: CaSR, Biological_Activity: Etelcalcetide (AMG 416) is a synthetic peptide as an activator of the calcium sensing receptor (CaSR). Etelcalcetide is effective in lowering parathyroid hormone (PTH) concentrations in patients receiving dialysis with secondary hyperparathyroidism receiving hemodialysis[1].

Name: JNJ-38877605, CAS: 943540-75-8, stock 10.7g, assay 98.3%, MWt: 377.35, Formula: C19H13F2N7, Solubility: DMSO : ≥ 30 mg/mL (79.50 mM), Clinical_Informat: Phase 1, Pathway: Protein Tyrosine Kinase/RTK, Target: c-Met/HGFR, Biological_Activity: JNJ-38877605 is an ATP-competitive inhibitor of c-Met with IC50 of 4 nM, 600-fold selective for c-Met than 200 other tyrosine and serine-threonine kinases.
IC50 value: 4 nM [1]
Target: c-Met
in vitro: JNJ-38877605 shows more than 600-fold selectivity for c-Met compared with more than 200 other diverse tyrosine and serine-threonine kinases and also potently inhibits HGF-stimulated and constitutively activated c-Met phosphorylation in vitro. [1] In EBC1, GTL16, NCI-H1993, and MKN45 cells, JNJ-38877605 (500 nM) leads to a significant reduction of phosphorylation of Met and RON, another key player in invasive growth [2]. A recent study shows that JNJ-38877605 is involved in modulating secretion of IL-8, GROa, uPAR and IL-6 in GTL16 cells [3].
in vivo: In mice bearing established GTL16 xenografts, JNJ-38877605, dosed orally with 40 mg/kg/day for 72 hours, results in a statistically significant decrease in the plasma levels of human IL-8 (from 0.150 ng/mL to 0.050 ng/mL) and GROα (from 0.080 ng/mL to 0.030 ng/mL). While concentrations of uPAR in the blood become reduced to more than 50% at the same dose [3].

Name: Ramucirumab, CAS: 947687-13-0, stock 33.9g, assay 98.8%, MWt: 6369.07, Formula: C285H434N74O88S2, Solubility: H2O, Clinical_Informat: Launched, Pathway: Protein Tyrosine Kinase/RTK, Target: VEGFR, Biological_Activity: Ramucirumab is a human VEGFR-2 antagonist for the treatment of solid tumors[1]. Ramucirumab is a recombinant human immunoglobulin G1 monoclonal antibody that binds to the extracellular binding domain of VEGFR-2 and prevents the binding of VEGFR ligands: VEGF-A, VEGF-C, and VEGF-D[2].
IC50 & Target: VEGFR[2]

Name: VU6005649, CAS: 2137047-43-7, stock 2.9g, assay 98.8%, MWt: 357.28, Formula: C16H12F5N3O, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein;Neuronal Signaling, Target: mGluR;mGluR, Biological_Activity: VU6005649 is a CNS penetrant mGlu7/8 receptor agonist with EC50s of 0.65 μM and 2.6 μM for mGlu7 receptor and mGlu8 receptor, respectively.
IC50 & Target: EC50: 0.65 μM (mGlu7 receptor ), 2.6 μM (mGlu8 receptor)[1]
In Vitro: VU6005649 is a CNS penetrant mGlu7/8 receptor agonist with EC50s of 0.65 μM and 2.6 μM for mGlu7 receptor and mGlu8 receptor, respectively. VU6005649 displays a terminal Kp of 2.43 with total brain levels ~9× above the mGlu7 positive allosteric modulator (PAM) in vitro EC50[1].
In Vivo: When VU6005649 (compound 9f) is dosed at 30 mg/kg IP in 10% Tween 80/H2O (0.75 mg/kg. s.c. amphetamine), no efficacy is observed in this assay. VU6005649 shows modest but significant pro-cognitive effects on associative learning in wild-type mice and the first example of efficacy of an mGlu7/8 positive allosteric modulator (PAM) in this model[1].

Name: FT671, CAS: 1959551-26-8, stock 36.4g, assay 98.5%, MWt: 533.48, Formula: C24H23F4N7O3, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Cell Cycle/DNA Damage, Target: Deubiquitinase, Biological_Activity: FT671 is a potent, non-covalent and selective USP7 inhibitor with an IC50 of 52 nM and binds to the USP7 catalytic domain with a Kd of 65 nM.
IC50 & Target: IC50: 52 nM (USP7)[1]
Kd: 65 nM (USP7)[1]
In Vitro: FT671 increases p53 protein levels in HCT116 or bone osteosarcoma (U2OS) cell lines, leading to induction of p53 target genes including BBC3 (which encodes PUMA), CDKN1A (p21), RPS27L (S27L) and MDM2. FT671 leads to the degradation of N-Myc and upregulation of p53 in the neuroblastoma cell line IMR-32. FT671 also stabilizes p53 in the MM.1S multiple myeloma cell line, which correlates with increased MDM2 ubiquitination and leads to expression of p53 target genes[1].
In Vivo: FT671 (100 mg/kg and 200 mg/kg, Oral gavage, daily) treatment in mice leads to a significant dose-dependent inhibition of tumor growth. And FT671 is well-torelated even at high doses[1].

Name: GNE-6776, CAS: 2009273-71-4, stock 19.7g, assay 98.4%, MWt: 348.40, Formula: C20H20N4O2, Solubility: DMSO : ≥ 100 mg/mL (287.03 mM), Clinical_Informat: No Development Reported, Pathway: Cell Cycle/DNA Damage, Target: Deubiquitinase, Biological_Activity: GNE-6776 is a selective USP7 inhibitor.
IC50 & Target: USP7[1]
In Vitro: GNE-6776 non-covalently targets USP7 12 Å distant from the catalytic cysteine. GNE-6776 attenuates ubiquitin binding and thus inhibits USP7 deubiquitinase activity. GNE-6776 interacts with acidic residues that mediate hydrogen-bond interactions with the ubiquitin Lys48 side chain. GNE-6776 targets cellular USP7, MDM2, and p53 signalling pathways.GNE-6776 selectively inhibits recombinant USP7 relative to 36 other deubiquitinases. GNE-6776 remains selective even at 100 μM, a more than sixfold higher concentration than used in cellular assays. GNE-6776 significantly inhibits USP7 while remaining selective against 44-47 other detected deubiquitinases[1].
In Vivo: Although efficacious exposure is only transiently achieved, GNE-6776 causes modest, although significant, EOL-1 xenograft growth delay[1].

Name: MK-3903, CAS: 1219737-12-8, stock 8.9g, assay 98.1%, MWt: 454.90, Formula: C27H19ClN2O3, Solubility: DMSO : 75 mg/mL (164.87 mM; Need ultrasonic and warming), Clinical_Informat: No Development Reported, Pathway: Epigenetics;PI3K/Akt/mTOR, Target: AMPK;AMPK, Biological_Activity: MK-3903 is a potent and selective AMP-activated protein kinase (AMPK) activator with an EC50 of 8 nM.
IC50 & Target: EC50: 8 nM (AMPK)[1]
In Vitro: MK-3903 (compound 42) is a potent and selective AMP-activated protein kinase (AMPK) activator with an EC50 of 8 nM. MK-3903 activates 10 of the 12 phosphorylated AMPK (pAMPK) complexes with EC50 values in the range of 8 to 40 nM and maximal activation >50%. MK-3903 partially activates pAMPK5 (36% max) and it does not activate pAMPK6. MK-3903 demonstrates low permeability (Papp=6×10-6 cm/s) in LLC-PK1 cells42 and is a substrate of human liver uptake transporters OATP1B1 and OATP1B3 (organic anion transporter proteins). Results show that MK-3903 binds moderately to the prostanoid DP2 (CRTH2) receptor (binding IC50=1.8 μM) but not in the presence of 10% human serum (binding IC50>86 μM)[1].
In Vivo: The pharmacokinetics of MK-3903 (compound 42) in C57BL/6 mice, Sprague to Dawley rats, and beagle dogs are characterized by moderate systemic plasma clearance (5.0 to13 mL/min/kg), a volume of distribution at steady state of 0.6 to 1.1 L/kg, and a terminal halflife of ~2h. Acute oral administration of MK-3903 (3, 10, and 30 mg/kg) to high-fructose fed db/+ mice results in significant inhibition of hepatic fatty acid synthesis (FAS) for all three doses[1].

Name: HIV-1 integrase inhibitor 3, CAS: 1638504-56-9, stock 0.4g, assay 99%, MWt: 432.42, Formula: C21H22F2N4O4, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease;Anti-infection, Target: HIV Integrase;HIV, Biological_Activity: HIV-1 integrase inhibitor 3 is a HIV-1 integrase strand transfer (INST) inhibitor with an IC50 of 2.7 nM.
IC50 & Target: IC50: 2.7 nM (INST)[1]
In Vitro: HIV-1 integrase inhibitor 3 (compound 4c) is a HIV-1 integrase strand transfer (INST) inhibitor with an IC50 of 2.7 nM. HIV-1 integrase inhibitor 3 also displays an antiviral inhibitory potency against the Q148H/G140S mutant with an EC50 of 7 nM[1].

Name: HIV-1 integrase inhibitor 4, CAS: 1638504-66-1, stock 34.5g, assay 98.3%, MWt: 514.50, Formula: C24H20F2N4O5S, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease;Anti-infection, Target: HIV Integrase;HIV, Biological_Activity: HIV-1 integrase inhibitor 4 is a HIV-1 integrase strand transfer (INST) inhibitor with an IC50 of 3.7 nM.
IC50 & Target: IC50: 3.7 nM (INST)[1]
In Vitro: HIV-1 integrase inhibitor 4 (compound 4f) is a HIV-1 integrase strand transfer (INST) inhibitor with an IC50 of 3.7 nM. HIV-1 integrase inhibitor 4 shows potent activity against recombinant HIV IN in biochemical assays and good efficacy in assays done in cell culture against a broad panel of viral mutants carrying the major RAL and DTG IN resistance mutations[1].

Name: Abatacept CTLA4lg;BMS-188667, CAS: 332348-12-6, stock 5.5g, assay 98.4%, MWt: 1000, Formula: N/A, Solubility: 10 mM in DMSO, Clinical_Informat: Launched, Pathway: Others, Target: Others, Biological_Activity: Abatacept (CTLA4lg) is a soluble fusion protein consisting of the extra-cellular domain of human CTLA4 and a fragment of the Fc portion of human IgG1 (hinge and CH2 and 3 domains)[1]. Abatacept is a selective T-cell co-stimulation modulator and a protein drug for the treatment of autoimmune diseases[2].
In Vivo: Abatacept reduces paw edema, and the SC Multiple-dose group shows significantly greater (tobs = 2.50) paw edema reduction compared with the IV dose group[2]. 
Abatacept exhibits linear PK across the studied doses. The NCA clearance (CL) is 20.8 mL/day/kg, volume (Vss) is 146 mL/kg, and bioavailability (F) of the SC dose dosing is 57.7%[2]. 
Abatacept (oral; 10 mg/kg; every 2 days) reduces the proportion of activated T cells (CD44highCD62L–) and inhibits the up-regulation of ICOS and CD71 in homozygous DO11.10 RAG-2–/– BALB/c (H-2d/d) mice[3].

Name: CADD522, CAS: 199735-88-1, stock 26.4g, assay 98.8%, MWt: 326.17, Formula: C15H13Cl2NO3, Solubility: DMSO : 250 mg/mL (766.47 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: CADD522 is a potent inhibitor of runt-related transcription factor-2 (RUNX2)-DNA binding with an IC50 of 10 nM. CADD522 exhibits antitumor activity[1].
IC50 & Target: RUNX2-DNA binding[1]

Name: Mavacamten MYK461;SAR439152, CAS: 1642288-47-8, stock 8.4g, assay 98.3%, MWt: 273.33, Formula: C15H19N3O2, Solubility: DMSO : ≥ 150 mg/mL (548.79 mM); H2O : < 0.1 mg/mL (insoluble), Clinical_Informat: Phase 3, Pathway: Cytoskeleton, Target: Myosin, Biological_Activity: Mavacamten is a modulator of cardiac myosin, with IC50s of 490, 711 nM for bovine cardiac and human cardiac, respectively.
IC50 & Target: IC50: 490 nM (bovine cardiac), 711 nM (human cardiac)[1].
In Vitro: Mavacamten is found to have an IC50 value of 490 nM in the bovine system, 711 nM in the human system, and 2140 nM in the rabbit system, indicating selectivity of >4-fold for cardiac myosin[1].
In Vivo: Treatment with Mavacamten reduces FS from 52±3% to 38±7%. Treatment with Mavacamten reduces FS from 81±7% to 60±13%, corresponding to a relative reduction of 25%. Across all measurements there is a linear correlation between FS and Mavacamten plasma concentrations with each 100 ng/mL increase in Mavacamten concentration lowering FS by 4.9%. Treatment with Mavacamten eliminates SAM in 5/5 subjects, whereas SAM persists in 3/3 subjects treated with vehicle alone. Pressure gradients across the LVOT drop to 11.1±5.0 mmHg with Mavacamten treatment; whereas vehicle treated cats maintain stable LVOT pressure gradients[2]. Mavacamten reduces contractility by decreasing the adenosine triphosphatase activity of the cardiac myosin heavy chain. Chronic administration of Mavacamten suppresses the development of ventricular hypertrophy, cardiomyocyte disarray, and myocardial fibrosis and attenuates hypertrophic and profibrotic gene expression in mice harboring heterozygous human mutations in the myosin heavy chain[3].

Name: DPPC 129Y83, CAS: 63-89-8, stock 23.6g, assay 98.4%, MWt: 734.04, Formula: C40H80NO8P, Solubility: DMSO : < 1 mg/mL (insoluble or slightly soluble), Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: DPPC is a zwitterionic phosphoglyceride that can be used for the preparation of liposomal monolayers.

Name: Halofantrine hydrochloride SKF-102886;WR-171669, CAS: 36167-63-2, stock 12g, assay 98.8%, MWt: 536.88, Formula: C26H31Cl3F3NO, Solubility: DMSO : 30 mg/mL (55.88 mM; Need ultrasonic), Clinical_Informat: Launched, Pathway: Anti-infection, Target: Parasite, Biological_Activity: Halofantrine hydrochloride (SKF-102886) is a blocker of delayed rectifier potassium current via the inhibition of human-ether-a-go-go-related gene (HERG) channel and a potent antimalarial compound[1][2].
IC50 & Target: Malaria[1].
HERG channel[2].

Name: Cephapirin (sodium) Cefapirin (sodium), CAS: 24356-60-3, stock 2.3g, assay 99%, MWt: 445.45, Formula: C17H16N3NaO6S2, Solubility: 10 mM in DMSO, Clinical_Informat: Launched, Pathway: Anti-infection, Target: Bacterial, Biological_Activity: Cephapirin sodium (Cefapirin sodium), a semisynthetic cephalosporin antibiotic, is bactericidal against strains of gram-positive and gram-negative bacteria[1].

Name: Tiludronate (disodium) Tiludronic Acid (disodium), CAS: 149845-07-8, stock 20.8g, assay 98.9%, MWt: 362.57, Formula: C7H7ClNa2O6P2S, Solubility: 10 mM in DMSO; H2O : 41.67 mg/mL (114.93 mM; Need ultrasonic), Clinical_Informat: Launched, Pathway: Others, Target: Others, Biological_Activity: Tiludronate disodium (Tiludronic Acid disodium) is a new bisphosphonate, which prevents postmenopausal bone loss. Tiludronate disodium (Tiludronic Acid disodium) presents antiresorptive and anti-inflammatory properties[1][2].

Name: N-Acetyl-DL-methionine, CAS: 1115-47-5, stock 33.3g, assay 98.3%, MWt: 191.25, Formula: C7H13NO3S, Solubility: , Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity:

Name: Leu-AMS, CAS: 288591-93-5, stock 17.2g, assay 98.6%, MWt: 459.48, Formula: C16H25N7O7S, Solubility: DMSO : ≥ 49.17 mg/mL (107.01 mM), Clinical_Informat: No Development Reported, Pathway: Anti-infection;Metabolic Enzyme/Protease, Target: Bacterial;Aminoacyl-tRNA Synthetase, Biological_Activity: Leu-AMS (compound 6), a leucine analogue, is a potent inhibitor of leucyl-tRNA synthetase (LRS) with an IC50 of 22.34 nM, which inhibits the catalytic activity of LRS but did not affect the leucine-induced mTORC1 activation. Leu-AMS shows cytotoxicity in cancer cells and normal cells, and inhibits the growth of bacteria[1].
IC50 & Target: IC50: 22.34 nM (LRS)[1]
In Vitro: Leu-AMS is proved to be a potent inhibitor of Leucyl-tRNA Synthetase (LRS) with an IC50 value of 22.34 nM. Leu-AMS is highly cytotoxic in both cancer cells and normal cells. Leu-AMS does not affect S6 kinase (S6K) phosphorylation at all. Leu-AMS inhibits the catalytic activity of LRS but does not affect the leucine-induced mTORC1 activation[1].

Name: Phenylacetylglutamine NSC 203800; Phenylacetyl-L-glutamine, CAS: 28047-15-6, stock 19.4g, assay 98.2%, MWt: 264.28, Formula: C13H16N2O4, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: Phenylacetylglutamine is a colonic microbial metabolite from amino acid fermentation.
In Vitro: Phenylacetylglutamine is a colonic microbial metabolite from amino acid fermentation. It results from glutamine conjugation of phenylacetic acid, which is almost exclusively derived from the microbial conversion of phenylalanine[1].

Name: (S)-3-Hydroxybutanoic acid (S)-β-Hydroxybutanoic acid; L-(+)-3-Hydroxybutyric acid; L-β-Hydroxybutyric acid, CAS: 6168-83-8, stock 30.9g, assay 98.8%, MWt: 104.10, Formula: C4H8O3, Solubility: H2O : 50 mg/mL (480.31 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: (S)-3-Hydroxybutanoic acid is a normal human metabolite, that has been found elevated in geriatric patients remitting from depression. In humans, 3-Hydroxybutyric acid is synthesized in the liver from acetyl-CoA, and can be used as an energy source by the brain when blood glucose is low.

Name: Farnesol, CAS: 4602-84-0, stock 20.9g, assay 98.5%, MWt: 222.37, Formula: C15H26O, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Anti-infection;Metabolic Enzyme/Protease, Target: Bacterial;Endogenous Metabolite, Biological_Activity: Farnesol is a sesquiterpene alcohol that modulates cell-to-cell communication in Candida albicans, and has the activity in inhibiting bacteria.
IC50 & Target: Bacterial[1].
In Vitro: Farnesol is a sesquiterpene alcohol that modulates cell-to-cell communication in Candida albicans. It is also shown that this molecule presents inhibitory effects against non-albicans Candida species, Paracoccidioides brasiliensis and bacteria. The minimum inhibitory concentrations (MICs) are determined in accordance with the M27-A3 protocol as described and Farnesol is tested at a concentration range of 0.29-150 μM. It is observed that Farnesol presents an inhibitory activity against C. neoformans and C. gattii (MIC range: 0.29-75.0 μM). Although Farnesol does not significantly alter phospholipase activity, a tendency to decrease this activity is observed[1].

Name: EHNA (hydrochloride), CAS: 58337-38-5, stock 26.8g, assay 98.8%, MWt: 313.83, Formula: C14H24ClN5O, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Adenosine Deaminase, Biological_Activity: EHNA hydrochloride is a specific inhibitor of adenosine deaminase, prevents dAdo degradation and increases mitochondrial dATP levels in fibroblasts[1].

Name: Tapinarof Benvitimod;WBI 1001;GSK2894512, CAS: 79338-84-4, stock 39.5g, assay 98.6%, MWt: 254.32, Formula: C17H18O2, Solubility: DMSO : ≥ 125 mg/mL (491.51 mM), Clinical_Informat: Phase 3, Pathway: Immunology/Inflammation, Target: Aryl Hydrocarbon Receptor, Biological_Activity: Tapinarof (Benvitimod; WBI 1001; GSK2894512) is a natural aryl hydrocarbon receptor (AhR) agonist with an EC50 of 13 nM.
IC50 & Target: EC50: 13 nM (AhR)[1]
In Vitro: Tapinarof activates the AhR pathway through direct binding. Tapinarof dose-dependently induces nuclear translocation of AhR in immortalized keratinocytes (HaCaT) (EC50=0.16 nM)[1].
In Vivo: Tapinarof acts through AhR to reduce inflammation in IMQ-treated mice. AhR-sufficient mice on a C57Bl/6 background exhibit a reduced clinical score after treatment with Tapinarof or 6-formylindolo(3,2-b)carbazole (FICZ). In contrast, AhR KO mice do not respond to the anti-inflammatory effects of Tapinarof. FICZ is used as a comparator in these studies and yields similar results, with dramatically reduced inflammatory responses in wild-type, but not AhR KO mice[1].

Name: Tulrampator CX-1632, CAS: 1038984-31-4, stock 9.5g, assay 98.5%, MWt: 380.37, Formula: C20H17FN4O3, Solubility: DMSO : 21.67 mg/mL (56.97 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Membrane Transporter/Ion Channel;Neuronal Signaling, Target: iGluR;iGluR, Biological_Activity: Tulrampator (CX-1632) is an orally bioavailable positive AMPAR (allosteric modulator of AMPA receptor). Antidepressant[1].
IC50 & Target: AMPAR[1]

Name: Adavivint SM04690;Lorecivivint, CAS: 1467093-03-3, stock 32.2g, assay 98.5%, MWt: 505.55, Formula: C29H24FN7O, Solubility: DMSO : 25 mg/mL (49.45 mM; Need ultrasonic and warming); H2O : < 0.1 mg/mL (insoluble), Clinical_Informat: Phase 2, Pathway: Stem Cell/Wnt, Target: Wnt, Biological_Activity: Adavivint (SM04690; Lorecivivint) is a potent and selective inhibitor of canonical Wnt signaling, with an EC50 of 19.5 nM via a high-throughput TCF/LEF-reporter assay in SW480 colon cancer cells.
IC50 & Target: EC50: 19.5 nM (Wnt, SW480 cell)[1]
In Vitro: Adavivint (SM04690) is a potent and selective inhibitor of Wnt signaling, with an EC50 of 19.5 nM via a high-throughput TCF/LEF-reporter assay in SW480 colon cancer cells, and shows no effect on SV40 luciferase reporter. Adavivint enhances aggregation of human mesenchymal stem cells (hMSCs) with an EC50 of 10 nM. Adavivint (30 nM) protects chondrocytes from catabolic breakdown in vitro[1].
In Vivo: Adavivint (0.3 μg) enhances cartilage repair and protection in the rat acute cruciate ligament tear and partial medial meniscectomy osteoarthritis (ACLT + pMMx OA) model[1].

Name: Alobresib GS-5829, CAS: 1637771-14-2, stock 25.3g, assay 98.2%, MWt: 437.49, Formula: C26H23N5O2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Epigenetics, Target: Epigenetic Reader Domain, Biological_Activity: Alobresib (GS-5829) is a BET bromodomain inhibitor, which represents a highly effective therapeutics agent against recurrent/chemotherapy resistant uterine serous carcinoma (USC) overexpressing c-Myc[1].
IC50 & Target: BET bromodomain[1]
In Vitro: Alobresib (0.1 nM-100 μM; 72 hours) inhibits cell proliferation in primary uterine serous carcinoma (USC) lines[1].
In Vivo: Alobresib (10 and 20 mg/kg; oral; twice-daily; for 28 days) impaires USC-ARK2 xenograft tumor growth in female CB17/lcrHsd-Prkd/scid mice. Alobresib exhibits a significantly slower rate of tumor growth in mice, compared with vehicle control and to mice undergoing daily treatment with JQ1 (50 mg/kg/day i.p.)[1]. 
Alobresib (10 and 20 mg/kg; oral; twice-daily; for 28 days) is well tolerated with no clear impact on body weight compared with vehicle control[1].

Name: RO1138452 CAY10441, CAS: 221529-58-4, stock 28.3g, assay 98.4%, MWt: 309.41, Formula: C19H23N3O, Solubility: DMSO : 33.33 mg/mL (107.72 mM; Need ultrasonic); H2O : < 0.1 mg/mL (insoluble), Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein, Target: Prostaglandin Receptor, Biological_Activity: RO1138452 is a potent and selective IP (prostacyclin) receptor antagonist. RO1138452 displays high affinity for IP receptors. In human platelets, pKi is 9.3±0.1; in a recombinant IP receptor system, pKi is 8.7±0.06.
IC50 & Target: IC50: 7 nM (rat I2 receptor), 52.9 nM (rabbit PAF), 724 nM (human α2A adrenoceptor), 3280 nM (rat α1B adrenoceptor), 1450 nM (human muscarinic M4 receptor), 2220 nM (human muscarinic M2 receptor), 2570 nM (human muscarinic M1 receptor), 3110 nM (human muscarinic M5 receptor), 1130 nM (rat 5-HT1B receptor ), 1190 nM (pig 5-HT2C receptor), 3040 nM (rat 5-HT2A receptor), 8580 nM (human 5-HT1A receptor ), 8910 nM (guinea-pig 5-HT4 receptor)[1] 
pKi: 5.87 (rat α1B adrenoceptor), 6.49 (human α2A adrenoceptor), 8.33 (rat I2 receptor), 5.66 (human muscarinic M1 receptor), 5.81 (human muscarinic M5 receptor), 5.88 (human muscarinic M2 receptor), 6.14 (human muscarinic M4 receptor), 7.9 (rabbit PAF), 5.35 (guinea-pig 5-HT4 receptor ), 5.37 (human 5-HT1A receptor ), 5.71 (rat 5-HT2A receptor) , 6.11 (rat 5-HT1B receptor), 6.11 (pig 5-HT2C receptor)[1]
In Vitro: RO1138452 is IP receptor antagonist. The pIC50 values of RO1138452 in attenuating cAMP accumulation is 7.0±0.07. Functional antagonism of RO1138452 is studied by measuring inhibition of carbaprostacyclin-induced cAMP accumulation in CHO-K1 cells stably expressing the human IP receptor. The antagonist affinity (pKi) of RO1138452 is 9.0±0.06. Selectivity profiles for RO1138452 are determined via a panel of receptor binding and enzyme assays. RO1138452 displays affinity at imidazoline2 (I2) (8.3) and platelet activating factor (PAF) (7.9) receptors[1]. RO1138452 (10 pM-10 μM) added to cells concurrently with a fixed concentration of Taprostene (1 μM) prevents, in a concentration-dependent manner, the inhibition of CXCL9 and CXCL10 release, with p[A]50 (molar) values of -8.73±0.11 and -8.47±0.16 (p>0.05), respectively[2].
In Vivo: RO1138452 is a potent and selective antagonist for both human and rat IP receptors and that is possesses analgesic and anti-inflammatory potential. RO1138452 (1-10 mg/kg, i.v.) significantly reduces acetic acid-induced abdominal constrictions. RO1138452 (3-100 mg/kg, p.o.) significantly reduces carrageenan-induced mechanical hyperalgesia and edema formation. One hour after administration of RO1138452 (5 mg/kg, i.v.) to rats, the total plasma concentration is 0.189 μg/mL, whereas the free plasma concentrations is calculated to be 0.009 μg/mL (28 nM)[1].

Name: Morphothiadin GLS4, CAS: 1092970-12-1, stock 40g, assay 98.2%, MWt: 509.39, Formula: C21H22BrFN4O3S, Solubility: DMSO : 100 mg/mL (196.31 mM; Need ultrasonic); H2O : < 0.1 mg/mL (insoluble), Clinical_Informat: Phase 2, Pathway: Anti-infection, Target: HBV, Biological_Activity: Morphothiadin is a potent inhibitor on the replication of both wild-type and adefovir-resistant HBV with an IC50 of 12 nM.
IC50 & Target: IC50: 12 nM (HBV)[1]
In Vitro: Morphothiadin is a potent inhibitor on the replication of both wild-type and adefovir-resistant HBV with an IC50 of 12 nM. Morphothiadin (GLS4) shows no toxicity up to 25 μM. The cytotoxic dose whereby 50% of cells die (CC50) for primary hepatocytes is 115 μM for Morphothiadin (P<0.001). The CC90 is 190 μM for Morphothiadin (P<0.01) in HepAD38 cells. Morphothiadin strongly inhibits virus accumulation in the supernatant of HepAD38 cells at 25 nM to 100 nM (P<0.02). Results show a concentration-dependent decrease of core protein in cells treated with Morphothiadin[2].
In Vivo: The area under the concentration-time curve from 0 to 24 h (AUC0-24) of Morphothiadin (GLS4) is 556 h•ng/mL. After intravenous administration of 10 mg/kg Morphothiadin, the total plasma clearance and apparent volume distribution are 4.2 liters/h/kg and 7.38 liters/kg, respectively. The bioavailability of Morphothiadin is 25.5%. It is found that virus titers have increased 83.5-fold in mice treated with 3.75 mg/kg per day of Morphothiadin, 28.3-fold among mice treated with 7.5 mg/kg per day, but only 3- to 6-fold among mice treated with the higher doses of Morphothiadin. There is generally an inverse relationship between Morphothiadin dose and virus titer, with the greatest rebound seen in mice treated with 3.75 mg/kg per day of Morphothiadin (540-fold) and the smallest rebound in mice treated with 60 mg/kg per day (23-fold) (P<0.001). The Morphothiadin doses of >7.5 mg/kg per day significantly suppresses the virus replication cycle throughout the treatment period, while Morphothiadin doses of >15 mg/kg per day suppresses virus for up to 2 weeks after the end of treatment[2].

Name: β-Endorphin, human, CAS: 61214-51-5, stock 36g, assay 98.4%, MWt: 3464.98, Formula: C158H251N39O46S, Solubility: 10 mM in H2O, Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein;Neuronal Signaling, Target: Opioid Receptor;Opioid Receptor, Biological_Activity: β-Endorphin, human, a prominent endogenous peptide, existing in the hypophysis cerebri and hypothalamus, is an agonist of opioid receptor, with preferred affinity for μ-opioid receptor and δ-opioid receptor; β-Endorphin, human exhibits antinociception activity.
IC50 & Target: Opioid receptor[1]
In Vitro: β-Endorphin, human is an agonist of opioid receptor, with preferred affinity for μ-opioid receptor and δ-opioid receptor. β-Endorphin exhibits anti-nociception activity by stimulating ε-opioid receptor, rather than μ-, δ-, and κ-opioid receptor[1]. β-Endorphin has anti-nociception activity. Firstly, β-Endorphin combines together with the opioid receptors in hyperalgesia. Further, β-Endorphin suppresses the release of substance P at the level of spinal cord and blocks the conduction of pain on the primary sensory neurons. Moreover, β-Endorphin activates the endogenous analgesia system located in the CNS. In addition, β-Endorphin inhibits the conduction of pain and agitation of nociceptors to exert an analgesic effect[2].

Name: Delgocitinib JTE-052, CAS: 1263774-59-9, stock 26.6g, assay 98.5%, MWt: 310.35, Formula: C16H18N6O, Solubility: DMSO : ≥ 58 mg/mL (186.89 mM), Clinical_Informat: Phase 2, Pathway: Epigenetics;Stem Cell/Wnt;JAK/STAT Signaling, Target: JAK;JAK;JAK, Biological_Activity: Delgocitinib is a novel and specific JAK inhibitor with IC50s of 2.8, 2.6, 13 and 58 nM for JAK1, JAK2, JAK3 and Tyk2, respectively.
IC50 & Target: IC50: 2.8 nM (JAK1), 2.6 nM (JAK2), 13 nM (JAK3), 58 nM (Tyk2)[1]
In Vitro: In the enzymatic assays, Delgocitinib potently inhibits all of the JAK subtypes with IC50 values of 2.8±0.6, 2.6±0.2, 13±0 and 58±9 nM for JAK1, JAK2, JAK3 and Tyk2, respectively. Lineweaver-Burk plots show that the inhibition mode of Delgocitinib toward all JAKs is competitive with ATP with Ki values of 2.1±0.3, 1.7±0.0, 5.5±0.3 and 14±1 nM for JAK1, JAK2, JAK3 and Tyk2, respectively. In these cell-based cytokine signaling assays, Delgocitinib inhibits the phosphorylation of Stat proteins induced by IL-2, IL-6, IL-23, GM-CSF, and IFN-α with IC50 values of 40±9, 33±14, 84±11, 304±22 and 18±3 nM, respectively. Delgocitinib also inhibits IL-2-induced proliferation of T cells in a concentration-dependent manner (IC50=8.9±3.6 nM), and its potency is similar to that of tofacitinib (IC50=16 nM)[1].
In Vivo: Delgocitinib decreases the IFN-γ production, but the potency of the 1-h prior administration is higher than that of the 6-h prior administration (ED50=0.24 versus 1.3 mg/kg). In the administration from day 1, Delgocitinib prevents the development of hind paw swelling and histological changes of inflammatory cell infiltration and synovial cell hyperplasia. Delgocitinib inhibits radiographic and histological changes of bone destruction and cartilage destruction. In the administration from day 15, Delgocitinib decreases the paw swelling in a dose-dependent manner. In addition, Delgocitinib ameliorates the inflammatory cell infiltration, synovial cell hyperplasia, and cartilage/bone destructions in the histological and radiographic examinations at the end of the study[1].

Name: 5α-Pregnane-3β,6α-diol-20-one, CAS: 21853-11-2, stock 31g, assay 98.9%, MWt: 334.49, Formula: C21H34O3, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: 5α-Pregnane-3β,6α-diol-20-one is a mitogenic metabolite of progesterone, and it can be produced in starved androgen-responsive prostate cancer cells.
In Vitro: Progesterone is converted to 5α-pregnane-3β,6α-diol-20-one in human fibroblasts[1]. Pregnenolone and progesterone are avidly metabolized to 5α-pregnan-3β,6α-diol-20-one in the C4.2 cell line, with nearly complete conversions at 24 h and 18 h, respectively. Preferential 5α-pregnan-3β,6α-diol-20-one formation from early steroid precursors is independent of CYP17A1 but rather relies on 3β-HSD activity[2].

Name: 1-Myristoyl-2-stearoyl-sn-glycero-3-phosphocholine, CAS: 76343-22-1, stock 39.4g, assay 98%, MWt: 734.04, Formula: C40H80NO8P, Solubility: , Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity:

Name: D-Erythro-dihydrosphingosine, CAS: 764-22-7, stock 6.3g, assay 98%, MWt: 301.51, Formula: C18H39NO2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease;Metabolic Enzyme/Protease, Target: Phospholipase;Endogenous Metabolite, Biological_Activity: D-Erythro-dihydrosphingosin directly inhibits cytosolic phospholipase A2α (cPLA2α) activity.
In Vitro: D-Erythro-dihydrosphingosine (D-erythro-DHS) significantly inhibits mastoparan-, but not Na3VO4-, stimulated arachidonic acid release in PC12 cells. D-Erythro-dihydrosphingosine at 100 AM slightly inhibits [3H]Arachidonic acid release, and 5 μM Ionomycin alone stimulates the release significantly. In the presence of 5 μM Ionomycin, 100 μM C2-ceramide stimulates the release, but D-Erythro-dihydrosphingosine (100 μM) inhibits the release. D-Erythro-dihydrosphingosine inhibits arachidonic acid release in cells and/or cPLA2α activity[1].

Name: 4-Bromo A23187, CAS: 76455-48-6, stock 32g, assay 99%, MWt: 602.52, Formula: C29H36BrN3O6, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Apoptosis;Membrane Transporter/Ion Channel;Neuronal Signaling, Target: Apoptosis;Calcium Channel;Calcium Channel, Biological_Activity: 4-Bromo A23187 is a halogenated analog of the highly selective calcium ionophore A-23187. 4-Bromo A23187，a calcium modulator, induces apoptosis in different cells, including HL-60 cells[1].

Name: Elenbecestat E2609, CAS: 1388651-30-6, stock 1.5g, assay 98.6%, MWt: 437.44, Formula: C19H18F3N5O2S, Solubility: 10 mM in DMSO, Clinical_Informat: Phase 3, Pathway: Neuronal Signaling, Target: Beta-secretase, Biological_Activity: Elenbecestat (E2609) is a potent, orally bioavailable and CNS-penetrant BACE-1 inhibitor for the treatment of Alzheimer's disease (AD)[1][2].
IC50 & Target: BACE-1[1]
In Vitro: E2609 is a potent BACE1 inhibitor with an IC50 of ~7 nmol/L in cell-based assay[2]. 
E2609 has been shown to reduce Ab production in the plasma, brain, and cerebrospinal fluid (CSF) of rodents[2]. 
In Vivo: E2609 displays the plasma half-life of 12-16 hours after once daily dosing[1]. 
E2609 (0.3-30 mg/kg; p.o.) potently inhibits Ab1-40 and Ab1-42 production in the plasma and CSF of non-human primates[2].

Name: Cyclosporin A-Derivative 1, CAS: 1487360-85-9, stock 35.9g, assay 98.5%, MWt: 1364.50, Formula: C65H118BF4N11O14, Solubility: H2O, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Cyclosporin A-Derivative 1 is a crystalline intermediate derived from the opening of cyclosporin A extracted from patent WO 2013167703 A1. Cyclosporin A is an immunosuppressive agent which can bind to the cyclophilin and inhibit calcineurin.
In Vitro: Cyclosporin A-Derivative 1 is a non-immunosuppressive Cyclosporine A derivative. The cyclosporin is acylated on the butenyl-methyl-threonine side chain and then subjected to a ring-opening reaction (the ring opens between the sarcosine and the N-methyl-leucine residues). Cyclosporin A-Derivative 1 is a linear peptide intermediate[1].

Name: Cyclosporin A-Derivative 2, CAS: 156047-45-9, stock 3.5g, assay 98.4%, MWt: 1149.51, Formula: C58H104N10O13, Solubility: H2O, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Cyclosporin A-Derivative 2 is a novel derivative from cyclosporin A. Cyclosporin A is an immunosuppressive agent which can bind to the cyclophilin and inhibit calcineurin.

Name: Alisporivir intermediate-1, CAS: 882506-05-0, stock 22.4g, assay 98.1%, MWt: 1461.91, Formula: C74H132N12O17, Solubility: H2O, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Alisporivir intermediate-1 is an intermediate in the synthesis of Alisporivir. Alisporivir is used for the treatment of inflammatory and viral diseases.

Name: Gemcabene PD-72953, CAS: 183293-82-5, stock 2.6g, assay 99%, MWt: 302.41, Formula: C16H30O5, Solubility: DMSO : ≥ 125 mg/mL (413.35 mM), Clinical_Informat: Phase 2, Pathway: Others, Target: Others, Biological_Activity: Gemcabene (PD-72953), a first-in-class lipid-lowering agent, lowers low-density lipoprotein cholesterol (LDL-C), decreases triglycerides, and raises high-density lipoprotein cholesterol (HDL-C) and lowers pro-inflammatory acute-phase protein, C-reactive protein (CRP), exerting anti-inflammatory activity[1][2][3].
In Vitro: Gemcabene calcium (PD-72953 calcium) significantly downregulates hepatic mRNA markers of inflammation (TNF-α, MCP-1, MIP-1β, CCR5, CCR2, NF-κB), lipogenesis and lipid modulation (ApoC-III, ACC1, ADH-4, Sulf-2), and fibrosis (TIMP-1 and MMP-2)[3].

Name: Lanosterol, CAS: 79-63-0, stock 3.3g, assay 98.3%, MWt: 426.72, Formula: C30H50O, Solubility: DMSO : < 1 mg/mL (insoluble or slightly soluble), Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: Lanosterol is a key triterpenoid intermediate in the biosynthesis of Cholesterol.

Name: DL-alpha-Tocopherol DL-α-Tocopherol, CAS: 10191-41-0, stock 17.3g, assay 98.2%, MWt: 430.71, Formula: C29H50O2, Solubility: 10 mM in DMSO, Clinical_Informat: Launched, Pathway: Apoptosis, Target: Ferroptosis, Biological_Activity: DL-alpha-Tocopherol is a synthetic vitamin E, with antioxidation effect. DL-alpha-Tocopherol protects human skin fibroblasts against the cytotoxic effect of UVB[1].

Name: Cot inhibitor-1, CAS: 915365-57-0, stock 32g, assay 98.8%, MWt: 553.46, Formula: C27H27Cl2FN8, Solubility: H2O : < 0.1 mg/mL (insoluble); DMSO : 25 mg/mL (45.17 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: MAPK/ERK Pathway, Target: MAP3K, Biological_Activity: Cot inhibitor-1 is a COT/Tpl2 inhibitor.

Name: 3'-Hydroxypterostilbene, CAS: 475231-21-1, stock 38.4g, assay 98.3%, MWt: 272.30, Formula: C16H16O4, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Apoptosis;Autophagy, Target: Apoptosis;Autophagy, Biological_Activity: 3'-Hydroxypterostilbene, a natural pterostilbene analogue, effectively inhibits the growth of human colon cancer cells (IC50s of 9.0, 40.2, and 70.9 µM for COLO 205, HCT-116, and HT-29 cells, respectively) by inducing apoptosis and autophagy. 3'-Hydroxypterostilbene inhibits the PI3K/Akt/mTOR/p70S6K, and p38MAPK pathways and activates the ERK1/2, JNK1/2 MAPK pathways[1].
IC50 & Target: Apoptosis[1] 
Autophagy[1]

Name: Galgravin, CAS: 528-63-2, stock 14.9g, assay 98.1%, MWt: 372.45, Formula: C22H28O5, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Galgravin is an active compound in Nectandra megapotamica, with anti-inflammatory activity. Galgravin displays in vitro cytotoxic activity and induce apoptosis in leukemia cells[1][2].
In Vitro: Galgravin has cytotoxic activity against human leukemia tumor cells with an IC50 of 16.5 µg/mL[2].

Name: Macranthoside B, CAS: 146100-02-9, stock 33.9g, assay 98.4%, MWt: 1075.24, Formula: C53H86O22, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Anti-infection, Target: Bacterial, Biological_Activity: Macranthoside B, isolated from Flos Lonicerae, possesses anti-bacterial activity[1].

Name: Eurycomanone Pasakbumin A, CAS: 84633-29-4, stock 7.1g, assay 98.5%, MWt: 408.40, Formula: C20H24O9, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Eurycomanone could increases spermatogenesis by inhibiting the activity of phosphodiesterase and aromatase in steroidogenesis.
In Vitro: Eurycomanone (EN) significantly increased testosterone production dose-dependently at 0.1, 1.0 and 10.0 μM, but the two lower doses when combined with 3-isobutyl-1-methylxanthine (IBMX), the phosphodiesterase inhibitor were not significantly higher than EN or IBMX alone, except at a higher concentration. The molecular docking studies indicated EN and IBMX were binding at different sites of the enzyme. EN has no reversal of inhibition by aminoglutethimide, ketoconazole or nifedipine at the respective steroid oogenesis enzyme. The quassinoid was also non-responsive to the inhibition of oestrogen receptor by tamoxifen, but displayed improved for mestane inhibition of aromatase in reducing oestrogen production. The molecular docking studies further supported that EN and formestane bound to aromatase with similar orientations and free energy binding values[1].

Name: Rosmanol, CAS: 80225-53-2, stock 32.1g, assay 98.1%, MWt: 346.42, Formula: C20H26O5, Solubility: DMSO : 150 mg/mL (433.00 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Rosmanol could inhibit the oxidation of low density lipoprotein (LPL) and significantly inhibit lipopolysaccharide induced iNOS and COX-2 expression, with anti-inflammatory effect.
In Vitro: Rosmanol exhibits the strongest inhibition on cell viability with IC50 approximately 42 μM. Rosmanol might suppress cancer cell proliferation or induce cancer cell undergoing apoptosis that lead to cell growth-inhibition. With 50 μM of Rosmanol treatment, the percentage of COLO 205 cells undergoing apoptosis increase dramatically from 9 h (29%) to 24 h (51%). Within 24 h of treatment with 50 μM Rosmanol, COLO 205 cells exhibit significant morphological changes and chromosomal condensation, which is indicative of apoptotic cell death[1]. Carnosol is a lipid protector against attack by O2[2].

Name: Nepodin Musizin, CAS: 3785-24-8, stock 6.4g, assay 98.7%, MWt: 216.23, Formula: C13H12O3, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Epigenetics;PI3K/Akt/mTOR;Anti-infection, Target: AMPK;AMPK;Parasite, Biological_Activity: Nepodin (Musizin) is a quinone oxidoreductase (PfNDH2) inhibitor isolate from Rumex crispus[1].Nepodin (Musizin) stimulates the translocation of GLUT4 to the plasma membrane by activation of AMPK[2].Nepodin (Musizin) has antidiabetic and antimalarial activities.
In Vitro: Nepodin (Musizin) exhibits significant IC50 values that are 0.74 and 0.79 μg/ml against P. falciparum chloroquine-sensitive (3D7) and P. falciparum chloroquine-resistant (S20), respectively[1].
In Vivo: Nepodin (Musizin) (orally administration; 2-10 mg/kg; 4 weeks) improves the impaired glucose tolerance of db/db mice, also decreases an increase in plasma insulin concentration of db/db mice in a dose-dependent manner[2].

Name: Vitexin 4'-glucoside 4'-O-Glucosylvitexin, CAS: 38950-94-6, stock 18.8g, assay 98.2%, MWt: 594.52, Formula: C27H30O15, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Vitexin 4'-glucoside is a leaf flavonoid identified from Briza stricta[1].

Name: Demethoxydeacetoxypseudolaric acid B analog, CAS: 500736-17-4, stock 39.5g, assay 98.1%, MWt: 446.49, Formula: C24H30O8, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Demethoxydeacetoxypseudolaric acid B analog (Compound 13b) is semi-synthesized by efficient routines from Pseudolaric acid B. It has potent activities against HMEC-1, HL-60, A-549, MB-MDA-468, BEL-7402, HCT116, and Hela cells with IC50s ranging from 0.136 to 1.162 μM[1].

Name: Platycodin D2, CAS: 66663-90-9, stock 9.7g, assay 98.4%, MWt: 1387.46, Formula: C63H102O33, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Platycodin D2 is a saponin isolated from Platycodon grandiflorum, with anti-cancer activity[1].

Name: Notoginsenoside S, CAS: 575446-95-6, stock 22.4g, assay 98.2%, MWt: 1343.50, Formula: C63H106O30, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Notoginsenoside S is a compound isolated from Panax notoginseng.

Name: Carabrone, CAS: 1748-81-8, stock 38.6g, assay 98.1%, MWt: 248.32, Formula: C15H20O3, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Anti-infection, Target: Bacterial, Biological_Activity: Carabrone is isolated from the fruits of Carpesium abrotanoides , is a well-known sesquiterpene and exhibits significant anti-bacterial and anti-tumor activities[1].
Carabrone exhibits antifungal activities in vitro and in vivo against Botrytis cinerea, Colletotrichum lagenarium(EC50=7.10 μg/mL) and Erysiphe graminis[2].
IC50 & Target: EC50: 7.10 μg/mL (Colletotrichum lagenarium)[1]

Name: Quercetin 3-gentiobioside, CAS: 7431-83-6, stock 14.4g, assay 98.7%, MWt: 626.52, Formula: C27H30O17, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Aldose Reductase, Biological_Activity: Quercetin 3-gentiobioside is isolated from A. iwayomogi, AR and AGE formation inhibitor, demonstrates biological activities against Aldose reductase (AR) and the formation of advanced glycation endproducts (AGEs)[1].

Name: Vicenin 3, CAS: 59914-91-9, stock 38.1g, assay 98.9%, MWt: 564.49, Formula: C26H28O14, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Angiotensin-converting Enzyme (ACE), Biological_Activity: Vicenin 3 is an angiotensin-converting enzyme (ACE) inhibitor (IC50=46.91 μM) from the aerial parts of Desmodium styracifolium[1].

Name: Gambogenic acid, CAS: 173932-75-7, stock 6.9g, assay 98.7%, MWt: 630.77, Formula: C38H46O8, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Epigenetics, Target: Histone Methyltransferase, Biological_Activity: Gambogenic acid is an active ingredient in gamboge, with anticancer activity. Gambogenic acid acts as an effective inhibitor of EZH2, specifically and covalently binds to Cys668 within the EZH2-SET domain, and induces EZH2 ubiquitination[1].
IC50 & Target: EZH2[1]

Name: Astringin trans-Astringin, CAS: 29884-49-9, stock 38.2g, assay 98.9%, MWt: 406.38, Formula: C20H22O9, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Astringin (trans-Astringin) is a natural glycoside found in the bark of Picea sitchensis and Picea abies (Norway spruce), in Vitis vinifera cell cultures and in wine. Astringin has potent antioxidant capacity and cancer-chemopreventive activity[1].

Name: Brevifolincarboxylic acid, CAS: 18490-95-4, stock 36.1g, assay 98.8%, MWt: 292.20, Formula: C13H8O8, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease;Immunology/Inflammation, Target: Glucosidase;Aryl Hydrocarbon Receptor, Biological_Activity: Brevifolincarboxylic acid is extracted from Polygonum capitatum[1], has inhibitory effect on the aryl hydrocarbon receptor (AhR)[2]. Brevifolincarboxylic acid is an α-glucosidase inhibitor with an IC50 of 323.46 μM[3].
IC50 & Target: IC50: 323.46 μM (α-glucosidase) (Brevifolincarboxylic acid)[3]

Name: Incensole, CAS: 22419-74-5, stock 8.2g, assay 98.9%, MWt: 306.48, Formula: C20H34O2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Incensole, a 14-membered diterpenoid, is isolated from both essential oils and resins of frankincense. Incensole has shown anti-inflammatory and anti-depression activities due to their ability to activate ion channels in the brain to alleviate anxiety or depression[1].

Name: Incensole Acetate, CAS: 34701-53-6, stock 11.8g, assay 98.3%, MWt: 348.52, Formula: C22H36O3, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Apoptosis, Target: Apoptosis, Biological_Activity: Incensole acetate is a main constituent of Boswellia carterii resin, has neuroprotective effects against neuronal damage in traumatic and ischemic head injury. Incensole acetate reduces Aβ25–35-triggered apoptosis in hOBNSCs[1].
In Vitro: Incensole acetate (100 μM; pre-treatment 4 hours) significantly ameliorates Aβ 25–35-induced cell death, a 48–52% decrease in cell viability at Aβ25–35 is restored to 85–89% upon pre-treatment with IA[1].
Incensole acetate (5-100 μM) pretreatment reverses increase in the mRNA and protein level of Bax, caspase 8, cyto c and decrease in the mRNA and protein level of Bcl2 induced by Aβ 25–35 in hOBNSCs[1].

Name: Luteolin-3-O-beta-D-glucuronide, CAS: 53527-42-7, stock 23.9g, assay 98.2%, MWt: 462.36, Formula: C21H18O12, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Luteolin-3-O-beta-D-glucuronide is a luteolin glucosiduronic acid consisting of luteolin having a beta-D-glucosiduronic acid residue attached at the 3'-position.

Name: 5,7-Dihydroxy-4-methylcoumarin, CAS: 2107-76-8, stock 15.1g, assay 98.2%, MWt: 192.17, Formula: C10H8O4, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: 5,7-Dihydroxy-4-methylcoumarin is a coumarin derivative from Mexican tarragon[1].

Name: Fucosterol, CAS: 17605-67-3, stock 19g, assay 98.4%, MWt: 412.69, Formula: C29H48O, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Epigenetics;Cell Cycle/DNA Damage, Target: PARP;PARP, Biological_Activity: Fucosterol is isolated from E. stolonifera with anti-adipogenic, anti-diabetic and anti-cancer activities. Fucosterol regulates adipogenesis via modulation of PPARαand C/EBPαexpression.
IC50 & Target: PPARα; C/EBPα[1]
In Vitro: Fucosterol (0-50 μM; 7 days) suppresses the expression of PPARα and C/EBPα when compared to fully differentiated control adipocytes[1].
Fucosterol shows cytotoxicity against T47D and HT29 cell lines with IC50 values of 27.94 and 70.41 μg/ml, respectively[3].
Fucosterol decreases cell HEK293, MCF-7, and SiHa cells proliferation with IC50 values of 185.4, 43.3, and 34.0 µg/ml, respectively[4].
In Vivo: Fucosterol (orally adminstratin; 30mg/kg) causes a significant decrease in serum glucose concentrations, and exhibits an inhibition of sorbitol accumulations in the lenses[2].

Name: Oxyberberin Berlambine; 8-Oxoberberine; Ketoberberine, CAS: 549-21-3, stock 25.2g, assay 98.4%, MWt: 351.35, Formula: C20H17NO5, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Berlambine is a natural alkaloid isolated from many plants[1].

Name: Dihydroartemisinic acid Dihydroqinghao acid, CAS: 85031-59-0, stock 15.1g, assay 98.8%, MWt: 236.35, Formula: C15H24O2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Anti-infection;Apoptosis, Target: Parasite;Ferroptosis, Biological_Activity: Dihydroartemisinic acid (Dihydroqinghao acid), isolated as a natural product from Artemisia annua, is a biosynthetic precursor to the antimalarial agent Artemisinin[1].

Name: Decursinol, CAS: 23458-02-8, stock 15.2g, assay 98.1%, MWt: 246.26, Formula: C14H14O4, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Decursinol, isolated from the roots of Angelica gigas, possesses antinociceptive effect with orally bioavailability. Decursinol possesses anti-tumor and anti-metastasis activity[1].

Name: L-Fucitol 1-Deoxy-D-galactitol, CAS: 13074-06-1, stock 39.7g, assay 98.5%, MWt: 166.17, Formula: C6H14O5, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: L-Fucitol (1-Deoxy-D-galactitol) is a sugar alcohol isolated from Nutmeg[1].

Name: Glycycoumarin, CAS: 94805-82-0, stock 5g, assay 99%, MWt: 368.38, Formula: C21H20O6, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Autophagy, Target: Autophagy, Biological_Activity: Glycycoumarin is a major bioactive coumarin of licorice. Glycycoumarin inhibits hepatocyte lipoapoptosis through activation of autophagy and inhibition of ER stress-mediated JNK and GSK-3-mediated mitochondrial pathway. Glycycoumarin exerts anti-liver cancer activity by directly targeting T-LAK cell-originated protein kinase [1] [2].

Name: Xanthyletin, CAS: 553-19-5, stock 6.7g, assay 98.6%, MWt: 228.24, Formula: C14H12O3, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Anti-infection, Target: Fungal, Biological_Activity: Xanthyletin is a coumarin isolated from Citrus, with anti-tumor and anti-bacterial activities. Xanthyletin also inhibits symbiotic fungus cultivated by leaf-cutting ants[1].
IC50 & Target: Fugal[1][2]
In Vitro: Xanthyletin inhibits symbiotic fungus cultivated by leaf-cutting ants[1]. 
Xanthyletin (25, 50, and 100 µg/mL) shows a total inhibition on the fungus[2].

Name: Cephaeline, CAS: 483-17-0, stock 14.9g, assay 98.6%, MWt: 466.61, Formula: C28H38N2O4, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Cephaeline is a phenolic alkaloid in Indian Ipecac roots. Cephaeline exhibits potent inhibition of both Zika virus (ZIKV) and Ebola virus (EBOV) infections[1][2].

Name: 1,3,6-Tri-O-galloyl-beta-D-glucose 1,3,6-Tri-O-galloyl-β-D-glucose, CAS: 18483-17-5, stock 1.6g, assay 98.2%, MWt: 636.47, Formula: C27H24O18, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: 1,3,6-Tri-O-galloyl-beta-D-glucose (1,3,6-Tri-O-galloyl-β-D-glucose) is a phenolic compound in Black Walnut Kernels[1].

Name: Dehydroeburicoic acid monoacetate 3-O-Acetyldehydroeburicoic acid, CAS: 77035-42-8, stock 31.8g, assay 98.5%, MWt: 510.75, Formula: C33H50O4, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Dehydroeburicoic acid monoacetate (Compound 18) is a lanostane triterpenoid isolated from Wolfiporia cocos[1].

Name: 6-Demethoxytangeretin, CAS: 6601-66-7, stock 39.2g, assay 98.6%, MWt: 342.34, Formula: C19H18O6, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Epigenetics, Target: Epigenetic Reader Domain, Biological_Activity: 6-Demethoxytangeretin is a citrus flavonoid isolated from Citrus depressa. 6-Demethoxytangeretin exerts anti-inflammatory activity and anti-allergic activity, suppresses production and gene expression of interleukin-6 in human mast cell-1 via anaplastic lymphoma kinase (ALK) and mitogen-activated protein kinase (MAPK) pathways[1]. 6-Demethoxytangeretin facilitates the CRE-mediated transcription associated with learning and memory in cultured hippocampal neurons[2].

Name: 7-O-Methyl morroniside, CAS: 41679-97-4, stock 1.7g, assay 98.4%, MWt: 420.41, Formula: C18H28O11, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: 7-O-Methyl morroniside is an iridoid glycoside (IG) extracted from Cornus officinalis fructus, used in many traditional Chinese medicines[1].

Name: 8-Deoxygartanin, CAS: 33390-41-9, stock 35.2g, assay 98.6%, MWt: 380.43, Formula: C23H24O5, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Anti-infection;NF-κB, Target: Parasite;NF-κB, Biological_Activity: 8-Deoxygartanin, a prenylated xanthones from G. mangostana, is a selective inhibitor of butyrylcholinesterase (BChE)[1]. 8-Deoxygartanin exhibits antiplasmodial activity with an IC50 of 11.8 μM for the W2 strain of Plasmodium falciparum[2]. 8-Deoxygartanin inhibits NF-κB (p65) activation with an IC50 of 11.3 μM[3].
IC50 & Target: IC50: 11.3 μM (NF-κB,p65)[2]

Name: 9-Methoxycamptothecin, CAS: 39026-92-1, stock 32.7g, assay 98.8%, MWt: 378.38, Formula: C21H18N2O5, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Apoptosis;Cell Cycle/DNA Damage, Target: Apoptosis;Topoisomerase, Biological_Activity: 9-Methoxycamptothecin (MCPT), isolated from Nothapodytes foetida, has antitumor activities through topoisomerase inhibition. 9-Methoxycamptothecin (MCPT) induces strong G2/M arrest and apoptosis in cancer[1][2].
IC50 & Target: Topoisomerase[1]. 
Apoptosis[2].

Name: Alkannin, CAS: 517-88-4, stock 15.8g, assay 99%, MWt: 288.30, Formula: C16H16O5, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Apoptosis, Target: Apoptosis, Biological_Activity: Alkannin, found in Alkanna tinctoria, is used as a food coloring. Alkannin shows anticancer activity, arrests cell cycle, and induces apoptosis. Alkannin improves hepatic inflammation in a Rho-kinase pathway[1][2][3].
In Vitro: Alkannin inhibits HCT-116 and SW-480 cells growth with IC50s of 2.38 and 4.53 µM, respectively[1].

Name: 3'-Demethylnobiletin, CAS: 112448-39-2, stock 16.3g, assay 99%, MWt: 388.37, Formula: C20H20O8, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: 3'-Demethylnobiletin, a derivative of Nobiletin, is a polymethoxyflavonoid in citrus fruits[1]. Nobiletin exhibits anticancer activity and inhibits tumor angiogenesis by regulating Src, FAK, and STAT3 signaling[2].

Name: 4''-methyloxy-Daidzin Daidzein 7-O-Β-D-glucoside 4''-O-methylate, CAS: 1195968-02-5, stock 28.1g, assay 98.5%, MWt: 430.40, Formula: C22H22O9, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: 4''-methyloxy-Daidzin (Daidzein 7-O-Β-D-glucoside 4''-O-methylate), an isoflavone methyl-glycoside, is isolated from Cordyceps militaris grown on germinated soybeans. Isoflavones possess immunomodulating and antiallergic activities[1].

Name: 4''-methyloxy-Genistin, CAS: 950910-16-4, stock 35.1g, assay 98.7%, MWt: 446.40, Formula: C22H22O10, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: 4''-methyloxy-Genistin, an isoflavone methyl-glycoside, is isolated from Cordyceps militaris grown on germinated soybeans. Isoflavones possess immunomodulating and antiallergic activities[1].

Name: Ilexoside D, CAS: 109008-27-7, stock 39.2g, assay 98.8%, MWt: 766.95, Formula: C41H66O13, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Ilexoside D is isolated from the roots of Ilex pubescens Hook. et Arn. Ilexoside D has the anti-tissue factor activity as well as the antithrombotic activity[1].

Name: Mauritianin, CAS: 109008-28-8, stock 6.2g, assay 98.3%, MWt: 740.66, Formula: C33H40O19, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Cell Cycle/DNA Damage, Target: Topoisomerase, Biological_Activity: Mauritianin is a kaempferol glycoside isolated from the flowers and leaves of Acalypha indica. Mauritianin is a topoisomerase I inhibitor[1][2].
IC50 & Target: Topoisomerase I[2]

Name: 25R-Inokosterone, CAS: 19682-38-3, stock 34.5g, assay 98.8%, MWt: 480.63, Formula: C27H44O7, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: 25R-Inokosterone is a phytoecdysone isolated from Achyranthis Radix[1].

Name: 17-Hydroxyisolathyrol, CAS: 93551-00-9, stock 21.1g, assay 98.7%, MWt: 350.45, Formula: C20H30O5, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: 17-Hydroxyisolathyrol is a macrocychc lathyrol derivative isolated from seeds of Euphorbla luthyrrs[1].

Name: Forsythoside I, CAS: 1177581-50-8, stock 17g, assay 98.4%, MWt: 624.59, Formula: C29H36O15, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Forsythoside I, a caffeoyl phenylethanoid glycoside (CPG) isolated from the fruits of Forsythia suspense (Thunb.) Vahl, may possesses anti-inflammatory activities[1].

Name: Ciwujianoside A1, CAS: 120768-65-2, stock 23g, assay 98.2%, MWt: 1221.38, Formula: C59H96O26, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Ciwujianoside A1 is isolated from the Eleutherococcus senticosus leaf[1].

Name: Forsythoside H, CAS: 1178974-85-0, stock 4.2g, assay 98.5%, MWt: 624.59, Formula: C29H36O15, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Forsythoside H, a caffeoyl phenylethanoid glycoside (CPG) isolated from the fruits of Forsythia suspense (Thunb.) Vahl, may possesses anti-inflammatory activities[1].

Name: Ciwujianoside C3, CAS: 114906-74-0, stock 34.2g, assay 98.1%, MWt: 1059.24, Formula: C53H86O21, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Immunology/Inflammation, Target: NO Synthase, Biological_Activity: Ciwujianoside C3, an orally active and brain penetrated compound, is isolated the leaves of Acanthopanax henryi Harms. Ciwujianoside C3 has anti-inflammatory effect and can reinforces object recognition memory[1][2].

Name: Acanthopanaxoside B, CAS: 915792-03-9, stock 19.4g, assay 98.6%, MWt: 1263.41, Formula: C61H98O27, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Acanthopanaxoside B is a triterpenoid saponin isolated from the leaves of Acanthopanax senticosus[1].

Name: Bacopasaponin C, CAS: 178064-13-6, stock 9.8g, assay 98.5%, MWt: 899.07, Formula: C46H74O17, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Bacopasaponin C is an indigenous glycoside isolated from Bacopa monniera, with antitumor and anti-leishmanial activities[1][2].

Name: Jionoside A1, CAS: 120444-60-2, stock 26.1g, assay 98.3%, MWt: 800.75, Formula: C36H48O20, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Jionoside A1 isolated from Radix Rehmanniae Praeparata displays dose dependent immune-enhancement activity and possesses moderate protective activities on H2O2-treated SH-SY5Y cells[1].

Name: Orientin-2''-O-p-trans-coumarate, CAS: 1229437-75-5, stock 32.7g, assay 98.6%, MWt: 594.52, Formula: C30H26O13, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Orientin-2''-O-p-trans-coumarate is a flavonoid found in Trigonella foenum-graecum, with potent antioxidant activity[1].

Name: Bacopaside II, CAS: 382146-66-9, stock 0.1g, assay 98.2%, MWt: 929.10, Formula: C47H76O18, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Apoptosis, Target: Apoptosis, Biological_Activity: Bacopaside II, an extract from the medicinal herb Bacopa monnieri, blocks the Aquaporin-1 (AQP1) water channel and impairs migration of cells that express AQP1. Bacopaside II induces cell cycle arrest and apoptosis[1][2].

Name: Beta-Eudesmol, CAS: 473-15-4, stock 14.2g, assay 98.4%, MWt: 222.37, Formula: C15H26O, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Membrane Transporter/Ion Channel;Neuronal Signaling, Target: TRP Channel;TRP Channel, Biological_Activity: Beta-Eudesmol is a natural oxygenated sesquiterpene, activates hTRPA1, with an EC50 of 32.5 μM. Beta-Eudesmol increases appetite through TRPA1[1].

Name: Alcesefoliside, CAS: 124151-38-8, stock 30.2g, assay 98.4%, MWt: 756.66, Formula: C33H40O20, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Alcesefoliside is a flavonoid isolated from Nitraria sibirica Pall, with antioxidant activity[1].

Name: Byakangelicin, CAS: 482-25-7, stock 10.5g, assay 98.1%, MWt: 334.32, Formula: C17H18O7, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Byakangelicin, one of the active compounds found in the roots of Angelica gigas, can serve as a modulator to improve brain accumulation of diverse active compounds (Umb, Cur, and Dox) and enhance therapeutic effects[1]. Byakangelicin is likely to increase the expression of all PXR target genes (such as MDR1) and induce a wide range of drug-drug interactions. Byakangelicin can inhibit the effects of sex hormones, it may increase the catabolism of endogenous hormones[2].
IC50 & Target: PXR[2]

Name: Darutoside, CAS: 59219-65-7, stock 2.7g, assay 98.3%, MWt: 484.62, Formula: C26H44O8, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Darutoside is a diterpenoid isolated from Siegesbeckia[1].

Name: Dehydroevodiamine (hydrochloride), CAS: 111664-82-5, stock 37.8g, assay 98.6%, MWt: 337.80, Formula: C19H16ClN3O, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Dehydroevodiamine hydrochloride is isolated from the leaves of Evodia rutaecarpa[1].

Name: (Rac)-Dencichin 2-Amino-3-(carboxyformamido)propanoic acid, CAS: 7554-90-7, stock 1g, assay 98.9%, MWt: 176.13, Formula: C5H8N2O5, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: (Rac)-Dencichin (2-Amino-3-(carboxyformamido)propanoic acid) is the racemate of Dencichin. Dencichin is a non-protein amino acid originally extracted from Panax notoginseng, and can inhibit HIF-prolyl hydroxylase-2 (PHD-2) activity[1].

Name: Asiaticoside B, CAS: 125265-68-1, stock 34.8g, assay 98.6%, MWt: 975.12, Formula: C48H78O20, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Asiaticoside B is a triterpene glycoside isolated from Actaea asiatica, with anti-cancer activity[1].

Name: Dendrophenol, CAS: 108853-14-1, stock 19.8g, assay 98.9%, MWt: 304.34, Formula: C17H20O5, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: NF-κB, Target: NF-κB, Biological_Activity: Dendrophenol, isolated from the stem of Dendrobium loddigesii Rolfe, act as a NF-κB inhibitor[1]. Antineoplastic activity[1].
IC50 & Target: NF-κB[1]

Name: Przewalskinic acid A, CAS: 136112-75-9, stock 3.1g, assay 98.5%, MWt: 358.30, Formula: C18H14O8, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Przewalskinic acid A is a rare, water-soluble phenolic acid thus far only found in the Salvia przewalskii Maxim herb. Phenolic acids show potent antioxidant activities and potential effects in protecting against brain and heart damage caused by ischemia reperfusion[1].

Name: Gardenin B, CAS: 2798-20-1, stock 19.2g, assay 98.9%, MWt: 358.34, Formula: C19H18O7, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Apoptosis, Target: Apoptosis, Biological_Activity: Gardenin B is a flavonoid isolated from Baccharis scandens. Gardenin B induces cell death in human leukemia cells involves multiple caspases[1].

Name: Proanthocyanidin A4, CAS: 111466-29-6, stock 14.6g, assay 98.3%, MWt: 576.50, Formula: C30H24O12, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Proanthocyanidin A4, isolated from the root of E. sinica, is a polyphenol found in a variety of plants. Proanthocyanidin A4 possesses anti-inflammatory effects[1].

Name: Hernandesine, CAS: 6681-13-6, stock 34.7g, assay 98.5%, MWt: 652.78, Formula: C39H44N2O7, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Hernandesine is isolated from T. flavum L[1].

Name: Dehydroeffusol, CAS: 137319-34-7, stock 22.5g, assay 99%, MWt: 250.29, Formula: C17H14O2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Apoptosis, Target: Apoptosis, Biological_Activity: Dehydroeffusol is a phenanthrene from medicinal herb Juncus effuses. Dehydroeffusol inhibits gastric cancer cell growth and tumorigenicity by selectively inducing tumor-suppressive endoplasmic reticulum stress and a moderate apoptosis. It shows very low toxicity[1][2].
In Vitro: Dehydroeffusol suppresses the expression of vasculogenic mimicry key gene VE-cadherin[2]. 
Dehydroeffusol decreases the MMP2 expression and activity in gastric cancer cells[2].

Name: Hydroxytyrosol acetate, CAS: 69039-02-7, stock 26.5g, assay 98%, MWt: 196.20, Formula: C10H12O4, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Hydroxytyrosol acetate is found in the olive oil with an antioxidant activity. Hydroxytyrosol acetate had a weaker DPPH radical scavenging activity than hydroxytyrosol[1].

Name: Purpureaside C, CAS: 108648-07-3, stock 38.3g, assay 98.9%, MWt: 786.73, Formula: C35H46O20, Solubility: DMSO : 125 mg/mL (158.89 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Purpureaside C is a phenolic glycoside and has significant proinflammatory action.

Name: Quercetagetin 6-Hydroxyquercetin, CAS: 90-18-6, stock 18.7g, assay 98.2%, MWt: 318.24, Formula: C15H10O8, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: JAK/STAT Signaling, Target: Pim, Biological_Activity: Quercetagetin (6-Hydroxyquercetin) is the major flavonoid isolated from Citrus unshiu (C. unshiu) peel[1]. Quercetagetin is a moderately potent and selective, cell-permeable pim-1 kinase inhibitor (IC50, 0.34 μM)[2]. Anti-inflammatory and anticancer properties.
IC50 & Target: IC50: 0.34 μM (PIM1), 3.45 μM (PIM2), 2.82 μM (RSK2), 21.2 μM (PKA)[1]
In Vitro: Quercetagetin also inhibits PIM2, PKA, and RSK2 with IC50s of 3.45, 21.2, and 2.82 µM, respectively[2]. 
Quercetagetin (0.1, 1, 10, and 100 μM, 72 hours) inhibits growth of RWPE2 prostate cancer cells with average ED50 is 3.8 μM[2].
In Vivo: Quercetagetin significantly inhibits UVB-induced skin cancer development. Topical application of 4 or 20 nmol of Quercetagetin to mouse skin reduces tumor incidence by 32.0% and 46.7%, respectively[3].

Name: Quercetagitrin Quercetagetin-7-O-glucoside, CAS: 548-75-4, stock 29.2g, assay 98.2%, MWt: 480.38, Formula: C21H20O13, Solubility: DMSO : 250 mg/mL (520.42 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Quercetagitrin (Quercetagetin-7-O-glucoside), isolated from the flowers of the African Marigold (Tagetes erecta), has anti-inflammatory activity[1][2].

Name: Chrysophanein, CAS: 4839-60-5, stock 6.2g, assay 98.5%, MWt: 416.38, Formula: C21H20O9, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Chrysophanein is a chrysophanol glycoside from leaves and roots of Aloe hijazensis. Chrysophanein shows a moderate cytotoxic activity against several carcinoma cells lines[1].

Name: (-)-Maackiain, CAS: 2035-15-6, stock 6.8g, assay 98.4%, MWt: 284.26, Formula: C16H12O5, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Anti-infection, Target: Fungal, Biological_Activity: (-)-Maackiain is a pterocarpan phytoalexin produced from Red clover (Trifolium pretense L.). (-)-Maackiain is toxic to several genera of fungal pathogens of legume and non legume hosts[1].

Name: (rel)-Myrislignan, CAS: 52190-21-3, stock 3.8g, assay 98.9%, MWt: 374.43, Formula: C21H26O6, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: (rel)-Myrislignan, a relative configuration of Myrislignan, is a lignan isolated from Myristica fragrans Houtt.

Name: Nuezhenidic acid, CAS: 183238-67-7, stock 28.5g, assay 98.4%, MWt: 452.36, Formula: C17H24O14, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Nuezhenidic acid, isolated from the fruits of Ligustrum lucidum, posseses inhibitory activities against influenza A virus[1].

Name: Pentanoic acid, CAS: 109-52-4, stock 11.2g, assay 98.6%, MWt: 102.13, Formula: C5H10O2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: TGF-beta/Smad;Stem Cell/Wnt;Cell Cycle/DNA Damage;Metabolic Enzyme/Protease, Target: ROCK;ROCK;ROCK;Endogenous Metabolite, Biological_Activity: Pentanoic acid, a short-chain fatty acid, is a product of bacterial metabolism and are associated with allergic skin disorders. Pentanoic acid activates ROCK signaling pathway.
IC50 & Target: ROCK[1]
In Vitro: Pentanoic acid, a short-chain fatty acid, is a product of bacterial metabolism and are associated with allergic skin disorders. Pentanoic acid (0-2 mM) strongly and dose-dependently induces thymic stromal lymphopoietin (TSLP) production in PAM212 cells. Pentanoic acid slightly induces the expression of Tnfa, Il1b and Il6 mRNA, but does not induce the protein levels of TNF-α expression. Pentanoic acid (2 mM) induced-TSLP production in keratinocytes is not related to FFAR2 and FFAR3, but mediated by activating ROCK signaling pathway, and is competetely inhibited by co-inhibition of Gq/11 and the ROCK signaling pathway[1].

Name: Salvianolic acid F, CAS: 158732-59-3, stock 21.9g, assay 98.3%, MWt: 314.29, Formula: C17H14O6, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Salvianolic acid F is a synthesized polyphenolic acid[1].

Name: Aminoacyl tRNA synthetase-IN-1, CAS: 219931-45-0, stock 18.2g, assay 98.2%, MWt: 459.48, Formula: C16H25N7O7S, Solubility: DMSO : 65 mg/mL (141.46 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Anti-infection;Metabolic Enzyme/Protease, Target: Bacterial;Aminoacyl-tRNA Synthetase, Biological_Activity: Aminoacyl tRNA synthetase-IN-1 is a bacterial aminoacyl tRNA synthetase (aaRS) inhibitor.
IC50 & Target: aaRS[1]

Name: GlyRS-IN-1, CAS: 112921-11-6, stock 4.4g, assay 98.9%, MWt: 403.37, Formula: C12H17N7O7S, Solubility: DMSO : 100 mg/mL (247.91 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Anti-infection;Metabolic Enzyme/Protease, Target: Bacterial;Aminoacyl-tRNA Synthetase, Biological_Activity: GlyRS-IN-1 is a glycyl-tRNA synthase (GlyRS) inhibitor extracted from patent WO 2017066459 A1. GlyRS-IN-1 can also inhibit the growth of bacteria.
IC50 & Target: GlyRS[1], Bacterial[1]

Name: Salicyl-AMS, CAS: 863238-55-5, stock 2.3g, assay 98.8%, MWt: 466.43, Formula: C17H18N6O8S, Solubility: DMSO : ≥ 90.5 mg/mL (194.03 mM), Clinical_Informat: No Development Reported, Pathway: Anti-infection, Target: Bacterial, Biological_Activity: Salicyl-AMS is a mycobactin biosynthesis inhibitor which can also inhibit M. tuberculosis growth in vitro under iron-limited conditions.
IC50 & Target: Bacterial[1]

Name: Ophiopogonin C, CAS: 65586-25-6, stock 14.5g, assay 98.3%, MWt: 915.07, Formula: C46H74O18, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Ophiopogonin C, isolated from the tubers of Ophiopogon japonicus, is a rare naturally occurring C29 steroidal glycoside. Ophiopogonin C shows cytotoxic activity against two human tumor cell lines MG-63 and SNU387 with IC50s of 19.76 μM and 15.51 μM, respectively[1].

Name: IRAK4-IN-7, CAS: 1801343-74-7, stock 11.7g, assay 99%, MWt: 417.42, Formula: C21H19N7O3, Solubility: DMSO : 13.89 mg/mL (33.28 mM; Need ultrasonic); H2O : < 0.1 mg/mL (insoluble), Clinical_Informat: No Development Reported, Pathway: Immunology/Inflammation;Protein Tyrosine Kinase/RTK, Target: IRAK;IRAK, Biological_Activity: IRAK4-IN-7 is a selective and potent IRAK4 inhibitor extracted from patent WO2015104688A1, Compound example 1. IRAK4-IN-7 is useful for treatment of cancer and inflammatory diseases[1].
IC50 & Target: IRAK4[1]

Name: (+)-Peusedanol, CAS: 20516-23-8, stock 5.8g, assay 98.2%, MWt: 264.27, Formula: C14H16O5, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: (+)-Peusedanol is a coumarin isolated from Peucedanumjaponicum[1].

Name: Polygalacin D, CAS: 66663-91-0, stock 20.4g, assay 98.7%, MWt: 1209.32, Formula: C57H92O27, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Apoptosis;Apoptosis, Target: Apoptosis;IAP, Biological_Activity: Polygalacin D (PGD) is a bioactive compound isolated from Platycodon grandiflorum (Jacq.) with anticancer and anti-proliferative properties.
PGD suppresses the expression of the IAP family of proteins including survivin, cIAP-1 and cIAP-2 and blocks the PI3K/Akt pathway by inhibiting the phosphorylation of GSK3β, Akt and the expression of PI3K. Polygalacin D induces apoptosis[1]
IC50 & Target: IC50: IAP[1]
In Vitro: Polygalacin D (0-40 µM; 48 hours) inhibits cell proliferation with IC50s of 26.49 µM in the A549 cells and 20.52 µM in the H460 cells[1].
Polygalacin D (0-20 µM; 48 hours) increases the proportion of early and late apoptotic cells, and nuclear condensation is observed in A549 and H460 cells[1].
Polygalacin D (0-20 µM; 48 hours) may exerts its apoptotic effects by regulating the apoptotic proteins and the IAP family of proteins in A549 and H460 cells[1].

Name: Acoforestinine, CAS: 110011-77-3, stock 13.3g, assay 98.9%, MWt: 645.78, Formula: C35H51NO10, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Acoforestinine is a diterpenoid alkaloid isolated from Aconitum handelianum[1].

Name: Praeruptorin A, CAS: 73069-27-9, stock 6.8g, assay 98.9%, MWt: 386.40, Formula: C21H22O7, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: NF-κB, Target: NF-κB, Biological_Activity: Praeruptorin A is a main bioactive constituent of Peucedanum praeruptorum (also known as Bai-Hua Qian Hu). Praeruptorin A exerts anti-inflammatory effects in vitro through inhibition of NF-κB activation[1].

Name: Schinifoline, CAS: 80554-58-1, stock 4.1g, assay 98.9%, MWt: 257.37, Formula: C17H23NO, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Schinifoline, a 4-quinolinone derivative isolated from Zanthoxylum schinifolium Sieb, improves radiosensitizing effect, and effects cell cycle and apoptotic-inducing effects in cancer [1].

Name: Praeruptorin E, CAS: 78478-28-1, stock 36g, assay 98.4%, MWt: 428.47, Formula: C24H28O7, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Membrane Transporter/Ion Channel;Neuronal Signaling, Target: Calcium Channel;Calcium Channel, Biological_Activity: Praeruptorin E is a main bioactive constituent of Peucedanum praeruptorum (also known as Bai-Hua Qian Hu). Praeruptorin C is a calcium antagonist with pD2′ value of 5.2[1].

Name: 3-O-Methylgalangin Galangin 3-methyl ether;3-Methylgalangin, CAS: 6665-74-3, stock 3.9g, assay 98.6%, MWt: 284.26, Formula: C16H12O5, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: 3-O-Methylgalangin (Galangin 3-methyl ether) is a natural flavonoid compound from the rhizome of Alpinia officinarum (AO) with antibacterial activities, which also inhibits pancreatic lipase[1][2].

Name: Desmethylglycitein 4',6,7-Trihydroxyisoflavone, CAS: 17817-31-1, stock 0.9g, assay 98.8%, MWt: 270.24, Formula: C15H10O5, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: PI3K/Akt/mTOR;TGF-beta/Smad;Epigenetics;Cell Cycle/DNA Damage, Target: PI3K;PKC;PKC;CDK, Biological_Activity: Desmethylglycitein (4',6,7-Trihydroxyisoflavone), a metabolite of daidzein, sourced from Glycine max with antioxidant, and anti-cancer activities.
Desmethylglycitein binds directly to CDK1 and CDK2 in vivo, resulting in the suppresses CDK1 and CDK2 activity[1]. Desmethylglycitein is a direct inhibitor of protein kinase C (PKC)α, against solar UV (sUV)-induced matrix matrix metalloproteinase 1 (MMP1)[2]. Desmethylglycitein binds to PI3K in an ATP competitive manner in the cytosol, where it inhibits the activity of PI3K and downstream signaling cascades, leading to the suppression of adipogenesis in 3T3-L1 preadipocytes[3].
In Vitro: Desmethylglycitein (4',6,7-Trihydroxyisoflavone)(0-100 μM; 24-72 hours) suppesses anchorage-dependent growth of HCT-116 and DLD1 cells in a dose- and time-dependent manner without cytotoxicity [1].
Desmethylglycitein (4',6,7-Trihydroxyisoflavone)(0-100 μM; 24-72 hours) suppresses CDK1 activity in a dose-dependent manner and inhibits CDK2 activity in HCT-116 cells[1].
Desmethylglycitein (4',6,7-Trihydroxyisoflavone)(0-100 μM; 24-72 hours) induces cell cycle arrest at the S and G2/M phases, the percentage of cells in S phase is higher in the 100 μM 6,7,4′-THIF-treated group, and the same pattern is observed in G2/M phase (29.5% versus 19.1% ) [1].
In Vivo: Desmethylglycitein (4',6,7-Trihydroxyisoflavone) (intraperitoneally injection; 5 or 25 mg/kg; once daily; 20 days) suppresses tumor development in mice and serves as an effective anticancer treatment with the potential to inhibit or delay the tumorigenicity of HCT-116 cells in an in vivo system[1].

Name: Terrestrosin D, CAS: 179464-23-4, stock 38.2g, assay 98.5%, MWt: 1049.16, Formula: C50H80O23, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Apoptosis, Target: Apoptosis, Biological_Activity: Terrestrosin D, a steroidal saponin from Tribulus terrestris L., induces cell cycle arrest and cancer cells apoptosis. Terrestrosin D has antiangiogenic activities[1].

Name: Chebulic acid, CAS: 23725-05-5, stock 12.8g, assay 98.5%, MWt: 356.24, Formula: C14H12O11, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Chebulic acid, a phenolcarboxylic acid compound isolated from Terminalia chebula, has potent anti-oxidant activity,
which breaks the cross-links of proteins induced by advanced glycation end-products (AGEs) and inhibits the formation of AGEs. Chebulic acid is effective in controlling elevated metabolic parameters, oxidative stress and renal damage, supporting its beneficial effect in diabetic nephropathy[1][2].

Name: Picfeltarraenin IV, CAS: 184288-35-5, stock 26.7g, assay 98.8%, MWt: 925.06, Formula: C47H72O18, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Neuronal Signaling, Target: AChE, Biological_Activity: Picfeltarraenin IV, a triterpenoid obtained from Picriafel-terrae Lour (P.fel-terrae), is an acetylcholinesterase (AChE) inhibitor. Picfeltarraenin IV can be used for the treatment of herpes infections, cancer and inflammation[1].
IC50 & Target: AChE[1]

Name: Sinapine, CAS: 18696-26-9, stock 30.8g, assay 98.7%, MWt: 310.36, Formula: C16H24NO5, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Membrane Transporter/Ion Channel, Target: P-glycoprotein, Biological_Activity: Sinapine is an alkaloid from seeds of the cruciferous species which shows favorable biological activities such as antioxidant and radio-protective activities.
IC50 & Target: P-glycoprotein[1]
In Vitro: Sinapine increases the sensitivity of Caco-2 cells to doxorubicin in a dose-dependent manner, whereas no or less effect is observed in the cells treated with doxorubicin alone. The combination of Sinapine and doxorubicin has a synergistic effect and increased the cytotoxicity of doxorubicin against Caco-2 cells. Results indicate that Sinapine plays an important role in the down-regulation of P-glycoprotein expression through suppression of FGFR4-FRS2a-ERK1/2 signaling pathway[1]. Sinapine can effectively protect against OH-induced damages to DNA and MSCs, thereby it may have a therapeutic potential in MSCs transplantation[2].
In Vivo: During the first 8 days, the dry matter intake and live weight gain of the rats are significantly reduced by the intake of sinapine and other phenolic compounds. However, after this adaptation period their performances are similar to those of the control group[3].

Name: Ricinoleic acid, CAS: 141-22-0, stock 6.2g, assay 98.4%, MWt: 298.46, Formula: C18H34O3, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Ricinoleic acid, from castor (Ricinus communis) seed oil, is a high-value hydroxy fatty acid with broad industrial applications. Ricinoleic acid is an attractive feedstock for the production of high-performance lubricants, cosmetics, polymers, surfactants, and coatings[1].

Name: Terrestrosin K, CAS: 193605-07-1, stock 5.2g, assay 98.8%, MWt: 1079.18, Formula: C51H82O24, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Terrestrosin K, a steroidal saponin from Tribulus terrestris L., has potential to treat cardiovascular and cerebrovascular diseases[1].

Name: Tectorigenin 7-O-Xylosyl Glucoside, CAS: 231288-19-0, stock 11.9g, assay 98.5%, MWt: 594.52, Formula: C27H30O15, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Tectorigenin 7-O-Xylosyl Glucoside is a glycosidic isoflavone isolated from Pueraria thomsonii flower[1].

Name: Secoisolariciresinol, CAS: 29388-59-8, stock 24.6g, assay 98.8%, MWt: 362.42, Formula: C20H26O6, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Secoisolariciresinol, isolated from water extract of silver fir (Abies alba) wood, is a lignan, a type of phenylpropanoids.

Name: Ginkgolide K, CAS: 153355-70-5, stock 25.5g, assay 98.3%, MWt: 406.38, Formula: C20H22O9, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Autophagy, Target: Autophagy, Biological_Activity: Ginkgolide K, isolated from Ginkgo biloba, induces protective autophagy through the AMPK/mTOR/ULK1 signaling pathway. Ginkgolide K possesses neuroprotective activity[1].

Name: Isopropylidenylacetyl-marmesin (±)-Prantschimgin, CAS: 35178-20-2, stock 12.8g, assay 98.2%, MWt: 328.36, Formula: C19H20O5, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Isopropylidenylacetyl-marmesin ((±)-Prantschimgin) is a coumarin isolated from the roots of F. bracteata[1].

Name: N-Caffeoylputrescine,(E)-, CAS: 29554-26-5, stock 25.3g, assay 98.5%, MWt: 250.29, Formula: C13H18N2O3, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: N-Caffeoylputrescine,(E)- is a caffeic acid amide found in the tobacco plants (Nicotiana tabacum L.)[1].

Name: Aurantio-obtusin β-D-glucoside Glucoaurantio-obtusin, CAS: 129025-96-3, stock 35.4g, assay 98%, MWt: 492.43, Formula: C23H24O12, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Aurantio-obtusin β-D-glucoside (Glucoaurantio-obtusin), isolated from Cassiae Semen (seeds of Cassia tora), is a glucoside of aurantio-obtusin[1].

Name: Clemaphenol A, CAS: 362606-60-8, stock 20g, assay 98.9%, MWt: 358.39, Formula: C20H22O6, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Clemaphenol A is a chemical constituent of the flower of Fritillaria pallidiflora[1].

Name: Pennogenin 3-O-beta-chacotrioside, CAS: 55916-52-4, stock 35.3g, assay 98.5%, MWt: 885.04, Formula: C45H72O17, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Autophagy, Target: Autophagy, Biological_Activity: Pennogenin 3-O-beta-chacotrioside is an active component isolated from Paris polyphylla, modulates autophagy via increasing the expressions of autophagy-related proteins LC3 and Beclin-1. Anti-colorectal cancer activity[1].
IC50 & Target: Autophagy[1]

Name: Kanzonol C, CAS: 151135-82-9, stock 30.1g, assay 98.2%, MWt: 392.49, Formula: C25H28O4, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Anti-infection;Anti-infection, Target: Fungal;Bacterial, Biological_Activity: Kanzonol C, a flavonoid isolated from the twigs of Dorstenia barteri (Moraceae), has potential to treat bacterial and fungal infections[1].

Name: Licochalcone E, CAS: 864232-34-8, stock 32.5g, assay 98%, MWt: 338.40, Formula: C21H22O4, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: MAPK/ERK Pathway;PI3K/Akt/mTOR;Autophagy, Target: p38 MAPK;Akt;Autophagy, Biological_Activity: Licochalcone E, a flavonoid compound isolated from Glycyrrhiza inflate, inhibits NF-κB and AP-1 transcriptional activity through the inhibition of AKT and MAPK activation[1].
IC50 & Target: AKT, MAPK, NF-κB[1].

Name: Licoflavone C, CAS: 72357-31-4, stock 11.4g, assay 98.5%, MWt: 338.35, Formula: C20H18O5, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Licoflavone C is a prenyl-flavone extracted from Genista ephedroides, reduces the genotoxicity of cancer drugs in human peripheral lymphocytes[1].

Name: (E)-Flavokawain A, CAS: 37951-13-6, stock 12.2g, assay 98.7%, MWt: 314.33, Formula: C18H18O5, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Apoptosis, Target: Apoptosis, Biological_Activity: (E)-Flavokawain A, a chalcone extracted from Kava, has anticarcinogenic effect. (E)-Flavokawain A induces apoptosis in bladder cancer cells by involvement of bax protein-dependent and mitochondria-dependent apoptotic pathway and suppresses tumor growth in mice[1].

Name: Licoflavone B, CAS: 91433-17-9, stock 32.4g, assay 98.4%, MWt: 390.47, Formula: C25H26O4, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Anti-infection, Target: Parasite, Biological_Activity: Licoflavone B is a flavonoid isolated from Glycyrrhiza inflata, inhibits S. mansoni ATPase (IC50, 23.78 µM) and ADPase (IC50, 31.50 µM) activity. Anti-schistosomiasis activity[1].
IC50 & Target: IC50: 23.78 µM (S. mansoni ATPase), 31.50 µM (S. mansoni ADPase)[1]

Name: Licoflavone A, CAS: 61153-77-3, stock 3.8g, assay 98.5%, MWt: 322.35, Formula: C20H18O4, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Phosphatase, Biological_Activity: Licoflavone A is a flavonoid isolated from the roots of Glycyrrhiza uralensis, inhibits protein tyrosine phosphatase-1B (PTP1B), with an IC50 of 54.5 μM[1].
IC50 & Target: IC50: 54.5 μM (PTP1B)[1]

Name: Licochalcone D, CAS: 144506-15-0, stock 1.6g, assay 98.3%, MWt: 354.40, Formula: C21H22O5, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: NF-κB, Target: NF-κB, Biological_Activity: Licochalcone D, a flavonoid compound mainly existing in the root of Glycyrrhiza inflate, is a potent inhibitor of NF-kappaB (NF-κB) p65. Licochalcone D possesses antioxidant, anti-inflammatory, anti-cancer properties[1][2].
IC50 & Target: NF-κB p65[1].

Name: Toringin, CAS: 1329-10-8, stock 34.4g, assay 98.1%, MWt: 416.38, Formula: C21H20O9, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Toringin, a bioflavonoid, is isolated from the bark of Docyniopsis tschonoski. Toringin progressively decreases not only the cis-effect of the expanded CTG repeats but cytotoxicity as well. Exposure to isosakuranetin, Toringin rescues PC12 neuronal cells. Flavonoids are efficacious for ameliorating the RNA gain of function caused by expanded CTG repeats, and have various biological activities and beneficial actions against cancers, coronary heart disease, among other pathologies[1].

Name: Glabrol, CAS: 59870-65-4, stock 11.2g, assay 98.5%, MWt: 392.49, Formula: C25H28O4, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Acyltransferase, Biological_Activity: Glabrol (Compound 1), One isoprenyl flavonoid was isolated from ethanol extract of licorice roots, is a potent and non-competitive Acyl-coenzyme A: cholesterol acyltransferase (ACAT) inhibitor with an IC50 value of 24.6 μM for rat liver microsomal ACAT activity[1].
In Vitro: Glabrol (Compound 1) decreases cholesteryl ester formation with an IC50 value of 26.0 μM in HepG2 cells[1].

Name: Pinocembrin 7-O-[3''-O-galloyl-4'',6''-hexahydroxydiphenoyl]-β-D-glucoside, CAS: 205370-59-8, stock 4.7g, assay 98.9%, MWt: 872.69, Formula: C42H32O21, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Pinocembrin 7-O-[3''-O-galloyl-4'',6''-hexahydroxydiphenoyl]-β-D-glucoside is a flavanone compound.

Name: S-Dihydrodaidzein, CAS: 879559-75-8, stock 5g, assay 98.5%, MWt: 256.25, Formula: C15H12O4, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: S-Dihydrodaidzein is the (S)-enantiomer of dihydrodaidzein which is one of the most prominent dietary phytoestrogens[1][2].

Name: β-Hydroxyisovalerylshikonin, CAS: 7415-78-3, stock 29.5g, assay 98.4%, MWt: 388.41, Formula: C21H24O7, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Protein Tyrosine Kinase/RTK;JAK/STAT Signaling;Protein Tyrosine Kinase/RTK, Target: Src;EGFR;EGFR, Biological_Activity: Beta-hydroxyisovalerylshikonin is a natural product isolated from Lithospermium radix, acts as a potent inhibitor of protein tyrosine kinases (PTK), with IC50s of 0.7μM and 1μM for EGFR and v-Src receptor, respectively. Beta-hydroxyisovalerylshikonin is effective against a wide variety of tumor cell lines, and most efficiently induces cell-death in NCI-H522 and DMS114 cells[1].
IC50 & Target: IC50: 0.7 μM (EGFR), 1 μM (v-Src)[1]

Name: Dihydrorotenone, CAS: 6659-45-6, stock 31.3g, assay 98.4%, MWt: 396.43, Formula: C23H24O6, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Apoptosis;Metabolic Enzyme/Protease, Target: Apoptosis;Mitochondrial Metabolism, Biological_Activity: Dihydrorotenone, a natural pesticide, is a potent mitochondrial inhibitor. Dihydrorotenone probably induces Parkinsonian syndrome. Dihydrorotenone induces human plasma cell apoptosis by triggering endoplasmic reticulum stress and activating p38 signaling pathway[1].

Name: Daidzein diacetate, CAS: 3682-01-7, stock 0.3g, assay 98.4%, MWt: 338.31, Formula: C19H14O6, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Daidzein diacetate is a derivative of Daidzein that is a soy isoflavone[1][2].

Name: Chimonanthine (-)-Chimonanthine, CAS: 5545-89-1, stock 26.1g, assay 98.4%, MWt: 346.47, Formula: C22H26N4, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Chimonanthine is an alkaloid of Chimonanthus praecox, inhibits tyrosinase and tyrosine-related protein-1 mRNA expression, amd inhibits melanogenesis[1].

Name: Taccalonolide AJ, CAS: 1349904-82-0, stock 14.6g, assay 98.3%, MWt: 676.70, Formula: C34H44O14, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Cell Cycle/DNA Damage;Cytoskeleton, Target: Microtubule/Tubulin;Microtubule/Tubulin, Biological_Activity: Taccalonolide AJ is a semi-synthesis compound with cellular microtubule stabilizing activity. Taccalonolide AJ exhibits high potency antiproliferative activity against cancer cells, with an IC50 of 4.2 nM for HeLa cells[1].
IC50 & Target: microtubule[1]

Name: Yadanziolide A, CAS: 95258-14-3, stock 18.9g, assay 98.1%, MWt: 426.41, Formula: C20H26O10, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Yadanziolide A, isolated from the cultivated dry seeds of Brucea javanica, has strong antiviral activities with IC50 of 5.5 μM against tobacco mosaic virus. Yadanziolide A shows significant antitumor effects[1][2].
IC50 & Target: IC50: 5.5 μM (Tobacco mosaic virus)[1]

Name: Calycanthine, CAS: 595-05-1, stock 15.2g, assay 98.7%, MWt: 346.47, Formula: C22H26N4, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Calycanthine, the principal alkaloid of the order Calycanthaceae, has been isolated from a species of the genus Psychotria, and is a central nervous system toxin, causing convulsions[1][2].

Name: Saikosaponin E, CAS: 64340-44-9, stock 5.5g, assay 98.4%, MWt: 764.98, Formula: C42H68O12, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Saikosaponin E is a saikosaponin isolated from Bupleurum yinchowense[1].

Name: Astraganoside, CAS: 1011711-05-9, stock 19.5g, assay 98.5%, MWt: 480.46, Formula: C23H28O11, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Astraganoside, an isoflavane compound, isolated from the roots of Astragalus membranaceus (known as ‘‘Huangqi’’)[1].

Name: Anemarrhenasaponin I, CAS: 163047-21-0, stock 35g, assay 99%, MWt: 758.93, Formula: C39H66O14, Solubility: DMSO : ≥ 50 mg/mL (65.88 mM), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Anemarrhenasaponin I, a traditional Chinese medicine, is isolated from Anemarrhena asphodeloides Bunge.
In Vitro: Six steroidal saponins are isolated from Anemarrhena asphodeloides Bunge (Liliaceae), a traditional chinese medicine, and named Anemarrhenasaponin I (An-I), Anemarrhenasaponin Ia (An-Ia), Timosaponin B-I (TB-I), Timosaponin B-II (TB-II), Timosaponin B-III (TB-III), and Timosaponin A-III (TA-III)[1].

Name: Isoastragaloside IV, CAS: 136033-55-1, stock 5.3g, assay 98.7%, MWt: 784.97, Formula: C41H68O14, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Isoastragaloside IV is a triterpene oligoglycoside isolated from Astragali Radix.

Name: 11(α)-Methoxysaikosaponin F, CAS: 104109-37-7, stock 14.5g, assay 98.9%, MWt: 959.16, Formula: C49H82O18, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: 11(α)-Methoxysaikosaponin F is a triterpenoid saponin isolated from Bupleurum marginatum Wall.ex DC(ZYCH) which is a promising therapeutic for liver fibrosis. 11(α)-Methoxysaikosaponin F has an IC50 of 387.7 nM with viability of hepatic stellate cells-T6 (HSCs-T6). Triterpenoid saponins have numerous targets, important network positions, and strong inhibitory activity[1].

Name: Saikosaponin G, CAS: 99365-19-2, stock 7.5g, assay 98.3%, MWt: 780.98, Formula: C42H68O13, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Saikosaponin G is a triterpene glycoside isolated from Bupleuri Radix[1].

Name: Saikosaponin B4, CAS: 58558-09-1, stock 24.6g, assay 99%, MWt: 813.02, Formula: C43H72O14, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Saikosaponin B4 is a member of saikosaponins isolated from the roots of B. falcatum, selectively inhibits ACTH-induced lipolysis[1].

Name: 6'-O-Cinnamoyl harpagide, CAS: 1245572-24-0, stock 32.8g, assay 98.7%, MWt: 494.49, Formula: C24H30O11, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: 6'-O-Cinnamoyl harpagide is an iridoid glycoside isolated from the roots of Scrophularia ningpoensis[1].

Name: Acetyl Perisesaccharide C, CAS: 110764-09-5, stock 9.6g, assay 99%, MWt: 794.88, Formula: C37H62O18, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Acetyl Perisesaccharide C is an oligosaccharide, which is isolated from the root barks of Periploca sepium.

Name: Aaptamine, CAS: 85547-22-4, stock 27g, assay 98.1%, MWt: 228.25, Formula: C13H12N2O2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein;Neuronal Signaling, Target: Adrenergic Receptor;Adrenergic Receptor, Biological_Activity: Aaptamine, a spongean alkaloid isolated from a sea sponge Aaptos aaptos, is a competitive antagonist of α-adrenoceptor and activates the p21 promoter in a p53-independent manner[1][1].

Name: 1-Methyl-6-oxo-1,6-dihydropyridine-3-carboxylic acid, CAS: 3719-45-7, stock 34.8g, assay 98.2%, MWt: 153.14, Formula: C7H7NO3, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: 1-Methyl-6-oxo-1,6-dihydropyridine-3-carboxylic acid is from Cordyceps bassiana, which is one of Cordyceps species with anti-oxidative, anti-cancer, anti-inflammatory, anti-diabetic, anti-obesity, anti-angiogenic, and anti-nociceptive activities. 1-Methyl-6-oxo-1,6-dihydropyridine-3-carboxylic acid targets to block AP-1-mediated luciferase activity, implying it has an anti-inflammatory function[1].

Name: 6-Methoxy Dihydrosanguinarine, CAS: 151890-26-5, stock 4.7g, assay 98.4%, MWt: 363.36, Formula: C21H17NO5, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: 6-Methoxy Dihydrosanguinarine is an lkaloid isolated from the fruits of M.cordata. 6-Methoxy Dihydrosanguinarine shows strong cytotoxicity against MCF-7 and SF-268 cell lines with IC50 values of 0.61 μM and 0.54 μM, respectively[1].

Name: Angelol B, CAS: 83156-04-1, stock 18.6g, assay 98.4%, MWt: 376.40, Formula: C20H24O7, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Angelol B is a coumarin isolated from the roots of Angelica pubescens f. biserrata, which is passive diffusion as the dominating process in Caco-2 cell monolayer model[1].

Name: Angelol A, CAS: 19625-17-3, stock 0.3g, assay 98.1%, MWt: 376.40, Formula: C20H24O7, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Angelol A is a coumarin isolated from the roots of Angelica pubescens f. biserrata, which is passive diffusion as the dominating process in Caco-2 cell monolayer model[1].

Name: Dehydrocorydaline (nitrate), CAS: 13005-09-9, stock 20.5g, assay 98.7%, MWt: 428.44, Formula: C22H24N2O7, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Anti-infection, Target: Parasite, Biological_Activity: Dehydrocorydaline nitrate is isolated from Corydalis edulis Maxim with anti-malarial effects. Dehydrocorydaline nitrate shows strong anti-malarial effects (IC50 =38 nM), and low cytotoxicity (cell viability > 90%) using P. falciparum 3D7 strain[1].
IC50 & Target: IC50: 38 nM (P. falciparum 3D7 strain)[1]

Name: 13-Methylberberine (chloride) 13-Methylberberinium (chloride), CAS: 54260-72-9, stock 30.6g, assay 98.1%, MWt: 385.84, Formula: C21H20ClNO4, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: 13-Methylberberine chloride (13-Methylberberinium chloride), a berberine analogue, has anti-adipogenic and antitumor activities. 13-Methylberberine chloride (13-Methylberberinium chloride) increases production of IL-12 and inhibits the expression of iNOS at posttranscriptional level in macrophages activated with LPS[1][2][3].

Name: Dihydropalmatine, CAS: 26067-60-7, stock 32.3g, assay 98.6%, MWt: 353.41, Formula: C21H23NO4, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Dihydropalmatine is a alkaloid isolated from Berberis aristata[1].

Name: Soyasapogenol A, CAS: 508-01-0, stock 2.4g, assay 98.6%, MWt: 474.72, Formula: C30H50O4, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Apoptosis, Target: Apoptosis, Biological_Activity: Soyasapogenol A, a triterpene compound, isolated from the roots of Abrus cantoniensis. Soyasapogenol A directly prevents apoptosis of hepatocytes, and secondly, inhibits the elevation of plasma TNF-α, which consequently results in the prevention of liver damage in the Concanavalin A-induced hepatitis model[1][2].

Name: Soyasapogenol B, CAS: 595-15-3, stock 37.7g, assay 98.3%, MWt: 458.72, Formula: C30H50O3, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Apoptosis;Autophagy, Target: Apoptosis;Autophagy, Biological_Activity: Soyasapogenol B, an ingredient of soybean, exerts anti-proliferative, anti-metastatic activities. Soyasapogenol B triggers endoplasmic reticulum stress, which mediates apoptosis and autophagy in colorectal cancer[1][2].

Name: Specneuzhenide Nuezhenide, CAS: 449733-84-0, stock 1.1g, assay 98.3%, MWt: 686.65, Formula: C31H42O17, Solubility: DMSO : ≥ 100 mg/mL (145.63 mM), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Specneuzhenide (Nuezhenide) is a phenol glycoside isolated from Ligustrum sinense. Specneuzhenide (Nuezhenide) possesses anti-tumor activity[1][2].

Name: Timosaponin A1, CAS: 68422-00-4, stock 33g, assay 98.4%, MWt: 578.78, Formula: C33H54O8, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Timosaponin A1 is a coprostane type steroidal saponin isolated from Rhizoma Anemarrhenae.

Name: Hypocrellin C, CAS: 149457-83-0, stock 33.1g, assay 98.8%, MWt: 528.51, Formula: C30H24O9, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Hypocrellin C is a pigment isolated from the fungi Hypocrella bambusae and Shiraia bambusicola[1].

Name: (+)-Columbianetin acetate (S)-Columbianetin acetate, CAS: 23180-65-6, stock 35.1g, assay 98.3%, MWt: 288.30, Formula: C16H16O5, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: (S)-Columbianetin acetate is an isomer of Columbianetin. Columbianetin is a phytoalexin associated with celery (Apium graveolens) resistance to pathogens during storage. Columbianetin exhibits excellent anti-fungal and anti-inflammatory activity[1][2].

Name: Angelic anhydride, CAS: 94487-74-8, stock 8g, assay 98.9%, MWt: 182.22, Formula: C10H14O3, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Angelic anhydride is an aliphatic acid anhydride from unsaturated hydrocarbon acid anhydrides[1].

Name: Dihydroguaiaretic acid, CAS: 66322-34-7, stock 29g, assay 98.9%, MWt: 330.42, Formula: C20H26O4, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Dihydroguaiaretic acid, is isolated from the fruits of Schisandra chinensis with an anti-cancer activty[1].
In Vitro: Dihydroguaiaretic acid shows inhibitory effect on Human ovarian cancer cells and A2780 Human endometrial cancer cells Ishikawa with IC50 values of 27.17 μM and 45.46 μM, respectively[1].

Name: Neocurdione, CAS: 108944-67-8, stock 39.9g, assay 98.7%, MWt: 236.35, Formula: C15H24O2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Neocurdione is a hepatoprotective sesquiterpene isolated from Curcuma zedoaria rhizome. Neocurdione exerts potent effect on D-galactosamine- (D-Gain) and lipopolysaccharide- (LPS) induced acute liver injury in mice[1].

Name: Kakkalide, CAS: 58274-56-9, stock 11.3g, assay 98.5%, MWt: 608.54, Formula: C28H32O15, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Kakkalide is an isoflavone derived from the flowers of Pueraria lobata. Kakkalide ameliorates endothelial insulin resistance by suppressing reactive oxygen species (ROS)-associated inflammation[1].

Name: 5'-Guanylic acid 5'-GMP;5'-guanosine monophosphate, CAS: 85-32-5, stock 29.3g, assay 98.3%, MWt: 363.22, Formula: C10H14N5O8P, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: 5'-Guanylic acid (5'-GMP) is involved in several metabolic disorders, including the AICA-ribosiduria pathway, adenosine deaminase deficiency, adenine phosphoribosyltransferase deficiency (aprt), and the 2-hydroxyglutric aciduria pathway.

Name: Bacopaside I, CAS: 382148-47-2, stock 34.3g, assay 98.7%, MWt: 979.13, Formula: C46H74O20S, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Bacopaside I, a saponin isolated from Bacopa monniera, exbibits antioxidant properties and free radical scavenging capacity and exerts antidepressant-like effect[1].

Name: Kuwanon G, CAS: 75629-19-5, stock 17.5g, assay 99%, MWt: 692.71, Formula: C40H36O11, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein;Anti-infection, Target: Bombesin Receptor;Bacterial, Biological_Activity: Kuwanon G is a flavonoid isolated from Morus alba, acts as a bombesin receptor antagonist, with potential antimicrobial activity[1][2].

Name: Perisesaccharide C, CAS: 1311473-28-5, stock 34.1g, assay 98.8%, MWt: 752.84, Formula: C35H60O17, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Perisesaccharide C is an oligosaccharide isolated from the root barks of Periploca sepium.

Name: Perisesaccharide B, CAS: 1095261-93-0, stock 2.9g, assay 98.9%, MWt: 780.85, Formula: C36H60O18, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Perisesaccharide B is an oligosaccharide isolated from the root barks of Periploca sepium.

Name: Yadanzioside A, CAS: 95258-15-4, stock 30.6g, assay 98.7%, MWt: 684.68, Formula: C32H44O16, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Yadanziolide A, a quassinoid glycoside from Brucea javanica, has antitumor activity[1].

Name: Ginsenoside Ra3, CAS: 90985-77-6, stock 6.8g, assay 98.4%, MWt: 1241.41, Formula: C59H100O27, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Ginsenoside Ra3, isolated from Panax ginseng, possesses anti-cancer activity[1].

Name: α-Terpineol, CAS: 98-55-5, stock 37.3g, assay 98.9%, MWt: 154.25, Formula: C10H18O, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Anti-infection, Target: Bacterial, Biological_Activity: α-Terpineol is isolated from Eucalyptus globulus Labill, exhibits strong antimicrobial activity against periodontopathic and cariogenic bacteria[1].
α-Terpineol possesses antifungal activity against T. mentagrophytes, and the activity might lead to irreversible cellular disruption[2].

Name: Dehydronuciferine, CAS: 7630-74-2, stock 35.9g, assay 98.7%, MWt: 293.36, Formula: C19H19NO2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Neuronal Signaling, Target: AChE, Biological_Activity: Dehydronuciferine is isolated from the leaves of Nelumbo nucifera Gaertn, a acetylcholinesterase (AChE) inhibitor with an IC50 of 25 μg/mL[1].
IC50 & Target: IC50: 25 μg/mL (AChE)[1]

Name: Amyloid β Peptide (42-1)(human), CAS: 317366-82-8, stock 20.2g, assay 98.6%, MWt: 4514.04, Formula: C203H311N55O60S, Solubility: H2O : 0.5 mg/mL (0.11 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Neuronal Signaling, Target: Amyloid-β, Biological_Activity: Amyloid β Peptide (42-1)(human) is the inactive form of Amyloid β Peptide (1-42). Amyloid β Peptide (42-1) is a 42-amino acid peptide which plays a key role in the pathogenesis of Alzheimer disease.

Name: Amyloid β-Peptide (1-42) (human) β-Amyloid (1-42), human, CAS: 107761-42-2, stock 27.2g, assay 98.9%, MWt: 4514.04, Formula: C203H311N55O60S, Solubility: DMSO : 50 mg/mL (11.08 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Neuronal Signaling, Target: Amyloid-β, Biological_Activity: Amyloid β-Peptide (1-42) human is a 42-amino acid peptide which plays a key role in the pathogenesis of Alzheimer disease.
In Vitro: Amyloid β-Peptide (1-42) human is a 42-amino acid peptide which plays a key role in the pathogenesis of Alzheimer disease. Application of Amyloid β-Peptide (1-42) human (1 to 10 μM) in the bathing solution does not change delayed rectifier K+-current and leakage current, but enhances inactivation of Са2+-current and blocks Са2+-dependent К+-current[1]. At 2.5 μM concentration, Amyloid β-Peptide (1-42) human reduces viability of SH-SY5Y cells to 65%. Results show that Amyloid β-Peptide (1-42) human localizes in both the cytoplasm and nucleus of SH-SY5Y cells after 30 min of incubation and after 8 h. In the latter, large accumulations of Amyloid β-Peptide (1-42) human are seen in the cytoplasm and in the nucleus. Increased APP mRNA levels are also detected upon Amyloid β-Peptide (1-42) human treatment[2].

Name: BRL-50481, CAS: 433695-36-4, stock 37.3g, assay 98.2%, MWt: 244.27, Formula: C9H12N2O4S, Solubility: DMSO : 300 mg/mL (1228.15 mM; Need ultrasonic and warming); H2O : < 0.1 mg/mL (insoluble), Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Phosphodiesterase (PDE), Biological_Activity: BRL-50481 is a novel and selective inhibitor of PDE7 with IC50s of 0.15, 12.1, 62 and 490 μM for PDE7A, PDE7B, PDE4 and PDE3, respectively.
IC50 & Target: IC50: 0.15 μM (PDE7A), 12 μM (PDE7B), 62 μM (PDE4), 490 μM (PDE3)[1]
In Vitro: BRL-50481 increases the cAMP content (19.1±6.2% of IBMX response at 300 μM) but is considerably less potent. BRL-50481 (30 μM) fails to suppress proliferation by itself but significantly potentiates the effect of rolipram. BRL-50481 (30 μM) has no effect on IL-15-induced proliferation but augments the inhibitory effect of rolipram. Pretreatment (30 min) of human monocytes with BRL-50481 has, by itself, a negligible (~2 to 10%) inhibitory effect on TNFα output at all concentrations tested. BRL-50481 also potentiates the inhibitory effect of PGE2 on LPS-induced TNFα release. BRL-50481 has no significant effect by itself on κB-dependent transcription (5.6±1.9% inhibition at 30 μM) and fails to enhance the effect of rolipram (maximum inhibition, 52.9±2.7%; pIC30 value of 5.33±0.12). BRL-50481 suppresses, in a concentration-dependent manner, LPS-induced TNFα release in monocytes in which PDE7A1 is induced (21.7±1.6% inhibition at 30 μM at the 12-h time point)[2].

Name: Vinaginsenoside R4, CAS: 156009-80-2, stock 2g, assay 98.4%, MWt: 963.15, Formula: C48H82O19, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Vinaginsenoside R4, isolated from the leaves of hydroponic Panax ginseng. It has an inhibitory effect on melanin biosynthesis without any cytotoxic effects on the melan-a cells, and enhances the depigmentation on the zebrafish[1].

Name: Vinaginsenoside R8, CAS: 156042-22-7, stock 14.5g, assay 98.4%, MWt: 963.15, Formula: C48H82O19, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Vinaginsenoside R8, a triterpenoid glycoside isolated from the rhizomes of Panacis majoris. Vinaginsenoside R8 displays activities against adenosine diphosphate (ADP)-induced platelet aggregation (IC50=25.18 μM)[1].

Name: Yangambin, CAS: 13060-14-5, stock 35.4g, assay 98.9%, MWt: 446.49, Formula: C24H30O8, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Membrane Transporter/Ion Channel;Neuronal Signaling, Target: Calcium Channel;Calcium Channel, Biological_Activity: Yangambin, a furofuran lignan, is already isolated from plants such as member of the Annonaceae family, including species of the genus Rollinia: R. pickeli, R. exalbidaand R. mucosa, as well from the Magnolia biondii. Yangambin, a selective PAF receptor antagonist, inhibits Ca2+ influx through voltage-gated Ca2+ channels, leading to the reduction in [Ca2+]i in vascular smooth muscle cells and consequent peripheral vasodilation[1]. Yangambin exhibits the antiallergic activity against β-hexosaminidase release with an IC50 of 33.8 μM and for anti-inflammatory activity with an IC50 of 37.4 μM[2].
IC50 & Target: PAF, Ca2+ channels[1]

Name: Tenuifoliside B, CAS: 139726-36-6, stock 38.3g, assay 98.6%, MWt: 668.60, Formula: C30H36O17, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Tenuifoliside B, a component isolated from Polygalae Radix, inhibits potassium cyanide (KCN)-induced hypoxia and scopolamine-induced memory impairment. Tenuifoliside B shows potential cognitive improvement and cerebral protective effects. Tenuifoliside B has potential to become an anti-AD lead compound[1][2].

Name: Sabinene, CAS: 3387-41-5, stock 6.8g, assay 98.4%, MWt: 136.23, Formula: C10H16, Solubility: DMSO : 33.33 mg/mL (244.66 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Sabinene is a perfume additive which is being explored as the component for the next generation aircraft fuel.

Name: Methyl protogracillin NSC-698793, CAS: 54522-53-1, stock 1.6g, assay 98.8%, MWt: 1079.23, Formula: C52H86O23, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Methyl protogracillin (NSC-698793), isolated from the roots of Dioscorea opposite Thunb, exhibits strong anti-cancer activity[1].

Name: Huangjiangsu A, CAS: 1026020-27-8, stock 15.7g, assay 98.6%, MWt: 1047.18, Formula: C51H82O22, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease;NF-κB;Immunology/Inflammation, Target: Reactive Oxygen Species;Reactive Oxygen Species;Reactive Oxygen Species, Biological_Activity: Huangjiangsu A, pseudoprotodioscin, methyl protobioside, protodioscin, and protodeltonin, isolated from D. villosa.
Huangjiangsu A has hepatoprotective potential against H2O2-induced cytotoxicity and ROS generation and could be promising as potential therapeutic agents for liver diseases[1].

Name: Gentisin, CAS: 437-50-3, stock 8.5g, assay 98.6%, MWt: 258.23, Formula: C14H10O5, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Gentisin is a natural compound isolated from Gentianae radix (Gentianaceae) with mutagenic activities[1].

Name: 7,8-Dimethoxycoumarin, CAS: 2445-80-9, stock 37g, assay 98.2%, MWt: 206.19, Formula: C11H10O4, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: 7,8-Dimethoxycoumarin (Daphnetin dimethyl ether) is a coumarin from Artemisia caruifolia[1].

Name: Cenicriviroc Mesylate TAK-652 Mesylate;TBR-652 Mesylate, CAS: 497223-28-6, stock 1.5g, assay 98.4%, MWt: 793.05, Formula: C42H56N4O7S2, Solubility: DMSO : ≥ 107.5 mg/mL (135.55 mM), Clinical_Informat: Phase 3, Pathway: Immunology/Inflammation;GPCR/G Protein;Anti-infection, Target: CCR;CCR;HIV, Biological_Activity: Cenicriviroc Mesylate (TAK-652 Mesylate) is a dual CCR2/CCR5 antagonist, also inhibits both HIV-1 and HIV-2, and displays potent anti-inflammatory and antiinfective activity.
IC50 & Target: CCR2/CCR5[1]
In Vitro: Migration of mouse monocytes in response to carbon tetrachloride (CCL2) is reduced following pre-treatment with Cenicriviroc Mesylate (CVC) at a concentration of 1 μM. Compare to untreated and unstimulated cells, the average fold change in migrating cells (±SD) is 0.8±0.2 (p>0.05) and 0.7±0.4 (p>0.05) for CCL2-stimulated cells treated with Cenicriviroc Mesylate and unstimulated cells treated with Cenicriviroc Mesylate, respectively[1]. Phenotypic susceptibility testing shows, for the four R5-tropic HIV-2 isolates, a median EC50 for Cenicriviroc Mesylate of 0.39 nM (0.03, 0.33, 0.45 and 0.98 nM). The dual-tropic and the X4-tropic HIV-2 strains are resistant to Cenicriviroc Mesylate with EC50 at >1000 nM, and Maximum percentages of inhibition (MPI) at 33% and 4%, respectively[2].
In Vivo: Cenicriviroc Mesylate (CVC) treatment leads to dose-related decrease in monocyte/macrophage recruitment, and achieving statistical significance at doses ≥20 mg/kg/day (p<0.05). Compare to the vehicle-control group, peritoneal lavage monocyte/macrophage counts are decreased by: 5.7%, 45.2%, 76.5% and 26.0% for Cenicriviroc Mesylate 5 twice daily (BID), Cenicriviroc Mesylate20 twice daily (BID), Cenicriviroc Mesylate100 BID, Cenicriviroc Mesylate 20 once-daily (QD), respectively. Exposure to Cenicriviroc Mesylate is dose-related and correlated with the decrease in monocyte/macrophage recruitment, with Cenicriviroc Mesylate appearing to be more effective when given BID versus QD, in line with the higher plasma concentrations achieved with BID dosing and the known short half-life in mice (~2 hours)[1].

Name: Coniferyl alcohol, CAS: 458-35-5, stock 0.5g, assay 98.6%, MWt: 180.20, Formula: C10H12O3, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Anti-infection, Target: Fungal, Biological_Activity: Coniferyl alcohol is an intermediate in biosynthesis of eugenol and of stilbenoids and coumarin[1]. Coniferyl alcohol specifically inhibits fungal growth[1].
IC50 & Target: Fungal[1]

Name: BM635, CAS: 1493762-74-5, stock 6.7g, assay 98.5%, MWt: 392.51, Formula: C25H29FN2O, Solubility: DMSO : 31 mg/mL (78.98 mM; Need ultrasonic and warming), Clinical_Informat: No Development Reported, Pathway: Anti-infection, Target: Bacterial, Biological_Activity: BM635 is a MmpL3 inhibitor with outstanding anti-mycobacterial activity. BM635 has an MIC50 of 0.12 μM against M. tuberculosis H37Rv.
IC50 & Target: MIC50: 0.12 μM (M. tuberculosis H37Rv)[1]
In Vivo: BM635 has potent MIC (0.12 µM), Tox50:MIC ratio of >100, and good microsomal stability in mice (1.4 mL/min/g). When tested in an acute murine infection model at multiple doses, BM635 exhibits potent anti-tubercular activity, with an ED99 of 49 mg/Kg (IC95%: 43–54 mg/Kg)[1]. The half-life in vivo of BM635 is 1h, allowing a reasonable maximum concentration (Cmax=1.62 μM) and a moderate bioavailability (46%). Its poor aqueous solubility together with its high lipophilicity leads to low exposure in vivo[2].

Name: NITD-349, CAS: 1473450-62-2, stock 9.8g, assay 98.4%, MWt: 306.35, Formula: C17H20F2N2O, Solubility: DMSO : ≥ 310 mg/mL (1011.91 mM), Clinical_Informat: No Development Reported, Pathway: Anti-infection, Target: Bacterial, Biological_Activity: NITD-349 is an MmpL3 inhibitor that shows highly potent anti-mycobacterial activity with MIC50 of 23 nM against virulent Mycobacterium tuberculosis H37Rv.
IC50 & Target: MIC50: 23 nM (Mycobacterium tuberculosis H37Rv)[1]
In Vitro: NITD-349 shows bactericidal activity against in vitro replicating Mycobacterium tuberculosis (Mtb) and also are active against intramacrophage Mtb. Kill kinetic analysis of these compounds showed both concentration- and time-dependent killing of Mtb cells with 3- to 4-log colony-forming unit (CFU) reductionwithin 3 days of treatment. The cidal activity profile of NITD-304 is similar to that of isoniazid for which rapid killing is noticed at concentrations greater than 0.2 μM. The MIC activity of NITD349 against various MDR Mtb strains ranges from 0.04 to 0.08 μM. NITD-349 shows high permeability and moderate in vitro metabolic clearance in mouse and human hepatic microsomes[1].
In Vivo: In the acute murine efficacy modelNITD-349 shows favorable oral pharmacokinetic (PK) properties in rodents and dogs and are efficacious in mouse models of both acute and chronic Mycobacterium tuberculosis infection. In the acute murine efficacy model, treatment of mice with NITD-349 at doses of 12.5 and 50 mg/kg resulted in 0.9- and 3.4-log CFU reduction in lung tissue. In an established infection mouse model, after 2 weeks of treatment, the efficacy of NITD-349 is comparable to the first-line TB drug rifampicin and is better than ethambutol. Four weeks of treatment at 100 mg/kg with NITD-349 results in 2.38-log CFU reductions[1].

Name: 4-Methyldaphnetin, CAS: 2107-77-9, stock 14.9g, assay 98.4%, MWt: 192.17, Formula: C10H8O4, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Apoptosis, Target: Apoptosis, Biological_Activity: 4-Methyldaphnetin is a precursor in the synthesis of derivatives of 4-methyl coumarin. 4-Methyldaphnetin has potent, selective anti-proliferative and apoptosis-inducing effects on several cancer cell lines. 4-Methyldaphnetin possesses radical scavenging property and strongly inhibits membrane lipid peroxidation[1][2][3].

Name: 4-Methylesculetin, CAS: 529-84-0, stock 12.8g, assay 98.3%, MWt: 192.17, Formula: C10H8O4, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Glutathione Peroxidase, Biological_Activity: 4-Methylesculetin is an orally active natural coumarin derivative, with potent anti-oxidant and anti-inflammatory activities. 4-Methylesculetin inhibits myeloperoxidase activity and reduces IL-6 level[1].

Name: 3-Epiursolic Acid, CAS: 989-30-0, stock 18.4g, assay 98.2%, MWt: 456.70, Formula: C30H48O3, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Cathepsin, Biological_Activity: 3-Epiursolic Acid is a triterpenoid isolated from Myrtaceae, acts as a competitive inhibitor of cathepsin L (ICIC50, 6.5 μM; Ki, 19.5 μM), with no obvious effect on cathepsin B[1].
IC50 & Target: IC50: 6.5 μM (Cathepsin L)[1] 
Ki: 19.5 μM (Cathepsin L)[1]

Name: 3-Epioleanolic acid, CAS: 25499-90-5, stock 7.7g, assay 98.4%, MWt: 484.75, Formula: C32H52O3, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: 3-Epioleanolic acid is an active component of Verbena officinalis Linn, with anti-inflammatory activity[1].

Name: 1,7-Dihydroxy-2,3-methylenedioxyxanthone, CAS: 183210-63-1, stock 16.2g, assay 99%, MWt: 272.21, Formula: C14H8O6, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: 1,7-Dihydroxy-2,3-methylenedioxyxanthone is isolated from Polygala cyparissias which is a small herb found in Brazil, Argentina and Uruguay. Polygala cyparissias are used in folk medicine as an anaesthetic[1].

Name: 1,2,3,7-Tetramethoxyxanthone, CAS: 22804-52-0, stock 36.1g, assay 98.3%, MWt: 316.31, Formula: C17H16O6, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: 1,2,3,7-Tetramethoxyxanthone is a xanthone isolated from Polygala tenuifolia[1].

Name: Arjungenin, CAS: 58880-25-4, stock 27.5g, assay 98.7%, MWt: 504.70, Formula: C30H48O6, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Arjungenin, a triterpene isolated from Terminalia arjuna, is an insect feeding-deterrent and growth inhibitor[1][2].

Name: Bacopaside V, CAS: 620592-16-7, stock 29.9g, assay 98.7%, MWt: 766.95, Formula: C41H66O13, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Bacopaside V is a bioactive triterpenoid glycoside of Bacopa monniera, a herb having confirmed nervine tonic activity[1].

Name: Isosakuranin, CAS: 491-69-0, stock 9.7g, assay 98%, MWt: 448.42, Formula: C22H24O10, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Isosakuranin is a natural product derived from the fruits of Paliurus ramosissimus[1].

Name: Baicalin methyl ester, CAS: 82475-03-4, stock 14.3g, assay 98.8%, MWt: 460.39, Formula: C22H20O11, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Baicalin methyl ester is a constituent of the roots of S. baicalmsis[1].

Name: Epitheaflagallin 3-O-gallate, CAS: 102067-92-5, stock 0.3g, assay 98.3%, MWt: 552.44, Formula: C27H20O13, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Epitheaflagallin 3-O-gallate is a minor polyphenol in black tea. Epitheaflagallin 3-O-gallate exhibits versatile physiological functions in vivo and in vitro, including antioxidative activity, pancreatic lipase inhibition, Streptococcus sorbinusglycosyltransferase inhibition, and an inhibiting effect on the activity of matrix metalloprotease-1 and -3 and their synthesis by human gingival fibroblasts[1].

Name: Caesappanin C, CAS: 1913319-59-1, stock 19.4g, assay 98%, MWt: 608.59, Formula: C32H32O12, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Caesappanin C, a biphenyl dimer from the ethanolic extract of the heartwood of Indonesian Caesalpinia sappan L., shows strong proliferation stimulating activity against the primary osteoblastic cells in vitro. Caesappanin C has the potential to stimulate bone formation and regeneration[1].

Name: 4'-O-Methylochnaflavone, CAS: 49619-87-6, stock 38.5g, assay 98.6%, MWt: 552.48, Formula: C31H20O10, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: 4'-O-Methylochnaflavone is a biflavonoid isolated from Lonicera japonica, suppresses mouse lymphocyte proliferation[1].

Name: Kojic acid, CAS: 501-30-4, stock 16.3g, assay 98.1%, MWt: 142.11, Formula: C6H6O4, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Anti-infection, Target: Parasite, Biological_Activity: Kojic acid is a natural substance produced by Aspergillus oryzae, also used as an anti-oxidant and radio-protective agent[1].

Name: 5-Ethoxy-10-Gingerol, CAS: 121771-98-0, stock 3.7g, assay 98.9%, MWt: 378.55, Formula: C23H38O4, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: 5-Ethoxy-10-Gingerol is a derivate of gingerol.

Name: Gambogellic acid, CAS: 173867-04-4, stock 2.6g, assay 98.7%, MWt: 628.75, Formula: C38H44O8, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Gambogellic acid is an xanthone isolated from the processed gamboge, with antitumor activity[1].

Name: Notoginsenoside FP2, CAS: 1004988-75-3, stock 23.6g, assay 98.2%, MWt: 1211.38, Formula: C58H98O26, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Notoginsenoside FP2, a dammarane-Type Bisdesmoside isolated from the Fruit Pedicels of Panax notoginseng, has potential to treat cardiovascular disease[1][2].

Name: Laetanine, CAS: 72361-67-2, stock 28g, assay 98.7%, MWt: 313.35, Formula: C18H19NO4, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Anti-infection, Target: Parasite, Biological_Activity: Laetanine, a noraporphine alkaloid from Litsea laeta, exhibits antiplasmodial activity[1].

Name: Hexamethylquercetagetin Hexa-O-methylquercetagetin; Quercetagetin hexamethyl ether;3,5,6,7,3',4'-Hexamethoxyflavone, CAS: 1251-84-9, stock 24.9g, assay 98.1%, MWt: 402.39, Formula: C21H22O8, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Hexamethylquercetagetin is a polymethoxylated flavone in peels of citrus cultivars.

Name: 2,3,4,5-Tetracaffeoyl-D-Glucaric acid, CAS: 1419478-52-6, stock 18.8g, assay 98.4%, MWt: 858.71, Formula: C42H34O20, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: 2,3,4,5-Tetracaffeoyl-D-Glucaric acid is a caffeoyl-D-glucaric acid derivative isolated from the Genus Gnaphalium[1].

Name: Bryodulcosigenin, CAS: 4965-97-3, stock 9.2g, assay 98.8%, MWt: 474.72, Formula: C30H50O4, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Bryodulcosigenin is an extract of the roots of Bryoniadioica with anti-inflammatory effect[1].

Name: Eriosematin, CAS: 168010-17-1, stock 7.7g, assay 98.2%, MWt: 312.36, Formula: C19H20O4, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Apoptosis, Target: Apoptosis, Biological_Activity: Eriosematin is a compound from the roots of Flemingia philippinensis with antiproliferative activity and apoptosis-inducing property[1].

Name: Scutellarein tetramethyl ether 4',5,6,7-Tetramethoxyflavone, CAS: 1168-42-9, stock 6.8g, assay 99%, MWt: 342.34, Formula: C19H18O6, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Scutellarein tetramethyl ether (4',5,6,7-Tetramethoxyflavone) is a bioactive component of Siam weed extract. Scutellarein tetramethyl ether (4',5,6,7-Tetramethoxyflavone) exhibits anti-inflammatory activity through NF-κB pathway[1]. Scutellarein tetramethyl ether (4',5,6,7-Tetramethoxyflavone) modulats of bacterial drug resistance via efflux pump inhibition[2]. Scutellarein tetramethyl ether (4',5,6,7-Tetramethoxyflavone) can enhance blood coagulation[3].

Name: Pomiferin NSC 5113, CAS: 572-03-2, stock 38.6g, assay 98.8%, MWt: 420.45, Formula: C25H24O6, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: PI3K/Akt/mTOR;Epigenetics;Cell Cycle/DNA Damage, Target: mTOR;HDAC;HDAC, Biological_Activity: Pomiferin (NSC 5113), a flavonoid from the fruits of Maclura pomifera, acts as an potential inhibitor of HDAC, with an IC50 of 1.05 μM, and also potently inhibits mTOR (IC50, 6.2 µM).
IC50 & Target: IC50: 1.05 μM (HDAC)[1], 6.2 µM (mTOR)[2]
In Vitro: Pomiferin is an potential inhibitor of HDAC, with an IC50 of 1.05 μM. Pomiferin shows cytotoxic effects on human tumor cell lines, with GI50s of 1.32 ± 0.02 μM (HCT-15 cells), 2.92 ± 0.09 μM (MDA-MB-231 cells), 3.18 ± 0.05 μM (ACHN cells), 3.34 ± 0.11 μM (LOX-IMVI cells), 3.95 ± 0.05 μM (PC-3 cells), 5.14 ± 0.06 μM (NCI-H23 cells), and 123 μM (Hepatocyte cells)[1]. Pomiferin is a highly specific mTOR inhibitor, with an IC50 of 6.2 µM. Pomiferin triacetate only affects two PI3Kα mutants, E542K and E545K. Pomiferin triacetate (0.3125-20 µM) stabilizes Pdcd4 from TPA-induced degradation in HEK293 cells. Pomiferin triacetate (20 µM) inhibits IGF-1-induced signaling downstream of Akt activation[2].
In Vivo: Pomiferin (5, 10 and 20 mg/kg, p.o.) shows protective effects on the treatment of reperfusion injury. Pomiferin also increases SOD activities and total antioxidative capacity, and decreases malondialdehyde in rats[3].

Name: Flemiphilippinin A, CAS: 140366-64-9, stock 35.3g, assay 98.2%, MWt: 488.57, Formula: C30H32O6, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Flemiphilippinin A is a prenylated isoflavone isolated from Flemingia philippinensis[1].
In Vivo: Flemiphilippinin A 是一种异黄酮异黄酮，分离于 Flemingia philippinensis 中。

Name: Ethoxysanguinarine, CAS: 28342-31-6, stock 9.8g, assay 98.4%, MWt: 377.39, Formula: C22H19NO5, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Apoptosis, Target: Apoptosis, Biological_Activity: Ethoxysanguinarine is a benzophenanthridine alkaloid natural product that is mainly found in Macleaya cordata. Ethoxysanguinarine inhibits viability and induces apoptosis of colorectal cancer cells by inhibiting protein phosphatase 2A (CIP2A)[1].

Name: Graveobioside A, CAS: 506410-53-3, stock 27.8g, assay 98.9%, MWt: 580.49, Formula: C26H28O15, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Graveobioside A is an anthoxanthin glycoside[1].

Name: 3-Feruloyl-1-Sinapoyl sucrose, CAS: 98942-06-4, stock 37.5g, assay 98.2%, MWt: 724.66, Formula: C33H40O18, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: 3-Feruloyl-1-Sinapoyl sucrose (compound 1) is a glycoside isolated from the aerial parts of Polygala chamaebuxus[1].

Name: Glucotropaeolin (potassium) Benzylglucosinolate (potassium), CAS: 5115-71-9, stock 19.5g, assay 99%, MWt: 447.52, Formula: C14H18KNO9S2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Glucotropaeolin potassium (Benzylglucosinolate potassium) , a glucosinolate contained in cruciferous vegetables, causes a moderate decrease in spontaneous DNA damage in animals[1].

Name: Decursinol angelate, CAS: 130848-06-5, stock 9.1g, assay 98.8%, MWt: 328.36, Formula: C19H20O5, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: TGF-beta/Smad;Epigenetics, Target: PKC;PKC, Biological_Activity: Decursinol angelate, a cytotoxic and protein kinase C (PKC) activating agent from the root of Angelica gigas, possesses anti-tumor and anti-inflammatory activities[1][2].
IC50 & Target: PKC[1].

Name: 14-Deoxyandrographolide, CAS: 4176-97-0, stock 29.3g, assay 98.8%, MWt: 334.45, Formula: C20H30O4, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: 14-Deoxyandrographolide, a bioactive compound of Andrographis paniculata, has hepatoprotective efficacy. 14-Deoxyandrographolide desensitizes hepatocytes to TNF-α-mediated apoptosis through the release of TNFRSF1A release[1].

Name: cis-p-Menthan-1,8-diol 4-p-Menthan-1,8-diol, CAS: 565-48-0, stock 1.3g, assay 98.9%, MWt: 172.26, Formula: C10H20O2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: cis-p-Menthan-1,8-diol is a natural menthane monoterpenoid[1].

Name: Onjisaponin Z, CAS: 1078708-72-1, stock 29.8g, assay 98.6%, MWt: 1471.58, Formula: C71H106O32, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Onjisaponin Z is a natural product isolated from Radix Polygalae.

Name: 14,15 β-Dihydroxyklaineanone, CAS: 137359-82-1, stock 7.1g, assay 98.1%, MWt: 396.43, Formula: C20H28O8, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: 14,15 D-dihydroxyklaineanone, a quassinoid isolated from the root of Eurycoma longifolia, possesses anti-cancer activity[1].

Name: Eurycomalactone, CAS: 23062-24-0, stock 17.9g, assay 98.1%, MWt: 348.39, Formula: C19H24O6, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: NF-κB, Target: NF-κB, Biological_Activity: Eurycomalactone is a natural product found in Eurycoma longifolia Jack., acts as a potent NF-κB inhibitor, with an IC50 of 0.5 μM. Eurycomalactone inhibits protein synthesis, depletes cyclin D1, but does not affect TNFα-induced degradation of IκBα or the phosphorylation of IKKα/β and IκBα[1].
IC50 & Target: IC50: 0.5 μM (NF-κB)[1]

Name: Arachidonic acid Immunocytophyt;Immunocytophyte;Vevodar, CAS: 506-32-1, stock 9.9g, assay 98.2%, MWt: 304.47, Formula: C20H32O2, Solubility: DMSO : ≥ 50 mg/mL (164.22 mM); Ethanol : ≥ 50 mg/mL (164.22 mM); H2O : < 0.1 mg/mL (insoluble), Clinical_Informat: Phase 4, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: Arachidonic acid is an essential fatty acid and a major constituent of biomembranes.
In Vivo: Arachidonic acid (ARA) is converted into various lipid mediators, such as prostaglandin E2 (PGE2), which is involved in the development of rheumatoid arthritis (RA)[1].

Name: Daphylloside, CAS: 14260-99-2, stock 38.7g, assay 98.1%, MWt: 446.40, Formula: C19H26O12, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Daphylloside is an iridoid isolated from the aerial parts of Galium verum.
In Vitro: Daphylloside may show some antioxidant effects.

Name: Asperulosidic Acid, CAS: 25368-11-0, stock 29.6g, assay 98.5%, MWt: 432.38, Formula: C18H24O12, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Stem Cell/Wnt;MAPK/ERK Pathway;NF-κB, Target: ERK;ERK;NF-κB, Biological_Activity: Asperulosidic Acid (ASPA), a bioactive iridoid glycoside, is extracted from the herbs of Hedyotis diffusa Willd. Asperulosidic Acid (ASPA) has anti-tumor, anti-oxidant, and anti-inflammatory activities[1].
ASPA is related to the inhibition of inflammatory cytokines (TNF-α, IL-6) and mediators via suppression of the NF-κB and mitogen-activated protein kinase (MAPK) signaling pathways[2].
In Vitro: Asperulosidic Acid (ASPA) (40-160 μg/mL; pre- 1 hour) significantly down-regulates the mRNA levels of TNF-α and IL-6 in LPS-induced RAW 264.7 cells compared with the group treated with LPS alone [1].
Asperulosidic Acid (ASPA) (40-160 μg/mL; pre- 1 hour) decreases IκB-α phosphorylation in a concentration-dependent manner, decreases Erk1/2 phosphorylation at all concentration levels, but there was no effect on p-p38 [1].

Name: Fuscaxanthone C, CAS: 15404-76-9, stock 34.9g, assay 98.3%, MWt: 438.51, Formula: C26H30O6, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Fuscaxanthone C is an xanthone isolated from the stem bark of Garcinia fusca[1].

Name: Cowaxanthone B, CAS: 212842-64-3, stock 13.2g, assay 98.5%, MWt: 424.49, Formula: C25H28O6, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Anti-infection, Target: Bacterial, Biological_Activity: Cowaxanthone B is a xanthone isolated from the fruits of Garcinia cowa. Cowaxanthone B has weak antibacterial activity[1].

Name: Feretoside, CAS: 27530-67-2, stock 5g, assay 98.4%, MWt: 404.37, Formula: C17H24O11, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease;Cell Cycle/DNA Damage, Target: HSP;HSP, Biological_Activity: Feretoside, a phenolic compound extracted from the barks of E. ulmoides, is a HSP inducer which act as cytoprotective agent.
IC50 & Target: HSP[1]
In Vitro: The barks of Eucommia ulmoides (Eucommiae Cortex, Eucommiaceae) have been used as a traditional medicine in Korea, Japan, and China to treat hypertension, reinforce the muscles and bones, and recover the damaged liver and kidney functions. Feretoside increases expression of HSF1 by a factor of 1.214, 1.144, 1.153, 1.114, 1.159, 1.041, and 1.167 at 3 mm, respectively[1].

Name: Cratoxylone, CAS: 149155-01-1, stock 4.3g, assay 98.6%, MWt: 428.47, Formula: C24H28O7, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Anti-infection, Target: Parasite, Biological_Activity: Cratoxylone, isolated from the bark of Cratoxylum Cochinchinense, possesses antiplasmodial activity[1][2].

Name: Gypenoside XLVI, CAS: 94705-70-1, stock 39.2g, assay 98.3%, MWt: 963.15, Formula: C48H82O19, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Gypenoside XLVI is one of the major dammarane-type triterpenoid saponins from Gynostamma pentaphallum[1]. Gypenoside XLVI has a tetracyclic triterpene structure and possess potent non-small cell lung carcinoma A549 cell inhibitory activity[2].

Name: Moluccanin, CAS: 116521-73-4, stock 9.6g, assay 98.1%, MWt: 386.35, Formula: C20H18O8, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Moluccanin is a coumarinolignoid from Aleurites moluccana[1].

Name: Cafestol, CAS: 469-83-0, stock 9.3g, assay 98.5%, MWt: 316.43, Formula: C20H28O3, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Stem Cell/Wnt;MAPK/ERK Pathway;Immunology/Inflammation;Immunology/Inflammation;NF-κB, Target: ERK;ERK;COX;PGE synthase;NF-κB, Biological_Activity: Cafestol, one of the major components of coffee, is a coffee-specific diterpene from. Cafestol is a ERK inhibitor for AP-1-targeted activity against PGE2 production and the mRNA expression of cyclooxygenase (COX)-2 in LPS-activated RAW264.7 cells. Cafestol has strong inhibitory activity on PGE2 production by suppressing the NF-kB activation pathway. Cafestol contributes to its beneficial effects through various biological activities such as chemopreventive, antitumorigenic, hepatoprotective, antioxidative and antiinflammatory effects[1].

Name: Kahweol, CAS: 6894-43-5, stock 10.3g, assay 99%, MWt: 314.42, Formula: C20H26O3, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Apoptosis;Epigenetics;PI3K/Akt/mTOR, Target: Apoptosis;AMPK;AMPK, Biological_Activity: Kahweol is one of the consituents of the coffee from Coffea Arabica with anti-inflammatory anti-angiogenic, and anti-cancerous activities. Kahweol inhibits adipogenesis and increase glucose uptake by AMP-activated protein kinase (AMPK) activation. Kahweol induces apoptosis.
IC50 & Target: AMPK; adipogenesis; apoptosis[1]
In Vitro: Kahweol (20-40 μM; 24 hours) decreases TGF-β-induced CTGF protein expression in AML12 and LX2 cells[1].
Kahweol (20-40 μM; 1 hour) decreases TGF-β-induced phospho-Smad2/3 expression in AML12 cells, but does not affect expression in LX2 cells[1].
Kahweol (20-40 μM) significantly decreased TGF-β-stimulated phospho-ERK and JNK expression in primary hepatocytes only[1].
kahweol (0-25 μg/ml; 6-24 hours) increased the phosphorylation of AMPK and its downstream target Acetyl-CoA carboxylase (ACC) in a time-dependent manner in 3T3-L1 cells[2].
kahweol (0-25 μg/ml) significantly affects protein expression of PPARγ, C/EBPα, FABP4, and FASN, that regulate adipocyte differentiation and lipid metabolism[2].

Name: 5,7,3'-Trihydroxy-6,4',5'-trimethoxyflavone, CAS: 78417-26-2, stock 18.1g, assay 98.2%, MWt: 360.31, Formula: C18H16O8, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: 5,7,3'-Trihydroxy-6,4',5'-trimethoxyflavone is a methylated flavones from Artemisia frigida.

Name: 4-O-beta-Glucopyranosyl-cis-coumaric acid, CAS: 117405-48-8, stock 10.9g, assay 98.6%, MWt: 326.30, Formula: C15H18O8, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: 4-O-beta-Glucopyranosyl-cis-coumaric acid is a natural compound isolated formn Nelumbo nucifera Gaertn.

Name: Epimagnolin B, CAS: 1134188-26-3, stock 15.1g, assay 98.5%, MWt: 416.46, Formula: C23H28O7, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Epimagnolin B is a bisepoxylignan isolated from Magnolia fargesii, with anti-inflammatory activity and antiallergic effects. Epimagnolin B inhibits NO production in LPS-activated microglia. Epimagnolin B exhibited antiallergic effects[1][2].
In Vitro: Epimagnolin B exhibits antiallergic effects without affecting the viability of BMMCs[1].

Name: 20(S),24(R)-Ocotillol, CAS: 69926-31-4, stock 18.8g, assay 98.5%, MWt: 492.73, Formula: C30H52O5, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: 20(S),24(R)-Ocotillol is isolated from Panax ginseng[1].

Name: EGCG Octaacetate, CAS: 148707-39-5, stock 12.6g, assay 98.8%, MWt: 794.67, Formula: C38H34O19, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Anti-infection, Target: Bacterial, Biological_Activity: EGCG Octaacetate is a prodrug of Green tea epigallocatechin-3-gallate (EGCG), utilized to enhance the stability and bioavailability of EGCG in vivo. EGCG Octaacetate has high efficacy, bioavailability, anti-oxidation and anti-angiogenesis capacities[1]. EGCG octaacetate is the potential antibacterial compound for gram-positive bacteria (GPB) and gram-negative bacteria (GNB) [2].

Name: 27-Deoxyactein, CAS: 264624-38-6, stock 30.3g, assay 98.9%, MWt: 660.83, Formula: C37H56O10, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: 27-Deoxyactein is a constituent isolated from Cimicifuga racemosa, prevents TCDD-induced osteoblasts damage. 27-Deoxyactein inhibits increased AhR, CYP1A1 and ERK levels[1].

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 2350

举报滥用情况

2016 China CPHI meet