EOS Med Chem, Medicinal Chemical is Big: EOS Med Chem Building block stock list 2352

EOS Med Chem is TOP 100 of China CRO & CMO company, mainly in custom synthesis.
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Name: C3a (70-77) Complement 3a (70-77), CAS: 63555-63-5, stock 18.7g, assay 98.6%, MWt: 823.94, Formula: C35H61N13O10, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Immunology/Inflammation, Target: Complement System, Biological_Activity: C3a (70-77) is an octapeptide corresponding to the COOH terminus of C3a, exhibits the specificity and 1 to 2% biologic activities of C3a.
IC50 & Target: Complement system[1]
In Vitro: The direct interaction of C3a(70-77) with human mononuclear leukocytes in culture results in a concentration-dependent inhibition of the generation of LIF evoked by mitogens and by the antigen SK-SD. The extent of suppression of LIF generation by C3a(70-77) is significant at concentrations of 10-7 M or higher and exceeds 75% at 10-6 M, irrespective of the stimulus[1]. 
C3a (70-77) induces histamine release and degranulation of rat mast cells, promotes contraction of guinea pig ileal tissue, and enhances vascular permeability in human skin. C3a (70-77) selectively desensitizes ileal smooth muscle to C3a but not to human C5a, a related anaphylatoxin. Conversely, C3a-(70-77) is unable to contract ileal smooth muscle pretreated with natural C3a. This cross-desensitization indicates a specific interaction of C3a (70-77) with cellular C3a binding sites[2].

Name: [Nle11]-Substance P, CAS: 57462-42-7, stock 5.5g, assay 98.4%, MWt: 1329.59, Formula: C64H100N18O13, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Neuronal Signaling;GPCR/G Protein, Target: Neurokinin Receptor;Neurokinin Receptor, Biological_Activity: [Nle11]-Substance P is a substance P analog that avoids methionine oxidation problems.
In Vitro: Substance P and its analog, [Nle11]-Substance P have shown similar potency in tests. The spasmogenic activity of Substance P and [Nle11]-Substance P are preserved in the same potency order on stimulated guinea-pig ileum[1].

Name: Fibrinogen Binding Inhibitor Peptide, CAS: 89105-94-2, stock 24.8g, assay 98.9%, MWt: 1189.28, Formula: C50H80N18O16, Solubility: H2O, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Fibrinogen Binding Inhibitor Peptide is a dodecapeptide (HHLGGAKQAGDV, H12), which is a fibrinogen γ-chain carboxy-terminal sequence (γ400-411). Fibrinogen Binding Inhibitor Peptide is a specific binding site of the ligand for activated glycoprotein (GP) IIb/IIIa.
In Vitro: Glycoprotein (GP) IIb/IIIa, which exists on the membrane of platelets, changes its form from inactive to active when platelets adhere to collagen exposed on sites of vascular injury. In the circulation, platelet aggregation is mediated by fibrinogen by bridging adjacent platelets through GPIIb/IIIa in an activation-dependent manner. A dodecapeptide HHLGGAKQAGDV (H12), corresponding to the fibrinogen γ-chain carboxy-terminal sequence (γ400-411), is a specific binding site of the ligand for activated GPIIb/IIIa<su>[1].

Name: Bactenecin Bactenecin, bovine, CAS: 116229-36-8, stock 3.3g, assay 98.6%, MWt: 1483.89, Formula: C63H118N24O13S2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Anti-infection;Anti-infection, Target: Fungal;Bacterial, Biological_Activity: Bactenecin is a cyclic antimicrobial peptide isolated from bovine neutrophils with potent activity against Bacterial and Fungal species.
IC50 & Target: Bacterial, Fungal[1]
In Vitro: Bactenecin inhibits the growth of Escherichia coli and Staphylococcus aureus at the same concentration. Bactenecin inhibits the growth of other medically important bacteria and yeast, and it kills the fungus Trichophyton rubrum. Acetylation and amidation of the amino- and carboxy-termini of bactenecin do not change its potency, while replacement of its two cysteine residues with serine decreases the potency[1]. Bactenecin, a dodecapeptide, is strongly cytotoxic to rat embryonic neurons, fetal rat astrocytes and human glioblastoma cells. This neurotoxicity is unique to bactenecin, as a panel of antibacterial peptides from vertebrates and invertebrates, like defensins corticostatin, indolicidin, cecropin P1, tachyplesin I, the magainins, or apidaecins did not impair neuronal viability[2].

Name: β-amyloid (1-11), CAS: 190436-05-6, stock 11.8g, assay 98.5%, MWt: 1325.30, Formula: C56H76N16O22, Solubility: 10 mM in H2O, Clinical_Informat: No Development Reported, Pathway: Neuronal Signaling, Target: Amyloid-β, Biological_Activity: β-amyloid (1-11) is a fragment of Amyloid-β peptide, maybe used in the research of neurological disease.

Name: Peptide YY (PYY), human, CAS: 118997-30-1, stock 28.7g, assay 98.8%, MWt: 4309.75, Formula: C194H295N55O57, Solubility: 10 mM in H2O, Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein;Neuronal Signaling, Target: Neuropeptide Y Receptor;Neuropeptide Y Receptor, Biological_Activity: Peptide YY (PYY) is a gut hormone that regulates appetite and inhibits pancreatic secretion. Peptide YY (PYY) can mediate its effects through the Neuropeptide Y receptors.
IC50 & Target: Neuropeptide Y receptor[1]
In Vitro: The gut hormone peptide YY ( PYY) belongs to the pancreatic polypeptide (PP) family along with PP and neuropeptide Y (NPY). These peptides mediate their effects through the NPY receptors of which there are several subtypes (Y1, Y2, Y4, and Y5)[1]. Pancreatic polypeptide YY (Peptide YY), a small peptide consisting of 36 amino acids, is originally isolated from porcine intestine and is secreted from the neuroendocrine cells (L cells) in the mucosa of the gastrointestinal tract, but it has been localized to other locations associated with the digestive system[2].
In Vivo: Peptide YY is capable of strongly inhibiting secretin-stimulated pancreatic secretion. A very low dose of Peptide YY (10-20 pmol/kg) significantly decreases the pancreatic secretion of bicarbonate as well as fluid that is stimulated by a single dose of secretin (0.1 unit/kg). A dose of Peptide YY of 100-200 pmol/kg causes a 70-80% reduction of the pancreatic bicarbonate and fluid secretion[3]. Peptide YY is localised to blood vessels and atherosclerotic plaques of rabbits. It causes vasoconstriction of the vascular tree[2].

Name: Angiotensin II (3-8), human, CAS: 12676-15-2, stock 23.9g, assay 98.9%, MWt: 774.91, Formula: C40H54N8O8, Solubility: 10 mM in H2O, Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein, Target: Angiotensin Receptor, Biological_Activity: Angiotensin II (3-8), human is a less effective agonist at the angiotensin AT1 receptor.
IC50 & Target: Angiotensin AT1 receptor[1]
In Vivo: Human Angiotensin II (3-8) causes endothelium-dependent renal cortical vasodilatation, in anaesthetized rats. At doses up to 125 pmol/kg, human Angiotensin II (3-8) is without any cardiovascular effects, but with doses of 1.25 and 12.5 nmol/kg there are dose-dependent increases in mean arterial blood pressure and reductions in renal and mesenteric flows and vascular conductances[1].

Name: Angiogenin (108-122), CAS: 112173-49-6, stock 18.8g, assay 98.5%, MWt: 1780.98, Formula: C78H125N25O23, Solubility: H2O, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Angiogenin (108-122) is an angiogenin peptide.
In Vitro: Angiogenin (108-122) effects on the ribonucleolytic activity of angiogenin using tRNA as substrate with 39% inhibition[1]. Angiogenin (108-122) acts as a therapeutic agent for the prophylaxis and/or treatment of cancer, an infectious disease, a fibrotic disease, an inflammatory disease, a neurodegenerative disease, an autoimmune disease, or a heart and vascular disease[2].

Name: β-Amyloid (31-35), CAS: 149385-65-9, stock 12.6g, assay 98.6%, MWt: 545.74, Formula: C25H47N5O6S, Solubility: 10 mM in H2O, Clinical_Informat: No Development Reported, Pathway: Neuronal Signaling, Target: Amyloid-β, Biological_Activity: β-Amyloid (31-35) is the shortest sequence of native Amyloid-β peptide that retains neurotoxic activity.
In Vitro: β-Amyloid (31-35) is a functional cytotoxic domain of Aβ peptide. β-Amyloid (31-35) increases the phosphorylation of biotinylated Aβ(1-40), enhances CDK-1 activity, and also inhibits binding of Aβ to cyclin B1. β-Amyloid (31-35) is cytotoxic, and such an effect can be inhibited by olomoucine in differentiated human teratocarcinoma cell line, Ntera 2/cl-D1 (NT-2) neurons[1]. β-Amyloid (31-35) shows cytotoxic effect on cerebellar granule cells (CGC). β-Amyloid (31-35) also increases caspase-3 activity in a time-dependent manner (4-24 h) at 40 μM[2].

Name: Glutaminyl Cyclase Inhibitor 1, CAS: 2110449-60-8, stock 31.3g, assay 98.7%, MWt: 369.43, Formula: C21H24FN3O2, Solubility: DMSO : 83.33 mg/mL (225.56 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Neuronal Signaling, Target: Amyloid-β, Biological_Activity: Glutaminyl Cyclase Inhibitor 1 is a glutaminyl cyclase inhibitor with an IC50 of 0.5 μM.
IC50 & Target: IC50: 0.5 μM (Glutaminyl cyclase)[1]
In Vitro: Glutaminyl Cyclase Inhibitor 1 is compound 23[1].

Name: Adrenocorticotropic Hormone (ACTH) (1-10), human, CAS: 2791-05-1, stock 16.7g, assay 98.9%, MWt: 1299.41, Formula: C59H78N16O16S, Solubility: H2O : 1 mg/mL (0.77 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Adrenocorticotropic Hormone (ACTH) (1-10), human, an adrenocorticotropin hormone fragment, possesses a weak α-melanocyte stimulating hormone (α-MSH) potency only at high doses (100 and 1000 nM).
In Vitro: α-melanocyte stimulating hormone (MSH) induces the differentiation of mouse epidermal melanocytes in vivo and in vitro. Adrenocorticotropic hormone (ACTH) possesses the same amino acid sequence as MSH does[1].

Name: Brain Natriuretic Peptide (BNP) (1-32), rat, CAS: 133448-20-1, stock 4.7g, assay 98.7%, MWt: 3452.94, Formula: C146H239N47O44S3, Solubility: H2O, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Brain Natriuretic Peptide (BNP) (1-32), rat is a 32 amino acid polypeptide secreted by the ventricles of the heart in response to excessive stretching of heart muscle cells (cardiomyocytes).
In Vitro: B-type natriuretic peptide (BNP) combats cardiac stress by reducing blood pressure and ventricular fibrosis. Rat BNP BNP (1-32) (rBNP (1-32)) is an amino-truncated form of the 45 residue natural rat form of BNP[1]. Atrial natriuretic peptide-(1-28) (ANP), brain natriuretic peptide-(1-32) (BNP) and C-Type natriuretic polypeptide (CNP) occur in the brain, are concentrated in the anteroventral area of the third cerebral ventricle and participate in the regulation of body fluid homeostasis. The ANP(1-28), BNP (1-32) and CNP(1-32) function in the mammalian brain to regulate salt and water homeostasis via their receptors NPR-A and NPR-B[2].
In Vivo: The depressor, natriuretic and cyclic GMP responses to several species of brain natriuretic peptide (BNP) are compared to atrial natriureticpeptide (ANP) 99-126 in conscious spontaneously hypertensive rats (SHR) and in conscious cynomolgus monkeys treated with vehicle or the selective neutral endopeptidase inhibitor SQ 28603. In the conscious SHR, the natriuretic and cyclic GMP responses to 3 nmol/kg i.v. rat BNP (1-32) greater than rat ANP 99-126 greater than pig BNP-26 and sre significantly potentiated by 100 mumol/kg i.v. SQ 28,603. Human BNP-32 is inactive in the SHR treated with either vehicle or SQ 28,603. In contrast, 1 nmol/kg i.v. of human BNP (1-32) stimulates renal and depressor responses in the conscious monkeys that are greater than or equal to those elicited by human ANP 99-126, whereas 3 nmol/kg i.v. rat BNP (1-32) reduces mean arterial pressure without affecting renal function[3]

Name: β-Amyloid (29-40) Amyloid beta-protein(29-40), CAS: 184865-04-1, stock 36g, assay 98.5%, MWt: 1085.36, Formula: C49H88N12O13S, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Neuronal Signaling, Target: Amyloid-β, Biological_Activity: β-Amyloid (29-40) is a fragment of Amyloid-β peptide.
IC50 & Target: Amyloid-β[1]
In Vitro: β-Amyloid (29-40) is a fragment of Amyloid-β peptide, unsoluble in water, acetonitrile or in a mixture of both in different ratios. Cationic arginine residues is introduced at β-Amyloid (29-40) C-terminus to solubilize β-Amyloid (29-40) and introduce cationicity in this Aβ stretch to enable it to interact with the negatively charged membrane of bacteria. β-Amyloid (29-40) variants shows antimicrobial effect[1]. Single chain variable fragments (scFv's) binds the 17-28 region of Abeta and effectively inhibits in vitro aggregation of Abeta, but binding the carboxyl-terminal region of β-Amyloid (29-40) does not inhibit aggregation[2].

Name: Leptin (22-56), human, CAS: 183598-56-3, stock 29.1g, assay 98.7%, MWt: 3950.52, Formula: C171H298N50O56, Solubility: H2O, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Leptin (22-56), human is the fragment of leptin, mediated via several isoforms of receptors (Ob-Rs).
IC50 & Target: Ob-Rs[1]
In Vitro: Leptin (22-56), human is the fragment of leptin, inhibits corticosterone production, but shows no effect on the proliferation of cultured adrenocortical cells. Leptin (22-56) may be responsible for the direct inhibitory effect on secretion and growth of leptin on cultured rat adrenocortical cells[1]. Leptin (22-56) inhibits food intake, and may favour erythropoiesis[2].

Name: Melanin Concentrating Hormone, salmon MCH (salmon), CAS: 87218-84-6, stock 25.8g, assay 98.1%, MWt: 2099.48, Formula: C89H139N27O24S4, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein;Neuronal Signaling, Target: MCHR1 (GPR24);MCHR1 (GPR24), Biological_Activity: Melanin Concentrating Hormone, salmon is a 19-amino-acid neuropeptide initially identified in the pituitary gland of teleost fish, which regulates food intake, energy balance, sleep state, and the cardiovascular system. Melanin-concentrating hormone is a ligand for an orphan G protein-coupled receptor (SLC-1/GPR24) and MCHR2.
IC50 & Target: SLC-1/GPR24, MCHR2[1]
In Vitro: An orphan G protein-coupled receptor (SLC-1/GPR24) has been identified as a receptor for MCH (MCHR1). MCHR2 has higher protein sequence homology to MCHR1 than any other G protein-coupled receptor. MCHR2 is specifically activated by nanomolar concentrations of MCH, binds to MCH with high affinity, and signals through Gq protein[1].
In Vivo: Melanin Concentrating Hormone stimulates appetite. Continuous infusion of Melanin Concentrating Hormone into the ventricular system increases food intake for 7-8 days[2]. Intracerebroventricular infusion of Melanin Concentrating Hormone (10 μg/day) causes a slight but significant increase in body weight in mice maintained on the regular diet. Chronic stimulation of the brain Melanin Concentrating Hormone system could cause obesity in mice[3].

Name: M443, CAS: 1820684-31-8, stock 34.7g, assay 98.4%, MWt: 589.61, Formula: C31H30F3N7O2, Solubility: DMSO : 55 mg/mL (93.28 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: M443 is an irreversible and specific inhibitor of MRK, with an IC50<125 nM.
IC50 & Target: IC50: <125 nM (MRK)[1].
In Vitro: MRK depletion decreases cell viability after IR by 33% of control at 3 Gy. Similarly, the clonogenic assay shows a significant decrease in survival with a dose enhancement factor (DEF) of 1.6 at 10% viability. MRK activation by IR is maximal at 30 minutes after exposure to radiation. Therefore, for subsequent analysis, this time point is used. In both cell cultures, the IR-stimulated activation of MRK, Chk2, and p38 is greatly inhibited by 500 nM M443. Cells are seeded on coverslips, pretreated with 500 nM M443 or vehicle, exposed to 6 Gy of IR, fixed at different times after IR and processed for immunofluorescence with the MPM2 phospho-specific antibody that specifically stains mitotic cells. In contrast to control cells, the M443-treated cells fail to arrest after IR and maintained a similar mitotic index as the nonirradiated cells. Thus, inhibition of MRK leads to inhibition of Chk2 and failure to arrest in the cell cycle in response to IR-induced DNA damage[1].
In Vivo: Control mice survive with a median of 32 days after tumor cell implantation. Treatment with M443 alone adds 5.5 days to this survival, whereas the chosen low dose of radiation does not significantly increase survival. In contrast, the combination of M443 and IR extend survival with a median of 16 days longer than control. Treatment with M443 does not affect the animal weight, as the weight loss observed is observed in all groups just a few days before the animals became moribund. It is showed that the tumor-containing fraction has elevated levels of both total and active MRK (lane RB in the vehicle-treated brain). In contrast, the tumor-containing fraction from the M443-treated brain shows total loss of MRK activity. Interestingly, the fractions containing normal brain, which in the control brain show some level of MRK protein, in the treated brain also has lost MRK, suggesting that diffusion of M443 across the whole cerebellum inhibit normal MRK as well[1].

Name: TLK117 TER117, CAS: 152684-53-2, stock 34.9g, assay 98.5%, MWt: 473.54, Formula: C23H27N3O6S, Solubility: DMSO : 150 mg/mL (316.76 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Gutathione S-transferase, Biological_Activity: TLK117, the active metabolite of TLK199, selective inhibits Glutathione S-transferase P1–1 (GSTP1-1) with a Ki of 0.4 μM for GSTP. TLK117 also competitively inhibits glyoxalase I with a Ki of 0.56 μM.
IC50 & Target: Ki: 0.4 μM[1], 0.56 μM (glyoxalase I)[2]
In Vitro: TLK117 is the most specific GSTP inhibitor to date, with a binding affinity greater than GSH itself and a selectivity for GSTP over 50-fold greater than the GSTM and GSTA classes (Ki=0.4 μM)[1]. TER 117 is developed as a GST P1-1 isoenzyme inhibitor to circumvent the indicated contribution of GST P1-1 to drug resistance of tumor cells. To facilitate the cellular uptake of TER 117, it is delivered as a diethyl ester (TER 117 DEE, also called TER 199). TER 117 is found to be a competitive inhibitor of both GST P1-1 and glyoxalase I[2].
In Vivo: Oropharyngeal administration of the GSTP inhibitor, TLK117, at a time when fibrosis is already apparent, attenuated bleomycin- and AdTGFβ-induced remodeling, α-SMA, caspase activation, FAS S-glutathionylation, and total protein S-glutathionylation. Four hours after administration of 50 mg/kg TLK117, GSTP activity is strongly decreased and remains decreased by about 60% for at least 24 hours[2].

Name: Beryllon II, CAS: 51550-25-5, stock 1.3g, assay 98.8%, MWt: 738.52, Formula: C20H10N2Na4O15S4, Solubility: DMSO : ≥ 64 mg/mL (86.66 mM), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Beryllon II is a widely used chromogenic reagent that is used to determine many elements, such as Mo, Mg and Co, and also used for the determination of proteins.
In Vitro: Beryllon II is a widely used chromogenic reagent that has been used to determine many elements, such as Mo, Mg and Co. Beryllon II-Al3+ complex with the addition of protein can potently enhance the Rayleigh light scattering, and used to determine proteins[1].

Name: GNE-131, CAS: 1629063-81-5, stock 19.8g, assay 98.7%, MWt: 442.57, Formula: C23H30N4O3S, Solubility: DMSO : 125 mg/mL (282.44 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Membrane Transporter/Ion Channel, Target: Sodium Channel, Biological_Activity: GNE-131 is a potent and selective inhibitor of human sodium channel NaV1.7, with an IC50 of 3 nM.
IC50 & Target: IC50: 3 nM (hNaV1.7)[1].
In Vitro: GNE-131 (Compound 13) shows moderate clearance in human liver microsomes and excellent functional activity against human NaV1.7 with an IC50 of 0.003±0.001 μM. GNE-131 shows excellent potency, good in vitro metabolic stability[1].
In Vivo: GNE-131 shows low in vivo clearance in mouse, rat, and dog. GNE-131 also displays excellent efficacy in a transgenic mouse model of induced pain[1].

Name: C188-9, CAS: 432001-19-9, stock 2.3g, assay 99%, MWt: 471.52, Formula: C27H21NO5S, Solubility: DMSO : ≥ 62 mg/mL (131.49 mM), Clinical_Informat: No Development Reported, Pathway: JAK/STAT Signaling;Stem Cell/Wnt, Target: STAT;STAT, Biological_Activity: C188-9 is a Stat3 inhibitor, with a Kd of 4.7 nM.
IC50 & Target: Kd: 4.7 nM (Stat3)[1].
In Vitro: C188-9 is a Stat3 inhibitor, with a Kd of 4.7 nM[1]. The IC50s of C188-9 to inhibit Stat3 activation in AML cell lines are in the range of 4-7 μM, and in primary AML samples the IC50s are in the range of 8-18 μM. For apoptosis studies, AML cell lines and primary samples are treated for 24 hours with C188-9, then apoptotic cells are quantified by FACS analysis for annexin V-labeled cells. The EC50s for apoptosis induction are quite variable, ranging from 6 μM to over 50 μM[2].
In Vivo: Of the approximately 13,528 discernible genes, levels of 37 gene transcripts are altered by C188 (17 down and 20 up-regulated, fdr <0.01, fold change≥1.5), of which 7 are known STAT3 gene targets. In comparison, C188-9 affects a much greater number of genes involved in oncogenesis (384 total, 95 down- and 289 up-regulated), including 76 genes previously reported as regulated by STAT3 (38 down-regulated and 38 up-regulated). Among the 38 genes previously shown to be upregulated by STAT3, 24 (63%) genes are downregulated by C188-9 treatment, as expected. Additionally, 10 more genes downregulated by C188-9 (fdr <0.01, fold change≥1.5) that previously are shown to be upregulated by STAT1. Thus, 40 of 48 (83.3%) genes downregulated by C188-9 previously are shown to be positively regulated by STAT1, including sixteen genes shown to be co-regulated by STAT3 and STAT1. This analysis raises the possibility that the effect of C188-9 on gene transcript levels in HNSCC tumors is mediated by its effects on both STAT3 and STAT1[3].

Name: IDH889, CAS: 1429179-07-6, stock 3.7g, assay 98.6%, MWt: 436.48, Formula: C23H25FN6O2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Isocitrate Dehydrogenase (IDH), Biological_Activity: IDH889 is an orally available, brain penetrant, allosteric and mutant specific inhibitor of isocitrate dehydrogenase 1 (IDH1). IDH889 has potent selectivity for IDH1 R132* mutations, with IC50s of 0.02 μM, 0.072 μM and 1.38 μM for IDH1R132H, IDH1R132C and IDH1wt, respectively. IDH889 shows potent cellular inhibition of R-2-hydroxyglutarate (2-HG) production with an IC50 of 0.014 μM[1].
IC50 & Target: IC50: 0.02 μM (IDH1R132H), 0.072 μM (IDH1R132C), 1.38 μM (IDH1wt)[1]

Name: GW806742X, CAS: 579515-63-2, stock 25.5g, assay 98.2%, MWt: 573.55, Formula: C25H22F3N7O4S, Solubility: DMSO : ≥ 125 mg/mL (217.94 mM), Clinical_Informat: No Development Reported, Pathway: Protein Tyrosine Kinase/RTK;MAPK/ERK Pathway, Target: VEGFR;Mixed Lineage Kinase, Biological_Activity: GW806742X is a Mixed Lineage Kinase Domain-Like protein (MLKL) inhibitor which binds the MLKL pseudokinase domain with a Kd value of 9.3 μM and has anti-necroptosis activity. GW806742X has activity against VEGFR2[1][2].
IC50 & Target: Kd: 9.3 μM (MLKL)[1]
In Vitro: GW806742X (0.1-10000 nM) rescues 50% of wild-type mouse dermal fibroblasts (MDFs) from TSQ-induced necroptosis with an IC50< 50 nM when 1 ng/mL TNF is used[1]. 
GW806742X (1 μM) retards MLKL translocation to the membrane[1].

Name: Dxd Exatecan derivative for ADC, CAS: 1599440-33-1, stock 13.9g, assay 98.9%, MWt: 493.48, Formula: C26H24FN3O6, Solubility: H2O : < 0.1 mg/mL (insoluble); DMSO : 50 mg/mL (101.32 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Cell Cycle/DNA Damage;Antibody-drug Conjugate/ADC Related, Target: Topoisomerase;ADC Cytotoxin, Biological_Activity: Dxd (Exatecan derivative for ADC) is a potent DNA topoisomerase I inhibitor, with an IC50 of 0.31 μM, used as a conjugated drug of HER2-targeting ADC (DS-8201a).
IC50 & Target: IC50: 0.31 μM (0.31 μM)[1]
In Vitro: Dxd (Exatecan derivative for ADC) is a potent DNA topoisomerase I inhibitor, with an IC50 of 0.31 μM, used as a conjugated drug of HER2-targeting ADC (DS-8201a). Dxd is cytotoxic to human cancer cell lines of KPL-4, NCI-N87, SK-BR-3, and MDA-MB-468 with IC50s of 1.43 nM-4.07 nM, but the control IgG-ADC (Dxd is the payload) shows no inhibition on the four cell lines (with HER2 expression). DS-8201a (Dxd is the payload) displays significant suppression on the HER2-positive KPL-4, NCI-N87, and SK-BR-3 cell lines, with IC50 values of 26.8, 25.4, and 6.7 ng/mL, respectively, but with no such inhibition on MDA-MB-468 (IC50, >10,000 ng/mL)[1].
In Vivo: DS-8201a (Dxd is the payload, 10 mg/kg, i.v.) shows potent antitumor activity in HER2-positive models with KPL4, JIMT-1, and Capan-1 and in HER2 low-expressing ST565 and ST313 models with HER2 IHC 1+/FISH-negative expression[1].

Name: TAS6417, CAS: 1661854-97-2, stock 31.1g, assay 98.6%, MWt: 396.44, Formula: C23H20N6O, Solubility: DMSO : ≥ 125 mg/mL (315.31 mM), Clinical_Informat: No Development Reported, Pathway: JAK/STAT Signaling;Protein Tyrosine Kinase/RTK, Target: EGFR;EGFR, Biological_Activity: TAS6417 is an EGFR inhibitor and an efficacious drug candidate for patients with NSCLC, with IC50 values ranging from 1.1-8.0 nM.
IC50 & Target: 1.1-8.0 nM (EGFR)[1].
In Vitro: TAS6417 inhibits the in vitro phosphorylation activity of EGFR and its mutants including an exon 20 insertion mutation, with IC50 values ranging from 1.1±0.1 to 8.0±1.1 nM. TAS6417 suppresses the growth of cells expressing exon 20 insertion mutations of the EGFR gene, with a GI50 value of 86.5±28.5 nM for LXF 2478L cells and 45.4±2.6 nM for NCI-H1975 EGFR D770_N771insSVD cells. TAS6417 also potently inhibits proliferation in other cell lines harboring activating mutations or acquired resistance mutations, with mean GI50 values of 1.92±0.21 nM to 7.12±0.60 nM. In contrast, the effect of TAS6417 on cell proliferation in normal human epidermal keratinocytes (NHEK-Neo), of which WT EGFR is implicates in the growth and survival, is moderate[1].
In Vivo: TAS6417 causes persistent tumor regression in vivo in EGFR exon 20 insertion-driven tumor models. TAS6417 inhibits mutant EGFR in tumors but not WT EGFR in skin tissues. TAS6417 prolongs survival of animals bearing lung cancer[1].

Name: Pralsetinib BLU-667, CAS: 2097132-94-8, stock 0.4g, assay 98.2%, MWt: 533.60, Formula: C27H32FN9O2, Solubility: H2O : < 0.1 mg/mL (insoluble); DMSO : ≥ 100 mg/mL (187.41 mM), Clinical_Informat: Phase 1, Pathway: Protein Tyrosine Kinase/RTK, Target: RET, Biological_Activity: Pralsetinib (BLU-667) is a highly potent, selective RET inhibitor. Pralsetinib (BLU-667) inhibits WT RET, RET mutants V804L, V804M, M918T and CCDC6-RET fusion with IC50s of 0.4, 0.3, 0.4, 0.4, and 0.4 nM, respectively[1].
IC50 & Target: IC50: 0.4 nM (Wild type RET), 0.3 nM (RET V804L), 0.4 nM (RET V804M), 0.4 nM (RET M918T), 0.4 nM (CCDC6-RET)[1]
In Vitro: Pralsetinib (BLU-667) demonstrates more than 10-fold increased potency over approved MKIs against oncogenic RET variants and resistance mutants[1]. 
Pralsetinib (BLU-667) demonstrates potent activity (IC50=0.4 nM) against common oncogenic RET alterations, including RET M918T, an activating mutation found in MTC, as well as the CCDC6-RET fusion observed in PTC and NSCLC[1]. 
Pralsetinib (BLU-667) suppresses RET pathway signaling in a panel of RET-driven cell lines: LC2/ad (CCDC6-RET, NSCLC), MZ-CRC-1 (RET M918T, MTC), and TT (RET C634W, MTC)[1].
In Vivo: Pralsetinib (BLU-667) potently inhibits growth of NSCLC and thyroid cancer xenografts driven by various RET mutations and fusions without inhibiting vascular endothelial growth factor receptor 2 (VEGFR-2)[1]. 
Pralsetinib (BLU-667) shows dose dependent activity against both KIF5B-RET Ba/F3 and KIF5B-RET V804L Ba/F3 allograft tumors with doses as low as 10 mg/kg twice-daily[1].

Name: HC-070, CAS: 1628291-95-1, stock 31.8g, assay 98.4%, MWt: 475.32, Formula: C22H20Cl2N4O4, Solubility: DMSO : ≥ 62.5 mg/mL (131.49 mM), Clinical_Informat: No Development Reported, Pathway: Membrane Transporter/Ion Channel;Neuronal Signaling, Target: TRP Channel;TRP Channel, Biological_Activity: HC-070 is an antagonist of TRPC4/TRPC5, with IC50s of 9.3 nM and 46 nM for hTRPC5 and hTRPC4 in cells, respectively.
IC50 & Target: IC50: 9.3 nM (hTRPC5, cell assay), 46 nM (hTRPC4, cell assay)[1]
In Vitro: HC-070 is an antagonist of TRPC4/TRPC5, with IC50s of 9.3 nM and 46 nM for hTRPC5 and hTRPC4, respectively. HC-070 weakly inhibits TRPC3 (IC50, 1 μM), and is at least 400-fold selective for human TRPC4 and TRPC5-containing channels versus the other channels examined. HC-070 inhibits lanthanum-activated hTRPC5-, mTRPC5-, rTRPC5-mediated currents with IC50s of 0.52 nM, 0.55 nM, and 0.32 nM in whole-cell manual patch clamp. Furthermore, HC-070 blocks M2R-activated human TRPC1/TRPC4 channels with an IC50 of 1.3 nM and La3+- and M1R-activated human TRPC1/5 channels with IC50s of 1.4 nM and 4.4 nM. HC-070 inhibits human TRPC5 currents activated via muscarinic type 1 (M1R) with an IC50 of 2.0 nM. HC-070 also suppresses hTRPC4 currents via M2R with an IC50 of 0.49 nM. HC-070 (20 nM) reduces CCK-4 evoked neuronal activity in the amygdala slices[1].
In Vivo: HC-070 (1 mg/kg, p.o.) affects mice with increased evoked anxiety (CCK-4), but shows no effects in the absence of CCK-4. HC-070 (0.3, 1 or 3 mg/kg, p.o.) decreases anxiety in a standard EPM (more light/high anxiety). HC-070 (1 mg/kg) reduces the increased capacity for fear memory in mice subjected to chronic social stress on days 1-15. In addition, HC-070 (1, 3, 10 mg/kg, p.o.) causes reduction in marble burying behavior. HC-070 (0.3, 1, 3, 10 mg/kg, p.o.) also reduces time of immobility in a tail suspension test but does not impact locomotor activity in mice[1].

Name: (S,R,S)-AHPC-PEG4-NH2 VH032-PEG4-NH2;VHL Ligand-Linker Conjugates 4 ;E3 ligase Ligand-Linker Conjugates 7 Free Base, CAS: 2010159-57-4, stock 22.6g, assay 98.7%, MWt: 663.83, Formula: C32H49N5O8S, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: PROTAC, Target: E3 Ligase Ligand-Linker Conjugate, Biological_Activity: (S,R,S)-AHPC-PEG4-NH2 is a synthesized E3 ligase ligand-linker conjugate that incorporates the (S,R,S)-AHPC based VHL ligand and 4-unit PEG linker used in PROTAC technology.
IC50 & Target: E3 Ligase Ligand-Linker Conjugate[1]
In Vitro: E3 ligase Ligand-Linker Conjugates 7 Free Base, extracted from patent US20170008904A1, can be used in the synthesis of compound A1895 in example 3[1].

Name: (S,R,S)-AHPC-PEG2-NH2 VH032-PEG2-NH2 ;VHL Ligand-Linker Conjugates 3 ;E3 ligase Ligand-Linker Conjugates 6 Free Base, CAS: 2010159-60-9, stock 26.1g, assay 98.6%, MWt: 575.72, Formula: C28H41N5O6S, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: PROTAC, Target: E3 Ligase Ligand-Linker Conjugate, Biological_Activity: (S,R,S)-AHPC-PEG2-NH2 is a synthesized E3 ligase ligand-linker conjugate that incorporates the (S,R,S)-AHPC based VHL ligand and 2-unit PEG linker used in PROTAC technology.
IC50 & Target: E3 Ligase Ligand-Linker Conjugate[1]

Name: (S,R,S)-AHPC-PEG3-NH2 VH032-PEG3-NH2;VHL Ligand-Linker Conjugates 1;E3 ligase Ligand-Linker Conjugates 5 Free Base, CAS: 2010159-56-3, stock 37.8g, assay 98.1%, MWt: 619.77, Formula: C30H45N5O7S, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: PROTAC, Target: E3 Ligase Ligand-Linker Conjugate, Biological_Activity: (S,R,S)-AHPC-PEG3-NH2 is a synthesized E3 ligase ligand-linker conjugate that incorporates the (S,R,S)-AHPC based VHL ligand and 3-unit PEG linker used in PROTAC technology.
IC50 & Target: E3 Ligase Ligand-Linker Conjugate[1]

Name: Thyrotropin-Releasing Hormone (TRH), Free Acid TRH-OH, CAS: 24769-58-2, stock 13.3g, assay 98.6%, MWt: 363.37, Formula: C16H21N5O5, Solubility: H2O, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Thyrotropin-Releasing Hormone (TRH), Free Acid (TRH-OH) is a physiological metabolite of Thyrotropin-Releasing Hormone.
In Vitro: TRH degradation products have been shown to be associated with a number of endocrine- and central nervous system-related biological functions. TRH (pGlu-His-Pro-NH2) can be enzymatically degraded in plasma and brain tissue to yield TRH-OH. TRH and hGHRH stimulate the release of [3H]GH into the culture medium to 435 and 464%, respectively, when compared to the control, but TRH-OH has no effect[1]. TRH-OH, produced after cleavage of the C-terminal amide group by a specific proline endopeptidase, is one of the most stable derivatives of TRH and is found at high levels in numerous brain regions. TRH-OH inhibits Na+ channel activity in mammalian septal neurons. In about 60% of the cells tested, TRH-OH at concentrations between 0.01 and 2.5 μM produces a dose-dependent reversible attenuation of Na+ currents. With 2 μM TRH-OH, peak Na+ current amplitude is reduced by 20-50%[2].

Name: Prolactin Releasing Peptide (12-31), human, CAS: 235433-36-0, stock 37.5g, assay 98.9%, MWt: 2272.57, Formula: C104H158N32O26, Solubility: H2O, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Prolactin Releasing Peptide (12-31), human is a fragment of the prolactin releasing peptide (PrRP). Prolactin Releasing Peptide (1-31), human is a high affinity GPR10 ligand that cause the release of the prolactin.
IC50 & Target: GPR10[1]
In Vitro: The Prolactin Releasing Peptide (PrRP) is a C-terminally amidated, 31-amino acid peptide derived from a 98-amino acid precursor. Radioiodinated PrRP-(1-31) binds to its receptor with high affinity (1 nM) and stimulates calcium mobilization in CHOK1 cells stably transfected with the receptor. A series of N-terminal deletions reveals that the Prolactin Releasing Peptide (12-31) amino acid is equipotent to PrRP-(1-31). Further N-terminal deletions reduce the affinity of the ligand considerably[1]. Prolactin Releasing Peptide (PrRP) has been identified as a specific, high affinity endogenous ligand for GPR10. Prolactin Releasing Peptide (PrRP) preproprotein can be cleaved at two different positions to give rise to two forms of 31 or 20 amino acids; Prolactin Releasing Peptide (PrRP)-31 and Prolactin Releasing Peptide (PrRP)-20 respectively. Rat Prolactin Releasing Peptide (PrRP) has also been identified and occurs as 31 or 20 amino acid forms; these peptides are highly conserved between species. Human PrRP‐20, human PrRP‐31, rat PrRP‐20 and rat PrRP‐31 display high affinity for GPR10 receptors, with Ki values of 0.26±0.07, 1.03±0.41, 0.22±0.06 and 0.33±0.11 nM, respectively[2].
In Vivo: Following intracerebroventricular injection of Prolactin Releasing Peptide (1-31), human 5 nM there is a highly significant simulation of plasma LH that began at 10 minutes and is maintained over the course of the experiment. Plasma FSH increased at 20 minutes following ICV injection. Total plasma testosterone increased at 60 minutes post injection[3].

Name: Pancreatic Polypeptide, rat Rat pancreatic polypeptide, CAS: 90419-12-8, stock 37.8g, assay 98.8%, MWt: 4398.87, Formula: C195H298N58O57S, Solubility: 10 mM in H2O, Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein;Neuronal Signaling, Target: Neuropeptide Y Receptor;Neuropeptide Y Receptor, Biological_Activity: Pancreatic Polypeptide, rat is an agonist of NPY receptor, with high affinity at NPYR4.
IC50 & Target: NPYR4[1]
In Vitro: Pancreatic Polypeptide, rat is an agonist of NPY receptor, with high affinity at NPYR4. Pancreatic Polypeptide (1 μM) does not alter proliferation in BRIN BD11 or 1.1B4 beta-cells, but reverses the decreased cell viability in BRIN BD11 cells induced by streptozotocin. Pancreatic Polypeptide (0.1 nM-1 μM) shows no effect on insulin secretion from isolated mouse islets, and does not affect the membrane potential and (Ca2+)i levels in BRIN BD11 cells at 1 μM[1].
In Vivo: Pancreatic Polypeptide (25 nmol/kg bw, i.p.) reduces glucose-stimulated insulin concentrations but shows no effect on acute feeding behaviour in overnight fasted mice[1].

Name: CRF, bovine Corticotropin Releasing Factor bovine, CAS: 92307-52-3, stock 17.1g, assay 98%, MWt: 4697.34, Formula: C206H340N60O63S, Solubility: 10 mM in H2O, Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein, Target: CRFR, Biological_Activity: CRF, bovine is a potent agonist of CRF receptor, and displaces [125I-Tyr]ovine CRF with a Ki of 3.52 nM.
IC50 & Target: Ki: 3.52 nM (CRF receptor)[1]
In Vitro: CRF, bovine is a potent agonist of CRF receptor, and displaces [125I-Tyr]ovine CRF with a Ki of 3.52 nM[1]. CRF shows pEC50s of 11.16, 8.53 and 8.70 for human CRF1, human CRF2 and rat CRF2α[2]. CRF is released from hypothalamic-pituitary-adrenal (HPA) axis induced by stress, and leads to production of glucocorticoids which down regulate immune responses. CRF also has proinflammatory effects. CRF affects brain microvessel endothelial cells (BMEC) structure or function, CRF (100 nM) significantly increases cAMP in BMEC[3].

Name: Secretin, porcine Porcine secretin (acetate), CAS: 17034-34-3, stock 8.4g, assay 98.2%, MWt: 1000, Formula: C130H220N44O41.xC2H4O2, Solubility: H2O, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Secretin, porcine (Porcine secretin acetate) is a 27-amino acid peptide, acting on pancreatic acinar cells and ductal epithelial cells stimulating the production of bicarbonate rich fluid.
In Vitro: Secretin, porcine is equivalent to the synthetic porcine and human forms of secretin, and they can be used interchangeably in pancreatic function testing[1].

Name: Thrombin Receptor Activator for Peptide 5 (TRAP-5), CAS: 141685-53-2, stock 31.5g, assay 98.5%, MWt: 634.77, Formula: C30H50N8O7, Solubility: 10 mM in H2O, Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein, Target: Protease-Activated Receptor (PAR), Biological_Activity: Thrombin Receptor Activator for Peptide 5 (TRAP-5) is also called Coagulation Factor II Receptor (1-5) or Proteinase Activated Receptor 1 (1-5), used in the research of coronary heart disease (CHD).
IC50 & Target: Protease-Activated Receptor

Name: Pancreatic Polypeptide, bovine, CAS: 179986-89-1, stock 27.7g, assay 98.4%, MWt: 4225.78, Formula: C186H287N53O56S2, Solubility: 10 mM in H2O, Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein;Neuronal Signaling, Target: Neuropeptide Y Receptor;Neuropeptide Y Receptor, Biological_Activity: Pancreatic Polypeptide, bovine, a 36-amino acid, straight chain polypeptide derived primarily from the pancreas, inhibits secretin- and cholecystokinin-stimulated pancreatic secretion; Pancreatic Polypeptide, bovine acts as an agonist of NPY receptor, with high affinity at NPYR4.
IC50 & Target: NPYR4[1]
In Vitro: Pancreatic Polypeptide, bovine is an agonist of NPY receptor, with high affinity at NPYR4. Pancreatic Polypeptide (1 μM) does not alter proliferation in BRIN BD11 or 1.1B4 beta-cells, but reverses the decreased cell viability in BRIN BD11 cells induced by streptozotocin. Pancreatic Polypeptide (0.1 nM-1 μM) shows no effect on insulin secretion from isolated mouse islets, and does not affect the membrane potential and (Ca2+)i levels in BRIN BD11 cells at 1 μM[1]. Pancreatic Polypeptide, bovine inhibits secretin- and cholecystokinin-stimulated pancreatic secretion. 125I-Pancreatic Polypeptide, bovine shows no specific binding to pancreatic acini[2].
In Vivo: Pancreatic Polypeptide (25 nmol/kg bw, i.p.) reduces glucose-stimulated insulin concentrations but shows no effect on acute feeding behaviour in overnight fasted mice[1]. Pancreatic Polypeptide, bovine (BPP; 40 μg/kg) inhibits CCK-33-induced pancreatic protein output during the entire bovine Pancreatic Polypeptide infusion period, but shows no effect on biliary protein output during CCK-33 or CCK-8 infusion[2].

Name: Ripretinib DCC-2618, CAS: 1442472-39-0, stock 37.7g, assay 98.5%, MWt: 510.36, Formula: C24H21BrFN5O2, Solubility: DMSO : 45 mg/mL (88.17 mM; Need ultrasonic), Clinical_Informat: Phase 3, Pathway: Apoptosis;Protein Tyrosine Kinase/RTK;Protein Tyrosine Kinase/RTK;Protein Tyrosine Kinase/RTK;Protein Tyrosine Kinase/RTK, Target: Apoptosis;VEGFR;FLT3;PDGFR;c-Kit, Biological_Activity: Ripretinib (DCC-2618) is an orally bioavailable, selective KIT and PDGFRA switch-control inhibitor. Ripretinib (DCC-2618) targets and binds to both wild-type and mutant forms of KIT and PDGFRA specifically at their switch pocket binding sites, thereby preventing the switch from inactive to active conformations of these kinases and inactivating their wild-type and mutant forms. Ripretinib (DCC-2618) also inhibits multiple other kinase targets, such as FLT3 and KDR (or VEGFR-2)[1][2]. DCC-2618 exerts antineoplastic effect and induces apoptosis[3].
IC50 & Target: KIT, PDGFRA, FLT3, KDR[1][2]
In Vitro: Ripretinib (DCC-2618) suppresses phosphorylation of KIT and decreases the expression of phosphosphorylated (p)STAT5, pAKT and pERK1/2 in neoplastic mast cells. Ripretinib inhibits the growth of ROSAKIT K509I cells with an IC50 of 34 ± 10 nM, and also induces apoptosis in these cells. Ripretinib (0.1-1.0 μM) inhibits IgE-dependent histamine release from basophils and spontaneous tryptase release from neoplastic mast cells, and also counteracts growth and survival of leukemic monocytes and blast cells at 0.01-5 μM[2]. 
Ripretinib (DCC-2618) is a pan-KIT and PDGFRA inhibitor, shows cytotoxic activity against gastrointestinal stromal tumors[4].

Name: Fibrinopeptide A, human Human fibrinopeptide A, CAS: 25422-31-5, stock 27.3g, assay 98.5%, MWt: 1536.56, Formula: C63H97N19O26, Solubility: H2O, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Fibrinopeptide A, human is a 16-residue short polypeptide cleaved from fibrinogen by thrombin. Fibrinopeptide A, human locates at the NH2-termini of the Aα chain.
In Vitro: The conversion of monomeric fibrinogen into polymeric fibrin is mediated by thrombin, which binds to the central region of fibrinogen and catalyzes cleavage of the 2 short peptides, the 16-residue fibrinopeptide A (FpA) and the 14-residue fibrinopeptide B (FpB), located at the NH2-termini of the Aα and Bβ chains, respectively[1].
In Vivo: Fibrinopeptide A (FPA) is a small polypeptide cleaved from fibrinogen by thrombin, has a short half-life, and is considered a sensitive biochemical marker of thrombin activity, fibrin generation, and ongoing thrombosis[2].

Name: Cecropin A, CAS: 80451-04-3, stock 9.9g, assay 98.9%, MWt: 4003.78, Formula: C184H313N53O46, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Anti-infection, Target: Bacterial, Biological_Activity: Cecropin A is a linear 37-residue antimicrobial polypeptide, with anticancer and anti-inflammatory activity.
IC50 & Target: Bacterial[2]
In Vitro: Cecropin A shows anticancer activity. Cecropin A (10-50 μM) dose-dependently reduces the viability of HL-60 cells. Cecropin A (30 μM) promotes ROS production, causes mitochondrial membrane potential (Δψm) collapse, and generates morphological changes in nuclear chromatin in HL-60 cells. Cecropin A (30 μM) also leads to an early apoptosis and cuases caspase-independent cell death in HL-60 cells[1]. Cecropin A has cytotoxicity on gram negative bacteria, including A. baumanii (CCARM 12005, CCARM 12035, CCARM 12036, CCARM 12037) with minimal inhibitory concentration (MIC) of 0.5-1 μM. Cecropin A (25 μM) significantly blocks the expression of mTNF-α, mIL-1β, and mMIP-2 mRNA and slightly inhibited the expression of mMIP-1 mRNA in RAW264.7 cells. Cecropin A (0.1, 0.25, 0.5, 1, 2.5, 5 μM) also inhibits NO production and reduces mTNF-α cytokine levels in LPS-stimulated RAW264.7 cells, and exihibits anti-inflammatory activity[2].

Name: Angiotensin III, human, mouse, CAS: 13602-53-4, stock 22.2g, assay 98.1%, MWt: 931.09, Formula: C46H66N12O9, Solubility: 10 mM in H2O, Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein, Target: Angiotensin Receptor, Biological_Activity: Angiotensin III, human, mouse is a heptapeptide, acts as an endogenous angiotensin type 2 receptor (AT2R) agonist, with IC50s of 0.648 nM and 21.1 nM for AT2R and AT1R, respectively.
IC50 & Target: IC50: 0.648 nM (AT2R), 21.1 nM (AT1R)[1]
In Vitro: Angiotensin III, human, mouse is a heptapeptide, acts as an endogenous angiotensin type 2 receptor (AT2R) agonist, with IC50s of 0.648 nM and 21.1 nM for AT2R and AT1R, respectively[1].
In Vivo: Angiotensin III (7, 14 and 28 nmol/kg/min) increases urine sodium excretion (UNaV), fractional excretion of sodium (FENa), and fractional excretion of lithium (FELi) in SD rat[2]. In RAS (renin-angiotensin system), Angiotensin III increases sympathetic nerve activity and vasopressin release and decreases the baroreflex leading to higher blood pressure in rats[3].

Name: Motilin, canine Motilin (canine), CAS: 85490-53-5, stock 8.8g, assay 98.2%, MWt: 2685.05, Formula: C120H194N36O34, Solubility: H2O, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Motilin, canine is a 22-amino acid peptide. Motilin is a potent agonist for gastrointestinal smooth muscle contraction.
In Vivo: Motilin is a potent agonist for gastrointestinal smooth muscle contraction and has been proposed to regulate the onset of phase III of the migrating motor complex (MMC) in dogs and humans. In the dog, but not in the human, Motilin also contracts the gallbladder and sphincter of Oddi and induces pancreatic secretion. Motilin activates L-type Ca2+ channel (IcaL) in canine jejunal circular smooth muscle cells through a G protein-coupled mechanism. At 1 μM, Motilin increases IcaL in canine jejunal circular smooth muscle cells by 43±20[1].

Name: Urotensin I Catostomus urotensin I, CAS: 83930-33-0, stock 33.8g, assay 98%, MWt: 4869.46, Formula: C210H340N62O67S2, Solubility: 10 mM in H2O, Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein, Target: CRFR, Biological_Activity: Urotensin I is, 41-aa neuropeptide, acts as an agonist of CRF receptor with pEC50s of 11.46, 9.36 and 9.85 for human CRF1, human CRF2 and rat CRF2α receptors in CHO cells, and Kis of 0.4, 1.8, and 5.7 nM for hCRF1, rCRF2α and mCRF2β receptors, respectively.
IC50 & Target: pEC50: 11.46 (human CRF1, CHO cells), 9.36 (human CRF2, CHO cells), 9.85 (rat CRF2α, CHO cells)[1] 
Ki: 0.4 nM (hCRF1, cell assay), 1.8 nM (rCRF2α, cell assay), and 5.7 nM (mCRF2β, cell assay)[2]
In Vitro: Urotensin I is a 41-aa neuropeptide, acts as an agonist of CRF receptor with pEC50s of 11.46, 9.36 and 9.85 for human CRF1, human CRF2 and rat CRF2α receptors in CHO cells[1] and with Kis of 0.4, 1.8, and 5.7 nM for hCRF1, rCRF2α and mCRF2β receptors in cell assay, respectively[2]. Urotensin I exhibits a striking sequence homology with ovine corticotropin-releasing factor and with frog sauvagine, and has potent hypotensive activity and corticotropin-releasing activity[3]. Urotensin I stimulates the release of ACTH from an isolated dispersed goldfish anterior pituitary cell column[4].

Name: NCGC00247743, CAS: 1435192-04-3, stock 23.8g, assay 98.4%, MWt: 391.51, Formula: C24H29N3O2, Solubility: H2O : < 0.1 mg/mL (insoluble); DMSO : 62.5 mg/mL (159.64 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Epigenetics, Target: Histone Demethylase, Biological_Activity: NCGC00247743 is a histone lysine demethylase KDM4 inhibitor.
IC50 & Target: KDM4[1]
In Vitro: Based on structure-activity relationship studies, a series of chemical compounds are derived from 8-hydroxyquinoline (8HQ) and shown to be active inhibitors of KDM4E and KDM4A. The effect of these compounds is tested on the growth of LNCaP cells and NCGC00247751 (A1), NCGC00244536 (B3), and NCGC00247743 (I9) are selected. These inhibitors inhibit LNCaP cell growth with IC50s in the μM range. These compounds also inhibit the enzymatic activity of other KDM4 isoforms although, interestingly, the potency and efficacy of B3 and A1 for KDM4A, 4C, and 4D are lower compared to that of NCGC00247743 (I9), suggesting a potential selectivity of the inhibitors for different isoforms of KDM4[1].

Name: (±) Anabasine, CAS: 13078-04-1, stock 3.6g, assay 98.3%, MWt: 162.23, Formula: C10H14N2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: (±) Anabasine is a biphasic muscle relaxant.

Name: TPCA-1, CAS: 507475-17-4, stock 40g, assay 98.6%, MWt: 279.29, Formula: C12H10FN3O2S, Solubility: DMSO : ≥ 100 mg/mL (358.05 mM), Clinical_Informat: No Development Reported, Pathway: Apoptosis;JAK/STAT Signaling;Stem Cell/Wnt;NF-κB, Target: Apoptosis;STAT;STAT;IKK, Biological_Activity: TPCA-1 is a potent and selective inhibitor of IKK-2 with IC50 of 17.9 nM. TPCA-1 is an effective inhibitor of STAT3 phosphorylation, DNA binding, and transactivation.
IC50 & Target: IC50: 17.9 nM (IKK)[1][2]. 
STAT3[3].
In Vitro: TPCA-1 inhibits lipopolysaccharide-induced human monocyte production of TNF-α, IL-6, and IL-8 with an IC50 of 170 to 320 nM[1][2]. 
TPCA-1 (0-2 μM) inhibits STAT3 phosphorylation and transactivation induced by cytokines and nonreceptor tyrosine kinase in dose- and time-dependent manner. TPCA-1 completely inhibits STAT3 phosphorylation without changing total STAT3 levels[3]. 
TPCA-1 increased sensitivity to ZD1839 in both TKI sensitive cells and insensitive cells[3].
In Vivo: TPCA-1 (3, 10, or 20 mg/kg, i.p.) results in a dose-dependent reduction in the severity of murine collagen-induced arthritis (CIA)[2]. 
TPCA-1(10 mg/kg, i.p. daily) inhibits growth of NSCLC with EGFR mutation and potentiates antitumor effect of ZD1839 in xenograft models[3].

Name: Exendin-3, CAS: 130357-25-4, stock 36.2g, assay 98.7%, MWt: 4202.57, Formula: C184H282N50O61S, Solubility: H2O, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Exendin-3 is a biologically active peptides isolated from venoms of the Gila monster lizards, Heloderma horridurn .
IC50 & Target: VIP receptor, putative exendin receptor[1]
In Vitro: Exendin-3 interacts with at least two receptors on guinea pig pancreatic acini; at high concentrations (>100 nM) the peptide interacts with VIP receptors, thereby causing a large increase in cAMP and stimulating amylase release; at lower concentrations (0.1-3 nM) the peptide interacts with a putative exendin receptor, thereby causing a smaller increase in cAMP of undetermined function[1].

Name: Cerebellin, CAS: 94071-26-8, stock 13.1g, assay 98.6%, MWt: 1632.78, Formula: C69H113N23O23, Solubility: H2O, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Cerebellin is a neuromodulatory peptide widely distributed in the central nervous system.
In Vitro: Cerebellin concentration-dependently (from 1 to 100 nM) increases norepinephrine (but not epinephrine) and cyclic-AMP production by adrenomedullary tissue in vitro[1].
In Vivo: Cerebellin potently stimulates norepinephrine release by rat adrenal medulla, acting through adenylate-cyclase/PKA-coupled receptors, and enhances adrenocortical steroid secretion in vivo (i.e. when the integrity of adrenal gland is preserved) through an indirect paracrine mechanism involving the release of medullary catecholamines[1]. Cerebellin reduces plasma insulin levels in rats after 1 and 2 h. Cerebellin decreases insulin secretion from isolated rat pancreatic islets at high (11 mM), but not at low (3.33 mM) glucose concentration. Cerebellin inhibits stimulated insulin secretion from clonal rat insulinoma (INS-1) cells, reduces forskolin-induced production of cAMP and intracellular calcium concentration[2].

Name: ACTH (1-17) α1-17-ACTH, CAS: 7266-47-9, stock 2.2g, assay 98.7%, MWt: 2093.41, Formula: C95H145N29O23S, Solubility: H2O, Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein;Neuronal Signaling, Target: Melanocortin Receptor;Melanocortin Receptor, Biological_Activity: ACTH (1-17), an adrenocorticotropin analogue, is a potent human melanocortin 1 (MC1) receptor agonist with a Ki of 0.21 nM.
IC50 & Target: Ki: 0.21 nM (human MC1 receptor)[1]
In Vitro: ACTH (1-17) is a potent agonist at the hMC1R. ACTH (1-17) shows high affinity for the hMC1R with a Ki value of 0.21±0.03 nM which is slightly higher than that of 0.13±0.005 nM for alpha-MSH[1]. ACTH (1-17) induces a slight and not significant increase in growth hormone secretion even when micromolar concentrations of the peptide are employed in rat pituitary cultures[2].
In Vivo: Inhibition of DNA labeling is noted when the ACTH (1-17) is administered at 2 hr after the beginning of the daily dark span when nocturnal animals become active. When administered at this circadian stage, the larger dose in particular is associated with an inhibition of DNA labeling lasting for 24 hr. The inhibitory effect is much shorter when the same dose is injected 4 hr earlier[3].

Name: Bombinin-Like Peptide (BLP-1), CAS: 138220-00-5, stock 23.6g, assay 98.8%, MWt: 2580.98, Formula: C115H194N34O33, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Anti-infection, Target: Bacterial, Biological_Activity: Bombinin-Like Peptide (BLP-1) is an antimicrobial peptide from Bombina species.
IC50 & Target: Bacterial[1]
In Vitro: Bombinin-like peptides, BLP-1, 2, 3 share considerable, but not complete, homology with bombinin, an antimicrobial, hemolytic peptide first isolated from the skin of Bombina uariegata. The BLPs have been assayed for antibiotic and hemolytic activity and found to be more potent than magainin 2 (a related antimicrobial peptide from Xenopus laeuis) in their ability to kill bacteria[1].

Name: Deruxtecan, CAS: 1599440-13-7, stock 5.3g, assay 99%, MWt: 1034.05, Formula: C52H56FN9O13, Solubility: H2O : < 0.1 mg/mL (insoluble); DMSO : ≥ 50 mg/mL (48.35 mM), Clinical_Informat: Phase 3, Pathway: Antibody-drug Conjugate/ADC Related, Target: Drug-Linker Conjugates for ADC, Biological_Activity: Deruxtecan is an ADC drug-linker conjugate composed of a derivative of DX-8951 (DXd) and a
maleimide-GGFG peptide linker, used for synthesizing DS-8201 and U3-1402.
IC50 & Target: Drug-linker conjugates for ADC[1]
In Vitro: Antibody-drug conjugates deliver anticancer agents selectively and efficiently to tumor tissue and have significant antitumor efficacy with a wide therapeutic window[2].

Name: Somatostatin-25, CAS: 76461-17-1, stock 3g, assay 98.5%, MWt: 2876.30, Formula: C127H191N37O34S3, Solubility: H2O, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Somatostatin-25 is a endogenous neuropeptide hormone that shows inhibitory activity against secretion of growth hormone.
In Vitro: Somatostatin-25 (0.1 pM-1 nM) significantly inhibits secretion of growth hormone in the in vitro system, and is 3-14 times more effective than the tetradecapeptide. Somatostatin-25 (0.1 nM-1pM) also inhibits secretion of growth hormone induced by the addition of prostaglandin 2 (PGE2). However, Somatostatin-25 shows no effect on the secretion of prolactin[1].

Name: β-CGRP, human Human β-CGRP;CGRP-II (Human), CAS: 101462-82-2, stock 22.1g, assay 98.3%, MWt: 3793.41, Formula: C162H267N51O48S3, Solubility: 10 mM in H2O, Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein;Neuronal Signaling, Target: CGRP Receptor;CGRP Receptor, Biological_Activity: β-CGRP, human is one of calcitonin peptides, acts via the complex of calcitonin-receptor-like receptor (CRLR) and receptor-activity-modifying protein (RAMP), with IC50s of 1 nM and 300 nM for CRLR/RAMP1 and CRLR/RAMP2 in cells.
IC50 & Target: IC50: 1 nM (CRLR/RAMP1, cell assay), 300 nM (CRLR/RAMP2, cell assay)[1]
In Vitro: β-CGRP, human is one of calcitonin peptides, acts via complex of calcitonin-receptor-like receptor (CRLR) and receptor-activity-modifying protein (RAMP), with IC50s of 1 nM in both SK-N-MC and Swiss 3T3 cells express CRLR and RAMP1, and 130 nM and 300 nM in NG108-15 and HEK293T cells expressing CRLR and RAMP2[1]. CGRP is a potent vasodilator and also shows pro- and -anti-inflammatory activity[2].

Name: S107 hydrochloride, CAS: 1357476-46-0, stock 25.3g, assay 98.9%, MWt: 245.77, Formula: C11H16ClNOS, Solubility: H2O : ≥ 132 mg/mL (537.09 mM), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: S107 hydrochloride is a RyR-selective 1,4-benzothiazepine derivative that stabilizes RyR2 channels by enhancing the binding affinity of calstabin2 to mutant and/or PKA-phosphorylated channels.
In Vitro: S107 is a small compound that enhances calstabin2 binding to RyR2 at low nanomolar concentrations and failed to interact with over 400 receptors, enzymes, and ion channels in screens using up to 10 μM of the compound. S107 has no effect on cardiac ion channels including the voltage-gated Na+, K+, and Ca2+ channels at concentrations up to 10 μM, and S107 had no effect on normal Ca2+ signaling in cells[1]. S107 is a promising candidate drug for treating catecholaminergic polymorphic ventricular tachycardia (CPVT). S107 exerts an antiarrhythmic effect on CPVT-hiPSC-CMs. Pre-incubation with 10 μM S107, which stabilizes the closed state of the ryanodine receptor 2, significantly decreases the percentage of CPVT-hiPSC-CMs presenting DADs to 25%[2]. S107 is thought to improve skeletal muscle function by stabilizing the RyR1-FKBP12 complex. S107 increases FKBP12 binding to RyR1 in SR vesicles in the presence of reduced glutathione and the NO-donor NOC12, with no effect in the presence of oxidized glutathione. S107 can reverse the harmful effects of redox active species on SR Ca2+ release in skeletal muscle by binding to RyR1 low affinity sites[3].
In Vivo: S107, which prevents a leak in the channel but does not block the channel or alter normal Ca2+ signaling, is able to inhibit both seizures and arrhythymias in the mutant mice[1].

Name: AMG 925 (HCl), CAS: 1401034-19-2, stock 21.7g, assay 98.8%, MWt: 508.02, Formula: C26H30ClN7O2, Solubility: DMSO : 1 mg/mL (1.97 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Cell Cycle/DNA Damage;Protein Tyrosine Kinase/RTK, Target: CDK;FLT3, Biological_Activity: AMG 925 HCl is a potent, selective, and orally available FLT3/CDK4 dual inhibitor with IC50s of 2±1 nM and 3±1 nM, respectively.
IC50 & Target: IC50: 2±1 nM (FLT 3), 3±1 nM (CDK4), 8±2 nM (CDK6), 375±150 nM (CDK2), 1.90±0.51 μM(CDK1)[1]
In Vitro: AMG 925 also inhibits CDK6, CDK2, and CDK1 in kinase assays with IC50s of 8±2 nM, 375±150 nM, 1.90±0.51 μM, respectively. A fair overall kinase selectivity of AMG 925 is as determined by KinomScan against a panel of 442 various kinases. Cellular selectivity (on-target vs. off-target activity) of AMG 925 is about 50-fold as evaluated by comparison of its growth-inhibiting activity in RB-positive (RB+) and RB-negative (RB-) non- acute myeloid leukemia (AML) cancer cell lines. AMG 925 potently inhibits growth of AML cell lines MOLM13 (FLT3-ITD; IC50=19 μM) and Mv4-11 (FLT3-ITD; IC50=18 μM)[1].
In Vivo: MOLM13 tumor-bearing mice are dosed twice daily by oral administration 6 hours apart with 12.5, 25, or 37.5 mg/kg AMG 925. Tumors are then harvested 3, 9, 12, and 24 hours after the first dose, and analyzed for levels of P-STAT5 and P-RB. Maximum inhibition of P-STAT5 and P-RB is achieved at 6 and 12 hours respectively at the 37.5 mg/kg dose of AMG 925. Interestingly, a rebound of P-STAT5 at 24 hours is observed, possibly as a result of compensational feedback. The pharmacodynamic responses of P-STAT5 and P-RB inhibition correlated with plasma concentrations of AMG 925. AMG 925 inhibits AML xenograft tumor growth by 96% to 99% without significant body weight loss. The antitumor activity of AMG 925 correlates with the inhibition of STAT5 and retinoblastoma protein (RB) phosphorylation, the pharmacodynamic markers for inhibition of FLT3 and CDK4, respectively. In addition, AMG 925 is also found to inhibit FLT3 mutants (e.g., D835Y) that are resistant to the current FLT3 inhibitors (e.g., AC220 and Sorafenib)[1].

Name: ACTH (1-13) Adrenocorticotropic Hormone (1-13), CAS: 22006-64-0, stock 0.2g, assay 98.2%, MWt: 1623.83, Formula: C75H106N20O19S, Solubility: H2O, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: ACTH (1-13) is a 13-aa peptide, with cytoprotective effects in the model of ethanol induced gastric lesions in rats.
In Vitro: Adrenocorticotropic hormone (ACTH) is a tropic hormone produced by the anterior pituitary, regulates cortisol and androgen production and is associated with Addison disease, Cushing syndrome and Cushing disease[2].
In Vivo: ACTH (1-13) alone or in combination with met-enkephalin shows potent cytoprotective effects in the model of ethanol induced gastric lesions in rats, and has immunomodulatory effects[1].

Name: Somatostatin-28 (1-12) 1-12-Somatostatin-28, CAS: 81286-16-0, stock 22.7g, assay 98.6%, MWt: 1244.33, Formula: C49H81N17O19S, Solubility: H2O, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Somatostatin-28 (1-12) is a somatostatin fragment that is monitored in brain tissue to track processing of somatostatin.

Name: ACTH (11-24) Adrenocorticotropic Hormone (11-24), CAS: 4237-93-8, stock 21.4g, assay 99%, MWt: 1652.04, Formula: C77H134N24O16, Solubility: H2O, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: ACTH (11-24) is a fragment of adrenocorticotrophin, acts as an antagonist of adrenocorticotropic hormone (ACTH) receptor, and induces cortisol release.
IC50 & Target: Adrenocorticotropic hormone receptor[1]
In Vitro: ACTH (11-24) acts as an antagonist of adrenocorticotropic hormone receptor[1]. ACTH (11-24) induces cortisol secretion submaximally in freshly dispersed or cultured beef adrenal cortical cells. The maximal cortisol release by ACTH (11-24) is enhanced by forskolin but inhibited by calcium channel blockers[2].
In Vivo: ACTH (11-24) blocks electroacupuncture (EA) anti-edema but not EA anti-hyperalgesia in rats[1].

Name: GRGDSPC, CAS: 91575-26-7, stock 34.7g, assay 98%, MWt: 690.73, Formula: C25H42N10O11S, Solubility: H2O, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: GRGDSPC, a 7-amino acid peptide, is a thiolated cell adhesion peptide.
In Vitro: GRGDSPC is conjugated to acrylated dextran via thiol-acrylate reaction to regulate the interactions of human mesenchymal stem cells (hMSCs) with the photocrosslinkable hydrogels. To determine the conjugation kinetics and efficiency of GRGDSPC peptide to DEX-MAES16, various GRGDSPC concentrations (i.e., 5, 10 and 20 mg/1 g DEX-MAES16) are conjugated to the acrylated Dextran (DEX) macromer over time (0.25, 0.5, 1 and 3h) in PBS at pH 7.8 and the free thiol groups of unreacted peptides are quantified using Ellman’s assay. In addition, the reaction kinetics of the thiol-peptide to acrylated (DEX-MAES16) and methacrylated (DEX-HEMA16) macromers are compared. As early as 15 min conjugation, with 5, 10 and 20 mg of GRGDSPC peptide/1 g modified DEX, the peptide conjugation efficiencies with DEX-MAES are 105.40, 94.10 and 87.45%, respectively, while for the reaction with the DEX-HEMA they are 0.73, 15.78 and 18.42%, respectively. After 1h, the GRGDSPC conjugation with DEX-MAES is completed with the peptide concentration of 10 mg, but only 35.66% of the thiol groups of the peptide react with DEX-HEMA. The reaction kinetics are also monitored at 3 h of conjugation, and all of the 20 mg GRGDSPC peptide reacts with acrylated DEX compared to only 32.53% for the methacrylated DEX at this time point[1].

Name: Allergen Gal d 4 (46-61), chicken Lysozyme C (46-61) (chicken), CAS: 62982-31-4, stock 24.1g, assay 98.9%, MWt: 1753.82, Formula: C72H116N22O29, Solubility: 10 mM in H2O, Clinical_Informat: No Development Reported, Pathway: Anti-infection, Target: Bacterial, Biological_Activity: Allergen Gal d 4 (46-61), chicken is a hen egg white lysozyme peptide.
In Vitro: Allergen Gal d 4 (46-61), chicken (HEL(46-61)) contains the immunodominant epitope recognized by mice of the k haplotype. The binding is shown to be specific, with a Kd of approximately 2 uM. The direct binding of a hen egg white lysozyme peptide, Allergen Gal d 4 (46-61), is examined to membrane I-Ak (protein encoded in the A locus of the I region) molecules in the presence of detergent. A number of synthetic peptide derivatives, which do not stimulate our T-cell reactive hybridomas, compete for the binding of Allergen Gal d 4 (46-61) to I-Ak and also inhibit the functional presentation of Allergen Gal d 4 (46-61). Inhibitors include a peptide lacking a tyrosine at position 53 and a peptide corresponding to the autologous lysozyme peptide. Presentation is examined with cells or with supported planar phospholipid membranes bearing only I-Ak and Allergen Gal d 4 (46-61)[1].

Name: Osteogenic Growth Peptide, OGP, CAS: 132996-61-3, stock 25.7g, assay 98.4%, MWt: 1523.74, Formula: C68H110N22O18, Solubility: H2O, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Osteogenic Growth Peptide, OGP is a short, naturally occurring 14-mer growth factor peptide found in serum at μM concentrations.
In Vitro: Osteogenic Growth Peptide (OGP) regulates proliferation, differentiation, and matrix mineralization in osteoblast lineage cells. The active portion of OGP, the OGP(10-14) region, is cleaved from the peptide and binds to the OGP receptor which activates the MAP kinase, the Src, and the RhoA pathways[1]. Osteogenic Growth Peptide (OGP) is a native molecule with a primary structure identical to the C-terminus of histone H4, whose sequence contains a highly conserved 14-amino acid motif (NH2-ALKRQGRTLYGFGG-OH). This peptide is isolated from blood during osteogenic remodeling of post-ablation of marrow regeneration. The osteogenic growth peptide (OGP) and its C-terminal pentapeptide OGP(10-14) have been shown to stimulate the proliferation, differentiation, alkaline phosphatase activity and matrix mineralization of osteoblastic lineage cells[2].

Name: [Sar1, Ile8]-Angiotensin II, CAS: 37827-06-8, stock 35.9g, assay 98.9%, MWt: 968.15, Formula: C46H73N13O10, Solubility: 10 mM in H2O, Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein, Target: Angiotensin Receptor, Biological_Activity: [Sar1, Ile8]-Angiotensin II is a peptide that has multiple effects on vascular smooth muscle, including contraction of normal arteries and hypertrophy or hyperplasia of cultured cells or diseased vessels.
In Vitro: Angiotensin II has multiple effects on vascular smooth muscle, including contraction of normal arteries and hypertrophy or hyperplasia of cultured cells or diseased vessels. Angiotensin II activates both the NADPH and NADH oxidases, and stimulates superoxide anion formation in vascular smooth muscle cells[1].

Name: BAY1238097, CAS: 1564268-08-1, stock 6.9g, assay 98.5%, MWt: 451.56, Formula: C25H33N5O3, Solubility: DMSO : 150 mg/mL (332.18 mM; Need ultrasonic), Clinical_Informat: Phase 1, Pathway: Epigenetics, Target: Epigenetic Reader Domain, Biological_Activity: BAY1238097 is a potent and selective inhibitor of BET binding to histones and has strong anti-proliferative activity in different AML (acute myeloid leukemia) and MM (multiple myeloma) models through down-regulation of c-Myc levels and its downstream transcriptome (IC50 <100 nM).
IC50 & Target: IC50: < 100 nM (BET in a TR-FRET assay)[1].
In Vitro: BAY 1238097 shows strong inhibitory activity (IC50 < 100 nM) in a TR-FRET assay using BET BRD4 bromodomain 1 and an acetylated peptide derived from histone H4. In the NanoBRET assay, the interaction between BRD4 (IC50=63 nM), BRD3 or BRD2 (IC50=609 nM) and H4 (IC50=2430 nM) is inhibited[1]. 
BAY 1238097 has in vitro anti-tumour activity in lymphoma models. BAY 1238097 affects the gene expression of GCB DLBCL cells. At the gene level, BTK, CCDC86, CCND2, CD19, CD27, FAIM, FCMR (FAIM3), IL7R, IRAK1, MAPK13, MYB, MYC, PDE4B, TNFRSF13B, TNFRSF17 are among the top downregulated genes. Beside histone-coding genes, the upregulated genes include CCL5, CDKN2C, CD69, JUN, and MKNK2[2].
In Vivo: BAY 1238097 shows strong efficacy in the AML and MM models. BAY 1238097 has in vivo anti-tumour activity in lymphoma models[1][2]. 
BAY 1238097 is well tolerated at 10-15 mg/kg applied daily over 9-14 days in different disease models, with no obvious toxicity[1][2].

Name: Transdermal Peptide TD 1 (peptide), CAS: 888486-23-5, stock 33.7g, assay 98.1%, MWt: 1061.15, Formula: C40H64N14O16S2, Solubility: H2O, Clinical_Informat: No Development Reported, Pathway: Membrane Transporter/Ion Channel, Target: Na+/K+ ATPase, Biological_Activity: Transdermal Peptide (TD 1 peptide) is a 11-amino acid peptide, binds toNa+/K+-ATPase beta-subunit (ATP1B1), and mainly interacts with the C-terminus of ATP1B1. Transdermal Peptide can enhance the transdermal delivery of many macromolecules[1].
In Vitro: In the presence of Transdermal Peptide, because of the specific binding of Transdermal Peptide to ATP1B1, cells will upregulate the level of ATP1B1 to maintain function and structure; as a result, the expression of ATP1B1 increases. However, as time goes on, some Transdermal Peptide molecules may be transported into cells by endocytosis; consequently, the expression of ATP1B1 then decreases. The interaction between Transdermal Peptide and ATP1B1 changes not only the expression of ATP1B1, but also the localization of ATP1B1 and then the structure of the epidermal layer. This interaction can be attenuated by inhibitors or competitors, which would result in the reduced delivery of macromolecular drugs across the skin[1].

Name: MPG, HIV related, CAS: 395069-92-8, stock 16.9g, assay 99%, MWt: 2766.22, Formula: C126H201N35O33S, Solubility: H2O, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: MPG, HIV related is 27-aa peptide, derived from both the nuclear localisation sequence of SV40 large T antigen and the fusion peptide domain of HIV-1 gp41 and is a potent delivery agent for the generalised delivery of nucleic acids and of oligonucleotides into cultured cells.
In Vitro: MPG, HIV related is 27-aa peptide vector, derived from both the nuclear localisation sequence of SV40 large T antigen and the fusion peptide domain of HIV-1 gp41 and is a potent delivery agent for the generalised delivery of nucleic acids and of oligonucleotides into cultured cells and for gene therapy. MPG enables complete expression of the gene produces encoded by the plasmids it delivers into cultured cell[1].

Name: β-Amyloid (10-35), amide, CAS: 181427-66-7, stock 21.4g, assay 98.6%, MWt: 2902.33, Formula: C133H205N35O36S, Solubility: 10 mM in H2O, Clinical_Informat: No Development Reported, Pathway: Neuronal Signaling, Target: Amyloid-β, Biological_Activity: β-Amyloid (10-35), amide is composed of 26 aa (10-35 residues of the Aβ peptide) and is the primary component of the amyloid plaques of Alzheimer’s disease.
In Vitro: β-Amyloid (10-35) is selected based on the following considerations: (1) β-Amyloid (10-35) incorporates the core region, point mutations of which significantly obstruct fibril formation and have been used to generate inhibitors of fibrillogenesis; (2) β-Amyloid (10-35) retains the ability to add to bona fide Alzheimer’s plaques, in contrast to other truncated peptides, and forms fibrils morphologically similar to those of the full length peptide; (3) Of most importance, the full length peptide, Aβ(1-42), is intractable for the controlled formation of fibrils from aqueous media because at the earliest time points, some of the peptide exists as an amorphous precipitate. In contrast, the use of β-Amyloid (10-35) allows the reproducible and controlled formation of fibrils from aqueous solutions, under defined conditions of pH, ionic strength, and peptide concentration and thus yields the required homogeneous fibrils[1].

Name: Flagelin 22 Flagellin 22, CAS: 304642-91-9, stock 23.3g, assay 98.8%, MWt: 2272.48, Formula: C93H162N32O34, Solubility: 10 mM in H2O, Clinical_Informat: No Development Reported, Pathway: Anti-infection, Target: Bacterial, Biological_Activity: Flagelin 22 (Flagellin 22), a fragment of bacterial flagellin, is an effective elicitor in both plants and algae.
In Vitro: Flagelin 22 (flg22) is a 22-amino-acid peptide, which corresponds to the highly conserved N-terminal region of flagellin, can induce immunity reaction in various plants such as tomato (Solanum lycopersicum), potato (Solanum tuberosum), tobacco (Nicotiana tabacum), and Arabidopsis thaliana. Flagelin 22 can induce oxidative bursts and hypersensitive responses (HR) in both female gametophytes and sporophytes of Saccharina japonica, indicating that algae and plants may share similar mechanisms for recognizing pathogens. After culturing the female gametophytes of S. japonica in the presence of Flagelin 22, flg15, flg14, and flg22D43A for 40 days, both Flagelin 22 and flg15 significantly induce growth inhibition of the algae at a concentration of 1 μM. The fresh weights of Flagelin 22- and flg15-challenged female gametophytes are less than one half of the control[1].

Name: LCMV gp33-41, CAS: 151705-84-9, stock 1.7g, assay 98.5%, MWt: 1044.22, Formula: C48H73N11O13S, Solubility: H2O, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: LCMV gp33-41, the carboxyl-extended 11-aa-long peptide, is an lymphocytic choriomeningitis virus sequence restricted by MHC class I H-2Db molecules and presented to cytotoxic T lymphocytes[1].

Name: Nucleoprotein (396-404) NP 396, CAS: 158475-79-7, stock 19.9g, assay 98.6%, MWt: 1078.18, Formula: C50H71N13O14, Solubility: H2O, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Nucleoprotein (396-404) is the 396 to 404 fragment of lymphocytic choriomeningitis virus (LCMV). Nucleoprotein (396-404) is the H-2D(b)-restricted immunodominant epitope and can be used as a molecular model of viral antigen.

Name: Handle region peptide, rat, CAS: 749227-53-0, stock 5.5g, assay 98.1%, MWt: 1184.54, Formula: C54H101N15O12 S, Solubility: 10 mM in H2O, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Renin, Biological_Activity: Handle region peptide, rat is a prorenin receptor antagonist, suppresses the progression of diabetic nephropathy and has anti-inflammatory in the eye.
IC50 & Target: Prorenin receptor[1]
In Vitro: Handle region peptide, rat is a (pro)renin receptor antagonist. Handle region peptide, rat (1 μM) reduces the ratio of active to total ERK1/2. Handle region peptide, rat (0.1-1 μM) reduces TGF-β1 mRNA level, and inhibits the mesangial cells proliferation in a dose-dependent manner. Handle region peptide, rat (0.01-1 μM) increases the MMP-2 activity[1].
In Vivo: Handle region peptide, rat (0.1 mg/kg) suppresses leukocyte adhesion in the endotoxin-induced uveitis (EIU) retina, and decreases the leukocyte counts in rats. Handle region peptide, rat (0.1 mg/kg) lowers the protein concentration in EIU rats induced by LPS, and reduces the mRNA expression and the protein levels of inflammatory mediators such as ICAM-1, CCL2/MCP-1, and IL-6 in rats[2].

Name: BNP-45 (rat) Brain natriuretic peptide-45 rat, CAS: 123337-89-3, stock 31.9g, assay 98.1%, MWt: 5040.67, Formula: C213H349N71O65S3, Solubility: H2O, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: BNP-45 (rat) is a circulating form of rat brain natriuretic peptide isolated from rat heart with potent hypotensive and natriuretic potency[1].
In Vivo: BNP-45 (rat) (0.1, 0.2, 0.5, 1.0 and 2.0 nmol/kg, i.v.) shows potent natriuretic and hypotensive activities in anesthetized spontaneously hypertensive rats (SHR) and Wistar-Kyoto rats (WKY). BNP-45 (rat) with high concentration decreases blood pressure in SHR. But WKY is more susceptible than SHR to BNP-45 for diuresis, natriuresis and urinary cGMP excretion. In addition, high dose of BNP-45 (rat) cuases prolonged lowering of blood pressure and urinary cGMP excretion in WKY[1].

Name: [Arg8]-Vasotocin, CAS: 113-80-4, stock 0.6g, assay 98.9%, MWt: 1050.22, Formula: C43H67N15O12S2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: [Arg8]-Vasotocin is a vertebrate neurohypophyseal peptide of the vasopressin/oxytocin hormone family[1].
In Vitro: [Arg8]-Vasotocin occurs throughout the vertebrate phyla, being present in primitive fish, the cyclostomes, and remaining unchanged in vertebrates up to and including birds[1].
[Arg8]-Vasotocin excites neurones in the dorsal vagal complex in vitro[2].

Name: TAT (48-57), CAS: 253141-50-3, stock 38.2g, assay 98.4%, MWt: 1396.65, Formula: C55H109N31O12, Solubility: H2O, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: TAT (48-57) is a cell-permeable peptide, derived from HIV-1 transactivator of transcription (Tat) protein residue 48-57.
In Vitro: TAT (48-57) is a cell-permeable peptide with short length, good at crossing cell membranes of different cell types, with overall low toxicity, and does not leak out from cells once internalised[1].

Name: AMARA peptide, CAS: 163560-19-8, stock 14.1g, assay 98.5%, MWt: 1542.81, Formula: C62H115N27O17S, Solubility: H2O, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: AMARA peptide is a substrate for SIK and AMPK.
In Vitro: AMARA peptide is a substrate for SIK and AMPK[1].

Name: Galanin (1-16), mouse, porcine, rat, CAS: 125118-77-6, stock 12.8g, assay 98.2%, MWt: 1669.88, Formula: C78H116N20O21, Solubility: 10 mM in H2O, Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein;Neuronal Signaling, Target: Neuropeptide Y Receptor;Neuropeptide Y Receptor, Biological_Activity: Galanin (1-16), mouse, porcine, rat is an agonist of the hippocampal galanin receptor, with a Kd of 3 nM.
IC50 & Target: Kd: 3 nM (Galanin receptor)[1]
In Vitro: Galanin (1-16), mouse, porcine, rat is an agonist of the hippocampal galanin receptor, with a Kd of 3 nM[1]. Galanin (1-16), mouse, porcine, rat shows high biological activity on locus coeruleus neurons[2].

Name: TAT 2-4, CAS: 1159916-66-1, stock 12.2g, assay 98.1%, MWt: 3215.74, Formula: C132H240N66O29, Solubility: H2O, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: TAT 2-4 is a peptide derived from HIV-1 transactivator of transcription (Tat) protein.

Name: Carbacyclin Carbaprostacyclin;Carba-PGI2, CAS: 69552-46-1, stock 21.2g, assay 98.5%, MWt: 350.49, Formula: C21H34O4, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein, Target: Prostaglandin Receptor, Biological_Activity: Carbacyclin is a PGI2 analogue, acts as a prostacyclin (PGI2) receptor agonist and vasodilator, and potently inhibits platelet aggregation.
IC50 & Target: PGI2 receptor[1]
In Vitro: Carbacyclin is an agonist of prostacyclin (PGI2) receptor[1]. Carbacyclin acts as an inhibitor of platelet aggregation induced by ADP or collagen in vitro[2]. Carbacyclin is a PGI2 analogue, activates CPT-1 mRNA expression through PPARδ, independent of the IP receptor signaling pathway. Carbacyclin (0.02 μM to 20 μM) activates the IP receptor signaling pathway via PKA, and such an effect is inhibited by H-89, a PKA inhibitor. Carbacyclin (0.02-80 μM) increases PPRE promoter activity via PPARδ independent of the IP receptor signaling pathway in cardiomyocytes[3].
In Vivo: Carbacyclin is 0.03 times as active as prostacyclin on inhibiting platelet aggregation in human, dog or rabbit plasma[2]. Carbacyclin (100 μg, i.p.) induces CPT-1 mRNA expression in murine heart[3].

Name: PA (224-233), Influenza, CAS: 271573-27-4, stock 6.2g, assay 98.2%, MWt: 1185.29, Formula: C53H80N14O17, Solubility: 10 mM in H2O, Clinical_Informat: No Development Reported, Pathway: Anti-infection, Target: Influenza Virus, Biological_Activity: PA (224-233), Influenza is a 10-aa peptide, a fragment of polymerase 2 protein in influenza A virus.
In Vitro: PA (224-233), Influenza is a 10-aa peptide, a fragment of polymerase 2 protein in influenza A virus[1].

Name: Ceratotoxin A, CAS: 150671-04-8, stock 5.7g, assay 98.9%, MWt: 2868.59, Formula: C135H243N35O32, Solubility: 10 mM in H2O, Clinical_Informat: No Development Reported, Pathway: Anti-infection, Target: Bacterial, Biological_Activity: Ceratotoxin A, a 29-residue peptide isolated from the accessory gland secretion fluid, with strong anti-bacterial activity.
IC50 & Target: Bacterial[1]
In Vitro: Ceratotoxin A is a 29-residue peptide isolated from the accessory gland secretion fluid, shows anti-E.coli activity, and is heat stable[1]. Ceratotoxin A is effective against Escherichia coli ATCC 23739, Pseudomonas aeruginos ATCC 27853, and Bacillus subtilis ATCC 6633 with minimal inhibitory concentration (MIC) of 7, 7, and 3.5 µM[2].

Name: ACTH (1-14) Adrenocorticotropic Hormone Fragment 1-14, CAS: 25696-21-3, stock 36.5g, assay 98.3%, MWt: 1680.88, Formula: C77H109N21O20S, Solubility: H2O, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: ACTH (1-14) is a fragment of adrenocorticotrophin, which regulates cortisol and androgen production.
In Vitro: Adrenocorticotropic hormone (ACTH) is a tropic hormone produced by the anterior pituitary, regulates cortisol and androgen production and is associated with Addison disease, Cushing syndrome and Cushing disease[1].

Name: MARK Substrate, CAS: 847991-34-8, stock 16.3g, assay 98%, MWt: 1417.61, Formula: C60H108N18O21, Solubility: H2O, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: MARK Substrate is a MARK substrate peptide.

Name: Nucleoprotein (118-126) NP(118-126), CAS: 124454-83-7, stock 23.6g, assay 99%, MWt: 1008.15, Formula: C43H69N13O13S, Solubility: H2O, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Nucleoprotein (118-126) is a 9-aa peptide, a fragment of Nucleoprotein.

Name: Gp100 (25-33), human, CAS: 212370-40-6, stock 15.6g, assay 98.2%, MWt: 1155.31, Formula: C52H82N16O14, Solubility: H2O, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Gp100 (25-33), human is the amino acids 25-33 fragment of the human melanoma antigen. It is a 9-amino acid (AA) epitope restricted by H-2Db and recognized by the T cells[1].

Name: HIV-1 Rev (34-50) HIV-1 rev Protein (34-50), CAS: 141237-50-5, stock 32.9g, assay 98.3%, MWt: 2437.74, Formula: C97H173N51O24, Solubility: 10 mM in H2O, Clinical_Informat: No Development Reported, Pathway: Anti-infection, Target: HIV, Biological_Activity: HIV-1 Rev (34-50) is a 17-aa peptide derived from the Rev-responsive element (RRE)-binding domains of Rev in HIV-1, with anti-HIV-1 activity.
IC50 & Target: HIV[1]
In Vitro: HIV-1 Rev (34-50) is a 17-aa peptide derived from the Rev-responsive element (RRE)-binding domains of Rev in HIV-1, with anti-HIV-1 activity[1].

Name: IRBP (1-20), human, CAS: 298202-25-2, stock 37g, assay 98.4%, MWt: 2194.59, Formula: C101H164N24O28S, Solubility: H2O, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: IRBP (1-20), human is the 1-20 fragment of interphotoreceptor retinoid binding protein (IRBP).

Name: Scyliorhinin II, CAS: 112748-19-3, stock 3.8g, assay 98.3%, MWt: 1851.09, Formula: C77H119N21O26S3, Solubility: 10 mM in H2O, Clinical_Informat: No Development Reported, Pathway: Neuronal Signaling;GPCR/G Protein, Target: Neurokinin Receptor;Neurokinin Receptor, Biological_Activity: Scyliorhinin II is a selective neurokinin-3 receptor agonist, with a Ki of 2.5 nM for neurokinin-3 receptor in rat cerebral cortex.
IC50 & Target: Ki: 2.5 nM (Neurokinin-3 receptor)[1]
In Vitro: Scyliorhinin II is a neurokinin-3 selective tachykinin receptor, with a Ki of 2.5 nM for neurokinin-3 (NK-3) receptor in rat cerebral cortex. Scyliorhinin II has little effect on NK-1 and NK-2 receptors, with Ki (NK-1 receptor)/Ki (NK-3 receptor) and Ki (NK-2 receptor)/Ki (NK-3 receptor) of 176 and 200[1].
In Vivo: Scyliorhinin II produces potent, dose-related reciprocal hindlimb scratching about equipotently with an ED50 of 0.08 nmol via intracerebroventricularly (i.c.v.) administration in mice[2].

Name: β-catenin peptide, CAS: 265669-37-2, stock 16.4g, assay 98.9%, MWt: 1073.20, Formula: C49H76N12O15, Solubility: H2O, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: β-catenin peptide is a 8-aa peptide, and can promote thymocyte positive selection.
In Vitro: β-catenin peptide is a 8-aa peptide of β-catenin, and can promote thymocyte positive selection[1].

Name: Tyrosine Protein Kinase JAK 2 (Phospho-Tyr8, 9), CAS: 247171-44-4, stock 5.9g, assay 98.8%, MWt: 2082.10, Formula: C88H138N20O34P2, Solubility: H2O, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Tyrosine Protein Kinase JAK 2 (Phospho-Tyr8, 9) is a peptide corresponding to amino acids 475 to 491 of mouse JAK2.

Name: N-Formyl-Nle-Leu-Phe-Nle-Tyr-Lys For-Nle-Leu-Phe-Nle-Tyr-Lys-OH, CAS: 71901-21-8, stock 17.9g, assay 98.9%, MWt: 824.02, Formula: C43H65N7O9, Solubility: H2O, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: N-Formyl-Nle-Leu-Phe-Nle-Tyr-Lys TFA (For-Nle-Leu-Phe-Nle-Tyr-Lys-OH TFA) is a formyl peptide receptor (FPR) agonist[1].

Name: G3-C12, CAS: 848301-94-0, stock 31.2g, assay 98.4%, MWt: 1758.98, Formula: C74H115N23O23S2, Solubility: H2O, Clinical_Informat: No Development Reported, Pathway: Immunology/Inflammation, Target: Galectin, Biological_Activity: G3-C12 is a galectin-3 binding peptide, with Kd of 88 nM, and shows anticancer activity.
IC50 & Target: Kd: 88 nM (Galectin-3)[1]
In Vitro: G3-C12 is a galectin-3 binding peptide, with high affinity (Kd) of 88 nM, but shows no affinity for other galectin family members or to other lectins. G3-C12 bearing opolymers N-(2-hydroxypropyl)methacrylamide (HPMA) potently and selectively targets colorectal cancer (CRC) tumour cells over-expressing galectin-3 and displays superior targetability to galectin-3 compared to the galactose bearing copolymer[1].

Name: Mini Gastrin I, human, CAS: 54405-27-5, stock 27.8g, assay 98.1%, MWt: 1646.73, Formula: C74H99N15O26S, Solubility: 10 mM in H2O, Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein;Neuronal Signaling, Target: Cholecystokinin Receptor;Cholecystokinin Receptor, Biological_Activity: Mini Gastrin I, human is a shorter version of human gastrin, consists of amino acids 5-17 of the parent peptide.
IC50 & Target: CCK2i4svR[1]

Name: Dynorphin A (1-10), CAS: 79994-24-4, stock 34.5g, assay 98.9%, MWt: 1234.45, Formula: C57H91N19O12, Solubility: 10 mM in H2O, Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein;Neuronal Signaling;Membrane Transporter/Ion Channel;Neuronal Signaling, Target: Opioid Receptor;Opioid Receptor;iGluR;iGluR, Biological_Activity: Dynorphin A (1-10) an endogenous opioid neuropeptide, binds to extracellular loop 2 of the κ-opioid receptor. Dynorphin A (1-10) also blocks NMDA-activated current with an IC50 of 42.0 μM.
IC50 & Target: κ-opioid receptor[1] 
NMDA receptor[2]
In Vitro: Dynorphin A (1-10) binds in the transmembrane domain of the κ-receptor[1]. The non-opioid actions of various forms of Dynorphin A (DynA) are examined on N-methyl-D-aspartate (NMDA) receptor channels in isolated rat trigeminal neurons using the whole-cell patch recording technique. All the dynorphins tested blocked NMDA-activated currents. The blocking actions are voltage-independent. The IC50 is 42.0 μM for DynA(1-10). To determine if shorter dynorphins have the similar blocking property, we examined the action of DynA(1-10) at different membrane potentials. DynA(1-10) blocks INMDA to a similar extent as the membrane potentials changed from -80 to +60 mV. Thus, despite a 160-fold difference in the apparent affinities, DynA(1-32) and DynA(1-10) both exert voltage-independent actions on NMDA receptors[2].

Name: CREBtide, CAS: 149155-45-3, stock 3.4g, assay 98.7%, MWt: 1716.99, Formula: C73H129N29O19, Solubility: 10 mM in H2O, Clinical_Informat: No Development Reported, Pathway: Stem Cell/Wnt;Protein Tyrosine Kinase/RTK, Target: PKA;PKA, Biological_Activity: CREBtide, a synthetic 13 amino acid peptide, has been reported as a PKA substrate.
IC50 & Target: PKA[1]
In Vitro: delta-CREB is a spliced variant of cAMP response element binding protein (CREB). CREBtide (KRREILSRRPSYR), a synthetic peptide based on the phosphorylation sequence in delta-CREB. delta-CREB and CREBtide are tested as substrates of cAMP-dependent protein kinase (cAK). The apparent Km of CREBtide phosphorylation by cAK is 3.9 μM, which is 10-fold lower than that of Kemptide (Km=39 μM), the synthetic peptide substrate most often employed for cAK measurement. The Vmax values are 12.4 mumol/(min.mg) for CREBtide and 9.8 mumol/(min.mg) for Kemptide. The apparent Km of CREBtide phosphorylation by cGMP-dependent protein kinase (cGK) is 2.9 μM and the Vmax value is 3.2 mumol/(min.mg). Both delta-CREB and CREBtide are phosphorylated at a much slower rate by cGK as compared with cAK, implying that the high cAK/cGK specificity exhibits by delta-CREB is retained by the peptide[2].

Name: Gluten Exorphin C, CAS: 142479-62-7, stock 34.7g, assay 98.7%, MWt: 591.70, Formula: C29H45N5O8, Solubility: 10 mM in H2O, Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein;Neuronal Signaling, Target: Opioid Receptor;Opioid Receptor, Biological_Activity: Gluten exorphin C is an opioid peptide derived from wheat gluten. Its IC50 values are 40 μM and 13.5 μM for μ opioid and δ opioid activities in the GPI and MVD assays, respectively.
IC50 & Target: IC50: 40 μM (μ opioid), 13.5 μM (δ opioid)[1]
In Vitro: Gluten exorphin C, a novel opioid peptide, is isolated from the pepsin-trypsin-chymotrypsin digest of wheat gluten. Gluten exorphin C is evaluated its opioid activities by the GPI and MVD assays and its receptor affinities by radioreceptor assays. Its IC50s are 40 μM and 13.5 μM in the GPI and the MVD assays, respectively. Gluten exorphin C has a structure quite different from any of the endogenous and exogenous opioid peptides ever reported in that the N terminal Tyr is the only aromatic amino acid. The analogs containing Tyr-Pro-X-Ser-Leu are synthesized to study its structure-activity relationship. Peptides in which X is an aromatic amino acid or an aliphatic hydrophobic amino acid has opioid activity[1].

Name: Malantide, CAS: 86555-35-3, stock 25.2g, assay 98.4%, MWt: 1633.89, Formula: C72H124N22O21, Solubility: H2O, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Malantide is a dodecapeptide phosphorylated by cyclic AMP-dependent protein kinase (PKA), and increases PKA activity.
In Vitro: Malantide is a dodecapeptide, and increases PKA activity in a variety of tissues[1]. Malantide is phosphorylated by PKA[2].

Name: Valorphin, CAS: 144313-54-2, stock 32.5g, assay 98.1%, MWt: 892.01, Formula: C44H61N9O11, Solubility: 10 mM in H2O, Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein;Neuronal Signaling, Target: Opioid Receptor;Opioid Receptor, Biological_Activity: Valorphin is an endogenous hemoglobin β-chain (33-39) fragment with opioid analgesic activity, binds to rat mu-opioid receptor, with an IC50 of 14 nM; Valorphin also shows anti-tumor activity.
IC50 & Target: IC50: 14 nM (mu-opioid receptor), 200 nM (δ-opioid receptor)[1]
In Vitro: Valorphin is a derivative of dihydrovaltrate with opioid analgesic activity, binds to rat mu-opioid receptor, with an IC50 of 14 nM. Valorphin has low affinity for δ-opioid receptor (IC50, 200 nM) and shows no affinity for κ receptor (IC50, >10 μM). Valorphin (>10 μM) decreases spontaneous firing rate of cerebellar rat Purkinje cells[1]. Valorphin (1 μM) treatment 48 h prior to 0.1 μM epirubicin, or 0.1 μM vincristine, or 0.05 μM vincristine, causes 100% tumor cell death[2].
In Vivo: Valorphin exhibits pronounced analgesic activity in mice, rats and rhesus monkeys via s.c, with ED50s of ≤5.2 mg/kg, but barely active after oral administration[1]. Valorphin (1 mg/kg) causes 42% of tumor growth inhibition in female BLRB mice bearing syngeneic mammary carcinoma cells[2].

Name: Tyr-Somatostatin-14, CAS: 58100-03-1, stock 19.3g, assay 98.9%, MWt: 1801.05, Formula: C85H113N19O21S2, Solubility: H2O, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Tyr-Somatostatin-14 is a customized peptide that adds a Tyrosine amino acid to Somatostatin-14.

Name: Neuropeptide Y(29-64), CAS: 303052-45-1, stock 27.2g, assay 98.3%, MWt: 4272.70, Formula: C189H284N54O58S, Solubility: 10 mM in H2O, Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein;Neuronal Signaling, Target: Neuropeptide Y Receptor;Neuropeptide Y Receptor, Biological_Activity: Neuropeptide Y(29-64) is a 36 amino acid peptide, a fragment of Neuropeptide Y.
In Vitro: Neuropeptide Y(29-64) is a 36 amino acid peptide, a fragment of Neuropeptide Y[1].

Name: Apidaecin IB, CAS: 123276-94-8, stock 1.7g, assay 98.6%, MWt: 2108.41, Formula: C95H150N32O23, Solubility: 10 mM in H2O, Clinical_Informat: No Development Reported, Pathway: Anti-infection, Target: Bacterial, Biological_Activity: Apidaecin IB is a insect antimicrobial peptide, with minimum inhibitory concentration (MIC) values of 8 μM for E. coli (ML35, O18K1H7 and ATCC 25922).
IC50 & Target: Bacterial[1]
In Vitro: Apidaecin IB is an insect antimicrobial peptide, with minimum inhibitory concentration (MIC) values of 8 μM for E. coli (ML35, O18K1H7 and ATCC 25922), 64 μM for K. pneumoniae 22, 8-16 μM for S. enteritidis (D5, PD1) and 4−8 μM for S. typhimurium ATCC 14028[1].

Name: ACTH (22-39) Adrenocorticotropic Hormone (22-39), CAS: 37548-29-1, stock 36.2g, assay 98.8%, MWt: 1985.06, Formula: C90H125N19O32, Solubility: H2O, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: ACTH (22-39) is an adrenocorticotropic hormone (ACTH) fragment. ACTH (22-39) is the 22-39 sequence of ACTH.
In Vitro: ACTH (22-39) contains two proline residues at positions 3 and 15 from the N-terminus[1].

Name: SJ000291942, CAS: 425613-09-8, stock 16g, assay 98.4%, MWt: 318.30, Formula: C16H15FN2O4, Solubility: DMSO : ≥ 150 mg/mL (471.25 mM), Clinical_Informat: No Development Reported, Pathway: TGF-beta/Smad, Target: TGF-β Receptor, Biological_Activity: SJ000291942 is an activator of the canonical bone morphogenetic proteins (BMP) signaling pathway. BMPs are members of the transforming growth factor beta (TGFβ) family of secreted signaling molecules.
IC50 & Target: BMP[1]
In Vitro: Embryos treated with SJ000291942 display the most severe ventralization and SJ000291942 is also the most potent. SJ000291942 also causes more mortality, and at lower doses than controls and the other two compounds. This demonstrates our compounds cause ventralization of embryos consistent with increased BMP signaling activity. SJ000291942 causes an increase in bmp2b and szl expression. Zebrafish assays suggest that SJ000291942 activates the canonical BMP signaling pathway. To extend these observations, immunoblotting of protein lysates from C33A-2D2 cells stimulated with SJ000291942 at different times is performed. SJ000291942 activates phosphorylation of SMAD1/5/8 in serum-free medium. Like in zebrafish embryos, SJ000291942 is most active. SJ000291942 induces p-SMAD1/5/8 maximally at 1hr of treatment. Immunoblotting analysis of lysates from C33A-2D2 treated with SJ000291942 reveals clear induction of the phosphorylated Extracellular Signal-regulated protein Kinase, ERK1/2 (P-ERK1/2) by SJ000291942. The highest dose (100 and 300ng) BMP4 treatments generate a gene expression signature most similar to osteoblast expression. Low dose (10ng) BMP4 treatment aligns closely with 25μM compound 3 treatment and with 25μM SJ000291942[1].

Name: Gamitrinib TPP hexafluorophosphate, CAS: 1131626-47-5, stock 3.3g, assay 99%, MWt: 1036.03, Formula: C52H65F6N3O8P2, Solubility: DMSO : 50 mg/mL (48.26 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Gamitrinib TPP hexafluorophosphate is a Gamitrinib (GA) mitochondrial matrix inhibitor.
IC50 & Target: GA mitochondrial matrix[1].
In Vitro: Gamitrinib TPP (GamitrinibTPP, G-TPP), a small molecule that combines the Hsp90 ATPase inhibitory module of 17-allylamino geldanamycin (17-AAG) with the mitochondrial-targeting moiety of triphenylphosphonium. Gamitrinib TPP is selectively delivered to mitochondria and does not affect Hsp90 homeostasis outside the organelle. Within a 16-hour exposure, concentrations of Gamitrinib TPP of 15-20 μM indistinguishably kill patient-derived and cultured glioblastoma cell lines. This cell death response has the hallmarks of mitochondrial apoptosis, with loss of organelle inner membrane potential, release of cytochrome c in the cytosol, activation of initiator caspase-9 and effector caspase-3 and caspase-7, and cellular reactivity for annexin V[1].
In Vivo: Whether the combination of TRAIL plus Gamitrinib TPP (GamitrinibTPP, G-TPP) has activity against glioblastoma in vivo is studied. Luciferase-expressing U87 glioblastoma cells implanted in the right cerebral striatum of immunocompromised mice give rise to rapidly growing tumors by bioluminescence imaging, and treatment of these mice with vehicle, stereotactic delivery of TRAIL, or systemic administration of suboptimal concentrations of Gamitrinib TPP does not affect tumor growth in vivo. Similarly, systemic monotherapy with Gamitrinib TPP at concentrations (20 mg/kg as daily i.p. injections) that inhibit subcutaneous xenograft tumor growth in mice has no effect on orthotopic glioblastoma growth. In contrast, 2 cycles of intracranial TRAIL combined with systemic Gamitrinib TPP suppresses the growth of established glioblastomas, with no significant animal weight loss throughout treatment[1].

Name: TTA-Q6(isomer), CAS: 910484-32-1, stock 7.2g, assay 98.2%, MWt: 405.80, Formula: C20H15ClF3N3O, Solubility: DMSO : 125 mg/mL (308.03 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: TTA-Q6(isomer) is an isomer of TTA-Q6. TTA-Q6 is a selective T-type Ca2+ channel antagonist.

Name: Aurora Kinase Inhibitor 3, CAS: 879127-16-9, stock 24.8g, assay 98%, MWt: 413.40, Formula: C21H18F3N5O, Solubility: DMSO : 125 mg/mL (302.37 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Cell Cycle/DNA Damage;Epigenetics, Target: Aurora Kinase;Aurora Kinase, Biological_Activity: Aurora Kinase Inhibitor 3 is a strong and selective Aurora A kinase inhibitor with an IC50 of 42 nM, and weakly inhibits EGFR with an IC50>10 μM. Aurora Kinase Inhibitor 3 has a binding mode with the cyclopropanecarboxylic acid moiety directed towards the solvent exposed region of the ATP-binding pocket, and several induced structural changes in the active-site compared with other published AIK structures[1].

Name: MZP-54, CAS: 2010159-47-2, stock 37.4g, assay 98.3%, MWt: 1036.67, Formula: C55H66ClN7O9S, Solubility: Ethanol : 50 mg/mL (48.23 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Epigenetics;PROTAC, Target: Epigenetic Reader Domain;PROTAC, Biological_Activity: MZP-54 is a selective degrader of BRD3/4 based on PROTAC technology, with a Kd of 4 nM for Brd4BD2.
IC50 & Target: Kd: 4 nM (Brd4BD2)[1]
In Vitro: MZP-54 is a selective degrader of BRD3/4 based on PROTAC technology, with a Kd of 4 nM for Brd4BD2. MZP-54 binds to VHL-EloC-EloB protein (VCB) with a Kd of 105 ± 24 nM. MZP-54 shows an inhibitory activity against MV4;11 and HL60 cells, with pEC50s of 7.08 ± 0.05 and 6.37 ± 0.03, respectively. MZP-54 also exhibits high depletion of cMyc levels[1].

Name: MZP-55, CAS: 2010159-48-3, stock 28g, assay 98.3%, MWt: 1080.72, Formula: C57H70ClN7O10S, Solubility: DMSO : 50 mg/mL (46.27 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Epigenetics;PROTAC, Target: Epigenetic Reader Domain;PROTAC, Biological_Activity: MZP-55 is a selective degrader of BRD3/4 based on PROTAC technology, with a Kd of 8 nM for Brd4BD2.
IC50 & Target: Kd: 8 nM (Brd4BD2)[1]
In Vitro: MZP-55 is a selective degrader of BRD3/4 based on PROTAC technology, with a Kd of 8 nM for Brd4BD2. MZP-55 binds to VHL-EloC-EloB protein (VCB) with a Kd of 105 ± 24 nM. MZP-55 shows an inhibitory activity against MV4;11 and HL60 cells, with pEC50s of 7.31 ± 0.03 and 6.57 ± 0.02, respectively[1].

Name: GSK1379725A, CAS: 1802251-00-8, stock 31.5g, assay 98.5%, MWt: 450.47, Formula: C23H23FN6O3, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: GSK1379725A is a selective BPTF ligand with a Kd of 2.8 uM, showing no binding activity for Brd4[1].
In Vitro: From the NMR titration of GSK1379725A, the bound and unbound resonances are separated by 171 Hz, providing an upper bound for the chemical exchange rate. Assuming an association rate of 1×108 M-1 s-1 as a high end for a range of protein-small molecule interactions, (e.g., chymotrypsin: proflavin k1=1.2×108 M-1 s-1), an upper Kd of 8 μM is estimated from this experiment. For a more accurate determination with a non-fluorinated protein, ITC is used as a complementary direct binding assay using unlabeled BPTF. A Kd of 2.8 μM is obtained, consistent with our intermediate exchange resonance broadening by PrOF NMR. Although GSK1379725A has been demonstrated to be selective over Brd4, a full selectivity panel against other bromodomains will be needed. A database search using ChEMBL only showed GSK1379725A to be active in five cellular assays with an EC50 of 500 nM carried out. Additionally, no kinase activity has been reported for GSK1379725A despite the growing screening use of the PKIS library[1].

Name: Tafamidis meglumine Fx-1006A, CAS: 951395-08-7, stock 39.1g, assay 98.7%, MWt: 503.33, Formula: C21H24Cl2N2O8, Solubility: H2O : < 0.1 mg/mL (insoluble); DMSO : 12.5 mg/mL (24.83 mM; Need ultrasonic), Clinical_Informat: Launched, Pathway: Others, Target: Others, Biological_Activity: Tafamidis meglumine (Fx-1006A) is a potent and selective transthyretin (TTR) stabilizer, shows comparable potency and efficacy to the mutumant homotetramers V30M-TTR, V122I-TTR and wild type WT-TTR, with EC50s of 2.7-3.2 μM. Tafamidis meglumine inhibits amyloidogenesis[1].
IC50 & Target: EC50: 2.7-3.2 μM (TTR)[1]
In Vitro: Tafamidis binds selectively and with negative cooperativity (Kds ∼2 nM and ∼200 nM) to the two normally unoccupied thyroxine-binding sites of the tetramer, and kinetically stabilizes TTR[1]. 
Tafamidis (0-7.2 μM) dose-dependently inhibits WT-TTR amyloidogenesis after treatment for 72 hours at a pH of 4.4-4.5[1].

Name: Lith-O-Asp, CAS: 881179-02-8, stock 39g, assay 98.5%, MWt: 491.66, Formula: C28H45NO6, Solubility: DMSO : ≥ 106 mg/mL (215.60 mM), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Lith-O-Asp is a sialytransferase (ST) inhibitor, with IC50s of 12-37 μM.
IC50 & Target: IC50: 12-37 μM (ST)[1].
In Vitro: The results indicate that Lith-O-Asp shows no apparent growth inhibition effect toward different cancer cell lines at the tested doses of 10, 30, and 60 μM. By in vitro activity assay, it is revealed that the ability of Lith-O-Asp to inhibit the activities of ST3Gal I, ST3Gal III, and ST6GalI. The IC50 values ranged from 12 to 37 μM. Flow cytometry shows a significant decrease in the expression of cell surface a-2,3- and a-2,6-sialylated antigens on The results indicates that Lith-O-Asp decreased the activity of both a-2,3- and a-2,6-sialyltransferases, and thus inhibit the transfer of sialic acids to the targeted glycoproteins[1].
In Vivo: A significant amount of secondary metastatic cancer cells are observed in lung tissues of DMSO control mice detected using IVIS in vivo imaging system after 26 days of fat pad inoculation. However, Lith-O-Asp–treated mice show fewer lung metastases. All DMSO-treated mice confirm secondary lung metastasis, but only 3 of 8 Lith-O-Asp-treated mice show lung metastasis. Average tumor nodules per mouse are 11±9 nodules in DMSO-treated group, and 2±4 nodules in Lith-O-Asp-treated group. Additionally, significantly stronger 4T1-Luc illumination signals are shown in control mice than in those injected with Lith-O-Asp-treated cancer cells on days 7 and 9[1].

Name: BMS-345541 (hydrochloride), CAS: 547757-23-3, stock 17.8g, assay 98.4%, MWt: 291.78, Formula: C14H18ClN5, Solubility: DMSO : 20 mg/mL (68.54 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: NF-κB, Target: IKK, Biological_Activity: BMS-345541 hydrochloride is a selective inhibitor of the catalytic subunits of IKK (IKK-2 IC50=0.3 μM, IKK-1 IC50=4 μM). BMS-345541 binds at an allosteric site of IKK.
IC50 & Target: IC50: 0.3 μM (IKK2), 4 μM (IKK1)
In Vitro: BMS-345541 inhibits IKK-2 and IKK-1 in dose-dependent manner. BMS-345541 fails to inhibit a panel of both serine/threonine and tyrosine kinases at concentrations as high as 100 μM. MS-345541 at concentrations as high as 100 μM fails to block both the anisomycin-stimulated phosphorylation of c-Jun and LPS-stimulated activation of MAPKAP K2 in THP-1 cells, as well as the EGF-stimulated phosphorylation of STAT3 in H292 cells[1]. BMS-345541 treatment results in a concentration-dependent inhibition of melanoma cell proliferation in SK-MEL-5, A375, and Hs 294T cells. BMS-345541 (0, 100 μM) shows apoptotic features as revealed by TUNEL staining and nuclear condensation[2].
In Vivo: BMS-345541 (10 mg/kg, p.o.) results in prolonged serum drug levels, with concentrations sustained at or above 1 μM for many hours in mice. BMS-345541 dose-dependently inhibits the production of TNFα measured in the serum of animals challenged with an intraperitoneal administration of LPS[1]. BMS-345541 (0, 10, 25, and 75 mg/kg, p.o.) effectively inhibits SK-MEL-5 tumor growth in a dose-dependent manner in the mice. Tumor-bearing mice treated with 75 mg/kg of BMS-345541 show effective inhibition of growth of SK-MEL-5, A375, and Hs 294T tumors by 86±2.8%, 69±11% and 67±3.4%, respectively[2]. BMS-345541 (30 and 100 mg/kg, p.o.) is effective in blocking both clinical and histological endpoints of inflammation and injury in mice[3].

Name: Pyrotinib dimaleate SHR-1258 dimaleate, CAS: 1397922-61-0, stock 35.9g, assay 98.6%, MWt: 815.22, Formula: C40H39ClN6O11, Solubility: H2O : ≥ 106 mg/mL (130.03 mM), Clinical_Informat: Phase 3, Pathway: JAK/STAT Signaling;Protein Tyrosine Kinase/RTK, Target: EGFR;EGFR, Biological_Activity: Pyrotinib dimaleate (SHR-1258 dimaleate) is a potent and selective EGFR/HER2 dual inhibitor with IC50 s of 13 and 38 nM, respectively.
IC50 & Target: IC50: 13 nM (EGFR), 38 nM (HER-2)[1]
In Vitro: Pyrotinib dimaleate has high potency in HER2-dependent cell lines (BT474, SK-OV-3), while showing much weaker inhibition in the HER2 negative cell line (MDA-MB-231). Pyrotinib dimaleate inhibits BT474 and SK-OV-3 cells with IC50s of 5.1 and 43 nM, respectively. Pyrotinib dimaleate displays high selectivity as HKI-272 when tested in a panel of different kinases such as KDR, c-Kit, PDGFRβ, c-Src and C-Met (c-Src with an IC50 of 790 nM, and others >3000 nM)[1].
In Vivo: Pyrotinib dimaleate has acceptable bioavailability of 20.6%, 43.5% and 13.5% in nude mice, rats and dogs, respectively. Pyrotinib dimaleate has favorable drug-like physicochemical properties and shows relatively higher oral exposure in human subjects (oral; t1/2=15 h) with a much longer half life than that of preclinical animal species such as mouse (i.v.; t1/2=1.56 h; i.g.; t1/2=2.52 h) and rat (i.v.; t1/2=4.42 h; i.g.; t1/2=3.38 h)[1].

Name: ETC-206, CAS: 1464151-33-4, stock 9.5g, assay 98.5%, MWt: 408.45, Formula: C25H20N4O2, Solubility: DMSO : ≥ 50 mg/mL (122.41 mM), Clinical_Informat: No Development Reported, Pathway: MAPK/ERK Pathway, Target: MNK, Biological_Activity: ETC-206 is a selective MNK1 and MNK2 inhibitor with IC50s of 64 nM and 86 nM, respectively.
IC50 & Target: IC50: 64 nM (MNK1), 86 nM (MNK2)[1]
In Vitro: ETC-206 inhibits eIF4E phosphorylation in HeLa cell line with an IC50 of 321 nM. The anti-proliferative effects of ETC-206 are assessed in vitro, using CellTiter-Glo viability assay against 25 hematological cancer cell lines including the K562 cell line that overexpresses eIF4E (K562 o/e eIF4E). The IC50s are 1.71 μM, 3.36 μM, 3.70 μM, 4.81 μM, 5.13 μM, 5.05 μM, 6.70 μM, 9.76 μM, and 48.8 μM for SU-DHL-6, GK-5, MC 116, P3HR-1, DOHH2, MPC-11, Ramos.2G6.4C10, AHH-1, and K562 o/e eIF4E cells, respectively[1].
In Vivo: The antitumor effect of ETC-206 is then assessed in a K562 e/o eIF4E mouse xenograft model after oral administration at 25, 50, or 100 mg/kg alone or in combination with a 2.5 mg/kg fixed dose of Dasatinib throughout the study. Dasatinib at 2.5 mg/kg elicits a tumor growth inhibition (TGI) of 88% with one tumor-free animal. In contrast, ETC-206 alone only yields a maximum TGI of 23% at the highest administered dose of 100 mg/kg, which does not impede tumor growth, and is similar to the nontreated animals. ETC-206 with 2.5 mg/kg of Dasatinib not only increases tumor growth inhibition in a dose-dependent manner but, more importantly leads to 2, 5, and 8 out of 8 tumor-free animals at 25, 50, and 100 mg/kg, respectively. The combination of ETC-206 and Dasatinib inhibits tumor growth at all tested doses, and no weight loss is recorded. Both the combination of ETC-206 and Dasatinib and, on the other hand, the dual MNK1/2 and BCR-ABL1 inhibitors prevent tumor growth in the same mouse xenograft model. ETC-206 has moderate terminal elimination half-life (t1/2=1.7 h, and 1.77 h for mouse (1 mg/kg, i.v.), mouse (5 mg/kg, p.o.))[1].

Name: Sirt2-IN-1, CAS: 1862238-00-3, stock 21.7g, assay 98.9%, MWt: 557.69, Formula: C28H27N7O2S2, Solubility: H2O : < 0.1 mg/mL (insoluble); DMSO : 150 mg/mL (268.97 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Epigenetics;Cell Cycle/DNA Damage, Target: Sirtuin;Sirtuin, Biological_Activity: Sirt2-IN-1 (Compound 9) is a sirtuin 2 (Sirt2) inhibitor with an IC50 of 163 nM[1].

Name: HJB97, CAS: 2093391-24-1, stock 31.2g, assay 98.2%, MWt: 500.55, Formula: C26H28N8O3, Solubility: DMSO : 30 mg/mL (59.93 mM; Need ultrasonic); H2O : < 0.1 mg/mL (insoluble), Clinical_Informat: No Development Reported, Pathway: Epigenetics, Target: Epigenetic Reader Domain, Biological_Activity: HJB97 is a high-affinity BET inhibitor with Kis of 0.9 nM (BRD2 BD1), 0.27 nM (BRD2 BD2), 0.18 nM (BRD3 BD1), 0.21 nM (BRD3 BD2), 0.5 nM (BRD4 BD1), 1.0 nM (BRD4 BD2), respectively. HJB97 is employed for the design of potential PROTAC BET degrader and has antitumor activity[1].
In Vitro: HJB97 is a highly potent and efficacious bomodomain and extra terminal (BET) inhibitor with IC50s of 3.1 nM (BRD2 BD1), 3.9 nM (BRD2 BD2), 6.6 nM (BRD3 BD1), 1.9 nM (BRD3 BD2), 7.0 nM (BRD4 BD1), 7.0 nM (BRD4 BD2)[1]. 
HJB97 (10-1000 nM, 4 days) potently inhibits cell growth in RS4;11 and MOLM-13 acute leukemia cell lines with IC50s of 24.1 nM and 25.6 nM[1]. 
HJB97 can effectively down-regulate the level of c-Myc at concentrations of 300-1000 nM in the RS4;11 cell line (treated for 24 h)[1].

Name: TRPM8 antagonist 2, CAS: 259674-19-6, stock 7.9g, assay 98.8%, MWt: 398.50, Formula: C26H26N2O2, Solubility: DMSO : 160 mg/mL (401.51 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Membrane Transporter/Ion Channel;Neuronal Signaling, Target: TRP Channel;TRP Channel, Biological_Activity: TRPM8 antagonist 2 is a potent and selective TRPM8 antagonist, with an IC50 of 0.2 nM, used in the research of neuropathic pain syndromes.
IC50 & Target: IC50: 0.2 nM (TRPM8)[1]
In Vitro: TRPM8 antagonist 2 (Compound 14) is a potent and selective TRPM8 antagonist, with an IC50 of 0.2 nM, used in the research of neuropathic pain syndromes. TRPM8 antagonist 2 potently inhibits menthol-induced increase in intracellular Ca2+ levels in Ca2+ fluorimetric assays in HEK293 cells stably expressing the rat isoform of TRPM8 channels (IC50, 40 nM)[1].
In Vivo: TRPM8 antagonist 2 (1, 10, and 30 mg/kg, s.c.) shows a marked, dose-dependent antinociceptive activity, and inhibits wet-dog shakes (WDS)-like cold hypersensitivity in mice by 63% at 30 mg/kg. In addition, TRPM8 antagonist 2 (0.1 and 1 μg, s.c.) attenuates Oxaliplatin (OXP)-induced cold allodynia in mice[1].

Name: NIK SMI1, CAS: 1660114-31-7, stock 9.8g, assay 98.9%, MWt: 365.38, Formula: C20H19N3O4, Solubility: DMSO : 100 mg/mL (273.69 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: NF-κB, Target: NF-κB, Biological_Activity: NIK SMI1 is a potent, selective NF-κB inducing kinase (NIK) inhibitor, which inhibits NIK-catalyzed hydrolysis of ATP to ADP with IC50 of 0.23±0.17 nM.
IC50 & Target: NIK[1]
In Vitro: NIK SMI1 (Compound 4f) inhibits NIK-catalyzed hydrolysis of ATP to ADP (fluorescence polarization, FP) with an IC50 of 0.23±0.17 nM. NIK SMI1 inhibits the expression of NIK SMI1 response elementregulated firefly luciferase reporter gene in HEK293 cells with an IC50 of 34±6 nM. Consistent with expectations for a NIK inhibitor, NIK SMI1 is shown to inhibit nuclear translocation of p52 (RelB) (IC50=70 nM). NIK SMI1 inhibits BAFF-induced B cell (mouse) survival in vitro with an IC50 of 373±64 nM[1].
In Vivo: C57BL/6 mice are treated twice daily for 7 days with orally administered NIK SMI1 or with three injections of recombinant BAFF receptor fusion protein (Br3- mIgG2a) over the course of the 7-day experiment as a positive control. The nonlinearity of exposure relative to dose between 100 and 200 mg/kg is a result of saturation of clearance mechanisms. The pharmacology of NIK SMI1 is examined in SD rat, CD-1 mouse, beagle, and cynomologous monkey with 20, 32, 18, and 7.8 mL/kg per min, respectively. Volume of distribution (Vd, L/kg) is 1.35, 1.58, 0.778, and 1.39, respectively[1].

Name: MF-094, CAS: 2241025-68-1, stock 31.5g, assay 98.9%, MWt: 535.70, Formula: C30H37N3O4S, Solubility: DMSO : 125 mg/mL (233.34 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Cell Cycle/DNA Damage, Target: Deubiquitinase, Biological_Activity: MF-094 is a potent and selective USP30 inhibitor with an IC50 of 120 nM. MF-094 increases protein ubiquitination and accelerates mitophagy[1].
IC50 & Target: IC50: 120 nM (USP30)[1]
In Vitro: MF-094 has <30% inhibitory activity for a panel of 22 USPs assays at 10 uM[1].

Name: cFMS Receptor Inhibitor II, CAS: 959860-85-6, stock 6.8g, assay 98.8%, MWt: 368.43, Formula: C23H20N4O, Solubility: H2O : < 0.1 mg/mL (insoluble); DMSO : 83.33 mg/mL (226.18 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Protein Tyrosine Kinase/RTK, Target: c-Fms, Biological_Activity: cFMS Receptor Inhibitor II is a CSF1R kinase inhibitor. CSF-1 is a cytokine[1].
IC50 & Target: CSF1R[1]

Name: MK-2 Inhibitor III, CAS: 1186648-22-5, stock 34.1g, assay 98.8%, MWt: 358.39, Formula: C21H18N4O2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: MAPK/ERK Pathway, Target: MAPKAPK2 (MK2), Biological_Activity: MK-2 Inhibitor III (compound 16) is an orally active, selective, and ATP-competitive MAPKAP-K2 (MK-2) inhibitor with an IC50 of 0.85 nM, and is exceptional selectivity against MK-3 (IC50=0.21 μM), MK-5 (IC50=0.081 μM), ERK2 (IC50=3.44 μM), MNK1(IC50=5.7 μM) as well as CDK2, JNK2, IKK2, MSK1, and MSK2[1].
IC50 & Target: IC50: 0.85 nM (MK-2), 0.21 μM (MK-3), 0.081 μM (MK-5), 3.44 μM (ERK2), 5.7 μM (MNK1)[1]
In Vitro: MK-2 Inhibitor III suppresses TNFα production in U397 cells with an IC50 of 4.4 μM[1].

Name: NAV-2729, CAS: 419547-11-8, stock 17.3g, assay 98.7%, MWt: 456.88, Formula: C25H17ClN4O3, Solubility: DMSO : 2 mg/mL (4.38 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: NAV-2729 is a dual Arf1/Arf6 activation inhibitor.
IC50 & Target: Arf6[1][2] 
Arf1[2]
In Vitro: NAV-2729 directly binds to Arf6. Based on a structural homology model of the Arf6/Arf6-GEF complex, it is predicted that NAV-2729 associates with Arf6 at the Arf6 GEF-binding area, which is distinct from the guanine nucleotide-binding pocket of Arf6. NAV-2729 blocks ARNO- and GEP100-mediated guanine nucleotide exchange on Arf6. The treatment of uveal melanoma cells with NAV-2729 interferes with anchorage-independent growth of the cell[1]. NAV-2729 is a dual Arf1/Arf6 inhibitor and is more effective toward Arf1 than Arf6. NAV-2729 blocks spontaneous activation of Arf6 and its activation by cytohesins and BRAG. NAV-2729 is an inhibitor of the spontaneous activation of Arf6, and it also inhibits the activation of Arf6 by its GEFs, ARNO and BRAG2, in solution. The inhibitory profile of NAV-2729 is analyzed at a concentration of 25 μM, which is reported to result in almost total inhibition of spontaneous and GEF-stimulated Arf6 activation in vitro. Under the conditions used in assays, NAV-2729 inhibits spontaneous nucleotide exchange of Δ13Arf6 by ~15%. NAV-2729 inhibits the activation of Δ13Arf6 by BRAG2Sec7PH by 25%. Δ17Arf1 has no measurable spontaneous nucleotide exchange. Activation of Δ17Arf1 by BRAG2Sec7PH is inhibited by NAV-2729, and the efficiency is markedly higher than that for Arf6 (50%). In a dose-response experiment, nucleotide exchange rates are reduced by 50% by 10 μM NAV-2729 for Δ17Arf1 while 50% inhibition is not achieved even at 25 μM NAV-2729 for Δ13Arf6[2].
In Vivo: Systemic treatment of mice with NAV-2729 interfere with tumorigenesis and tumor growth in orthotopic xenograft mouse model of uveal melanoma[1].

Name: QX77, CAS: 1798331-92-6, stock 19.4g, assay 98.3%, MWt: 300.74, Formula: C16H13ClN2O2, Solubility: DMSO : ≥ 64 mg/mL (212.81 mM), Clinical_Informat: No Development Reported, Pathway: Autophagy, Target: Autophagy, Biological_Activity: QX77 is a chaperone-mediated autophagy (CMA) activator.
IC50 & Target: CMA[1]
In Vitro: Treatment with CMA activator QX77 rescues Rab11 down-regulation and trafficking deficiency in cystinotic cells. QX77 treatment also increases LAMP2A localization at the lysosomal membrane[1].

Name: RS-246204, CAS: 878451-87-7, stock 7.1g, assay 98.5%, MWt: 339.37, Formula: C16H13N5O2S, Solubility: H2O : < 0.1 mg/mL (insoluble); DMSO : 5 mg/mL (14.73 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: RS-246204 is a R-spondin-1 substitute compound that is able initiate small intestinal organoids without the use of the R-spondin-1 protein.
In Vitro: R-spondin-1 protein is added at a high concentration for the initiation and maintenance of the organoids. RS-246204 is a R-spondin-1 substitute that could promote the initial formation and growth of enteroids in the medium without R-spondin-1. The enteroids grown with RS-246204 had a similar differentiation capacity as well as self-renewal capacity as the enteroids grown with R-spondin-1. Furthermore, the RS-246204-derived enteroids could successfully produce the forskolin induced swelling and the organoid based epithelial to mesenchymal transition model[1].
In Vivo: RS-246204 significantly increased BrdU+ cells and body weight in the DSS induced colitis model. These results suggest that RS-246204 activates the R-spondin dependent pathway in Lgr5 stem cells, thereby enhancing proliferation or the anti-apoptotic effect, promoting regeneration of the intestinal epithelium and reducing the disease severity[1].

Name: GSK2807 Trifluoroacetate, CAS: 2245255-66-5, stock 39.1g, assay 98%, MWt: 566.53, Formula: C21H33F3N8O7, Solubility: H2O : ≥ 50 mg/mL (88.26 mM), Clinical_Informat: No Development Reported, Pathway: Epigenetics, Target: Histone Methyltransferase, Biological_Activity: GSK2807 Trifluoroacetate is a potent, selective and SAM-competitive inhibitor of SMYD3, with a Ki of 14 nM and an IC50 of 130 nM[1][2].
IC50 & Target: Ki: 14 nM (SMYD3)[1].
IC50: 130 nM (SMYD3)[2]
In Vitro: A high-resolution crystal structure reveals that GSK2807 bridges the gap between the SAM-binding pocket and the substrate lysine tunnel of SMYD3. GSK2807 is 24-fold selective for SMYD3 in comparison with the closely related enzyme SMYD2 (Ki=14±6 nM and 345±36 nM, respectively)[1].

Name: VH032-PEG5-C6-Cl HaloPROTAC 2, CAS: 1799506-06-1, stock 32g, assay 98.7%, MWt: 783.41, Formula: C38H59ClN4O9S, Solubility: DMSO : ≥ 50 mg/mL (63.82 mM), Clinical_Informat: No Development Reported, Pathway: PROTAC, Target: PROTAC, Biological_Activity: VH032-PEG5-C6-Cl (HaloPROTAC 2) is a small molecule HaloPROTAC that incorporates the VH032 based VHL ligand and 5-unit PEG linker. VH032-PEG5-C6-Cl is capable of inducing the degradation of GFP-HaloTag7 in cell-based assays[1].
In Vitro: Treatment (24 hour) with VH032-PEG5-C6-Cl leads to nearly 70% degradation of GFP-Halotag7 at 2.5 μM[1].

Name: Cl-C6-PEG4-O-CH2COOH PROTAC Linker 4, CAS: 1799506-30-1, stock 23.4g, assay 98.1%, MWt: 370.87, Formula: C16H31ClO7, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: PROTAC, Target: PROTAC Linker, Biological_Activity: Cl-C6-PEG4-O-CH2COOH (PROTAC Linker 4) is a PROTAC linker can be used in the synthesis of chloroalkane-containing PROTACs (HaloPROTACs).

Name: Menaquinone-7 Vitamin K2-7;Vitamin K2(35);Vitamin MK-7, CAS: 2124-57-4, stock 33.2g, assay 98.6%, MWt: 649.00, Formula: C46H64O2, Solubility: H2O : < 0.1 mg/mL (insoluble); DMSO : 5 mg/mL (7.70 mM; Need ultrasonic and warming), Clinical_Informat: Phase 2, Pathway: Others, Target: Others, Biological_Activity: Menaquinone-7 (Vitamin K2-7), belongs to a class of K2-vitamin homologs, is originally discovered as the anti-hemorrhagic factors[1]. Menaquinone-7 (Vitamin K2-7) is identified as the most bioactive cofactor for the carboxylation reaction of Gla-proteins [2]. Supplementation with Menaquinone-7 (Vitamin K2-7) is a pharmacological option for activating matrix Gla protein and intervening in the progression of calcific aortic valve stenosis (CAVS)[3].

Name: INCB054329, CAS: 1628607-64-6, stock 3.8g, assay 98.3%, MWt: 348.36, Formula: C19H16N4O3, Solubility: DMSO : ≥ 100 mg/mL (287.06 mM), Clinical_Informat: Phase 2, Pathway: Epigenetics, Target: Epigenetic Reader Domain, Biological_Activity: INCB054329 is a potent BET inhibitor.
IC50 & Target: BET[1]
In Vitro: INCB054329 is a bromodomain and extra-terminal motif (BET) inhibitor[1]. INCB054329 inhibits binding of BRD2, BRD3 and BRD4 to an acetylated histone H4 peptide with low nanomolar potency. In myeloma cell lines, treatment with INCB054329 inhibits expression of c-MYC and induced HEXIM1. The majority of myeloma, AML, and lymphoma cell lines tested are growth inhibited by INCB054329 with potencies less than 200 nM. Selectivity is seen when compared with nontransformed cells as the potency for growth inhibition of IL-2 stimulated T-cells from normal donors is greater than 1300 nM. Cell cycle analysis reveals treatment-induced G1 arrest. Furthermore in both AML and lymphoma cell lines, INCB054329 induces apoptosis consistent with increased expression of pro-apoptotic regulators[2].
In Vivo: Oral administration of INCB054329 inhibits tumor growth in several models of hematologic cancers. In the MM1.S multiple myeloma xenograft model, inhibition of tumor growth is correlated with reduction of c-MYC levels. PK-PD analysis shows c-MYC suppression is associated with an IC50 value of less than 100 nM in vivo[2].

Name: 1,2-Distearoyl-sn-glycero-3-phosphorylethanolamine DSPE, CAS: 1069-79-0, stock 27.9g, assay 98.1%, MWt: 748.07, Formula: C41H82NO8P, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: 1,2-Distearoyl-sn-glycero-3-phosphorylethanolamine (DSPE) is a phosphoethanolamine (PE) lipid that can be used in the synthesis of liposomes[1].
In Vitro: 1,2-Distearoyl-sn-glycero-3-phosphorylethanolamine (DSPE), one of many phosphoethanolamine (PE) lipids, cannot sustain a lamellar form at pH values below ∼8.5, the pKa of the ethanolamine moiety[1].

Name: GSTO-IN-2, CAS: 1202710-57-3, stock 29.4g, assay 98.9%, MWt: 620.77, Formula: C33H52N2O9, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Gutathione S-transferase, Biological_Activity: GSTO-IN-2 is a glutathione S-transferase inhibitor with IC50s of 3.6, 16.3, and 1.4 μM for GSTA2, GSTM1, and GSTP1-1.
IC50 & Target: IC50: 3.6 μM (GSTA2), 16.3 μM (GSTM1), 1.4 μM (GSTP1-1)[1]
In Vitro: GSTO-IN-2 is compound 3 in the reference. GSTO-IN-2 shows synergetic effect with chemotherapy drugs against two breast cancer cell lines through the inactivation of GST isozymes. The maximal enhancement of cisplatin-induced inhibition of cell viability is observed at 50 μM GSTO-IN-2, up to 640% against MCF-7 and up to 270% against MDA-MB-231. Viability inhibition of thiotepa is enhanced by GSTO-IN-2 (25 and 50 μM), up to 170-320% against MCF-7 and up to 180-270% against MDA-MB-231.[1].

Name: α-2,3-sialyltransferase-IN-1 Lith-O-Asp analog, CAS: 881179-06-2, stock 1.6g, assay 99%, MWt: 491.66, Formula: C28H45NO6, Solubility: DMSO : ≥ 103.7 mg/mL (210.92 mM), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: α-2,3-sialyltransferase-IN-1 (Lith-O-Asp analog) is a noncompetitive α-2,3-sialyltransferase inhibitor with an IC50 of 6 μM.
IC50 & Target: IC50: 6 μM (α-2,3-sialyltransferase)[1]
In Vitro: α-2,3-sialyltransferase-IN-1 is compound 17 in the reference[1].

Name: D-Glucose 6-phosphate, CAS: 56-73-5, stock 34g, assay 98.3%, MWt: 260.14, Formula: C6H13O9P, Solubility: H2O : ≥ 33.33 mg/mL (128.12 mM), Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: D-Glucose 6-phosphate is a glucose sugar phosphorylated at the hydroxy group on carbon 6.
In Vitro: This dianion is very common in cells as the majority of glucose entering a cell will become phosphorylated in this way.

Name: Lorglumide sodium salt CR-1409 (sodium salt), CAS: 1021868-76-7, stock 17.1g, assay 98.3%, MWt: 481.39, Formula: C22H31Cl2N2NaO4, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein;Neuronal Signaling, Target: Cholecystokinin Receptor;Cholecystokinin Receptor, Biological_Activity: Lorglumide sodium salt (CR-1409 sodium salt) is a potent cholecystokinin (CCK) receptor antagonist[1].
IC50 & Target: CCK[1]

Name: S119-8, CAS: 443639-96-1, stock 27.2g, assay 98.7%, MWt: 344.45, Formula: C23H24N2O, Solubility: DMSO : ≥ 150 mg/mL (435.48 mM), Clinical_Informat: No Development Reported, Pathway: Anti-infection, Target: Influenza Virus, Biological_Activity: S119-8 is a broad spectrum inhibitor of influenza A and B viruses.
IC50 & Target: Influenza A and B[1]
In Vitro: S119-8 is an analog of S119. S119-8 has acquired enhanced broad-spectrum activity with improved calculated physical properties, while maintaining significant potency (IC50=1.43 μM) at non-toxic (CC50=66.10 μM) concentrations, albeit somewhat higher (7-fold) than that of the parent S119 against influenza A/WSN/33 H1N1 (WSN) virus. S119-8 also shows activity against multiple influenza B viruses and an oseltamivir-resistant influenza A virus, but does not inhibit a non-influenza virus, vesicular stomatitis nirus (VSV). S119-8 has increased breadth of inhibition against influenza A and B viruses accompanied by only a small loss in potency. S119-8 inhibits influenza viruses A/Puerto Rico/8/1934 (H1N1) (PR8) with an IC50 of 6.05 μM. S119-8 inhibits influenza A/Vietnam/1203/2004 (H5N1) with an IC50 of 8.42 μM[1].

Name: AZ3451, CAS: 2100284-59-9, stock 26g, assay 98.9%, MWt: 571.46, Formula: C30H27BrN4O3, Solubility: H2O : < 0.1 mg/mL (insoluble); DMSO : ≥ 83.3 mg/mL (145.77 mM), Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein, Target: Protease-Activated Receptor (PAR), Biological_Activity: AZ3451 is a potent protease-activated receptor-2 (PAR2) antagonist with IC50 of 23 nM.
IC50 & Target: Protease-activated receptor-2 (IC50= 23 nM)[1]
In Vitro: Antagonist AZ3451 binds to a remote allosteric site outside the helical bundle of the protease-activated receptor 2. AZ3451 is highly lipophilic, which coincides with the hydrophobic nature of the binding pocket within the membrane. Antagonist binding prevents structural rearrangements required for receptor activation and signalling[1].

Name: GPR84 antagonist 8, CAS: 1445846-30-9, stock 4.3g, assay 98.1%, MWt: 421.45, Formula: C23H23N3O5, Solubility: DMSO : 5 mg/mL (11.86 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein, Target: GPR84, Biological_Activity: GPR84 antagonist 8 is a selective GPR84 antagonist.
IC50 & Target: GPR84[1]
In Vitro: GPR84 is a member of the metabolic G protein-coupled receptor family, and its expression has been described predominantly in immune cells. To test the hypothesis that blocking the activation of GPR84 can be a potential anti-inflammatory strategy in different inflammatory diseases, GPR84 antagonist 8 is used. The potency and specificity of GPR84 antagonist 8 is assessed tusing GPR84-CHO cells in the cAMP assay. GPR84 antagonist 8 effectively inhibits the action of 6-OAU in decreasing cAMP production in GPR84-CHO cells. To test GPR84 antagonist 8’s inhibition of the pro-inflammatory effects of GPR84 activation in macrophages, LPS pre-treated BMDMs are incubated with 10 µM GPR84 antagonist 8 for 30 min before adding 1 µM 6-OAU. Protein analysis by Western Blot shows that the GPR84 antagonist 8 partially blocks the phosphorylation of AKT and ERK induced by 6-OAU[1].

Name: JNJ-632, CAS: 1572510-42-9, stock 30.2g, assay 98.7%, MWt: 378.42, Formula: C18H19FN2O4S, Solubility: DMSO : 125 mg/mL (330.32 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Anti-infection, Target: HBV, Biological_Activity: JNJ-632 is a hepatitis B virus (HBV) capsid assembly modulator (CAM).
IC50 & Target: HBV[1]
In Vitro: JNJ-632 is a capsid assembly modulator inhibiting hepatitis B virus (HBV). JNJ-632 inhibits HBV DNA HepG2.2.15 and HBV DNA HepG2.117 with EC50s of 0.12 and 0.43 μM, respectively. In the high-content multiparameter cytotoxicity (HepG2), JNJ-632 shows EC20s in the 10-30 μM range (considered weakly cytotoxic)[1].
In Vivo: The single dose PK profile of JNJ-632 is evaluated in C57BL/6 mice following intravenous (iv) and oral (po) administration. JNJ-632 has a moderate plasma clearance of 34 mL/min/kg and a moderate volume of distribution of 1.3 L/kg. The oral bioavailability is 40% following oral administration of 10 mg/kg and 66% following oral administration of 50 mg/kg. JNJ-632 has moderate terminal elimination half-life with t1/2s of 0.42±0.06 h, 1.1±0.67 h, 2.4±2.3 h, and 5.3±0.1 h for 2.5 mg/kg (iv), 10 mg/kg (po), 50 mg/kg (po), and 50 mg/kg (sc).To circumvent the first pass metabolism, JNJ-632 is also dosed subcutaneously at 50 mg/kg in C57BL/6 mice and this results in a concentration in plasma after 24 h of dosing of 102 ng/mL and concentration in liver after 24 h of dosing of 1297 ng/g[1].

Name: INCB054329 Racemate, CAS: 1628607-62-4, stock 8.8g, assay 98.5%, MWt: 348.36, Formula: C19H16N4O3, Solubility: DMSO : ≥ 62.5 mg/mL (179.41 mM), Clinical_Informat: No Development Reported, Pathway: Epigenetics, Target: Epigenetic Reader Domain, Biological_Activity: INCB054329 Racemate is a BET protein inhibitor.
IC50 & Target: BET [1].

Name: MAT2A inhibitor 2, CAS: 13299-99-5, stock 20.1g, assay 98.2%, MWt: 365.85, Formula: C18H24ClN3O3, Solubility: DMSO : 75 mg/mL (205.00 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: MAT2A inhibitor 2 is a methionine adenosyltransferase 2A (MAT2A) inhibitor.
IC50 & Target: MAT2A.

Name: CC-90003, CAS: 1621999-82-3, stock 19.5g, assay 98.8%, MWt: 458.44, Formula: C22H21F3N6O2, Solubility: DMSO : ≥ 125 mg/mL (272.66 mM); H2O : < 0.1 mg/mL (insoluble), Clinical_Informat: Phase 1, Pathway: Stem Cell/Wnt;MAPK/ERK Pathway, Target: ERK;ERK, Biological_Activity: CC-90003 is an irreversible and selective inhibitor of ERK 1/2 with antitumor activity.
IC50 & Target: ERK 1/2[1]
In Vitro: CC-90003 is an irreversible and selective inhibitor of ERK 1/2 with antitumor activity[1].

Name: GSK319347A, CAS: 862812-98-4, stock 15.1g, assay 98.5%, MWt: 469.53, Formula: C22H19N3O5S2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: NF-κB, Target: IKK, Biological_Activity: GSK319347A is a dual inhibitor of TBK1 and IKKε with IC50s of 93 nM and 469 nM, respectively. GSK319347A also inhibits IKK2 with an IC50 of 790 nM.
IC50 & Target: IC50: 93 nM (TBK1), 469 nM (IKKε)[1] 
IC50: 790 nM (IKK2)[2]
In Vitro: GSK319347A (Compound 1) inhibits TBK1 enzyme with an IC50 of 93 nM, which also translates into good cell potency (72 nM). Moreover, IKK-3 Inhibitor exhibits excellent selectivity against cell-cycle kinases CDK2 and AurB[1]. IKK-3 Inhibitor (Compound 13) is a novel IκB kinase 2 (IKK2) inhibitor with an IC50 of 790 nM[2].

Name: Ceftobiprole Ro 63-9141;BAL 9141, CAS: 209467-52-7, stock 34.2g, assay 98.2%, MWt: 534.57, Formula: C20H22N8O6S2, Solubility: DMSO : 5 mg/mL (9.35 mM; Need ultrasonic), Clinical_Informat: Phase 3, Pathway: Anti-infection, Target: Bacterial, Biological_Activity: Ceftobiprole is a broad-spectrum cephalosporin with activity against Methicillin-resistant staphylococcus aureus (MRSA) with the MIC90 value of 2 mcg/mL.
IC50 & Target: MIC90: 2 mcg/mL (MRSA)[1]
In Vitro: Ceftobiprole has demonstrates activity against important gram-positive bacteria, including penicillin-resistant S. pneumonia (PRSP), Methicillin-resistant S. aureus (MRSA), and E. faecalis with MIC90 values of 0.25, 2, and 2 mcg/mL, respectively. Ceftobiprole has also demonstrated potent in vitro activity against several clinical isolates of community-associated Methicillin-resistant S. aureus (CA-MRSA), vancomycin-intermediate S. aureus (VISA), and Vancomycin-resistant S. aureus (VRSA), with a minimum inhibitory concentration (MIC) of 2 mcg/mL[1]. Ceftobiprole is highly active against S. aureus, withMICs ranging from 0.12 to 4 mg/L (only one resistant strain,MIC of 4 mg/L). Furthermore, Ceftobiprole is twice more active on Methicillin-susceptible S. aureus (MSSA) strains with MIC50 and MIC90 of 0.5 mg/L than on MRSA strains with MIC50 and MIC90 of 1 mg/L. Moreover, Panton-Valentine leukocidin (PVL)+MRSA are slightly more susceptible to Ceftobiprole (MIC50 of 0.5 mg/L and MIC90 of 1 mg/L) than PVL-MRSA (MIC50 and MIC90 of 1 mg/L)[2].

Name: dBET6, CAS: 1950634-92-0, stock 33g, assay 98.2%, MWt: 841.37, Formula: C42H45ClN8O7S, Solubility: H2O : < 0.1 mg/mL (insoluble); DMSO : ≥ 100 mg/mL (118.85 mM), Clinical_Informat: No Development Reported, Pathway: Apoptosis;Epigenetics;PROTAC, Target: Apoptosis;Epigenetic Reader Domain;PROTAC, Biological_Activity: dBET6 is a highly potent, selective and cell-permeable degrader of BET based on PROTAC, with an IC50 of 14 nM, and has antitumor activity.
IC50 & Target: IC50: 14 nM (BET)[1]
In Vitro: dBET6 is a highly potent, selective and cell-permeable degrader of BET with an IC50 of 14 nM. dBET6 (100 nM) exhibits antitumor activity against T cell acute lymphoblastic leukemia (T-ALL) lines via degradation of BRD4[1].
In Vivo: dBET6 (7.5 mg/kg, p.o., BID) reduces the leukemic burden in a disseminated mouse model of T-ALL[1].

Name: (R)-ADX-47273, CAS: 851881-59-9, stock 28.3g, assay 98.9%, MWt: 369.36, Formula: C20H17F2N3O2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein;Neuronal Signaling, Target: mGluR;mGluR, Biological_Activity: (R)-ADX-47273 is a potent mGluR5 positive allosteric modulator, with an EC50 of 168 nM for potentiation .
IC50 & Target: EC50: 168 nM (mGluR5)[1].
In Vitro: (R)-ADX-47273 (ADX-47273 (5)) is a potent mGluR5 positive allosteric modulator with an EC50 for potentiation of 168 nM and a 9-fold shift of the glutamate response curve at 1 μM[1].

Name: ML-290, CAS: 1482500-76-4, stock 34.8g, assay 98.9%, MWt: 506.49, Formula: C24H21F3N2O5S, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: ML-290 is a first-in-class and potent relaxin/insulin-like family peptide receptor (RXFP1) agonist and activator of anti-fibrotic genes, with an EC50 of 94 nM[1].
IC50 & Target: EC50: 94 nM (RXFP1)[1]
In Vitro: ML-290 is a first-in-class and potent relaxin/insulin-like family peptide receptor (RXFP1) agonist and activator of anti-fibrotic genes, with an EC50 of 94 nM[1]. 
ML290 (5 μM) shows anti-fibrotic, relaxin-like gene expression at 24 and 72 h in activated human hepatic stellate cells[1].

Name: Tubulin inhibitor 1, CAS: 2237054-53-2, stock 6.2g, assay 98.6%, MWt: 368.43, Formula: C21H24N2O4, Solubility: DMSO : ≥ 125 mg/mL (339.28 mM), Clinical_Informat: No Development Reported, Pathway: Cell Cycle/DNA Damage;Cytoskeleton;Apoptosis, Target: Microtubule/Tubulin;Microtubule/Tubulin;Apoptosis, Biological_Activity: Tubulin inhibitor 1 is a tubulin inhibitor, inhibits tubulin polymerization. Tubulin inhibitor 1 shows potent anti-tumor activity, casues cellular mitotic arrest in the G2/M phase, and induces cellular apoptosis[1].
IC50 & Target: Tubulin[1]
In Vitro: Tubulin inhibitor 1 (Compound 7a3) is a tubulin inhibitor, inhibits tubulin polymerization[1]. 
Tubulin inhibitor 1 has potent anti-proliferative activity against SK-OV-3, MDA-MB-231, HeLa, A549, CT26 and MCF-7 cells, with IC50s of 16.7 ± 3.0, 31.4 ± 0.7, 32.8 ± 2.9, 67.0 ± 0.8, 58.0 ± 2.4 and 35.4 ± 5.6 nM, respectively[1]. 
Tubulin inhibitor 1 (40, 80, and 160 nM, 48 hours) markedly causes cellular mitotic arrest in the G2/M phase, induces apoptosis in SK-OV-3 cells[1].
In Vivo: Tubulin inhibitor 1 (50 mg/kg, i.p., every two days three times for 20-25 days) is well tolerated, significantly reduces tumour growth in Balb/c nude mice bearing SK-OV-3 cells[1].

Name: CF53, CAS: 1808160-52-2, stock 8.3g, assay 98.9%, MWt: 443.50, Formula: C24H25N7O2, Solubility: DMSO : 110 mg/mL (248.03 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Epigenetics;Epigenetics, Target: Epigenetic Reader Domain;Histone Acetyltransferase, Biological_Activity: CF53 is a highly potent, selective and orally active inhibitor of BET protein, with a Ki of <1 nM, Kd of 2.2 nM and an IC50 of 2 nM for BRD4 BD1. CF53 binds to both the BD1 and BD2 domains of BRD2, BRD3, BRD4, and BRDT BET proteins with high affinities, very selective over non-BET bromodomain-containing proteins. CF53 shows potent anti-tumor activity both in vitro and in vivo[1].
IC50 & Target: IC50: 2 nM (BRD4 BD1)[1] 
Ki: <1 nM (BRD4 BD1)[1] 
Kd: 1.1 nM (BRD2 BD1), 0.6 nM (BRD2 BD2), 0.52 nM (BRD3 BD1), 0.49 nM (BRD3 BD2), 2.2 (BRD4 BD1), 0.8 nM (BRD4 BD2), 2 nM (BRDT BD1), 2.1 nM (BRDT BD2), 47 nM (CREBBP), 570 nM (CECR2), 110 nM (EP300)[1]
In Vitro: CF53 (Compound 28) binds to both the BD1 and BD2 domains of BRD2, BRD3, BRD4, and BRDT BET proteins with high affinities, Kds are 1.1 nM (BRD2 BD1), 0.6 nM (BRD2 BD2), 0.52 nM (BRD3 BD1), 0.49 nM (BRD3 BD2), 0.8 nM (BRD4 BD2), 2 nM (BRDT BD1), 2.1 nM (BRDT BD2), 47 nM (CREBBP), 570 nM (CECR2), 110 nM (EP300), respectively[1]. 
CF53 exhibits IC50s of 7, 85 nM against MOLM-13 acute leukemia and MDA-MB-231 breast cancer cell lines, respectively[1].
In Vivo: CF53 (25, 50 mg/kg, p.o.) exhibits potent anti-tumor activity both in MDA-MB-231 xenograft tumor model and in RS4;11 model in mice[1].

Name: H3B-5942, CAS: 2052128-15-9, stock 27.9g, assay 98.9%, MWt: 494.63, Formula: C31H34N4O2, Solubility: DMSO : 83.33 mg/mL (168.47 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Others, Target: Estrogen Receptor/ERR, Biological_Activity: H3B-5942 is a selective, irreversible and orally active estrogen receptor covalent antagonist, inactivates both wild-type and mutant ERα by targeting Cys530, with Kis of 1 nM and 0.41 nM, respectively. H3B-5942 reduces ERα target gene GREB1, shows potent antitumor activity both in multiple cell lines or animals bearing ERαWT or ERα mutations[1].
IC50 & Target: Ki: 1 nM (ERαWT), 0.41 nM (ERαY537S)[1]
In Vitro: H3B-5942 is a selective and irreversible estrogen receptor covalent antagonist, inactivates both wild-type and mutant ERα by targeting Cys530, with Kis of 1 nM and 0.41 nM, respectively[1]. 
H3B-5942 elevates ERα protein level distinct from SERMs/SERD, blocks ERα-dependent transcription in breast cancer cells. H3B-5942 (0.01-10 μM) reduces ERα target gene GREB1 in MCF7-ERαWT, various MCF7-ERαMUT lines, and the PDX-ERαY537S/WT line[1]. 
H3B-5942 also decreases proliferation of MCF7-Parental, MCF7-LTED-ERαWT, and MCF7-LTED-ERαY537C lines with GI50s of 0.5, 2, and 30 nM, respectively. H3B-5942 (10-25 nM) in combination with CDK4/6 inhibitors (≥25 pM) has synergic inhibitory effect on multiple cell lines bearing ERαWT or clinically frequent ERα mutations[1].
In Vivo: H3B-5942 (1, 3, 10, or 30 mg/kg, p.o, q.d. for 17 days) dose-dependently inhibits tumor growth in MCF7 xenograft model in athymic female nude mice[1]. 
H3B-5942 (3, 10, 30, 100, and 200 mg/kg, p.o, q.d.) exhibits similar anti-tumor activity in the ERαY537S/WT ST941 model in athymic female nude mice[1].

Name: UCB9608, CAS: 1616413-96-7, stock 24.1g, assay 98.3%, MWt: 410.47, Formula: C20H26N8O2, Solubility: DMSO : 65 mg/mL (158.36 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: PI3K/Akt/mTOR, Target: PI4K, Biological_Activity: UCB9608 is a potent, selective and orally active PI4KIIIβ inhibitor, with an IC50 of 11 nM, selective over PI3KC2 α, β, and γ lipid kinases. UCB9608 improves metabolic stability and exhibits excellent pharmacokinetic profile, acts as a potent immunosuppressive agent[1].
In Vitro: UCB9608 is a potent, selective and orally active PI4KIIIβ inhibitor, with an IC50 of 11 nM. UCB9608 is selective for PI4KIIIβ over PI3KC2 α, β, and γ lipid kinases[1]. 
UCB9608 inhibits human mixed lymphocyte reaction, the IC50 is 37 nM[1].

Name: GDC-0575 dihydrochloride ARRY-575 dihydrochloride;RG7741 dihydrochloride, CAS: 1657014-42-0, stock 9.7g, assay 98.1%, MWt: 451.19, Formula: C16H22BrCl2N5O, Solubility: DMSO : 65 mg/mL (144.06 mM; Need ultrasonic), Clinical_Informat: Phase 1, Pathway: Cell Cycle/DNA Damage, Target: Checkpoint Kinase (Chk), Biological_Activity: GDC-0575 dihydrochloride (ARRY-575 dihydrochloride) is an orally bioavailable CHK1 inhibitor, with an IC50 of 1.2 nM, and has antitumor activity.
IC50 & Target: IC50: 1.2 nM (CHK1)[1]
In Vitro: GDC-0575 dihydrochloride is a selective and orally bioavailable CHK1 inhibitor, with an IC50 of 1.2 nM. GDC-0575 (100 nM) suppressses CHK1 activation induced by AraC by decreasing the level of Tyr15-phosphorylated CDK2. GDC-0575 (100 nM) has no effect on the viability of AML cells, but significantly reduces cell viability and induces apoptosis in combination with AraC. In addition, GDC-0575 plus AraC shows no effect on normal hematopoietic stem and progenitor cells (HSPCs)[1]. GDC-0575 shows cytotoxic activity against most of 20 melanoma cell lines tested, but several cell lines grown as tumour sphere (TS) are relatively insensitive[2].
In Vivo: GDC-0575 (7.5 mg/kg, p.o.) in combination with AraC alomost completely eradicates leukemic burden in mice transplanted with U937-Luc cells, and shows more efficient activity than AraC alone. Furthermore, GDC-0575 elevates the cytotoxicity of AraC in different primary AML models in vivo[1]. GDC-0575 (25, 50 mg/kg, p.o.) dose-dependently inhibits the growth of tumor in D20 and C002 xenografts[2].

Name: Dehydronitrosonisoldipine, CAS: 87375-91-5, stock 32.5g, assay 98.7%, MWt: 370.40, Formula: C20H22N2O5, Solubility: DMSO : 100 mg/mL (269.98 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Membrane Transporter/Ion Channel;Neuronal Signaling, Target: Calcium Channel;Calcium Channel, Biological_Activity: Dehydronitrosonisoldipine is a calcium channel antagonist.
IC50 & Target: Calcium channel[1].

Name: BMS-509744, CAS: 439575-02-7, stock 31.5g, assay 98.3%, MWt: 623.83, Formula: C32H41N5O4S2, Solubility: DMSO : 21.9 mg/mL (35.11 mM; Need ultrasonic and warming), Clinical_Informat: No Development Reported, Pathway: Protein Tyrosine Kinase/RTK, Target: Itk, Biological_Activity: BMS-509744 is a potent, selective and ATP competitive Itk inhibitor with an IC50 of 19 nM.
IC50 & Target: IC50: 19 nM (Itk)[1]
In Vitro: BMS-509744 reduces T-cell receptor-induced functions including PLCγ1 tyrosine phosphorylation, calcium mobilization, IL-2 secretion, and T-cell proliferation in vitro in both human and mouse cells. BMS-488516 and BMS-509744 potently inhibit Itk in vitro with IC50 values of 96 and 19 nM, respectively. Both compounds exhibit competitive kinetics with respect to ATP, suggesting that they bind to the ATP binding site of the Itk kinase domain[1].
In Vivo: BMS-509744 and BMS-488516 suppress the production of IL-2 induced by anti-T-cell receptor antibody administered to mice. BMS-509744 exhibits a 50% inhibitory capacity when dosed at 50 mg/kg, irrespective of the amount of induction antibody. BMS-509744 also significantly diminishes lung inflammation in a mouse model of ovalbumin-induced allergy/asthma[1].

Name: AZD-1480, CAS: 935666-88-9, stock 19.9g, assay 98.7%, MWt: 348.77, Formula: C14H14ClFN8, Solubility: DMSO : 50 mg/mL (143.36 mM; Need ultrasonic), Clinical_Informat: Phase 1, Pathway: Epigenetics;Stem Cell/Wnt;JAK/STAT Signaling, Target: JAK;JAK;JAK, Biological_Activity: AZD-1480 is an ATP-competitive inhibitor of JAK1 and JAK2 with IC50s of 1.3 and <0.4 nM, respectively.
IC50 & Target: IC50: < 0.4 nM (JAK2)
In Vitro: AZD1480 (5μM) induces G2/M arrest and cell death by inhibiting Aurora kinases[1]. AZD1480 is a potent JAK2 inhibitor that can suppress growth, survival, as well as FGFR3 and STAT3 signaling and downstream targets including Cyclin D2 in human multiple myeloma cells. At low micromolar concentrations, AZD1480 blocks cell proliferation and induces apoptosis of myeloma cell lines[2]. AZD1480 effectively blocks constitutive and stimulus-induced JAK1, JAK2, and STAT-3 phosphorylation in both human and murine glioma cells, and leads to a decrease in cell proliferation and induction of apoptosis[3]. AZD1480 is a potent, competitive small-molecule inhibitor of JAK1/2 kinase, and that it is capable of inhibiting STAT3 phosphorylation and tumor growth in a STAT3-dependent manner. AZD1480 inhibits tumor angiogenesis and metastasis in part by affecting the tumor microenvironment[4].
In Vivo: AZD1480 inhibits the STAT3 phosphorylation in an xenograft model of human solid tumors and multiple myeloma[1]. In vivo, AZD1480 inhibits the growth of subcutaneous tumors and increases survival of mice bearing intracranial glioblastoma (GBM) tumors by inhibiting STAT-3 activity, indicating that pharmacologic inhibition of the JAK/STAT-3 pathway by AZD1480 should be considered for study in the treatment of patients with GBM tumors[3]. AZD1480 blocks lung infiltration of myeloid cells and formation of pulmonary metastases in both mouse syngeneic experimental and spontaneous metastatic models. Furthermore, AZD1480 reduces angiogenesis and metastasis in a human xenograft tumor model[4]. AZD1480 suppresses the growth of human solid tumor xenografts harboring persistent Stat3 activity[5].

Name: Fedratinib TG-101348;SAR 302503, CAS: 936091-26-8, stock 35.7g, assay 98.3%, MWt: 524.68, Formula: C27H36N6O3S, Solubility: H2O : < 0.1 mg/mL (insoluble); DMSO : ≥ 42 mg/mL (80.05 mM), Clinical_Informat: Phase 3, Pathway: Apoptosis;Epigenetics;Stem Cell/Wnt;JAK/STAT Signaling, Target: Apoptosis;JAK;JAK;JAK, Biological_Activity: Fedratinib (TG-101348) is a selective inhibitor of JAK2 with an IC50 of 3 nM, showing 35- and 334-fold selectivity over JAK1 and JAK3, respectively.
IC50 & Target: IC50: 3 nM (JAK2)[1]
In Vitro: Fedratinib (TG-101348) significantly inhibits JAK2 V617F, Flt3, and Ret with IC50 of 3 nM, 15 nM, and 48 nM, respectively. TG101348 has an IC50 appr 300-fold higher for the closely related JAK3 and is a less potent inhibitor of the JAK1 and TYK2 family members. Fedratinib (TG-101348) inhibits proliferation of a human erythroblast leukemia (HEL) cell line that harbors the JAK2V617F mutation, as well as a murine pro-B cell line expressing human JAK2V617F (Ba/F3 JAK2V617F), with IC50 of 305 nM and 270 nM, respectively. Fedratinib (TG-101348) also inhibits proliferation of parental Ba/F3 cells to a comparable level, with IC50 of appr 420 nM. Fedratinib (TG-101348) treatment reduces STAT5 phosphorylation at concentrations that parallel the concentrations required to inhibit cell proliferation. Fedratinib (TG-101348) induces apoptosis in both HEL and Ba/F3 JAK2V617F cells in a dose-dependent manner. Fedratinib does not show proapoptotic activity in control normal human dermal fibroblasts at concentrations up to 10 μM, and the antiproliferative IC50 against fibroblasts is >5 μM[1]. Fedratinib (TG-101348) treatment decreases GATA-1 expression, which is associated with erythroid-skewing of JAK2V617F+ progenitor differentiation, and inhibits STAT5 as well as GATA S310 phosphorylation[2]. Fedratinib (TG-101348) inhibits the proliferation of HMC-1.1 (KITV560G) cells, with somewhat lower potency than HMC-1.2 (KITD816V, KITV560G) cells, with IC50 of 740 nM and 407 nM, respectively[3].
In Vivo: Fedratinib (TG-101348) has potential for efficacious treatment of JAK2V617F-associated myeloproliferative diseases (MPD). In treated animals, there is a statistically significant reduction in hematocrit and leukocyte count, a dose-dependent reduction/elimination of extramedullary hematopoiesis, and, at least in some instances, evidence for attenuation of myelofibrosis, correlated with surrogate endpoints, including reduction/elimination of JAK2V617F disease burden, suppression of endogenous erythroid colony formation, and in vivo inhibition of JAK-STAT signal transduction. There are no apparent toxicities and no effect on T cell number[1]. Oral administration of Fedratinib (TG-101348) (120 mg/kg) significantly inhibits PV progenitor erythroid differentiation in vivo[2].

Name: DOV-216,303 (Free Base), CAS: 66504-40-3, stock 34.7g, assay 98.8%, MWt: 228.12, Formula: C11H11Cl2N, Solubility: DMSO : ≥ 125 mg/mL (547.96 mM); H2O : < 0.1 mg/mL (insoluble), Clinical_Informat: No Development Reported, Pathway: Neuronal Signaling;Neuronal Signaling, Target: Dopamine Transporter;Serotonin Transporter, Biological_Activity: DOV-216,303 (Free Base) is a potent triple serotonin, norepinephrine, and dopamine reuptake inhibitor, with IC50 values of 14 nM, 20 nM and 78 nM for hSERT, hNET and hDAT, respectively[1]. Has antidepressant-like effects and increases monoamine release in the prefrontal cortex of olfactory bulbectomized (OBX) rats[2].
IC50 & Target: IC50: 14 nM (serotonin), 20 nM (norepinephrine), 78 nM (dopamine)[1].
In Vivo: Acute treatment of DOV-216,303 (20 mg/kg, i.p.) significantly increases dopamine, norepinephrine and serotonin levels in both OBX and Sham animals[2]. 
Chronic treatment with DOV 216,303 (20 mg/kg, i.p., for 17 days) increases extracellular concentrations of dopamine, norepinephrine and serotonin in the medial prefrontal cortex of both OBX and Sham animals and significantly increases extracellular baseline serotonin concentrations[2].

Name: Momelotinib CYT387, CAS: 1056634-68-4, stock 13.6g, assay 98.5%, MWt: 414.46, Formula: C23H22N6O2, Solubility: DMSO : ≥ 40 mg/mL (96.51 mM), Clinical_Informat: Phase 3, Pathway: Apoptosis;Epigenetics;Stem Cell/Wnt;JAK/STAT Signaling;Autophagy, Target: Apoptosis;JAK;JAK;JAK;Autophagy, Biological_Activity: Momelotinib (CYT387) is an ATP-competitive inhibitor of JAK1/JAK2 with IC50a of 11 nM and 18 nM,respectively. CYT387 shows much less activity against JAK3.
IC50 & Target: IC50: 11 nM (JAK1), 18 nM (JAK2)
In Vitro: Momelotinib (CYT387) inhibits the proliferation of parental Ba/F3 cells (Ba/F3-wt) stimulated by IL-3 with IC50 of 1400 nM. Furthermore, Momelotinib (CYT387) also causes the inhibition of cell proliferation in cell lines constitutively activated by JAK2 or MPL signaling, including Ba/F3-MPLW515L cells, CHRF-288-11 cells and Ba/F3-TEL-JAK2 cells with IC50 of 200 nM, 1 nM and 700 nM, respectively. In addition, Momelotinib (CYT387) has been shown to inhibit erythroid colony growth in vitro from JAK2V617F-positive PV patients with similar potency with IC50 of 2 μM-4 μM[1]. Momelotinib (CYT387) inhibits PI3K/AKT and Ras/MAPK signaling induced by IL-6 and IGF-1. Moreover, Momelotinib (CYT387) induces apoptosis as a single agent and synergizes with the conventional anti-MM therapies PS-341 and L-PAM in primary multiple myeloma (MM) cells[2].
In Vivo: In a murine MPN model, Momelotinib (CYT387) normalizes white cell counts, hematocrit, spleen size, and restores physiologic levels of inflammatory cytokines[3].

Name: WHI-P97, CAS: 211555-05-4, stock 2.4g, assay 98.9%, MWt: 455.10, Formula: C16H13Br2N3O3, Solubility: DMSO : 5.88 mg/mL (12.92 mM; Need ultrasonic); H2O : < 0.1 mg/mL (insoluble), Clinical_Informat: No Development Reported, Pathway: Epigenetics;Stem Cell/Wnt;JAK/STAT Signaling, Target: JAK;JAK;JAK, Biological_Activity: WHI-P97 is a rationally designed potent inhibitor of JAK-3.
IC50 value:
Target: JAK3
Treatment of mast cells with WHI-P97 inhibited the translocation of 5-lipoxygenase (5-LO) from the nucleoplasm to the nuclear membrane and consequently 5-LO-dependent leukotriene (LT) synthesis after IgE receptor/FcepsilonRI crosslinking by >90% at low micromolar concentrations. WHI-P97 did not directly inhibit the enzymatic activity of 5-LO, but prevented its translocation to the nuclear membrane without affecting the requisite calcium signal. WHI-P97 was very well tolerated in mice, with no signs of toxicity at dose levels ranging from 5 microg/kg to 50 mg/kg, and LD(10) was not reached at a 50 mg/kg dose level when administered as a single i. p. or i.v. bolus dose.

Name: 2-(1-Methyl-1H-imidazol-4-yl)ethan-1-amine, CAS: 501-75-7, stock 3.6g, assay 98.3%, MWt: 125.17, Formula: C6H11N3, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: 2-(1-Methyl-1H-imidazol-4-yl)ethan-1-amine is a histamine (Him) metabolite.
In Vitro: 2-(1-Methyl-1H-imidazol-4-yl)ethan-1-amine (1-methylhistamine) is a histamine metabolite. It is a product of histamine 1-methyltransferase in the pathway of histidine metabolism.

Name: Dexloxiglumide, CAS: 119817-90-2, stock 33.7g, assay 98.3%, MWt: 461.38, Formula: C21H30Cl2N2O5, Solubility: DMSO : 50 mg/mL (108.37 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein;Neuronal Signaling, Target: Cholecystokinin Receptor;Cholecystokinin Receptor, Biological_Activity: Dexloxiglumide is a selective cholecystokinin type A (CCKA) receptor antagonist[1]. Dexloxiglumide, the active enantiomer of Loxiglumide, inhibits smooth muscle cell contractions induced by cholecystokinin-octapeptide (CCK-8)[2].

Name: BRAF inhibitor, CAS: 918505-61-0, stock 25.4g, assay 98.1%, MWt: 456.47, Formula: C22H18F2N4O3S, Solubility: DMSO : 50 mg/mL (109.54 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: MAPK/ERK Pathway, Target: Raf, Biological_Activity: BRAF inhibitor is a B-Raf inhibitor extracted from patent WO/2011103196 A1, Compound P-0850.

Name: GSK-923295, CAS: 1088965-37-0, stock 27.7g, assay 98.8%, MWt: 592.13, Formula: C32H38ClN5O4, Solubility: H2O : < 0.1 mg/mL (insoluble); DMSO : 30 mg/mL (50.66 mM; Need ultrasonic), Clinical_Informat: Phase 1, Pathway: Apoptosis;Cytoskeleton;Cell Cycle/DNA Damage, Target: Apoptosis;Kinesin;Kinesin, Biological_Activity: GSK-923295 is a special, allosteric inhibitor of centromere-associated protein-E (CENP-E) kinesin motor ATPase activity, with Ki of 3.2±0.2 nM and 1.6± 0.1 nM for human and canine, respectively.
IC50 & Target: Ki: 3.2 nM (human CENP-E), 1.6 nM (canine CENP-E)[1]
In Vitro: GSK-923295 (GSK923295) is a first-in-class, specific, allosteric inhibitor of CENP-E kinesin motor function. GSK923295 is uncompetitive with both ATP and MT, inhibiting CENP-E MT-stimulated ATPase activity with a Ki of 3.2±0.2 nM and 1.6±0.1 nM for human and canine, respectively. GSK923295 inhibits release of inorganic phosphate and stabilized CENP-E motor domain interaction with microtubules[1]. GSK923295 has broad growth inhibitory activity in a panel of 237 cancer cell lines and produces significant tumor growth-delay in 8 of the 11 mouse xenograft tumor models with IC50s of 17.2 nM, 55.6 nM, 42 nM, and 51.9 nM for SW48, RKO (BRAF mutant), SW620 (KRAS mutant), and HCT116 (KRAS mutant), respectively[2]. GSK923295 is a potent and selective small molecule inhibitor of human CENPE with a Ki of 3.2 nM. GSK923295 demonstrates broad efficacy against a panel of 19 human neuroblastoma derived cell lines with an average growth IC50 of 41 nM[3].
In Vivo: Xenografts of mice treated with GSK-923295 (GSK923295) shows significant tumor growth delay compared to the control arm (NB-EBc1 p<0.0001; NB-1643 p=0.018; NB-1691 p=0.0018)[3].

Name: A-770041, CAS: 869748-10-7, stock 31.5g, assay 98.8%, MWt: 621.73, Formula: C34H39N9O3, Solubility: DMSO : ≥ 100 mg/mL (160.84 mM), Clinical_Informat: No Development Reported, Pathway: Protein Tyrosine Kinase/RTK, Target: Src, Biological_Activity: A-770041 is selective and orally active Src-family Lck inhibitor; A-770041 is a 147 nM inhibitor of Lck (1 mM ATP) and is 300-fold selective against Fyn, the other Src family kinase involved in T-cell signaling.
IC50 value: 147 nM
Target: Lck

Name: CI-1040 PD 184352, CAS: 212631-79-3, stock 40g, assay 98.5%, MWt: 478.66, Formula: C17H14ClF2IN2O2, Solubility: DMSO : ≥ 150 mg/mL (313.37 mM), Clinical_Informat: Phase 2, Pathway: Apoptosis;MAPK/ERK Pathway, Target: Apoptosis;MEK, Biological_Activity: CI-1040 (PD184352) is an orally active, highly specific, small-molecule inhibitor of MEK with an IC50 of 17 nM for MEK1.
IC50 & Target: IC50: 17 nM (MEK)[1]
In Vitro: CI-1040 directly inhibits MEK1 with an IC50 of 17 nM. It has also been shown to have little activity against a panel of related kinases with IC50 values more than 2.5 orders of magnitude higher. Treatment of whole cells with CI-1040 completely inhibits the mitogen-stimulated phosphorylation of ERK. CI-1040 at a concentration of 1 μM is found to inhibit phosphorylation of ERK1 and ERK2 by 99% and 92%, respectively in MDA-MB-231 breast cancer cells[1]. CI-1040 induces apoptosis and inhibits proliferation in U-937 cells in a dose and time-dependent manner. CI-1040 induces a significant increase in PUMA mRNA and protein levels[2].
In Vivo: The systemic administration of the MEK inhibitor CI-1040 reduces adenoma formation to a third and significantly restores lung structure. The proliferation rate of lung cells of mice treated with CL-1040 is decreased without any obvious effects on differentiation of pneumocytes[3].

Name: Peptide T (TFA), CAS: 1610056-01-3, stock 17.6g, assay 98.3%, MWt: 971.89, Formula: C37H56F3N9O18, Solubility: 10 mM in DMSO, Clinical_Informat: Phase 2, Pathway: Anti-infection, Target: HIV, Biological_Activity: Peptide T (TFA) is an octapeptide from the V2 region of HIV-1 gp120. Peptide T is a ligand for the CD4 receptor and prevents binding of HIV to the CD4 receptor.
IC50 & Target: CD4, HIV[1]
In Vitro: Peptide T acts to block viral entry as it inhibits in the MAGI cell assay and blocks infection in the luciferase reporter assay using HIV virions pseudotyped with ADA envelope. Peptide T selectively inhibits HIV replication using chemokine receptor CCR5 compared to CXC4[2]. Peptide T at 10-8 M induces IL-10 production by the human Th2 cell line and PBMC. Also peptide T at 10-9 M concentration significantly inhibits IFN-g production by PBMC[3].
In Vivo: Peptide T is administered subcutaneously at different doses and phases of the experimental autoimmune encephalomyelitis (EAE) disease, but Peptide T neither prevents nor ameliorates EAE[4].

Name: Pomalidomide-PEG4-C2-NH2 Cereblon Ligand-Linker Conjugates 8;E3 Ligase Ligand-Linker Conjugates 22, CAS: 2225940-52-1, stock 37.3g, assay 98.2%, MWt: 492.52, Formula: C23H32N4O8, Solubility: DMSO : 50 mg/mL (101.52 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: PROTAC, Target: E3 Ligase Ligand-Linker Conjugate, Biological_Activity: Pomalidomide-PEG4-C2-NH2 is a synthesized E3 ligase ligand-linker conjugate that incorporates the Pomalidomide based cereblon ligand and 4-unit PEG linker used in PROTAC technology.

Name: Thalidomide-O-amido-PEG2-C2-NH2 (TFA) Cereblon Ligand-Linker Conjugates 10 (TFA);E3 Ligase Ligand-Linker Conjugates 24 (TFA), CAS: 1957235-75-4, stock 6.9g, assay 98.8%, MWt: 576.48, Formula: C23H27F3N4O10, Solubility: H2O : ≥ 150 mg/mL (260.20 mM), Clinical_Informat: No Development Reported, Pathway: PROTAC, Target: E3 Ligase Ligand-Linker Conjugate, Biological_Activity: Thalidomide-O-amido-PEG2-C2-NH2 TFA is a synthesized E3 ligase ligand-linker conjugate that incorporates the Thalidomide based cereblon ligand and 2-unit PEG linker used in PROTAC technology.
IC50 & Target: Ligand for E3 Ligase[1].

Name: Thalidomide-O-amido-C6-NH2 (TFA) Cereblon Ligand-Linker Conjugates 11 (TFA);E3 Ligase Ligand-Linker Conjugates 25 (TFA), CAS: 1950635-14-9, stock 38.9g, assay 98.3%, MWt: 544.48, Formula: C23H27F3N4O8, Solubility: DMSO : ≥ 105.5 mg/mL (193.76 mM), Clinical_Informat: No Development Reported, Pathway: PROTAC, Target: E3 Ligase Ligand-Linker Conjugate, Biological_Activity: Thalidomide-O-amido-C6-NH2 TFA (Cereblon Ligand-Linker Conjugates 11 TFA) is a synthesized E3 ligase ligand-linker conjugate that incorporates the Thalidomide based cereblon ligand and a linker used in PROTAC technology.
IC50 & Target: E3 Ligase Ligand-Linker Conjugate[1]

Name: TES-991, CAS: 1883602-20-7, stock 6.5g, assay 98.6%, MWt: 393.45, Formula: C17H11N7OS2, Solubility: H2O : < 0.1 mg/mL (insoluble); DMSO : 62.5 mg/mL (158.85 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: TES-991 is a potent and selective human α‑Amino-β-carboxymuconate-ε-semialdehyde Decarboxylase (ACMSD) inhibitor, with an IC50 of 3 nM.
IC50 & Target: IC50: 3 nM (hACMSD)[1].
In Vitro: TES-991 (compounds 21) is able to significantly increase intracellular NAD+ levels, providing further proof of their mechanism of action. TES-991 shows an inhibition of cytochrome P450 2C19, suggesting a possible involvement of the 2H-tetrazole motif in this interaction[1].
In Vivo: After the intravenous administration of 0.5 mg/kg, TES-991 (compound 21) shows low blood clearance, with low volumes of distribution and halflives (t1/2) of about 4.0 and 5.0 h, respectively, although after oral administration at 5 mg/kg, the blood concentrations of TES-991 is quantifiable for up to 8 h. A moderate systemic exposure is observed for the 2H-tetrazole analogue, TES-991, a good systemic exposure is recorded for the free acid[1].

Name: MS21570, CAS: 65373-29-7, stock 9.8g, assay 98.4%, MWt: 237.34, Formula: C10H11N3S2, Solubility: DMSO : 125 mg/mL (526.67 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: MS21570 is a selective GPR171 antagonist, with an IC50 of 220 nM.
IC50 & Target: IC50: 220 nM (GPR171)[1].
In Vivo: MS21570 significantly attenuates this CNO-mediated increase in food intake. Interestingly, MS21570 causes a significant increase in center time compared to vehicle suggesting an effect on the anxiety-like behavior. Intra-BLA administration of MS21570 leads to an increase in open arm time on the elevated plus maze although there is no effect on locomotor activity during this test. Interestingly, when administered before and immediately following fear conditioning, MS21570 significantly attenuates freezing measured 24 hours later. Behavioral differences between systemic and intra-BLA administration of MS21570 could be due to the pharmacokinetic and pharmacodynamic properties of the drug. Further studies are needed to characterize the GPR171 antagonist[1].

Name: Dextran Dextran 40, CAS: 9004-54-0, stock 34.6g, assay 98.9%, MWt: 40000.00, Formula: N/A, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Dextran (Dextran 40) has an inhibitory effect on thrombocyte aggregation and coagulation factors and is used as a plasma volume expander.

Name: CAY 10465, CAS: 688348-33-6, stock 39.4g, assay 99%, MWt: 317.13, Formula: C15H9Cl2F3, Solubility: DMSO : ≥ 100 mg/mL (315.33 mM), Clinical_Informat: No Development Reported, Pathway: Immunology/Inflammation, Target: Aryl Hydrocarbon Receptor, Biological_Activity: CAY 10465 is a selective and high-affinity AhR agonist, with a Ki of 0.2 nM, and shows no effect on estrogen receptor (Ki >100000 nM).
IC50 & Target: Ki: 0.2 nM (AhR)[1]
In Vitro: CAY 10465 (Compound 4i) is a selective and high-affinity AhR receptor agonist, with a Ki of 0.2 nM, and shows no effect on estrogen receptor (Ki >100000 nM)[1]. CAY 10465 (0.01 nM-100 μM) reduces apolipoprotein A-I (apo A-I) levels in HepG2 cells, and inhibits the synthesis of the protein[2].

Name: PDM2, CAS: 688348-25-6, stock 5.1g, assay 98.4%, MWt: 283.58, Formula: C14H9Cl3, Solubility: DMSO : 50 mg/mL (176.32 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Immunology/Inflammation, Target: Aryl Hydrocarbon Receptor, Biological_Activity: PDM2 is a selective, high-affinity aryl hydrocarbon receptor (AhR) antagonist with an Ki of 1.2±0.4 nM.
IC50 & Target: Ki: 1.2±0.4 nM(AhR)[1]
In Vitro: PDM2 (Compound 4b) exhibits a Ki of 1.2±0.4 nM for AhR and no affinity for estrogen receptor (ER), confirming that replacement of hydroxyl with chloride abolished binding on ER and increased dramatically the affinity for AhR[1].

Name: Elamipretide (TFA) MTP-131 (TFA); RX-31 (TFA); SS-31 (TFA), CAS: 1606994-55-1, stock 3.7g, assay 98.2%, MWt: 753.81, Formula: C34H50F3N9O7, Solubility: H2O, Clinical_Informat: Phase 3, Pathway: Metabolic Enzyme/Protease, Target: Mitochondrial Metabolism, Biological_Activity: Elamipretide TFA (MTP-131 TFA; RX-31 TFA; SS-31 TFA) is a cardiolipin peroxidase inhibitor and mitochondria-targeting peptide[1].
IC50 & Target: Cardiolipin peroxidase[1]

Name: SMN-C3, CAS: 1449597-34-5, stock 19.9g, assay 98.8%, MWt: 416.52, Formula: C24H28N6O, Solubility: DMSO : 5 mg/mL (12.00 mM; Need ultrasonic); H2O : < 0.1 mg/mL (insoluble), Clinical_Informat: No Development Reported, Pathway: Cell Cycle/DNA Damage, Target: DNA/RNA Synthesis, Biological_Activity: SMN-C3 is an orally active SMN2 splicing modulator and has the potential to treat spinal muscular atrophy (SMA).
IC50 & Target: SMN[1].
In Vivo: At P16, vehicle treated D7 mice are much smaller than heterozygous littermate controls and appear moribund. In contrast, D7 mice treated with the high dose of SMN-C3 show a phenotype similar to that of heterozygous controls. SMN-C3 treatment induces a dose-dependent bodyweight gain in the D7 mice, with some animals showing a body weight that is ~80% that of heterozygous controls. SMN-C3 normalizes the motor behavior of D7 mice, illustrated by the ability of the mice to right themselves as quickly as heterozygous controls and by their level of locomotor activity. Most importantly, whereas vehicle-treated mice die within 3 weeks after birth with a median survival of 18 days, SMN-C3 treatment increases survival in a dose-dependent manner to a median survival time of 28 days in the low-dose (0.3 mg/kg per day) group. In the two higher-dose groups (1 and 3 mg/kg per day), ~90% of animals survive beyond P65 when the study is completed[1].

Name: SIRT5 inhibitor 1, CAS: 2166487-21-2, stock 6g, assay 99%, MWt: 674.81, Formula: C31H39FN6O6S2, Solubility: DMSO : 125 mg/mL (185.24 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Epigenetics;Cell Cycle/DNA Damage, Target: Sirtuin;Sirtuin, Biological_Activity: SIRT5 inhibitor 1 is a potent Human Sirtuin 5 deacylase inhibitor, with an IC50 of 0.11 μM.
IC50 & Target: IC50: 0.11 μM (Sirtuin)[1].
In Vitro: SIRT5 inhibitor 1 (compound 49) is a very potent human sirtuin 5 deacylase inhibitor, with an IC50 of 0.11 μM, >100-fold from compound 1[1].

Name: [Des-Arg9]-Bradykinin (acetate), CAS: 23827-91-0, stock 39.1g, assay 98.2%, MWt: 964.07, Formula: C46H65N11O12, Solubility: H2O : 100 mg/mL (103.73 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein, Target: Bradykinin Receptor, Biological_Activity: [Des-Arg9]-Bradykinin acetate is a Bradykinin B1 receptor agonist that displays selectivity for B1 over B2 receptors.
IC50 & Target: Bradykinin B1 receptor[1]
In Vitro: [Des-Arg9]-Bradykinin acetate is a Bradykinin(B1) receptor agonist. The B2 receptor mediates the action of bradykinin (BK) and lysyl-bradykinin (Lys-BK), the first set of bioactive kinins formed in response to injury from kininogen precursors through the actions of plasma and tissue kallikreins, whereas the B1 receptor mediates the action of [Des-Arg9]-Bradykinin (des-Arg9-BK) and Lys-des-Arg Arg9-BK, the second set of bioactive kinins formed through the actions of carboxypeptidases on BK and Lys-BK, respectively[1].

Name: BAY-2402234, CAS: 2225819-06-5, stock 13.4g, assay 98.2%, MWt: 520.84, Formula: C21H18ClF5N4O4, Solubility: DMSO : 125 mg/mL (240.00 mM; Need ultrasonic), Clinical_Informat: Phase 1, Pathway: Others, Target: Others, Biological_Activity: BAY-2402234 is a selective dihydroorotate dehydrogenase (DHODH) inhibitor for the treatment of myeloid malignancies.
IC50 & Target: DHODH[1].
In Vitro: BAY-2402234 is a selective low-nanomolar inhibitor of human DHODH enzymatic activity. In vitro, it potently inhibits proliferation of AML cell lines in the sub-nanomolar to low-nanomolar range. BAY-2402234 induces differentiation of AML cell lines also in a sub-nanomolar to low-nanomolar range, demonstrating the anticipated mode of action in cellular mechanistic assays[1].
In Vivo: BAY-2402234 exhibits strong in vivo anti-tumor efficacy in monotherapy in several subcutaneous and disseminated AML xenografts as well as AML patient-derived xenograft (PDX) models. Target engagement of the novel DHODH inhibitor BAY-2402234 can be observed by increase of tumoral and plasma dihydroorotate levels after treatment with the inhibitor. Consistent with the in vitro data BAY-2402234 induces AML differentiation in vivo as detected by upregulation of differentiation cell surface markers in xenograft and PDX models after treatment with the inhibitor. Furthermore, differentiation-associated transcriptomic changes are evident following a single administration of BAY-2402234 in vivo[1].

Name: CG-806, CAS: 1370466-81-1, stock 11.6g, assay 98.6%, MWt: 509.45, Formula: C26H19F4N5O2, Solubility: DMSO : 7.2 mg/mL (14.13 mM; Need ultrasonic), Clinical_Informat: Phase 1, Pathway: Protein Tyrosine Kinase/RTK;Protein Tyrosine Kinase/RTK, Target: Btk;FLT3, Biological_Activity: CG-806 is an orally active, potent and non-covalent pan-FLT3/pan-BTK inhibitor with an IC50 of 0.08 µM for FLT3[1][2]. CG-806 has an IC50 of 11 nM against FLT3 wild type (WT)-transfected Ba/F3 cells[3].
IC50 & Target: FLT3/BTK[1].
In Vitro: In FLT3-ITD AML cells, CG-806 induces apoptosis through inhibition of FLT3 signaling (decreases phospho-FLT3, -STAT5 and -ERK) and promotion of G0/G1 cell cycle arrest. In FLT3-WT AML cell lines, or Ba/F3 cells transfected with FLT3-WT, D835Y, ITD+D835Y, or ITD+F691L, CG-806 markedly decreases phosphorylation of BTK, aurora kinases (AURK) and H3S10, resulting in G2/M arrest or polyploidy, and apoptosis with less or no effect on FLT3-WT activity. CG-806 decreases BTK phosphorylation in all malignant B cell lines tested and inhibits cell proliferation and colony formation.CG-806 equivalently inhibits BTK-WT and BTK-C481S in HEK293 transfected cells[3].
In Vivo: CG-806 (0-120 mg/kg; oral administration; for 28 days; CD-1 mice) treatment suppresses leukemia growth at all doses tested throughout the 28-day period of dosing, and has no adverse CG-806-related effects on body weight, ophthalmic, respiratory or neurological examinations, clinical pathology (coagulation, clinical chemistry, or urinalysis), organ weight or macroscopic evaluations in the subcutaneous MV4-11 xenograft model[1].

Name: IACS-8968 (R-enantiomer) IDO/TDO Inhibitor (R-enantiomer), CAS: 2239305-67-8, stock 18.8g, assay 98.8%, MWt: 381.35, Formula: C17H18F3N5O2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Indoleamine 2,3-Dioxygenase (IDO), Biological_Activity: IACS-8968 (R-enantiomer) is the R-enantiomer of IACS-8968. IACS-8968 is a dual IDO and TDO inhibitor, with pIC50s of 6.43 for IDO and <5 for TDO, respectively.
IC50 & Target: IDO, TDO[1].

Name: IACS-8968 (S-enantiomer) IDO/TDO Inhibitor (S-enantiomer), CAS: 2239305-70-3, stock 13.3g, assay 98.6%, MWt: 381.35, Formula: C17H18F3N5O2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Indoleamine 2,3-Dioxygenase (IDO), Biological_Activity: IACS-8968 (S-enantiomer) is the S-enantiomer of IACS-8968. IACS-8968 is a dual IDO and TDO inhibitor, with pIC50s of 6.43 for IDO and <5 for TDO, respectively.
IC50 & Target: IDO, TDO[1].

Name: TFLLR-NH2(TFA), CAS: 1313730-19-6, stock 38.2g, assay 98.6%, MWt: 761.83, Formula: C33H54F3N9O8, Solubility: H2O : 100 mg/mL (131.26 mM; Need ultrasonic); DMSO : 100 mg/mL (131.26 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein, Target: Protease-Activated Receptor (PAR), Biological_Activity: TFLLR-NH2 (TFA) is a selective PAR1 agonist with an EC50 of 1.9 μM.
IC50 & Target: EC50: 1.9 μM (PAR1)[1]
In Vitro: PAR1 agonists stimulate concentration-dependent increases in [Ca2+]i and in the proportions of neurones. The maximal increase in [Ca2+]i above basal is detected in response to 10 μm TF-NH2 (peak 196.5±20.4 nM, n=25) when 50–80% of identified neurones responded[1]. SW620 cells cultured in the supernatant of TFLLR-NH2-activated platelets upregulate E-cadherin expression and downregulate the vimentin expression. In the in vitro platelet culture system, a TFLLR-NH2 dose-dependent increase of secreted TGF-β1 is detected in the supernatant[2].
In Vivo: Injection of TF-NH2 into the rat paw stimulates a marked and sustained oedema. An NK1R antagonist and ablation of sensory nerves with capsaicin inhibit oedema by 44% at 1 h and completely by 5 h. In wild-type but not PAR1−/− mice, TF-NH2 stimulates Evans blue extravasation in the bladder, oesophagus, stomach, intestine and pancreas by 2–8 fold. Extravasation in the bladder, oesophagus and stomach is abolished by an NK1R antagonist[1]. TFp-NH2 produces notable contraction at 3-50 μM and relaxation at 0.3-50 μM, in the absence of apamin. The concentration-response curve for TFp-NH2-induced contraction is remarkably shifted left, when the TFp-NH2-induced relaxation is blocked by apamin at 0.1 μM[3].

Name: GSK4028, CAS: 2079886-19-2, stock 37.2g, assay 98.3%, MWt: 377.28, Formula: C17H21BrN4O, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Epigenetics;Epigenetics, Target: Epigenetic Reader Domain;Histone Acetyltransferase, Biological_Activity: GSK4028 is the enantiomeric negative control of GSK4027, which is a PCAF/GCN5 bromodomain chemical probe, the pIC50 of GSK4028 is 4.9 in a time-resolved fluorescence resonance energy transfer (TR-FRET) assay.
IC50 & Target: pIC50: 4.9 (PCAF/GCN5)[1].
In Vitro: GSK4028 is the enantiomeric negative control of GSK4027, which is a PCAF/GCN5 bromodomain chemical probe, the pIC50 of GSK4028 is 4.9. GSK4028 also demonstrates potency toward BRD4 BD1 and BRD9 inTR-FRET assay with pIC50s of <4.3 and 4.5±0.13, respectively[1].

Name: Nisin, CAS: 1414-45-5, stock 15.3g, assay 98.5%, MWt: 3354.07, Formula: C143H230N42O37S7, Solubility: H2O : < 0.1 mg/mL (insoluble); DMSO : 1 mg/mL (0.30 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Anti-infection, Target: Bacterial, Biological_Activity: Nisin is a bacteriocin produced by a group of Gram-positive bacteria that belongs to Lactococcus and Streptococcus species.
In Vitro: Nisin is classified as a Type A (I) lantibiotic that is synthesized from mRNA and the translated peptide contains several unusual amino acids due to post-translational modifications. Nisin is an antimicrobial peptide produced by certain Gram-positive bacteria that include Lactococcus and Streptococcus species[1].

Name: GCN2iB, CAS: 2183470-12-2, stock 20.4g, assay 98.5%, MWt: 451.83, Formula: C18H12ClF2N5O3S, Solubility: H2O : < 0.1 mg/mL (insoluble); DMSO : 16.67 mg/mL (36.89 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Cell Cycle/DNA Damage;Autophagy, Target: Eukaryotic Initiation Factor (eIF);Autophagy, Biological_Activity: GCN2iB is an ATP-competitive inhibitor of a serine/threonine-protein kinase general control nonderepressible 2 (GCN2), with an IC50 of 2.4 nM.
IC50 & Target: IC50: 2.4 nM (GCN2)[1].
In Vitro: GCN2iB shows an IC50 value of 2.4 nM for GCN2 and potent cellular activity. In a panel of 468 kinases, only GCN2 shows >99.5% inhibition, and three kinases (MAP2K5, STK10, and ZAK) show >95%inhibition at 1 μM GCN2iB, demonstrating high kinase selectivity[1].
In Vivo: In the antitumor activity study of the CCRF-CEM xenografts, ASNase or GCN2iB alone does not significantly affect tumor growth. Notably, a combination of ASNase and GCN2iB elicit potent antitumor activity (P=0.0002) with synergistic effects. In MV-4-11 and SU.86.86 xenografts, robust antitumor activity of the combination of GCN2iB and ASNase is observed with synergistic effect, respectively. ASNase/GCN2iB-treated tumors do not show significant growth even after drug cessation. The combination of ASNase and GCN2iB yield survival advantage compared with the vehicle treated control with synergistic effect[1].

Name: Selumetinib AZD6244;ARRY-142886, CAS: 606143-52-6, stock 20.3g, assay 98.7%, MWt: 457.68, Formula: C17H15BrClFN4O3, Solubility: DMSO : 20.83 mg/mL (45.51 mM; Need ultrasonic), Clinical_Informat: Launched, Pathway: Apoptosis;MAPK/ERK Pathway, Target: Apoptosis;MEK, Biological_Activity: Selumetinib (AZD6244) is selective, non-ATP-competitive oral MEK1/2 inhibitor, with an IC50 of 14 nM for MEK1. Selumetinib (AZD6244) inhibits ERK1/2 phosphorylation.
IC50 & Target: IC50: 12 nM (MEK)[4], 14 nM (MEK1)[3]
In Vitro: Selumetinib (AZD6244) causes a time- and dose-dependent reduction in DNA synthesis and cell viability in primary, induces growth arrest and apoptosis associated with the inactivation of ERK in primary 2-1318 cells[1]. 
Selumetinib (AZD6244) (1µM) shows anti-proliferative effects through G0/G1 arrest on H-441, H-1437 cells[2]. 
Selumetinib (AZD6244) results in the growth inhibition of several cell lines containing B-Raf and Ras mutations but has no effect on a normal fibroblast cell line[3].
In Vivo: Selumetinib (AZD6244, 50 and 100 mg/kg, p.o.) decreases the growth rate of 4-1318 xenografts in a dose-dependent manner; AZD6244 when given at the dose of 50 mg/kg also significantly suppresses the growth of the 5-1318, 2-1318, 26-1004, and 29-1104 xenografts[1]. Selumetinib (ARRY-142886, 10, 25, 50, or 100 mg/kg, p.o.) is capable of inhibiting both ERK1/2 phosphorylation and growth of HT-29 xenograft tumors in nude mice. Tumor regressions are also seen in a BxPC3 xenograft model[3].

Name: CU-CPT-9a, CAS: 2165340-32-7, stock 36.2g, assay 98.1%, MWt: 265.31, Formula: C17H15NO2, Solubility: DMSO : 135 mg/mL (508.84 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Immunology/Inflammation, Target: Toll-like Receptor (TLR), Biological_Activity: CU-CPT-9a is a specific TLR8 antagonist, with an IC50 of 0.5 nM.
IC50 & Target: IC50: 0.5 nM (TLR8)[1].
In Vitro: CU-CPT-9a is a specific TLR8 antagonist, with an IC50 of 0.5±0.1 nM. The elevation of the downstream protein levels induced by R848 can be reversed by CU-CPT-9a in a dose-dependent manner. By contrast, the expression of TRIF and IRF3 (cytoplasmic and nuclear) are only responsive to TLR4 and TLR3, independent of TLR837. The expression levels of TRIF and IRF3 do not show significant change in THP-1 cells upon treatment of R848, nor do they change with the treatment of CU-CPT-9a. CU-CPT8m and CU-CPT-9a both significantly suppress the TNF-α level in a dose-dependent manner, which is in agreement with previous reports of TLR8 involvement in these autoimmune diseases[1].

Name: Retagliptin Phosphate SP 2086, CAS: 1256756-88-3, stock 2.2g, assay 98.2%, MWt: 562.36, Formula: C19H21F6N4O7P, Solubility: DMSO : ≥ 150 mg/mL (266.73 mM), Clinical_Informat: Phase 3, Pathway: Metabolic Enzyme/Protease, Target: Dipeptidyl Peptidase, Biological_Activity: Retagliptin Phosphate is pharmaceutical composition of DPP-4 inhibitor for treating type-2 diabetes.
IC50 & Target: DPP-4[1].

Name: 5-Chloro-2'-deoxyuridine 5-Chlorodeoxyuridine;CldU, CAS: 50-90-8, stock 8.4g, assay 98.5%, MWt: 262.65, Formula: C9H11ClN2O5, Solubility: DMSO : ≥ 125 mg/mL (475.92 mM), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: 5-Chloro-2'-deoxyuridine, a thymine analog, is to study the potential of hypochlorous acid damage to DNA and DNA precursors.
In Vitro: When 5-Chloro-2’-deoxyuridine (ClDU) is placed into tissue culture medium, mammalian cells incorporate the analog into DNA. It is observed that 10 μM concentration of 5-Chloro-2’-deoxyuridine in the media does not alter cell division kinetics. Previously it has been shown that 5-Chloro-2’-deoxyuridine is metabolized and incorporated into DNA using antibodies that bind selectively to DNA containing halogenated bases. In the studies reported here, 5-Chloro-2’-deoxyuridine is more similar to BrdU in acting as a T analog. The toxicity of 5-Chloro-2’-deoxyuridine could in part be attributed to inhibition of thymidylate synthase[1].

Name: Exo1, CAS: 75541-83-2, stock 13.1g, assay 98.4%, MWt: 273.26, Formula: C15H12FNO3, Solubility: DMSO : 25 mg/mL (91.49 mM; Need ultrasonic); H2O : < 0.1 mg/mL (insoluble), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Exo1 is a chemical inhibitor of the exocytic pathway.
In Vitro: Exo1 is a modifier of Golgi ARF1 GTPase activity. Because Exo1 affects a subset of the membrane events that are blocked by BFA, but seems to have a different protein target (and presumably has different side effects), it provides an independent means to interfere with Golgi activity. Exo1 Disrupts Vesicular Traffic from the ER to the Golgi apparatus by disrupting Golgi structures. Exo1 inhibits exocytosis with an IC50 of ~20 μM. Exo1 prevents acquisition of endoglycosidase H resistance by newly synthesized proteins such as VSVGts-GFP, transferrin, and MHC class I[1].

Name: CDDO-dhTFEA RTA dh404, CAS: 1191265-33-4, stock 2.7g, assay 98.5%, MWt: 574.72, Formula: C33H45F3N2O3, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: NF-κB;NF-κB, Target: Keap1-Nrf2;NF-κB, Biological_Activity: CDDO-dhTFEA (RTA dh404) is a synthetic oleanane triterpenoid compound which potently activates Nrf2 and inhibits the pro-inflammatory transcription factor NF-κB[1]. CDDO-dhTFEA restores hypertension (MAP), increases Nrf2 and expression of its target genes, attenuates activation of NF-κB and transforming growth factor-β pathways, and reduces glomerulosclerosis, interstitial fibrosis and inflammation in the chronic kidney disease (CKD) rats[2].

Name: Tetradecanoylcarnitine, CAS: 25597-07-3, stock 23.3g, assay 98.1%, MWt: 371.55, Formula: C21H41NO4, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: Tetradecanoylcarnitine is a human carnitine involved in β-oxidation of long-chain fatty acids.

Name: Stearoylcarnitine, CAS: 25597-09-5, stock 38.4g, assay 98.2%, MWt: 427.66, Formula: C25H49NO4, Solubility: DMSO : < 1 mg/mL (insoluble or slightly soluble), Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: Stearoylcarnitine is a fatty ester lipid molecule.

Name: Phosphorylcholine Phosphocholine, CAS: 3616-04-4, stock 21.9g, assay 98.8%, MWt: 184.15, Formula: C5H15NO4P, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Phosphatidylcholine is the main phospholipid component in eukaryotic biofilms. Phosphatidylcholine exists in commensal or pathogenic bacteria associated with eukaryotes in prokaryotes. Phosphorylcholine exhibits a surprising range of immunomodulatory properties[1].

Name: N-Oleoyl glycine, CAS: 2601-90-3, stock 26.8g, assay 98.1%, MWt: 339.51, Formula: C20H37NO3, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: PI3K/Akt/mTOR;GPCR/G Protein;Metabolic Enzyme/Protease;Neuronal Signaling, Target: Akt;Cannabinoid Receptor;Endogenous Metabolite;Cannabinoid Receptor, Biological_Activity: N-Oleoyl glycine is a lipoamino acid, which stimulates adipogenesis associated with activation of CB1 receptor and Akt signaling pathway in 3T3-L1 adipocyte.
IC50 & Target: CB1 receptor, Akt[1]
In Vitro: N-Oleoyl glycine is a lipoamino acid, which stimulates adipogenesis associated with activation of CB1 receptor and Akt signaling pathway in 3T3-L1 adipocyte. N-Oleoyl glycine (1, 5, 10, 20, 50 μM) dose- and time-dependently stimulates 3T3-L1 adipogenesis after treatment for 1-10 days via activation of CB1R. N-Oleoyl glycine also elevates Akt signaling pathway during the differentiation of 3T3-L1 adipocytes[1].

Name: Methionine sulfoxide, CAS: 62697-73-8, stock 39.9g, assay 98.8%, MWt: 165.21, Formula: C5H11NO3S, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: Methionine sulfoxide is an oxidation product of methionine with reactive oxygen species and can be regarded as a biomarker of oxidative stress in vivo.

Name: 3-Hydroxyvaleric acid, CAS: 10237-77-1, stock 20g, assay 98.1%, MWt: 118.13, Formula: C5H10O3, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: 3-Hydroxyvaleric acid is a 5-carbon ketone body. 3-Hydroxyvaleric acid is anaplerotic, meaning it can refill the pool of TCA cycle intermediates.

Name: Hydroxyphenylacetylglycine, CAS: 28116-23-6, stock 31.9g, assay 98.5%, MWt: 209.20, Formula: C10H11NO4, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: Hydroxyphenylacetylglycine is an acyl glycine, and an endogenous human metabolite.
In Vitro: Hydroxyphenylacetylglycine (4-Hydroxyphenylacetylglycine) is an acyl glycine, and an endogenous human metabolite[1].

Name: Glutarylcarnitine, CAS: 102636-82-8, stock 19.5g, assay 98.7%, MWt: 275.30, Formula: C12H21NO6, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: Glutarylcarnitine is the diagnostic metabolite for malonic aciduria and glutaric aciduria type I monitored in most tandem mass spectrometry newborn screening programmes.
In Vitro: Malonylcarnitine and Glutarylcarnitine are important diagnostic metabolites in the screening of dried blood spots by tandem mass spectrometry[1].

Name: Ursocholic acid, CAS: 2955-27-3, stock 10g, assay 98.6%, MWt: 408.57, Formula: C24H40O5, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: Ursocholic acid, a bile acid found predominantly in bile of mammals, is transformed into deoxycholic acid by the intestinal microflora in mice. Ursodeoxycholic acid is an inhibitor of 7α-hydroxysteroid dehydrogenase and hepatocyte nuclear factor 1α[1].
IC50 & Target: 7α-hydroxysteroid dehydrogenase[1], hepatocyte nuclear factor 1α[2].

Name: Allotetrahydrocortisol 5a-Tetrahydrocortisol, CAS: 302-91-0, stock 18.6g, assay 98.7%, MWt: 366.49, Formula: C21H34O5, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: Allotetrahydrocortisol (5a-Tetrahydrocortisol) is a metabolite of Cortisol. Cortisol is the main glucocorticoid in human. It is produced in adrenal cortex and plays a crucial role in many physiological processes[1][2].
In Vitro: Allotetrahydrocortisol (5a-Tetrahydrocortisol) is a natural C21 steroid of animal origin, and has the axial configuration of its 3-hydroxyl group[1].

Name: Asymmetric dimethylarginine, CAS: 30315-93-6, stock 8.2g, assay 98.8%, MWt: 202.25, Formula: C8H18N4O2, Solubility: H2O : 100 mg/mL (494.44 mM; adjust pH to 2-3 with HCl), Clinical_Informat: No Development Reported, Pathway: Immunology/Inflammation;Metabolic Enzyme/Protease, Target: NO Synthase;Endogenous Metabolite, Biological_Activity: Asymmetric dimethylarginine is an endogenous inhibitor of nitric oxide synthase (NOS), and functions as a marker of endothelial dysfunction in a number of pathological states.
IC50 & Target: Nitric oxide synthase[1]
In Vitro: Asymmetric dimethylarginine is an endogenous inhibitor of nitric oxide synthase (NOS), and functions as a marker of endothelial dysfunction in a number of pathological states. Asymmetric dimethylarginine (ADMA) is elevated in HIV-1 infection[1].

Name: Cholesteryl oleate, CAS: 303-43-5, stock 3.2g, assay 98.3%, MWt: 651.10, Formula: C45H78O2, Solubility: DMS : 5.2 mg/mL (7.99 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: Cholesteryl oleate is a cholesteryl ester.

Name: Hydroxyphenyllactic acid, CAS: 306-23-0, stock 25.1g, assay 98.7%, MWt: 182.17, Formula: C9H10O4, Solubility: DMSO : 125 mg/mL (686.17 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Anti-infection;Metabolic Enzyme/Protease, Target: Fungal;Endogenous Metabolite, Biological_Activity: Hydroxyphenyllactic acid is an antifungal metabolite.
In Vitro: Hydroxyphenyllactic acid (4-hydroxyphenyllactic acid) is an antifungal metabolite[1].

Name: Monoisobutyl phthalic acid, CAS: 30833-53-5, stock 13.7g, assay 98.1%, MWt: 222.24, Formula: C12H14O4, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: Monoisobutyl phthalic acid is a phthalate metabolite that is in human semen and in meconium.
In Vitro: Monoisobutyl phthalic acid (Monoisobutyl phthalate) is a phthalate metabolite that is in human semen and in meconium[1].

Name: Urocanic acid, CAS: 104-98-3, stock 30.9g, assay 98.1%, MWt: 138.12, Formula: C6H6N2O2, Solubility: H2O : 2 mg/mL (14.48 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: Urocanic acid, produced in the upper layers of mammalian skin, is a major absorber of ultraviolet radiation (UVR).
In Vitro: Urocanic acid (UCA) is formed in the upper layers of the epidermis where filaggrin, a histidine-rich filamentous protein produced after caspase-14 cleavage of profilaggrin, is broken down by proteinases into component amino acids[1].

Name: Isovalerylcarnitine, CAS: 31023-24-2, stock 5.4g, assay 98.6%, MWt: 245.32, Formula: C12H23NO4, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: Isovalerylcarnitine is a product of the catabolism of L-leucine. It increases calpain activity.

Name: 1-Arachidoyl-sn-glycero-3-phosphocholine, CAS: 108341-80-6, stock 28.4g, assay 99%, MWt: 551.74, Formula: C28H58NO7P, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: 1-Arachidoyl-sn-glycero-3-phosphocholine is a lysophospholipid (LyP).

Name: Maltotriose, CAS: 1109-28-0, stock 23.6g, assay 98.4%, MWt: 504.44, Formula: C18H32O16, Solubility: H2O : ≥ 150 mg/mL (297.36 mM), Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: Maltotriose is a ligosaccharide metabolite found in human urine.

Name: Hydroxypyruvic acid, CAS: 1113-60-6, stock 30.8g, assay 98.7%, MWt: 104.06, Formula: C3H4O4, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: Hydroxypyruvic acid is an intermediate in the metabolism of Glycine, serine and threonine. It is a substrate for Serine--pyruvate aminotransferase and Glyoxylate reductase/hydroxypyruvate reductase.

Name: Orotidine, CAS: 314-50-1, stock 23.5g, assay 98.1%, MWt: 288.21, Formula: C10H12N2O8, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: Orotidine is an intermediate in pyrimidine nucleotide biosynthesis in RNA and DNA, and plays a crucial role in contemporary biology.

Name: Oxoadipic acid, CAS: 3184-35-8, stock 25.3g, assay 98.6%, MWt: 160.12, Formula: C6H8O5, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: Oxoadipic acid is a key metabolite of the essential amino acids tryptophan and lysine.

Name: Stearoylethanolamide, CAS: 111-57-9, stock 21.5g, assay 98.2%, MWt: 327.55, Formula: C20H41NO2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: Stearoylethanolamide is an endocannabinoid-like compound with pro-apoptotic activity.
In Vitro: Stearoylethanolamide (SEA) is present in human, rat and mouse brain in amounts comparable with those of the endocannabinoid anandamide (arachidonoylethanolamide; AEA). Stearoylethanolamide is an endocannabinoid-like compound with pro-apoptotic activity, which is regulated by NO in a way opposite to that reported for AEA[1].

Name: Tiglyl carnitine, CAS: 64681-36-3, stock 20.3g, assay 98%, MWt: 243.30, Formula: C12H21NO4, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: Tiglyl carnitine is found to be associated with celiac disease and mitochondrial acetoacetyl-CoA thiolase (T2) deficiency.

Name: Elaidic acid, CAS: 112-79-8, stock 9.3g, assay 98.7%, MWt: 282.46, Formula: C18H34O2, Solubility: DMSO : 13.5 mg/mL (47.79 mM; Need ultrasonic); H2O : < 0.1 mg/mL (insoluble), Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: Elaidic acid is the major trans fat found in hydrogenated vegetable oils and can be used as a pharmaceutical solvent.

Name: 21-Hydroxypregnenolone, CAS: 1164-98-3, stock 3.5g, assay 98.4%, MWt: 332.48, Formula: C21H32O3, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: 21-Hydroxypregnenolone is an essential intermediate in corticosterone synthesis.

Name: 3-Methylcrotonylglycine, CAS: 33008-07-0, stock 37.9g, assay 98.8%, MWt: 157.17, Formula: C7H11NO3, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: 3-Methylcrotonylglycine is an acyl glycine, a normal amino acid metabolite found in urine.

Name: p-Synephrine, CAS: 614-35-7, stock 33.2g, assay 98.6%, MWt: 167.21, Formula: C9H13NO2, Solubility: H2O : 2 mg/mL (11.96 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: p-Synephrine is an organic compound, found in multiple biofluids, such as urine and blood.

Name: Delta-Tocopherol, CAS: 119-13-1, stock 29.4g, assay 98.4%, MWt: 402.65, Formula: C27H46O2, Solubility: DMSO : 125 mg/mL (310.44 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: Delta-Tocopherol is an isomer of Vitamin E.

Name: p-Hydroxymandelic acid, CAS: 1198-84-1, stock 32.8g, assay 98.3%, MWt: 168.15, Formula: C8H8O4, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: p-Hydroxymandelic acid is a valuable aromatic fine chemical and widely used for production of pharmaceuticals and food additives.
In Vitro: p-Hydroxymandelic acid (4-Hydroxymandelic acid; 4-HMA) is widely used in production of aromatic drugs and flavors. It is employed for the preparation of 4-hydroxyphenylacetic acid, which is the synthetic precursor of selective β1-receptor antagonist drug atenolol. p-Hydroxymandelic acid can conjugate cytotoxic drug and enzyme substrate, and such a p-Hydroxymandelic acid based adaptor system showed promising application in the targeting drug delivery system[1].

Name: Hydroxycotinine, CAS: 34834-67-8, stock 36.4g, assay 98.1%, MWt: 192.21, Formula: C10H12N2O2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: Hydroxycotinine is the main nicotine metabolite detected in smokers urine.

Name: 3-Hydroxyisovaleric acid, CAS: 625-08-1, stock 32.9g, assay 98.3%, MWt: 118.13, Formula: C5H10O3, Solubility: DMSO : 50 mg/mL (423.26 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: 3-Hydroxyisovaleric acid is a normal human metabolite excreted in the urine.

Name: 3-Methylglutaric acid, CAS: 626-51-7, stock 18.7g, assay 98.3%, MWt: 146.14, Formula: C6H10O4, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: 3-Methylglutaric acid is a leucine metabolite.

Name: 3-Hydroxyglutaric acid, CAS: 638-18-6, stock 26.8g, assay 98.6%, MWt: 148.11, Formula: C5H8O5, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: 3-Hydroxyglutaric acid is a glutaric acid derivative.

Name: Imidazoleacetic acid Imidazolyl-4-acetic acid, CAS: 645-65-8, stock 5.4g, assay 98.9%, MWt: 126.11, Formula: C5H6N2O2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: Imidazoleacetic acid is an endogenous ligand that stimulates imidazole receptors.

Name: Deoxycorticosterone, CAS: 64-85-7, stock 22g, assay 98.1%, MWt: 330.46, Formula: C21H30O3, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: Deoxycorticosterone is a steroid hormone produced by the adrenal gland that possesses mineralocorticoid activity and acts as an aldosterone precursor.

Name: trans-trans-Muconic acid, CAS: 3588-17-8, stock 27.2g, assay 98.9%, MWt: 142.11, Formula: C6H6O4, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: trans-trans-Muconic acid is a urinary metabolite of benzene and has been used as a biomarker of exposure to benzene in human.

Name: Angiotensin III, CAS: 12687-51-3, stock 1.6g, assay 98.5%, MWt: 931.11, Formula: N/A, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein;Metabolic Enzyme/Protease, Target: Angiotensin Receptor;Endogenous Metabolite, Biological_Activity: Angiotensin III is an angiotensin 1 (AT1) and AT2 receptor agonist.

Name: Epipregnanolone, CAS: 128-21-2, stock 30.2g, assay 99%, MWt: 318.49, Formula: C21H34O2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: Epipregnanolone is an endogenous neurosteroid that has anesthetic, hypnotic, and sedative properties.

Name: 3-Nitro-L-tyrosine, CAS: 621-44-3, stock 37.9g, assay 98.6%, MWt: 226.19, Formula: C9H10N2O5, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: 3-Nitro-L-tyrosine is a biomarker of nitrogen free radical species modified proteins in systemic autoimmunogenic conditions.

Name: L-2-Hydroxyglutaric acid (S)-2-Hydroxyglutaric acid, CAS: 13095-48-2, stock 21.8g, assay 98.5%, MWt: 148.11, Formula: C5H8O5, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: L-2-Hydroxyglutaric acid is an epigenetic modifier and putative oncometabolite in renal cancer.

Name: 2-Methoxyestrone, CAS: 362-08-3, stock 23.9g, assay 98.3%, MWt: 300.39, Formula: C19H24O3, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: 2-Methoxyestrone is a methoxylated catechol estrogen and metabolite of estrone, with a pKa of 10.81.

Name: Uridine diphosphate glucose, CAS: 133-89-1, stock 37.4g, assay 98.4%, MWt: 566.30, Formula: C15H24N2O17P2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: Uridine diphosphate glucose is an important intermediate in several different metabolic pathways and biosynthetic reactions, including the biosynthesis of polysaccharides such as starch and glycogen, lipopolysaccharides, and glycosphingolipids.

Name: N8-Acetylspermidine dihydrochloride, CAS: 34450-15-2, stock 28.9g, assay 98.4%, MWt: 260.20, Formula: C9H23Cl2N3O, Solubility: H2O : 50 mg/mL (192.16 mM; Need ultrasonic); DMSO : 100 mg/mL (384.32 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: N8-Acetylspermidine dihydrochloride is a polyamine.

Name: Beta-Cortol, CAS: 667-65-2, stock 1.2g, assay 98.5%, MWt: 368.51, Formula: C21H36O5, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: Beta-Cortol is an androgen metabolite present in adults.

Name: 5-Methyltetrahydrofolic acid 5-Methyl THF, CAS: 134-35-0, stock 11.6g, assay 98.3%, MWt: 459.46, Formula: C20H25N7O6, Solubility: DMSO : 83.33 mg/mL (181.37 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: 5-Methyltetrahydrofolic acid (5-Methyl THF) is a biologically active form of folic acid. 5-Methyltetrahydrofolic acid is a methylated derivate of tetrahydrofolate. 5-Methyltetrahydrofolic acid is the predominant natural dietary folate and the principal form of folate in plasma and cerebrospinal fluid[1].

Name: 5,6-Dihydrouridine, CAS: 5627-05-4, stock 10.7g, assay 98.5%, MWt: 247.21, Formula: C8H13N3O6, Solubility: DMSO : ≥ 125 mg/mL (505.64 mM), Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: 5,6-Dihydrouridine is a modified base found in conserved positions in the D-loop of tRNA in Bacteria, Eukaryota, and some Archaea.
In Vitro: 5,6-Dihydrouridine (Dihydrouridine) is one of the posttranscriptionally modified nucleosides. It is a product of the reduction of uridine (U), and can be further modified to 5-methyldihydrouridine (m5D). 5,6-Dihydrouridine is commonly present in the tRNA from Bacteria, Eukaryota, and some Archaea. It is identified in six positions in the “D-loop” of the tRNA (16, 17, 20a, 20b) and in position 47 in the variable loop[1].

Name: Oleoylcarnitine, CAS: 38677-66-6, stock 36.7g, assay 98.7%, MWt: 425.64, Formula: C25H47NO4, Solubility: , Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity:

Name: 8-Hydroxyguanosine, CAS: 3868-31-3, stock 34.4g, assay 99%, MWt: 299.24, Formula: C10H13N5O6, Solubility: DMSO : ≥ 250 mg/mL (835.45 mM), Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: 8-Hydroxyguanosine is a systematic marker of oxidative stress and a marker of hydroxyl radical damage to RNA.

Name: 3-Hydroxycapric acid, CAS: 14292-26-3, stock 27g, assay 98.3%, MWt: 188.26, Formula: C10H20O3, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: 3-Hydroxycapric acid is an inhibitor for mitotic progression.
In Vitro: 3-Hydroxycapric acid (Myrmicacin) inhibits mitotic progression at any stage even after metaphase[1].

Name: Nepsilon-Acetyl-L-lysine, CAS: 692-04-6, stock 26.7g, assay 98.9%, MWt: 188.22, Formula: C8H16N2O3, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: Nepsilon-Acetyl-L-lysine is a derivative of the amino acid lysine.

Name: Valerylcarnitine, CAS: 40225-14-7, stock 16.9g, assay 98.7%, MWt: 245.32, Formula: C12H23NO4, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: Valerylcarnitine is an endogenous metabolite, belonging to the short-chain acylcarnitines.

Name: Dihydrofolic acid, CAS: 4033-27-6, stock 17.2g, assay 98.1%, MWt: 443.41, Formula: C19H21N7O6, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: Dihydrofolic acid is a folic acid derivative acted upon by dihydrofolate reductase to produce tetrahydrofolic acid.

Name: Pseudouridine, CAS: 1445-07-4, stock 12.3g, assay 98.8%, MWt: 244.20, Formula: C9H12N2O6, Solubility: DMSO : 125 mg/mL (511.88 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: Pseudouridine, the most abundant modified nucleoside in non-coding RNAs, enhances the function of transfer RNA and ribosomal RNA by stabilizing RNA structure.

Name: Biotin sulfone, CAS: 40720-05-6, stock 4.6g, assay 98.4%, MWt: 276.31, Formula: C10H16N2O5S, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: Biotin sulfone is first isolated as a natural metabolite of biotin.

Name: trans-Vaccenic acid, CAS: 693-72-1, stock 18.1g, assay 98.7%, MWt: 282.46, Formula: C18H34O2, Solubility: DMSO : ≥ 250 mg/mL (885.08 mM), Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: trans-Vaccenic acid is a precursor for the synthesis of saturated fatty acid in the rumen and of conjugated linoleic acid (CLA) at the tissue level.

Name: 3-Methyl-2-oxovaleric acid, CAS: 1460-34-0, stock 11g, assay 98.5%, MWt: 130.14, Formula: C6H10O3, Solubility: DMSO : 130 mg/mL (998.92 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: 3-Methyl-2-oxovaleric acid is a neurotoxin, an acidogen, and a metabotoxin, and also an abnormal metabolite that arises from the incomplete breakdown of branched-chain amino acids.

Name: Guanosine 5'-diphosphate, CAS: 146-91-8, stock 5.4g, assay 98.1%, MWt: 443.20, Formula: C10H15N5O11P2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: Guanosine 5'-diphosphate is a nucleoside diphosphate. Guanosine 5'-diphosphate is a potential iron mobilizer, which prevents the hepcidin-ferroportin interaction and modulating the interleukin-6 (IL-6)/stat-3 pathway[1].

Name: Pi-Methylimidazoleacetic acid, CAS: 4200-48-0, stock 22.3g, assay 98.4%, MWt: 140.14, Formula: C6H8N2O2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: Pi-Methylimidazoleacetic acid is a potential neurotoxin.

Name: Mevalonic acid, CAS: 150-97-0, stock 29.7g, assay 98.3%, MWt: 148.16, Formula: C6H12O4, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: Mevalonic acid, a precursor in the mevalonate pathway, is essential for cell growth and proliferation[1][2].

Name: 3-Methyladipic acid, CAS: 3058-01-3, stock 31.1g, assay 98.3%, MWt: 160.17, Formula: C7H12O4, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: 3-Methyladipic acid is the final metabolite in the ω-oxidation pathway.

Name: Leucyl-phenylalanine, CAS: 3063-05-6, stock 1.6g, assay 98.2%, MWt: 278.35, Formula: C15H22N2O3, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: Leucyl-phenylalanine belongs to the class of organic compounds known as dipeptides.

Name: 7-Dehydrocholesterol, CAS: 434-16-2, stock 38.1g, assay 98.2%, MWt: 384.64, Formula: C27H44O, Solubility: Ethanol : 16.67 mg/mL (43.34 mM; Need ultrasonic); DMSO : < 1 mg/mL (insoluble or slightly soluble), Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: 7-Dehydrocholesterol is biosynthetic precursor of cholesterol and vitamin D3.
In Vitro: 7-Dehydrocholesterol is a biosynthetic precursor of cholesterol and vitamin D3. 7-Dehydrocholesterol is present in relatively high concentration in skin where it is converted to pre-vitamin D3 upon UV irradiation and where it is also exposed to exogenous radical sources and oxygen[1].

Name: 1,5-Anhydrosorbitol, CAS: 154-58-5, stock 28.8g, assay 98.6%, MWt: 164.16, Formula: C6H12O5, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: 1,5-Anhydrosorbitol is a short-term marker for glycemic control.
In Vitro: 1,5-Anhydrosorbitol can indicate that metabolite score marks individuals at higher risk for developing diabetes or insulin resistance and thereby coronary heart disease(CHD)[1].

Name: Thiamine pyrophosphate, CAS: 154-87-0, stock 24g, assay 98%, MWt: 460.77, Formula: C12H19ClN4O7P2S, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: Thiamine pyrophosphate is the coenzyme form of Vitamin B1 and is a required intermediate in the pyruvate dehydrogenase complex and the ketoglutarate dehydrogenase complex.

Name: Argininic acid, CAS: 157-07-3, stock 10.3g, assay 98.8%, MWt: 175.19, Formula: C6H13N3O3, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: Argininic acid is an α-amino acid that is used in the biosynthesis of proteins.
In Vitro: Argininic acid (Arginine) contains an α-amino group, an α-carboxylic acid group, and a side chain consisting of a 3-carbon aliphatic straight chain ending in a guanidino group. In humans, arginine is classified as a semiessential or conditionally essential amino acid, depending on the developmental stage and health status of the individual.

Name: 1-Methyl-6-oxo-1,6-dihydropyridine-3-carboxamide, CAS: 701-44-0, stock 38.8g, assay 98.1%, MWt: 152.15, Formula: C7H8N2O2, Solubility: DMSO : 62.5 mg/mL (410.78 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: 1-Methyl-6-oxo-1,6-dihydropyridine-3-carboxamide is one of the end products of nicotinamide-adenine dinucleotide (NAD) degradation.

Name: Homogentisic acid, CAS: 451-13-8, stock 5.1g, assay 98.7%, MWt: 168.15, Formula: C8H8O4, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: Homogentisic acid is a specific metabolite in urine and serum, which is used for diagnosis of alkaptonuria.

Name: N-Acetylornithine, CAS: 6205-08-9, stock 38.1g, assay 98.4%, MWt: 174.20, Formula: C7H14N2O3, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: N-Acetylornithine is an intermediate in the enzymatic biosynthesis of the amino acid L-arginine from L-glutamate.

Name: Ureidopropionic acid, CAS: 462-88-4, stock 0.7g, assay 98.5%, MWt: 132.12, Formula: C4H8N2O3, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: Ureidopropionic acid is an intermediate in the metabolism of uracil.

Name: 1-Methyladenosine, CAS: 15763-06-1, stock 31.3g, assay 98.2%, MWt: 281.27, Formula: C11H15N5O4, Solubility: DMSO : 150 mg/mL (533.30 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: 1-Methyladenosine is an RNA modification originating essentially from two different reaction types, one catalyzed by enzymes and the other the result of the reaction of RNA with certain alkylating agents.

Name: 4-Guanidinobutanoic acid, CAS: 463-00-3, stock 10.8g, assay 98.1%, MWt: 145.16, Formula: C5H11N3O2, Solubility: H2O : 25 mg/mL (172.22 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: 4-Guanidinobutanoic acid is a normal metabolite present in low concentrations.

Name: 3-Hydroxyhippuric acid, CAS: 1637-75-8, stock 17.1g, assay 98.9%, MWt: 195.17, Formula: C9H9NO4, Solubility: DMSO : 83.33 mg/mL (426.96 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: 3-Hydroxyhippuric acid is an acyl glycine. Acyl glycines are normally minor metabolites of fatty acids.

Name: 8-Dehydrocholesterol, CAS: 70741-38-7, stock 31.3g, assay 98.8%, MWt: 384.64, Formula: C27H44O, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: 8-Dehydrocholesterol elevated concentration is one of the diagnostic biochemical hallmarks of classical Smith-Lemli-Opitz syndrome (SLOS).

Name: 1,2-Dipalmitoyl-sn-glycerol 3-phosphate, CAS: 7091-44-3, stock 21.9g, assay 98.2%, MWt: 648.89, Formula: C35H69O8P, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: 1,2-Dipalmitoyl-sn-glycerol 3-phosphate is a phosphatidic acid.

Name: 5'-Deoxyadenosine, CAS: 4754-39-6, stock 22.6g, assay 98.8%, MWt: 251.24, Formula: C10H13N5O3, Solubility: DMSO : 125 mg/mL (497.53 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: 5'-Deoxyadenosine is an oxidized nucleoside found in the urine of normal subjects.

Name: Citraconic acid, CAS: 498-23-7, stock 1.4g, assay 98.1%, MWt: 130.10, Formula: C5H6O4, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: Citraconic acid belongs to the class of organic compounds known as methyl-branched fatty acids.

Name: Propionylcarnitine, CAS: 17298-37-2, stock 30.5g, assay 98.4%, MWt: 217.26, Formula: C10H19NO4, Solubility: DMSO : 125 mg/mL (575.35 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: Propionylcarnitine is a propionyl ester of L-carnitine.

Name: Hexacosanoic acid, CAS: 506-46-7, stock 22.7g, assay 99%, MWt: 396.69, Formula: C26H52O2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: Hexacosanoic acid is a long-chain fatty acid related to various diseases such as adrenoleukodystrophy (ALD), adrenomyeloneuropathy (AMN) and atherosclerosis.

Name: Ethyl glucuronide, CAS: 17685-04-0, stock 22.2g, assay 98.8%, MWt: 222.19, Formula: C8H14O7, Solubility: , Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity:

Name: Paullinic acid, CAS: 17735-94-3, stock 4.9g, assay 98.2%, MWt: 310.51, Formula: C20H38O2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: Paullinic acid is a long-chain fatty acid that has been detected in multiple biofluids, such as blood and urine.

Name: (S)-3,4-Dihydroxybutyric acid, CAS: 51267-44-8, stock 26.7g, assay 98.7%, MWt: 120.10, Formula: C4H8O4, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: (S)-3,4-Dihydroxybutyric acid is a normal human urinary metabolite that is excreted in increased concentration in patients with succinic semialdehyde dehydrogenase (SSADH) deficiency.

Name: 1-Methyladenine, CAS: 5142-22-3, stock 3.9g, assay 98.3%, MWt: 149.15, Formula: C6H7N5, Solubility: H2O : 5.2 mg/mL (34.86 mM; ultrasonic and warming and heat to 80°C), Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: 1-Methyladenine is a product of alkylation damage in DNA which can be repaired by damage reversal by oxidative demethylation.

Name: Alloepipregnanolone, CAS: 516-55-2, stock 17.3g, assay 98.7%, MWt: 318.49, Formula: C21H34O2, Solubility: DMSO : 3.33 mg/mL (10.46 mM; Need ultrasonic); Ethanol : 10 mg/mL (31.40 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: Alloepipregnanolone, a pregnane with anesthetic, hypnotic, and sedative properties, interferes with the development of rapid tolerance to the anxiolytic effect of ethanol.
In Vivo: On day 2, pretreatment with a 0.20 mg/kg dose of Alloepipregnanolone blocks the development of rapid tolerance to the anxiolytic effect of ethanol. However, there is a significant decrease in the anxiolytic effect in the control groups that received ethanol on both days (EE), suggesting that the 1.5 g/kg dose of ethanol results in rapid tolerance. The post hoc analysis confirms that the 0.20 mg/kg pretreatment with Alloepipregnanolone blocks the rapid tolerance compared to the control groups, although the 0.10 mg/kg dose only partially blocks the development of such tolerance. However, the 0.05 mg/kg dose has no effect on the development of rapid tolerance to ethanol[1].

Name: 2-Oxovaleric acid, CAS: 1821-02-9, stock 9.9g, assay 98.1%, MWt: 116.12, Formula: C5H8O3, Solubility: DMSO : ≥ 250 mg/mL (2152.95 mM), Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: 2-Oxovaleric acid is a keto acid that is found in human blood.

Name: Indolelactic acid, CAS: 1821-52-9, stock 33.5g, assay 98.3%, MWt: 205.21, Formula: C11H11NO3, Solubility: DMSO : 86.67 mg/mL (422.35 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: Indolelactic acid is a tryptophan (Trp) catabolite in Azotobacter vinelandii cultures.

Name: N-Acetylputrescine hydrochloride, CAS: 18233-70-0, stock 12.7g, assay 98.9%, MWt: 166.65, Formula: C6H15ClN2O, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: N-Acetylputrescine hydrochloride is a putrescine derivative.

Name: 2-Hydroxyadipic acid, CAS: 18294-85-4, stock 18.4g, assay 98.7%, MWt: 162.14, Formula: C6H10O5, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: 2-Hydroxyadipic acid is an organic acid, formed by the reduction of 2-ketoadipic acid.

Name: Aldosterone, CAS: 52-39-1, stock 29.6g, assay 98.8%, MWt: 360.44, Formula: C21H28O5, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: Aldosterone is the primary mineralocorticoid. Aldosterone is a steroid hormone, and it is synthesized and secreted in response to renin-angiotensin system activation (RAS) or high dietary potassium by the zona glomerulosa (ZG) of the adrenal cortex. Aldosterone activity is dependent by the binding and activation of the cytoplasmic/nuclear mineralocorticoid receptor (MR) at cellular level[1][2].
In Vitro: Aldosterone (1-1000 nM; 24 hours) inhibits interleukin-1β-stimulated nitrite production by vascular smooth muscle cells in a dose-dependent manner[3].
In Vivo: Aldosterone (1 mg/Kg+1% NaCl; i.h.; once daily for 3 weeks) significantly increases systolic blood pressure (SBP), diastolic blood pressure (DBP), left ventricular systolic pressure (LVSP) and left ventricular end-diastolic pressure (LVEDP)[4]. 
Aldosterone (0.72 mg/kg/day; 14 days) causes a small increase ( 14 mmHg) in blood pressure in male mice[5].

Name: 3b-Hydroxy-5-cholenoic acid, CAS: 5255-17-4, stock 37.9g, assay 98.4%, MWt: 374.56, Formula: C24H38O3, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: 3b-Hydroxy-5-cholenoic acid is a monohydroxy bile acid of endogenous origin and could be found in children with the syndrome of hepatic ductular hypoplasia.

Name: 3-Hydroxydodecanoic acid, CAS: 1883-13-2, stock 25.9g, assay 98.7%, MWt: 216.32, Formula: C12H24O3, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: 3-Hydroxydodecanoic acid is a medium-chain fatty acid associated with fatty acid metabolic disorders.

Name: 10Z-Nonadecenoic acid, CAS: 73033-09-7, stock 11.5g, assay 98.7%, MWt: 296.49, Formula: C19H36O2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: 10Z-Nonadecenoic acid is a kind of long-chain fatty acid with anti-tumor activity.
In Vitro: 10Z-Nonadecenoic acid is a kind of long-chain fatty acid with anti-tumor activity[1]. 10Z-Nonadecenoic acid could also inhibit p53 activity[2].

Name: (R)-3-Hydroxyisobutyric acid, CAS: 1910-47-0, stock 22.7g, assay 99%, MWt: 104.10, Formula: C4H8O3, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: (R)-3-Hydroxyisobutyric acid is an intermediate in the pathways of l-valine and thymine and plays an important role in the diagnosis of the very rare inherited metabolic diseases 3-hydroxyisobutyric aciduria and methylmalonic semialdehyde dehydrogenase deficiency.

Name: Tetrahydrocortisone, CAS: 53-05-4, stock 35.8g, assay 98.2%, MWt: 364.48, Formula: C21H32O5, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: Tetrahydrocortisone is a stress-induced hormone. Tetrahydrocortisone is also a urinary metabolite of Cortisone derived from the reduction of Cortisone by 5-reductase[1].

Name: NADP, CAS: 53-59-8, stock 36.4g, assay 98.8%, MWt: 744.41, Formula: C21H29N7O17P3, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: NADP is nicotinamide adenine dinucleotide phosphate, acting as a key cofactor for electron transfer in the metabolism of all organisms, being alternately oxidized (NADP+) and reduced (NADPH).

Name: Aminoadipic acid, CAS: 542-32-5, stock 37.1g, assay 98.5%, MWt: 161.16, Formula: C6H11NO4, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: Aminoadipic acid is an intermediate in the metabolism of lysine and saccharopine.

Name: Turanose, CAS: 547-25-1, stock 34.2g, assay 98.6%, MWt: 342.30, Formula: C12H22O11, Solubility: H2O : ≥ 130 mg/mL (379.78 mM), Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: Turanose is a reducing disaccharide.

Name: LysoPC(14:0/0:0), CAS: 20559-16-4, stock 11g, assay 98.7%, MWt: 467.58, Formula: C22H46NO7P, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: LysoPC(14:0/0:0) is a lysophospholipid (LyP). It is a monoglycerophospholipid in which a phosphorylcholine moiety occupies a glycerol substitution site.

Name: 8-Hydroxyguanine, CAS: 5614-64-2, stock 6.9g, assay 98.5%, MWt: 167.13, Formula: C5H5N5O2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: 8-Hydroxyguanine is a major pre-mutagenic lesion generated from reactive oxygen species. It causes G-T and A-C substitutions.

Name: (S)-3-Hydroxyisobutyric acid, CAS: 2068-83-9, stock 28.8g, assay 98%, 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-Hydroxyisobutyric acid is an important interorgan metabolite, an intermediate in the pathways of l-valine and thymine and a good gluconeogenic substrate.

Name: Glycerol 3-phosphate, CAS: 17989-41-2, stock 14g, assay 98.1%, MWt: 172.07, Formula: C3H9O6P, Solubility: H2O : ≥ 50 mg/mL (290.58 mM), Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: Glycerol 3-phosphate is produced by cytosolic glycerol 3-phosphate dehydrogenase pathway through the reduction of dihydroxyacetone phosphate using NADH formed during glycolysis.

Name: Trametinib GSK1120212;JTP-74057, CAS: 871700-17-3, stock 16.6g, assay 98.9%, MWt: 615.39, Formula: C26H23FIN5O4, Solubility: DMSO : 33.33 mg/mL (54.16 mM; Need ultrasonic), Clinical_Informat: Launched, Pathway: Apoptosis;Autophagy;MAPK/ERK Pathway, Target: Apoptosis;Autophagy;MEK, Biological_Activity: Trametinib (GSK1120212;JTP-74057) is a potent MEK inhibitor that inhibits MEK1 and MEK2 with IC50s of about 2 nM.
IC50 & Target: IC50: 2 nM (MEK1/2)[1]
In Vitro: Trametinib (GSK1120212;JTP-74057) (0.1-100 nM) blocks tumor necrosis factor-α and interleukin-6 production from peripheral blood mononuclear cells (PBMCs). Trametinib (JTP-74057) inhibits the growth of 9 out of 10 human colorectal cancer cell lines, and they shows cell-cycle arrest at the G1 phase after drug tratment[1]. The combination of GSK2118436 and Trametinib (GSK1120212) effectively inhibits cell growth, decreases ERK phosphorylation, decreases cyclin D1 protein, and increases p27(kip1) protein in the resistant clones[2].
In Vivo: Adjuvant-induced arthritis (AIA) and type II collageninduced arthritis (CIA) development are suppressed almost completely by 0.1 mg/kg of Trametinib (GSK1120212;JTP-74057) or 10 mg/kg of Leflunomide[1]. Trametinib (0.3 mg/kg, 1 mg/kg, p.o.) is effective in inhibiting the HT-29 xenograft growth in a nude mouse xenograft model[2].

Name: Trametinib (DMSO solvate) GSK-1120212 (DMSO solvate);JTP-74057 (DMSO solvate), CAS: 1187431-43-1, stock 30.2g, assay 99%, MWt: 693.53, Formula: C28H29FIN5O5S, Solubility: DMSO : 69 mg/mL (99.49 mM; Need ultrasonic); H2O : < 0.1 mg/mL (insoluble), Clinical_Informat: Launched, Pathway: MAPK/ERK Pathway, Target: MEK, Biological_Activity: Trametinib DMSO solvate (GSK-1120212 (DMSO solvate);JTP-74057 (DMSO solvate)) is a potent MEK inhibitor that specifically inhibits MEK1/2, with an IC50 value of about 2 nM.
IC50 & Target: IC50: 2 nM (MEK1/2)[1]
In Vitro: In BRAF mutant SK-MEL-28 cells and KRAS mutant HCT116 cells, Trametinib (GSK1120212;JTP-74057) DMSO solvate causes dose-dependent inhibition of ERK1/2 phosphorylation as well as dose-dependent growth inhibition. In both SK-MEL-28 and HCT116 cells, Trametinib DMSO solvate inhibits 50% p-ERK1/2 at nearly equivalent concentrations (0.8 and 1.8 nM, respectively). However, as the slopes of the curves reflect, in SK-MEL-28 cells, Trametinib DMSO solvate inhibits 90% p-ERK1/2 at a lower concentration (3.4 nM) than in HCT116 (33.3 nM). Furthermore, in both cell lines, 50% growth inhibition is only achieved at concentrations Trametinib DMSO solvate that produces near complete ERK1/2 inhibition (85 and 90%, respectively)[2].
In Vivo: Trametinib (GSK1120212;JTP-74057) DMSO solvate is evaluated in vivo in an A549 (KRAS mutant cell line) xenograft model, orally dosing daily for 21 days (qd×21). In this study, near complete tumor growth inhibition is observed at 5.0 and 2.5 mg/kg [92 and 87% tumor growth inhibition (TGI), respectively] and to a lesser degree at 0.5 and 0.1 mg/kg (62 and 58% TGI). Although 5 mg/kg is the maximally tolerated dose (MTD) in this study, 3 mg/kg is the typically observed MTD. Dose-dependent antitumor activity with Trametinib DMSO solvate treatment has been similarly reported for several other KRAS and BRAF mutant tumor models[2].

Name: 25-Hydroxycholesterol, CAS: 2140-46-7, stock 37.5g, assay 98.2%, MWt: 402.65, Formula: C27H46O2, Solubility: DMSO : 5 mg/mL (12.42 mM; Need ultrasonic); Ethanol : 14.29 mg/mL (35.49 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: 25-Hydroxycholesterol is a metabolite of cholesterol that is produced and secreted by macrophages in response to Toll-like receptor (TLR) activation. 25-hydroxycholesterol is a potent (EC50≈65 nM) and selective suppressor of IgA production by B cells.
In Vitro: The synthesis of 25-hydroxycholesterol is catalyzed by the enzyme cholesterol 25-hydroxylase, which uses cholesterol and molecular oxygen as substrates and NADPH as a cofactor. 25-hydroxycholesterol is a potent bioactive lipid in the innate and adaptive immune systems[1].

Name: 5-Methylcytidine, CAS: 2140-61-6, stock 7.4g, assay 98.6%, MWt: 257.24, Formula: C10H15N3O5, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: 5-Methylcytidine is a pyrimidine nucleoside detected in multiple biofluids.

Name: 1-Methylguanosine, CAS: 2140-65-0, stock 2.4g, assay 98.7%, MWt: 297.27, Formula: C11H15N5O5, Solubility: DMSO : 125 mg/mL (420.49 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: 1-Methylguanosine is a methylated nucleoside.

Name: N2,N2-Dimethylguanosine, CAS: 2140-67-2, stock 35.9g, assay 98.8%, MWt: 311.29, Formula: C12H17N5O5, Solubility: DMSO : 15 mg/mL (48.19 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: N2,N2-Dimethylguanosine is an urinary nucleoside, a primary degradation product of tRNA.

Name: 3-Methyluridine, CAS: 2140-69-4, stock 5.2g, assay 98.3%, MWt: 258.23, Formula: C10H14N2O6, Solubility: DMSO : 160 mg/mL (619.60 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: 3-Methyluridine is a modified nucleoside of cellular RNA.

Name: RSV-IN-1, CAS: 861139-16-4, stock 11.7g, assay 98.1%, MWt: 427.48, Formula: C20H21N5O4S, Solubility: DMSO : 125 mg/mL (292.41 mM; Need ultrasonic); H2O : < 0.1 mg/mL (insoluble), Clinical_Informat: No Development Reported, Pathway: Anti-infection, Target: RSV, Biological_Activity: RSV-IN-1 is a human respiratory syncytical virus (hRSV) inhibitor, with an IC50 of 0.11 μM.
IC50 & Target: IC50: 0.11μM (hRSV)[1].
In Vitro: The concentration of P13 that reduces the number of RSV plaques in HEp-2 cells by 50% (IC50) is 0.11 μM. The concentration of P13 that reduces the viability of HEp-2 by 50% (CC50) is 310 μM. Note that some cytotoxicity of P13 observed at 500 μM might be due to DMSO solvent. Hence, the selective index (CC50/IC50) values is 2818 for P13. Note that even at the relatively high concentrations P13 does not completely block the development of RSV plaques. These escape plaques are of smaller size and of non-syncytial phenotype as compared to plaques formed in the absence of inhibitor[1].

Name: 1-Methylinosine N1-Methylinosine, CAS: 2140-73-0, stock 20.6g, assay 98.9%, MWt: 282.25, Formula: C11H14N4O5, Solubility: DMSO : 20.83 mg/mL (73.80 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Cell Cycle/DNA Damage;Metabolic Enzyme/Protease, Target: Nucleoside Antimetabolite/Analog;Endogenous Metabolite, Biological_Activity: 1-Methylinosine is a modified nucleotide found at position 37 in tRNA 3' to the anticodon of eukaryotic tRNA[1].

Name: 4-Hydroxynonenal 4-HNE, CAS: 75899-68-2, stock 22.6g, assay 98%, MWt: 156.22, Formula: C9H16O2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease;Metabolic Enzyme/Protease, Target: Aldehyde Dehydrogenase (ALDH);Endogenous Metabolite, Biological_Activity: 4-Hydroxynonenal (4-HNE) is an α,β unsaturated hydroxyalkenal and an oxidative/nitrosative stress biomarker. 4-Hydroxynonenal is a substrate and an inhibitor of acetaldehyde dehydrogenase 2 (ALDH2). 4-Hydroxynonenal can modulate a number of signaling processes mainly through forming covalent adducts with nucleophilic functional groups in proteins, nucleic acids, and membrane lipids. 4-Hydroxynonenal plays an important role in cancer through mitochondria[1][2][3].
IC50 & Target: Acetaldehyde dehydrogenase 2 (ALDH2)[1]
In Vitro: 4-Hydroxynonenal is both a substrate and an inhibitor of ALDH2; inhibition of ALDH2 by 4-Hydroxynonenal is reversible at low concentration and become irreversible when the concentration of 4-HNE reaches 10 µM[1]. 
4-Hydroxynonenal can induce antioxidant defense mechanisms to restrain its own production and to enhance the cellular protection against oxidative stress[1]. 
4-Hydroxynonenal, the product of lipid peroxidation, is mutagenic and genotoxic in viruses, bacteria and mammalian cells. It reacts with all four DNA bases but with different efficiency: G >C > A >T. 4-Hydroxynonenal-dG represents the best biomarker of the genotoxic effects of 4-Hydroxynonenal and these adducts are primarily found in nuclear DNA. A classic example of etiological relevance of 4-Hydroxynonenal-dG in human cancers is 4-Hydroxynonenal-dG induced p53 mutation. 4-Hydroxynonenal-dG adducts were preferentially formed at the third base of codon 249 in the p53 gene, causing gene mutation and affecting diverse biological processes including cell cycle arrest, apoptosis, DNA repair, and differentiation[1].
In Vivo: Following 24 h after fluid percussion injury (FPI), the mouse brain tissue is analyzed for the expression level of NADPH oxidase 1 (NOX1), inducible nitric oxide synthase (iNOS), 4-Hydroxynonenal (4-HNE. Both wild-type (Nrf2+/+) and Nrf2-deficient mice (Nrf2−/−) results in increased expression of 4-Hydroxynonenal following 15 psi injury (moderate injury) when compared to uninjured Nrf2+/+ and Nrf2−/− mice. Similar to iNOS result, in Nrf2−/− KO mice, the expression level of 4-Hydroxynonenal is significantly high when compared to corresponding injured and uninjured Nrf2+/+ WT animals[2].

Name: PD0325901 PD325901, CAS: 391210-10-9, stock 20.1g, assay 98.7%, MWt: 482.19, Formula: C16H14F3IN2O4, Solubility: DMSO : ≥ 56 mg/mL (116.14 mM), Clinical_Informat: Phase 2, Pathway: Apoptosis;Autophagy;MAPK/ERK Pathway, Target: Apoptosis;Autophagy;MEK, Biological_Activity: PD0325901 is a selective and cell permeable MEK inhibitor with an IC50 of 0.33 nM.
IC50 & Target: IC50: 0.33 nM (MEK)
In Vitro: PF0325901 shows higher permeability, and should be able to achieve higher systemic exposures than CI-1040[1]. PD0325901 is exquisitely specific and highly potent against purified MEK, revealing a Kiapp of 1 nM against activated MEK1 and MEK2. PD0325901 is roughly 500-fold more potent than CI-1040 with respect to its cellular effects on phosphorylation of ERK1 and ERK2, displaying subnanomolar activity. PD0325901 prevents the growth of melanoma cell lines. PD0325901 inhibits the growth of TPC-1 cells and K2 cells with GC50 of 11 nM and 6.3 nM, respectively. PD0325901 significantly prevents the the growth of PTC cells harboring a BRAF mutation at very low concentration (10 nM) and only moderately increases the growth of the PTC cells carrying the RET/PTC1 rearrangement at the same concentration. PD0325901 effectively inhibits the phosphorylation of ERK1/2 in multiple PTC cell lines[2].
In Vivo: PD0325901 (25 mg/kg, p.o.) inhibits phosphorylation of ERK by more than 50% at 24 hours post-dosing. The dose required to produce a 70% incidence of complete tumor responses (C26 model) is 25 mg/kg/day versus 900 mg/kg/day for PD0325901 and CI-1040, respectively. Anticancer activity of PD 0325901 has been demonstrated for a broad spectrum of human tumor xenografts. PD0325901 (20-25 mg/kg/day, p.o.) treatment in mice, shows no tumor growth inoculated with PTC cells bearing a BRAF mutation. For PTC with the RET/PTC1 rearrangement, the average tumor volume of the orthotopic tumor is decreased by 58% as compared with controls. PTC cells carrying a BRAF mutation are more sensitive to PD0325901 than are PTC cells carrying the RET/PTC1 rearrangement[2].

Name: Galactose 1-phosphate, CAS: 2255-14-3, stock 12.9g, assay 98.6%, MWt: 260.14, Formula: C6H13O9P, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: Galactose 1-phosphate is an intermediate in the galactose metabolism and nucleotide sugars.

Name: L-Hexanoylcarnitine, CAS: 22671-29-0, stock 6.9g, assay 98.4%, MWt: 259.34, Formula: C13H25NO4, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: L-Hexanoylcarnitine is an acylcarnitine and is found to be associated with celiac disease.

Name: 7-Methylguanine, CAS: 578-76-7, stock 1.5g, assay 98.8%, MWt: 165.15, Formula: C6H7N5O, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: 7-Methylguanine is a metabolite of DNA methylation. It can be generated by methylating agents, and used as a probe of protein–DNA interactions and a key component of DNA sequencing method.

Name: Nicotinuric acid, CAS: 583-08-4, stock 23.8g, assay 98.2%, MWt: 180.16, Formula: C8H8N2O3, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: Nicotinuric acid is an acyl glycine. Nicotinuric acid is a metabolite of nicotinic acid.

Name: L-Palmitoylcarnitine, CAS: 2364-67-2, stock 25.5g, assay 98.8%, MWt: 399.61, Formula: C23H45NO4, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: L-Palmitoylcarnitine is a fatty acid metabolite.

Name: Anserine, CAS: 584-85-0, stock 27.1g, assay 98.5%, MWt: 240.26, Formula: C10H16N4O3, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: Anserine is a dipeptide found in skeletal muscle of vertebrates.

Name: m-Tyramine, CAS: 588-05-6, stock 19g, assay 98.6%, MWt: 137.18, Formula: C8H11NO, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: m-Tyramine is an endogenous trace amine neuromodulator. m-Tyramine has effects on the adrenergic and dopaminergic receptor[1, 2].

Name: m-Coumaric acid, CAS: 588-30-7, stock 10.1g, assay 98.9%, MWt: 164.16, Formula: C9H8O3, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: m-Coumaric acid is a polyphenol metabolite from caffeic acid, formed by the gut microflora and the amount in human biofluids is diet-dependant.

Name: Petroselinic acid, CAS: 593-39-5, stock 27.7g, assay 98.5%, MWt: 282.46, Formula: C18H34O2, Solubility: DMSO : ≥ 100 mg/mL (354.03 mM), Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: Petroselinic acid, a positional isomer of oleic acid, is isolated from the vegetable oil of Coriandrum sativum fruits.

Name: Cholestenone, CAS: 601-57-0, stock 26.2g, assay 98.7%, MWt: 384.64, Formula: C27H44O, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: Cholestenone is the intermediate oxidation product of cholesterol.

Name: Suberylglycine, CAS: 60317-54-6, stock 39g, assay 98.7%, MWt: 231.25, Formula: C10H17NO5, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: Suberylglycine is an acyl glycine, which is a normally minor metabolite of fatty acid.

Name: Cholesteryl arachidonate, CAS: 604-34-2, stock 18.2g, assay 98.4%, MWt: 673.11, Formula: C47H76O2, Solubility: , Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity:

Name: Docosapentaenoic acid (22n-3), CAS: 24880-45-3, stock 33g, assay 98.3%, MWt: 330.50, Formula: C22H34O2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: Docosapentaenoic acid (22n-3) is a component of phospholipids found in all animal cell membranes.

Name: Guanidinosuccinic acid, CAS: 6133-30-8, stock 33.6g, assay 98.8%, MWt: 175.14, Formula: C5H9N3O4, Solubility: DMSO : 75 mg/mL (428.23 mM; Need ultrasonic); H2O : 6 mg/mL (34.26 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Guanidinosuccinic acid is a nitrogenous metabolite isolated in excess from serum and urine.
In Vivo: Guanidinosuccinic acid, a constituent of normal urine, is elevated in the urine and serum of azotemic patients[1]. Guanidinosuccinic acid (GSA), a guanidino compound found to be greatly increased in uremia, is administered by intraperitoneal (i.p.) injection to adult albino mice and to young mice 7, 14 and 21 days old. Epileptogenic and toxic properties are assessed and Guanidinosuccinic acid brain levels following i.p. injection ae determined. In adult mice, Guanidinosuccinic acid induces long-lasting generalized clonic and clonic-tonic convulsions in a dose-dependent manner with a CD50 (and 95% confidence interval) of 363 (287-458) mg/kg (n=35), and an LD50 of 579 (445-756) mg/kg. The CD50 of Guanidinosuccinic acid corresponded with a brain concentration of 56 nmol/g tissue. Electrocorticographic recording in five adult mice revealed epileptiform discharges (spikes, spike-waves, and polyspike-waves) which appeared concomitant with the convulsions, When young mice are i.p. injected with a (for adults) subconvulsive dose of Guanidinosuccinic acid (250 mg/kg), an age-dependent decrease is noted in Guanidinosuccinic acid-induced convulsions and in the resulting brain concentration[2].

Name: L-Octanoylcarnitine, CAS: 25243-95-2, stock 12.9g, assay 98.8%, MWt: 287.40, Formula: C15H29NO4, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: L-Octanoylcarnitine is the physiologically active form of octanoylcarnitine.

Name: Isobutyryl-L-carnitine, CAS: 25518-49-4, stock 39.7g, assay 98.4%, MWt: 231.29, Formula: C11H21NO4, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: Isobutyryl-L-carnitine is a product of the acyl-CoA dehydrogenases. Isobutyryl-L-carnitine is a member of the class of compounds known as acyl carnitines.

Name: Dodecanoylcarnitine, CAS: 25518-54-1, stock 39.7g, assay 98%, MWt: 343.50, Formula: C19H37NO4, Solubility: Methanol : 50 mg/mL (145.56 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: Dodecanoylcarnitine is present in fatty acid oxidation disorders such as long-chain acyl CoA dehydrogenase deficiency, carnitine palmitoyltransferase I/II deficiency, and is also associated with celiac disease.

Name: Butyrylcarnitine, CAS: 25576-40-3, stock 3g, assay 98.3%, MWt: 231.29, Formula: C11H21NO4, Solubility: H2O : ≥ 100 mg/mL (432.36 mM), Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: Butyrylcarnitine is a metabolite in plasma, acts as a biomarker to improve the diagnosis and prognosis of heart failure, and is indicative of anomalous lipid and energy metabolism.

Name: 3-Hydroxybutyric acid, CAS: 300-85-6, stock 24.2g, assay 99%, MWt: 104.10, Formula: C4H8O3, Solubility: H2O : 65 mg/mL (624.40 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: 3-Hydroxybutyric acid is a butyric acid substituted with a hydroxyl group in the beta or 3 position.

Name: 2,3-Diaminopropionic acid, CAS: 4033-39-0, stock 11g, assay 98%, MWt: 104.11, Formula: C3H8N2O2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: 2, 3-Diaminopropionic acid is a metabolite of b-oxalyl-L-a, b-diaminopropionic acid a neurotoxic amino acid (ODAP).

Name: (S)-b-aminoisobutyric acid, CAS: 4249-19-8, stock 36.2g, assay 98.9%, MWt: 103.12, Formula: C4H9NO2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: (S)-b-aminoisobutyric acid is a non-protein amino acid originating from the catabolism of thymine and valine.

Name: N-Methylhydantoin, CAS: 616-04-6, stock 18.9g, assay 98.2%, MWt: 114.10, Formula: C4H6N2O2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: N-Methylhydantoin is a product of degradation of creatinine by bacteria.

Name: 3,4-Dihydroxymandelic acid, CAS: 775-01-9, stock 23.3g, assay 98.7%, MWt: 184.15, Formula: C8H8O5, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: 3,4-Dihydroxymandelic acid is a metabolite of norepinephrine.

Name: Melanin, CAS: 8049-97-6, stock 19.2g, assay 98.5%, MWt: 318.28, Formula: C18H10N2O4, Solubility: DMSO : 20 mg/mL (62.84 mM; Need ultrasonic), Clinical_Informat: Phase 2, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: Melanin is a unique pigment with myriad functions. It is multifunctional, providing defense against environmental stresses such as ultraviolet (UV) light, oxidizing agents and ionizing radiation.
In Vitro: Melanin contributes to the ability of fungi to survive in harsh environments. In addition, it plays a role in fungal pathogenesis. Melanin is an amorphous polymer that is produced by one of two synthetic pathways. Fungi may synthesize melanin from endogenous substrate via a 1,8-dihydroxynaphthalene (DHN) intermediate. Alternatively, some fungi produce melanin from L-3,4-dihydroxyphenylalanine (L-dopa)[1].

Name: Lathosterol, CAS: 80-99-9, stock 31.4g, assay 98.7%, MWt: 386.65, Formula: C27H46O, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: Lathosterol is a cholesterol-like molecule. Serum Lathosterol concentration is an indicator of whole-body cholesterol synthesis.

Name: 4-Pyridoxic acid, CAS: 82-82-6, stock 24.5g, assay 98.7%, MWt: 183.16, Formula: C8H9NO4, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: 4-Pyridoxic acid is a catabolic product of vitamin B6 which is excreted in the urine.

Name: Stigmastanol, CAS: 83-45-4, stock 23g, assay 99%, MWt: 416.72, Formula: C29H52O, Solubility: DMSO : < 1 mg/mL (insoluble or slightly soluble), Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: Stigmastanol is a phytosterol found in a variety of plant sources.

Name: Sphingomyelin, CAS: 85187-10-6, stock 5.6g, assay 98.7%, MWt: 732.08, Formula: C41H84N2O6P, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: Sphingomyelin is a type of sphingolipid found in animal cell membranes and implicates in the regulation of trans-membrane signaling.

Name: N-Acetyl-L-aspartic acid, CAS: 997-55-7, stock 29.7g, assay 98%, MWt: 175.14, Formula: C6H9NO5, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: N-Acetyl-L-aspartic acid is a derivative of aspartic acid.

Name: 5-Hydroxydopamine hydrochloride, CAS: 5720-26-3, stock 26.5g, assay 98.5%, MWt: 205.64, Formula: C8H12ClNO3, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: 5-Hydroxydopamine is a naturally occurring amine in human urine.

Name: 4-Octyl Itaconate, CAS: 3133-16-2, stock 2g, assay 98.6%, MWt: 242.31, Formula: C13H22O4, Solubility: DMSO : ≥ 150 mg/mL (619.04 mM), Clinical_Informat: No Development Reported, Pathway: NF-κB, Target: Keap1-Nrf2, Biological_Activity: 4-Octyl Itaconate is a cell-permeable Itaconate derivative. Itaconate is an anti-inflammatory metabolite that activates Nrf2 via alkylation of KEAP1.
IC50 & Target: Nrf2[1]
In Vivo: 4-Octyl Itaconate (OI) is a cell-permeable itaconate derivative. 4-Octyl Itaconate is protective against lipopolysaccharide-induced lethality in vivo and decreases cytokine production[1].

Name: GLP-1 receptor agonist 2, CAS: 2230197-64-3, stock 11.8g, assay 98.3%, MWt: 580.05, Formula: C30H31ClFN5O4, Solubility: DMSO : ≥ 125 mg/mL (215.50 mM), Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein, Target: Glucagon Receptor, Biological_Activity: GLP-1 receptor agonist 2 is a glucagon-like peptide-1 receptor (GLP-1R) agonist.
IC50 & Target: GLP-1R[1].

Name: Glycogen, CAS: 9005-79-2, stock 0.8g, assay 98.5%, MWt: 666.57, Formula: C24H42O21, Solubility: H2O : 50 mg/mL (75.01 mM; Need ultrasonic), Clinical_Informat: Phase 4, Pathway: Metabolic Enzyme/Protease, Target: Endogenous Metabolite, Biological_Activity: Glycogen is a glycolytic intermediates and high-energy phosphates that can serve as a form of energy storage in humans, animals, fungi, and bacteria.

Name: PKC-theta inhibitor, CAS: 736048-65-0, stock 22g, assay 98.3%, MWt: 454.45, Formula: C20H25F3N6O3, Solubility: DMSO : 62.5 mg/mL (137.53 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: TGF-beta/Smad;Epigenetics, Target: PKC;PKC, Biological_Activity: PKC-theta inhibitor is a selective PKC-θinhibitor, with an IC50 of 12 nM.
IC50 & Target: IC50: 12 nM (PKC-θ)[1].

Name: V-9302, CAS: 1855871-76-9, stock 30.9g, assay 98.4%, MWt: 538.68, Formula: C34H38N2O4, Solubility: DMSO : 125 mg/mL (232.05 mM; Need ultrasonic); H2O : < 0.1 mg/mL (insoluble), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: V-9302 is a competitive antagonist of transmembrane glutamine flux. V-9302 selectively and potently targets the amino acid transporter ASCT2 (SLC1A5). V-9302 inhibits ASCT2-mediated glutamine uptake (IC50=9.6 µM) in HEK-293 cells[1].
IC50 & Target: ASCT2[1]
In Vitro: V-9302 inhibits ASCT2-mediated glutamine uptake in human cells in a concentration-dependent fashion and exhibits a 100-fold improvement in potency over gamma-L-glutamyl-p-nitroanilide[1].
In Vivo: Pharmacological blockade of ASCT2 with V-9302 results in attenuated cancer cell growth and proliferation, increases cell death, and increases oxidative stress, which collectively, contributes to anti-tumor responses in vitro and in murine models[1].

Name: H-Arg-4MβNA, CAS: 60285-94-1, stock 32.8g, assay 98.3%, MWt: 329.40, Formula: C17H23N5O2, Solubility: H2O : ≥ 125 mg/mL (379.48 mM), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: H-Arg-4MβNA is a substrate for cathepsin H, used for the detection of enzyme activity in gel electrophoresis.

Name: Stachyose tetrahydrate, CAS: 10094-58-3, stock 30.5g, assay 98.6%, MWt: 738.64, Formula: C24H50O25, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Stachyose is a prebiotic, a non-reducing tetrasaccharide in the rafnose family of oligosaccharides with few side efects.
In Vitro: Stachyose highly promotes proliferation of lactic acid bacteria (LAB) by inducing LAB to produce more α-galactosidase to hydrolyze stachyose[2].
In Vivo: Stachyose may improve bioavailability of genistein via inhibiting intestinal degradation and first-pass metabolism of soy genistein[1].

Name: MV1, CAS: 1001600-54-9, stock 4.5g, assay 98%, MWt: 576.73, Formula: C33H44N4O5, Solubility: DMSO : ≥ 125 mg/mL (216.74 mM), Clinical_Informat: No Development Reported, Pathway: Apoptosis, Target: IAP, Biological_Activity: MV1 is an antagonist of IAP (inhibitor of apoptosis protein), leads to protein knockdown of HaloTag-fused proteins when combined with HaloTag ligand[1].

Name: Chlorcyclizine (hydrochloride), CAS: 14362-31-3, stock 26.3g, assay 98.6%, MWt: 337.29, Formula: C18H22Cl2N2, Solubility: DMSO : 77.5 mg/mL (229.77 mM; Need ultrasonic), Clinical_Informat: Launched, Pathway: Immunology/Inflammation;GPCR/G Protein;Neuronal Signaling, Target: Histamine Receptor;Histamine Receptor;Histamine Receptor, Biological_Activity: Chlorcyclizine hydrochloride is a histamine H1 antagonist.
IC50 & Target: Histamine H1[1]
In Vivo: Pregnant rats administered 30, 60, and 90mg/kg Chlorcyclizine during the sensitive period for palate development survived until scheduled sacrifice on Gestation Days (GDs) 17 or 21. The rats administered 60 or 90mg/kg Chlorcyclizine have transient adverse clinical signs (chromorhinorrhea, red peri-oral substance, urogenital staining, and scant stool) and a concomitant body weight loss of 7% and 11%, respectively, over the dosing interval. Rats administered 30mg/kg Chlorcyclizine do not exhibit any adverse clinical signs, but do not gain weight over the dose interval as would be expected during pregnancy. Based on the testing facility’s historical control database (16 studies, n=380). pregnant rats typically gain about 6% body weight from GDs 12 to 15[1].

Name: KRN2 (bromide), CAS: 1390654-28-0, stock 7.8g, assay 98%, MWt: 524.38, Formula: C27H23BrFNO4, Solubility: DMSO : ≥ 60 mg/mL (114.42 mM), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: KRN2 (bromide) is a selective inhibitor of nuclear factor of activated T cells (NFAT5), with an IC50 of 0.1 μM.
IC50 & Target: IC50: 100 nM (NFAT5)[1]
In Vitro: KRN2 selectively suppresses the expression of pro-inflammatory genes, including Nos2 and Il6, without hampering high-salt-induced NFAT5 and its target gene expressions[1]. 
KRN2 dose-dependently inhibits the NF-κB p65 binding to Nfat5 promoter 1 and directly blocks the interaction between NF-κB p65 and its DNA binding sequence in the upstream site (base pairs -3000 to +1) of Nfat5 exon 1[1].
In Vivo: KRN2 (3 mg/kg, i.p., daily for 2 weeks) effectively suppresses AIA in which innate immune cells play a predominant role[1]. 
KRN2 (3 mg/kg, i.p., daily) effectively suppresses CIA as well as AIA in mice, decreasing the production of pro-inflammatory cytokines and autoantibodies as well as macrophage infiltration[1].

Name: H-151, CAS: 941987-60-6, stock 11.8g, assay 98.5%, MWt: 279.34, Formula: C17H17N3O, Solubility: H2O : < 0.1 mg/mL (insoluble); DMSO : 125 mg/mL (447.48 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Immunology/Inflammation, Target: STING, Biological_Activity: H-151 is a highly potent, selective and covalent antagonist of STING, reduces TBK1 phosphorylation and suppresses human STING palmitoylation[1].
IC50 & Target: STING[1]

Name: Cyclo(Arg-Gly-Asp-D-Phe-Val) (TFA), CAS: 199807-33-5, stock 39.7g, assay 98.6%, MWt: 688.65, Formula: C28H39F3N8O9, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Cytoskeleton, Target: Integrin, Biological_Activity: Cyclo(Arg-Gly-Asp-D-Phe-Val) (TFA) is an inhibitor of integrin αvβ3, with antitumor activity.
IC50 & Target: αvβ3[1]
In Vitro: Cyclo(Arg-Gly-Asp-D-Phe-Val) (TFA) is an inhibitor of integrin αvβ3. Cyclo(Arg-Gly-Asp-D-Phe-Val) [c(RGDfV); 35 nM] induces disruption of leukemia cell migration and adhesion to leukemia osteoblasts in the 3D and 2D culture systems, affects the leukemia cell cycle and induces apoptosis in leukemia cells[1].

Name: Pradefovir mesylate Remofovir mesylate, CAS: 625095-61-6, stock 5.6g, assay 98.3%, MWt: 519.90, Formula: C18H23ClN5O7PS, Solubility: H2O : ≥ 125 mg/mL (240.43 mM), Clinical_Informat: Phase 2, Pathway: Metabolic Enzyme/Protease, Target: Cytochrome P450, Biological_Activity: Pradefovir mesylate is a good substrate for liver CYP3A4. Pradefovir is converted to 9-(2-phosphonylmethoxyethyl)adenine (PMEA) in human liver microsomes with a Km of 60 μM.
In Vitro: Pradefovir is a cyclodiester prodrug of PMEA. It is one of the HepDirect prodrugs, which are designed to be efficiently and specifically activated through an oxidative reaction catalyzed by CYP3A4, which is located mainly in the liver. Pradefovir is converted to PMEA in human liver microsomes with a Km of 60 μM, a maximum rate of metabolism of 228 pmol/min/mg protein, and an intrinsic clearance of about 359 L/min[1].
In Vivo: Daily oral dosing of Pradefovir (300 mg/kg) to rats for 8 days does not affect body weight; liver weight; liver weight-body weight ratio; liver microsomal protein content; total CYP content; enzyme activities for CYP1A, CYP2B, and CYP3A; and apoprotein contents for CYP1A1, CYP2B1/2, CYP3A1/2, and CYP4A1/3, indicating that Pradefovir is not a CYP inducer in rats[1].

Name: L 888607 Racemate, CAS: 1030017-51-6, stock 36.9g, assay 98.2%, MWt: 375.84, Formula: C19H15ClFNO2S, Solubility: H2O : < 0.1 mg/mL (insoluble); DMSO : 6 mg/mL (15.96 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein, Target: Prostaglandin Receptor, Biological_Activity: L 888607 Racemate is a selective prostaglandin D2 receptor subtype 1 (DP1) antagonist, with Kis of 132 nM and 17 nM for DP1 and thromboxane A2 receptor (TP), respectively.
IC50 & Target: Ki: 132 nM (DP1), 17 nM (TP)[1].
In Vitro: L 888607 Racemate (compound 3) maintains a modest binding affinity for the DP1 receptor (Ki = 132 nM) and is actually 8-fold more potent on the TP receptor (Ki = 17 nM)[1].

Name: Protosappanin A PTA, CAS: 102036-28-2, stock 16.5g, assay 98.8%, MWt: 272.25, Formula: C15H12O5, Solubility: 10 mM in DMSO, Clinical_Informat: Phase 4, Pathway: Epigenetics;Stem Cell/Wnt;JAK/STAT Signaling;JAK/STAT Signaling;Stem Cell/Wnt, Target: JAK;JAK;JAK;STAT;STAT, Biological_Activity: Protosappanin A (PTA), an immunosuppressive ingredient and major biphenyl compound isolated from Caesalpinia sappan L, suppresses JAK2/STAT3-dependent inflammation pathway through down-regulating the phosphorylation of JAK2 and STAT3[1].
IC50 & Target: JAK2, STAT3[1].
In Vitro: Protosappanin A (PTA: 12.5, 25, 50 μM, 24 hours) significantly inhibits the production of TNF-α and IL-1β in LPS-activated BV2 microglia. And the mRNA expressions of IL-6, IL-1β, and MCP-1 are reduced by PTA in a dose-dependent manner in BV2 microglial cell line[1]. 
Protosappanin A (PTA: 12.5, 25, 50 μM, 24 hours) suppresses JAK2/STAT3-dependent inflammation pathway through down-regulating the phosphorylation of JAK2 and STAT3, as well as STAT3 nuclear translocation against LPS treatment[1]. 
Protosappanin A (PTA: 12.5, 25, 50 μM, 24 hours) shows obvious effect on disturbing the interaction of transmembrane protein CD14 with Toll-like receptor-4, resulting in the inhibition of NF-κB-dependent oxidative and nitrative stress in LPS-induced BV2 microglia[2].

Name: CA-5f, CAS: 1370032-19-1, stock 6.9g, assay 98.1%, MWt: 388.46, Formula: C24H24N2O3, Solubility: DMSO : 77.5 mg/mL (199.51 mM; Need ultrasonic); H2O : < 0.1 mg/mL (insoluble), Clinical_Informat: No Development Reported, Pathway: Apoptosis;Autophagy, Target: Apoptosis;Autophagy, Biological_Activity: CA-5f is a potent late-stage macroautophagy/autophagy inhibitor via inhibiting autophagosome-lysosome fusion. CA-5f increases LC3B-II (a marker to monitor autophagy) and SQSTM1 protein, and also increases ROS production. Anti-tumor activity[1].
IC50 & Target: Macroautophagy/autophagy[1]
In Vitro: CA-5f (0-40 μM, 6 hour) concentration- and time-dependently elevates the level of LC3B-II (a marker to monitor autophagy) and SQSTM1 protein both in A549 cells and HUVECs[1]. 
CA-5f (20 μM, 6 hours) inhibits the degradation of autophagosomes when treated alone or in combination Bafilomycin A1 (100 nM) or Chloroquine (30 μM) in A549 cells and HUVECs[1]. 
CA-5f (20 μM) neither impairs the hydrolytic function nor the quantity of lysosomes[1]. 
CA-5f (20 μM, 96 hours) inhibits the growth of A549 cells, and less cytotoxic to normal HUVECs[1]. 
In Vivo: CA-5f (40 mg/kg, i.p., every 2 days for up to 30 days) is well tolerated, and potently inhibits the growth of tumor in nude mice bearing A549 lung cancer cells[1]. 
CA-5f (40 mg/kg, i.p.) suppresses autophagic flux and induces apoptosis in nude mice bearing A549 lung cancer cells[1].

Name: AMG 333, CAS: 1416799-28-4, stock 11.7g, assay 98.6%, MWt: 453.32, Formula: C20H12F5N3O4, Solubility: DMSO : ≥ 125 mg/mL (275.74 mM), Clinical_Informat: Phase 1, Pathway: Membrane Transporter/Ion Channel;Neuronal Signaling, Target: TRP Channel;TRP Channel, Biological_Activity: AMG 333 is a potent and highly selective TRPM8 antagonist with an IC50 of 13 nM.
IC50 & Target: IC50: 13 nM (TRPM8)[1]

Name: VU0529331, CAS: 1286725-49-2, stock 7.5g, assay 98.6%, MWt: 384.43, Formula: C22H20N6O, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Membrane Transporter/Ion Channel, Target: Potassium Channel, Biological_Activity: VU0529331 is a modestly selective non-GIRK1-containing G protein-gated, inwardly-rectifying, potassium channel (non-GIRK1/X) activator, with EC50s of 5.1 µM and 5.2 µM for GIRK2 and GIRK1/2 in HEK293 cells, respectively, also effective on GIRK4 homomeric channel[1].
IC50 & Target: EC50: 5.1 µM (GIRK2), 5.2 µM (GIRK1/2)[1]

Name: PF-06747711, CAS: 1892576-58-7, stock 10.4g, assay 99%, MWt: 497.51, Formula: C26H26F3N5O2, Solubility: DMSO : 41.67 mg/mL (83.76 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: ROR, Biological_Activity: PF-06747711 is a potent, selective, and orally active retinoic acid receptor-related orphan C2 (RORC2, also known as RORγt) inverse agonist, with an IC50 of 4.1 nM. Anti-skin inflammatory activity[1].
IC50 & Target: IC50: 4.1 nM (RORC2)[1]
In Vitro: PF-06747711 (Compound 66) reduces IL-17 production by human Th17 cells with an IC50 of 9.5 nM[1].
In Vivo: PF-06747711 (10, 30, and 100 mg/kg, p.o., daily over 5 days) inhibits ear swelling in a dose-dependent manner in mice[1].

Name: SMS2-IN-2, CAS: 2241838-28-6, stock 36.6g, assay 98.4%, MWt: 369.78, Formula: C19H13ClFN3O2, Solubility: DMSO : 125 mg/mL (338.04 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: SMS2-IN-2 is a potent, highly selective and orally active sphingomyelin synthase 2 (SMS2) inhibitor, with IC50s of 100 nM and 56 μM for SMS2 and SMS1, respectively. Anti-chronic inflammatory activity[1].
IC50 & Target: IC50: 100 nM (SMS2), 56 μM (SMS1)[1]
In Vivo: SMS2-IN-2 (Compound 15w; 20, 50 mg/kg/day, p.o. for 6 weeks) reduces chronic inflammation in the db/db mice[1].

Name: PF-06700841, CAS: 1883299-62-4, stock 23.9g, assay 98.6%, MWt: 389.40, Formula: C18H21F2N7O, Solubility: 10 mM in DMSO, Clinical_Informat: Phase 2, Pathway: Epigenetics;Stem Cell/Wnt;JAK/STAT Signaling, Target: JAK;JAK;JAK, Biological_Activity: PF-06700841 is a potent dual Janus kinase 1 (JAK1) and TYK2 inhibitor with IC50s of 17 nM and 23 nM, respectively. PF-06700841 also inhibits JAK2 and JAK3 with IC50s of 77 nM and 6.49 μM, respectively[1].
IC50 & Target: IC50: 17 nM (JAK1), 23 nM (TYK2)[1]
In Vitro: PF-06700841 (Compound 23) potently inhibits TYK2/JAK2 mediated IL-12/pSTAT4 and IL-23/pSTAT3 (human whole blood (HWB) IC50s of 65 and 120 nM, respectively). PF-06700841 has good potency against IL6/pStat1 in the CD3+ cellular subset (IC50 of 81 nM), but lower inhibition of IL6/pSTAT3, again in the CD3+ cellular subset (IC50 of 641 nM). PF-06700841 also inhibits the JAK1/JAK3 driven γ-common chain cytokines, represented by IL-15/pStat5 and IL-21/pSTAT3 with reasonable potency (HWB IC50s of 238 and 204 nM, respectively). PF-06700841 inhibits EPO/pSTAT5 (JAK2 homodimer) in HWB spiked with CD34+ progenitor cells (IC50 of 577 nM). IL10/pSTAT3 (TYK2/JAK1) and IL27/pSTAT3 (JAK1/JAK2/TYK2) are also inhibited by PF-06700841 with IC50s of 305 nM and 86 nM, respectively[1].
In Vivo: PF-06700841 (Compound 23; 3-30 mg/kg; oral administration; for 7 consecutive days; female Lewis rats) treatment significantly reduces paw volume increase in a dose-dependent manner. The plasma concentrations in animals dosed with PF-06700841 at peak (30 min) and trough (24 h) time intervals post final dose respectively are as follows: 3 mg/kg, 3.54 μM, 0.0221 μM; 10 mg/kg, 10.95 μM, 0.06 μM; and 30 mg/kg, 23.89 μM, 0.06 μM[1].

Name: Monascin, CAS: 21516-68-7, stock 20.5g, assay 98.6%, MWt: 358.43, Formula: C21H26O5, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Monascin is a kind of azaphilonoid pigments extracted from Monascus pilosus-fermented rice (red-mold rice). Monascin also exhibits anti-tumor-initiating activity and anti-inflammatory activity with oral administration. Monascin inhibits the activation of NOR 1 (an NO donor)[1][2].
In Vivo: Monascin (0.0025% in drinking water; mice) appears effective for the inhibition of UVB-initiated carcinogenesis on mouse skin[1].

Name: Ankaflavin, CAS: 50980-32-0, stock 0.3g, assay 98.7%, MWt: 386.48, Formula: C23H30O5, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Cell Cycle/DNA Damage, Target: PPAR, Biological_Activity: Ankaflavin, isolated from Monascus-Fermented red rice, is a PPARγ agonist with anti-inlfammatory activity. Ankaflavin exhibits selective cytotoxic effect and induces cell death on cancer cells[1][2].
IC50 & Target: PPARγ[2].

Name: 2-O-Acetyl-20-hydroxyecdysone 20-Hydroxyeedysone 2-acetate, CAS: 19536-25-5, stock 9.2g, assay 98.8%, MWt: 522.67, Formula: C29H46O8, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: 2-O-Acetyl-20-hydroxyecdysone, an ecdysterones in insects and terrestrial plants, inhibits amyloid-β42 (Aβ42)-induced cytotoxicity. 2-O-Acetyl-20-hydroxyecdysone could decrease Aβ oligomer formation through promotion of fibrogenesis, transforming Aβ oligomers to the low-toxicity fibrils[1].

Name: ACT-709478, CAS: 1838651-58-3, stock 34g, assay 98%, MWt: 425.41, Formula: C22H18F3N5O, Solubility: DMSO : ≥ 125 mg/mL (293.83 mM), Clinical_Informat: Phase 2, Pathway: Membrane Transporter/Ion Channel;Neuronal Signaling, Target: Calcium Channel;Calcium Channel, Biological_Activity: ACT-709478 is a potent, selective, orally active, and brain penetrating T-type calcium channel blocker. ACT-709478 is used in the research of generalized epilepsies[1].
IC50 & Target: IC50: 6.4 nM (Cav3.1), 18 nM (Cav3.2), 7.5 nM (Cav3.3), 2410 nM (Cav1.2)[1]
In Vitro: ACT-709478 (Compound 66b) blocks Cav3.1, Cav3.2, Cav3.3, Cav1.2 with IC50s of 6.4, 18, 7.5 and 2410 nM, respectively. ACT-709478 blocks recombinant channel hCav3.3 potently with marked voltage-dependency (Kr≈1500 nM and Ki≈20 nM). ACT-709478 blocks currents through hKv11.1-hERG channels with an IC50 of 5.5 μM[1]. 
ACT-709478 also inhibits P450 enzymes with IC50s of 14, 15, 22, 25, 51 and 52 μM for CYP2C8,CYP2D6 CYP2C9, CYP2C19, CYP3A4, and CYP2B6, respectively[1].
In Vivo: ACT-709478 (Compound 66b, 100, 300 mg/kg, p.o., 12 hours) potently decreases the cumulative duration of absence-like seizures in mice[1].

Name: BRD 4354, CAS: 315698-07-8, stock 7.3g, assay 98.5%, MWt: 382.89, Formula: C21H23ClN4O, Solubility: DMSO : 125 mg/mL (326.46 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Epigenetics;Cell Cycle/DNA Damage, Target: HDAC;HDAC, Biological_Activity: BRD 4354 is a moderately potent inhibitor of HDAC5 and HDAC9, with IC50s of 0.85 and 1.88 μM, respectively.
IC50 & Target: IC50: 0.85 μM (HDAC5), 1.88 μM (HDAC9)[1].
In Vitro: BRD 4354 is a moderately potent inhibitor of HDAC5 and HDAC9, with BRD4354 having half-maximum inhibitory concentrations (IC50) of 0.85 μM and 1.88 μM, respectively. BRD 4354 also inhibits HDACs 4, 6, 7, and 8 at higher concentrations (3.88-13.8 μM) but demonstrates less of an inhibitory effect on other class I HDACs 1, 2, and 3 (IC50>40 μM) [1].

Name: AGL-2263, CAS: 638213-98-6, stock 24g, assay 98.6%, MWt: 322.27, Formula: C17H10N2O5, Solubility: DMSO : 125 mg/mL (387.87 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Protein Tyrosine Kinase/RTK, Target: Insulin Receptor, Biological_Activity: AGL-2263 is an insulin receptor (IR) blocker.
IC50 & Target: Insulin receptor[1].
In Vitro: AGL-2263 is an insulin receptor (IR) blocker[1].

Name: Arimoclomol maleate BRX-220, CAS: 289893-26-1, stock 34.3g, assay 98.7%, MWt: 429.85, Formula: C18H24ClN3O7, Solubility: DMSO : 250 mg/mL (581.60 mM; Need ultrasonic), Clinical_Informat: Phase 3, Pathway: Metabolic Enzyme/Protease;Cell Cycle/DNA Damage, Target: HSP;HSP, Biological_Activity: Arimoclomol maleate (BRX-220) is a co-inducer of heat shock proteins (HSP).
IC50 & Target: HSP[1]
In Vivo: The HSP coinducer Arimoclomol (BRX-220), administered for 5 d, has a protective effect against CCK-induced acute pancreatitis. Repeated CCK treatment results in the typical laboratory and morphological changes of experimentally induced pancreatitis. The pancreatic levels of HSP60 and HSP72 are significantly increased in the animals treated with Arimoclomol [1]. Arimoclomol is a coinducer of heat shock proteins for the potential treatment of amyotrophic lateral sclerosis (ALS), the most common form of motor neuron disease[2].

Name: FDI-6, CAS: 313380-27-7, stock 23.3g, assay 98.5%, MWt: 437.43, Formula: C19H11F4N3OS2, Solubility: DMSO : ≥ 50 mg/mL (114.30 mM), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: FDI-6 is an inhibitor of FOXM1. FDI-6 binds directly to FOXM1 protein, to displace FOXM1 from genomic targets in MCF-7 breast cancer cells, and induce concomitant transcriptional down-regulation.
IC50 & Target: FOXM1[1]
In Vitro: FDI-6 is characterized in depth and is shown to bind directly to FOXM1 protein, to displace FOXM1 from genomic targets in MCF-7 breast cancer cells, and induce concomitant transcriptional down-regulation. MDA-MB-231 ER-negative breast and PEO-1 ovarian cancer cells are sensitive to FDI-6 in cell viability assays (GI50=21.8 μM and 18.1 μM, respectively) and exhibit comparable down-regulation of CDC25B after a 3 h treatment with FDI-6. The transcription factor FOXM1 regulates a network of proliferation-associated genes critical to mitotic spindle assembly, chromosome segregation, and G2/M transition, with depletion leading to cell cycle arrest. Importantly, aberrant up-regulation of FOXM1 has been shown to be a key driver of cancer progression and has been proposed as an initiating factor of oncogenesis[1].

Name: Neurotoxin Inhibitor, CAS: 951571-70-3, stock 8.8g, assay 98.1%, MWt: 346.41, Formula: C19H14N4OS, Solubility: DMSO : 45 mg/mL (129.90 mM; Need ultrasonic); H2O : < 0.1 mg/mL (insoluble), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Neurotoxin Inhibitor is a neurotoxin inhibitor.

Name: Barnidipine Mepirodipine;YM-09730-5(Free base), CAS: 104713-75-9, stock 24g, assay 98.1%, MWt: 491.54, Formula: C27H29N3O6, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Membrane Transporter/Ion Channel;Neuronal Signaling, Target: Calcium Channel;Calcium Channel, Biological_Activity: Barnidipine (Mepirodipine) is an L-type calcium antagonist (CaA) with high affinity for [3H] initrendipine binding sites (Ki=0.21 nmol/l), has selective action against CaA receptors[1].
Barnidipine (Mepirodipine) is an antihypertensive drug and acts by the reduction of peripheral vascular resistance secondary to its vasodilatory action[2].
IC50 & Target: Ki: 0.21 nmol/l ([3H] initrendipine)[1]

Name: AZD2906, CAS: 1034148-15-6, stock 37.7g, assay 98.1%, MWt: 460.50, Formula: C26H25FN4O3, Solubility: DMSO : 125 mg/mL (271.44 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein, Target: Glucocorticoid Receptor, Biological_Activity: AZD2906 is a selective glucocorticoid receptor (GR) agonist, increases micronucleated immature erythrocytes in the bone marrow of rats. AZD2906 shows IC50s of 2.2, 0.3, 41.6 and 7.5 nM at GR in human, rat PBMC and human, rat whole blood, respectively[1].
IC50 & Target: IC50: 2.2 nM (Glucocorticoid receptor, Human PBMC), 0.3 nM (Glucocorticoid receptor, Rat PBMC), 41.6 nM (Glucocorticoid receptor, Human whole blood), 7.5 nM (Glucocorticoid receptor, Rat whole blood)[1]
In Vitro: AZD2906 is a selective glucocorticoid receptor (GR), with IC50s of 2.2, 0.3, 41.6 and 7.5 nM at GR in human, rat PBMC and human, rat whole blood, respectively[1].
In Vivo: AZD2906 (5, 25, 50 mg/kg, p.o.) increases micronucleated immature erythrocytes (MIE) in the bone marrow of rats after treatment for 2 days[1]. 
AZD2906 (5, 25 mg/kg, p.o.) induces an accumulation of glycogen in the liver of rats, and exhibits cortical lymphocytic atrophy of a moderate to marked degree in the thymus of rats[1].

Name: IACS-10759 Hydrochloride, CAS: 1807523-99-4, stock 20.8g, assay 98.1%, MWt: 599.02, Formula: C25H26ClF3N6O4S, Solubility: H2O : < 0.1 mg/mL (insoluble); DMSO : ≥ 100 mg/mL (166.94 mM), Clinical_Informat: No Development Reported, Pathway: Apoptosis, Target: Apoptosis, Biological_Activity: IACS-10759 Hydrochloride is a potent inhibitor of complex I of oxidative phosphorylation (OXPHOS).
IC50 & Target: OXPHOS[1]
In Vitro: IACS-10759 inhibits the conversion of NADH to NAD+ in an immunoprecipitated complex I assay at low nM concentrations[1].
In Vivo: IACS-10759 is orally bioavailable with excellent physicochemical properties in preclinical species and achieves significant in vivo efficacy with daily oral dosing of 10-25 mg/kg. There is a >50 day extension of median survival in an orthotopic AML cell line xenograft and robust regression in DLBCL and GBM xenograft models[1].

Name: HC-056456 3,4-Bis(2-thienoyl)-1,2,5-oxadiazole-N-oxide, CAS: 7733-96-2, stock 27.4g, assay 98.9%, MWt: 306.32, Formula: C12H6N2O4S2, Solubility: DMSO : ≥ 150 mg/mL (489.68 mM), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: HC-056456 is an effective but not perfectly-selective blocker of CatSper channels. The [Na+]i rise is slowed by HC-056456 (IC50~3 µM).
IC50 & Target: CatSper[1]
In Vitro: HC-056456 similarly slows the rise of [Ca2+]i that is evoked by alkaline depolarization and reported by fura-2. HC-056456 also selectively and reversibly decreased CatSper currents recorded from patch-clamped sperm. HC-056456 produces a pharmacological phenocopy of the CatSper-null sperm. Acute application of HC-056456 causes rapid loss of flagellar waveform asymmetry from hyperactivated sperm, indicating that continued entry of Ca2+ through CatSper channels is required to maintain hyperactivation. HC-056456 selectively and reversibly blocks CatSper currents. The specificity and reversibility of the blockade of CatSper-dependent currents by HC-056456 is examined by using patch clamp recordings. The observed current is blocked slightly more than 50% by 20 µM HC-056456 (estimated IC50 near 15 µM). In concept, it remains possible that CatSper channel heterogeneity explains residual HC-056456-resistant current. The action of HC-056456 on KSper channels, the other major cation channel observed in patch-clamped sperm, is also examined. Subsequent application of 50 µM HC-056456 results in partial blockade of this current. For HC-056456 action on KSper an IC50 near 40 µM is estimated[1].

Name: PEO-IAA 2-(1H-Indol-3-yl)-4-oxo-4-phenyl-butyric acid, CAS: 6266-66-6, stock 38.7g, assay 98.2%, MWt: 293.32, Formula: C18H15NO3, Solubility: DMSO : ≥ 150 mg/mL (511.39 mM), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: PEO-IAA is an indole-3-acetic acid (IAA) antagonist. PEO-IAA is an auxin antagonist that binds to transport inhibitor response 1/auxin signaling F-box proteins (TIR1/AFBs).
In Vitro: PEO-IAA is also an α-alkyl-IAA, and shows more potent anti-auxin activity in auxin-responsive gene expression and in the cell division and elongation pathway that is mediated via SCFTIR1/AFBs. PEO-IAA suppresses not only the expression of an auxin-responsive ZmSAUR2 gene, but also gravitropic curvature. PEO-IAA blocks the auxin response in Arabidopsis, rice, moss and maize[1].

Name: Rapamycin Sirolimus; AY 22989, CAS: 53123-88-9, stock 9.3g, assay 98.6%, MWt: 914.17, Formula: C51H79NO13, Solubility: H2O : < 0.1 mg/mL (insoluble); DMSO : 150 mg/mL (164.08 mM; Need ultrasonic), Clinical_Informat: Launched, Pathway: PI3K/Akt/mTOR;Autophagy;Immunology/Inflammation;Apoptosis;Autophagy, Target: mTOR;Autophagy;FKBP;FKBP;FKBP, Biological_Activity: Rapamycin (Sirolimus; AY 22989) is a potent and specific mTOR inhibitor with an IC50 of 0.1 nM in HEK293 cells. Rapamycin binds to FKBP12 and specifically acts as an allosteric inhibitor of mTORC1[1]. Rapamycin is an autophagy activator, an immunosuppressant[2].
IC50 & Target: IC50: 0.1 nM (mTOR)[1]
In Vitro: Rapamycin (12.5-100 nM; 24 hours) treatment exerts modest inhibitory effect on lung cancer cell proliferation in a dose-dependent manner in all cell lines (A549, SPC-A-1, 95D and NCI-H446 cells) tested, achieving about 30-40% reduction in cell proliferation at 100 nM vs. ~10% reduction at 12.5 nM[3]. 
Lung cancer cell line 95D cells are exposed to Rapamycin (10 nM, 20 nM) and RP-56976 (1 nM, 10 nM) alone or in combination (Rapamycin 20 nM+ RP-56976 10 nM). After 24 hours exposure to Rapamycin or RP-56976 alone does not significantly alter the level of expression or phosphorylation of ERK1/2, whereas cells treated with the combination of Rapamycin with RP-56976 exhibit a marked reduction in the phosphorylation levels of ERK1/2[3].
In Vivo: Rapamycin (2.0 mg/kg; intraperitoneal injection; every other day; 28 days) alone has a moderate inhibitory effect. However, the combination of Metformin and Rapamycin exerts a significantly increased inhibition of tumor growth compared with the control group, the Rapamycin monotherapy group and the Metformin monotherapy group[4].

Name: PF-05231023, CAS: 1037589-69-7, stock 14.9g, assay 98.3%, MWt: 528.55, Formula: C26H32N4O8, Solubility: DMSO : 125 mg/mL (236.50 mM; Need ultrasonic), Clinical_Informat: Phase 1, Pathway: Protein Tyrosine Kinase/RTK, Target: FGFR, Biological_Activity: PF-05231023, a long-acting fibroblast growth factor 21 (FGF21) analog, is a FGF21-receptor agonist, suitable for development as a potential treatment for T2DM[1][5].
IC50 & Target: FGF21-receptor[5].
In Vitro: PF-05231023 is a long-acting fibroblast growth factor 21 (FGF21) analog[2].
In Vivo: Administration of native FGF21 and PF-05231023 (3 mg/kg or 10 mg/kg; subcutaneously twice a week for two weeks) improves glucose tolerance and liver insulin sensitivity in Zucker rats[3]. PF-05231023 (10 mg/kg; intraperitoneally injected) decreases retinal inflammation in diabetic mice. PF-05231023 reduces retinal IL-1β mRNA expression in Akita mice. PF-05231023 increases cone-specific arrestin4 expression in Akita mice. PF-05231023 restores photoreceptor morphology in Akita mice. PF-05231023 inhibits oxidative-stress-induced inflammation in photoreceptors. PF-05231023 decreases the variability of retinal NRF2 levels and shows a trend (non-significant) towards increased NRF2 levels in Akita mice[4].

Name: TFAP N-(5-Aminopyridin-2-yl)-4-(trifluoromethyl)benzamide, CAS: 1011244-68-0, stock 0.7g, assay 98.8%, MWt: 281.23, Formula: C13H10F3N3O, Solubility: DMSO : ≥ 155 mg/mL (551.15 mM), Clinical_Informat: No Development Reported, Pathway: Immunology/Inflammation;Metabolic Enzyme/Protease, Target: COX;Endogenous Metabolite, Biological_Activity: TFAP is a selective cyclooxygenase-1 (COX-1) inhibitor, with an IC50 of 0.8 μM.
IC50 & Target: IC50: 0.8 μM (COX-1)[1].
In Vitro: TFAP is a selective cyclooxygenase-1 (COX-1) inhibitor, with an IC50 of 0.8 μM, while that against COX-2 is over 200 μM.

Name: 4'-Methylchrysoeriol, CAS: 4712-12-3, stock 39.9g, assay 98.3%, MWt: 314.29, Formula: C17H14O6, Solubility: DMSO : 20.83 mg/mL (66.28 mM; Need ultrasonic); H2O : < 0.1 mg/mL (insoluble), Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Cytochrome P450, Biological_Activity: 4'-Methylchrysoeriol is a potent inhibitor of Cytochrome P450 enzymes, with an IC50 of 19 nM for human P450 1B1-dependent EROD.
IC50 & Target: IC50: 19 nM ( human P450 1B1-dependent EROD)[1].
In Vitro: 4'-Methylchrysoeriol (34DM57DHF) is a potent inhibitor of P450 enzymes, particularly for P450 1B1, with an IC50 of 19 nM for human P450 1B1-dependent EROD[1].

Name: Hexadimethrine bromide 1,5-Dimethyl-1,5-diazaundecamethylene polymethobromide, CAS: 28728-55-4, stock 27.2g, assay 98.2%, MWt: 404.27, Formula: C15H36Br2N2, Solubility: DMSO : 5 mg/mL (12.37 mM; Need ultrasonic and warming); H2O : ≥ 125 mg/mL (309.20 mM), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Hexadimethrine bromide is a cationic polymer discovered to enhance retroviral transduction.
In Vitro: Hexadimethrine bromide inhibits human mesenchymal stem cell proliferation during lentiviral transduction. Hexadimethrine bromide is considered non-toxic at low concentrations, but has been found to negatively affect cell proliferation in some cell types at concentrations greater than 10 µg/mL. Trypsinized cells exposed to Hexadimethrine bromide are visibly larger in size when viewed under the microscope[1].

Name: PAT-1251 Hydrochloride, CAS: 2098884-53-6, stock 30.6g, assay 98.1%, MWt: 435.80, Formula: C18H18ClF4N3O3, Solubility: 10 mM in DMSO, Clinical_Informat: Phase 1, Pathway: Neuronal Signaling, Target: Monoamine Oxidase, Biological_Activity: PAT-1251 Hydrochloride is a potent, selective and oral lysyl oxidase-like 2 (LOXL2) inhibitor, with IC50s of 0.71 and 1.17 μM for hLOXL2 and hLOXL3, respectively, and also potently inhibits mouse, rat, and dog LOXL2 (IC50s, 0.10, 0.12, and 0.16 μM, respectively). PAT-1251 Hydrochloride is used in the research of fibrotic diseases.
IC50 & Target: IC50: 0.10 μM (Mouse LOXL2), 0.12 μM (Rat LOXL2), 0.16 μM (Dog LOXL2), 0.71 μM (hLOXL2), 1.17 μM (hLOXL3)[1]
In Vitro: PAT-1251 is a lysyl oxidase-like 2 (LOXL2) inhibitor, with IC50s of 0.71 and 1.17 μM for hLOXL2 and hLOXL3, respectively, and also potently inhibits mouse, rat, and dog LOXL2 (IC50s, 0.10, 0.12, and 0.16 μM, respectively). PAT-1251 shows highly selective for LOXL2 over other key members of the amine oxidase family, such as the copper-dependent amine oxidases semicarbazide-sensitive amine oxidase (SSAO) and diamine oxidase (DAO), in addition to the flavin-dependent monoamine oxidases A (MAO-A) and B (MAO-B), with <10% inhibition at 10 μM[1].

Name: LY223982 CGS23131;SKF107324, CAS: 117423-74-2, stock 26.2g, assay 98.9%, MWt: 502.56, Formula: C30H30O7, Solubility: DMSO : 100 mg/mL (198.98 mM; Need ultrasonic); H2O : < 0.1 mg/mL (insoluble), Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein, Target: Leukotriene Receptor, Biological_Activity: LY223982 is a potent and specific inhibitor of leukotriene B4 receptor, with an IC50 of 13.2 nM against [3H]LTB4 binding to LTB4 receptor.
IC50 & Target: IC50: 13.2 nM (LTB4 receptor)[1]
In Vitro: LY223982 is a potent and specific inhibitor of leukotriene B4 (LTB4) receptor, with an IC50 of 13.2 nM against [3H]LTB4 binding to LTB4 receptor. LY223982 is also a potent antagonist of the aggregation of human neutrophils by LTB4 (IC50, 100 nM)[1].
In Vivo: LY223982 inhibits transient leukopenia induced in rabbits with LTB4 (ED50, 3 mg/kg) but not with FMLP, and shows no agonist activity in any of the test systems[1].

Name: DLinDMA, CAS: 871258-12-7, stock 27.5g, assay 98%, MWt: 616.06, Formula: C41H77NO2, Solubility: Ethanol : ≥ 100 mg/mL (162.32 mM); DMSO : < 1 mg/mL (insoluble or slightly soluble), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: DLinDMA is a key lipid component of stable nucleic acid lipid particles as a benchmark.

Name: DLin-KC2-DMA, CAS: 1190197-97-7, stock 23g, assay 98.2%, MWt: 642.09, Formula: C43H79NO2, Solubility: DMSO : 5 mg/mL (7.79 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: DLin-KC2-DMA is a cationic/ionizable lipid for siRNA delivery[1].

Name: LHF-535, CAS: 1450929-77-7, stock 36.9g, assay 98.7%, MWt: 412.52, Formula: C27H28N2O2, Solubility: H2O : < 0.1 mg/mL (insoluble); DMSO : 96.67 mg/mL (234.34 mM; Need ultrasonic), Clinical_Informat: Phase 1, Pathway: Anti-infection, Target: Arenavirus, Biological_Activity: LHF-535 is an antiviral agent extracted from patent WO2013123215A2, Compound 38, has EC50s of <1 μM, <1 μM, <1 μM, and 1-10 μM for Lassa, Machupo, Junin, and VSVg virus, respectively[1].
In Vitro: LHF-535 is a small-molecule viral entry inhibitor that targets the arenavirus envelope glycoprotein (GP). LHF-535 exhibits potent antiviral activity against a broad array of hemorrhagic fever arenaviruses. LHF-535 inhibits Lassa GP-pseudotyped lentivirus with an IC50 of 0.1-0.3 nM[2].
In Vivo: LHF-535 (3, 10 or 30 mg/kg; orally; daily; 14 days) protectes mice from a lethal challenge with Tacaribe virus and dramatically reduces viral titers in plasma, spleen, and liver[2]. 
An increase in survival is also observed when the first dose of LHF-535 (10 mg/kg) is delayed by 1, 2, or 3 days after infection, demonstrating that LHF-535 is efficacious as a post-exposure therapeutic in mice[2].

Name: EX229, CAS: 1219739-36-2, stock 10.3g, assay 98.8%, MWt: 431.87, Formula: C24H18ClN3O3, Solubility: DMSO : 13 mg/mL (30.10 mM; Need ultrasonic and warming), Clinical_Informat: No Development Reported, Pathway: Epigenetics;PI3K/Akt/mTOR, Target: AMPK;AMPK, Biological_Activity: EX229, a Benzimidazole derivative, is a potent and allosteric activator of AMP-activated protein kinase (AMPK), with Kds of 0.06 μM, 0.06 μM and 0.51 μM for α1β1γ1, α2β1γ1 and α1β2γ1 in biolayer interferometry, respectively.
IC50 & Target: Kd: 0.06 μM (α1β1γ1), 0.06 μM (α2β1γ1), 0.51 μM (α1β2γ1)[1].
In Vitro: EX229 is a potent and allosteric activator of AMP-activated protein kinase (AMPK), with Kds of 0.06 μM, 0.06 μM and 0.51 μM for α1β1γ1, α2β1γ1 and α1β2γ1, respectively.[1]. Treatment of hepatocytes with EX229 (991) alone results in a slight increase in the phosphorylation of AMPK and RAPTOR only at 0.3 μM, whereas a robust increase in ACC phosphorylation is readily observed and saturated at a concentration of 0.03 μM EX229. AICAR or C13 alone robustly increases T172 phosphorylation of AMPKα, and when EX229 is coincubated, there is a modest additional dose-dependent increase in AMPKα phosphorylation. RAPTOR phosphorylation is modestly increased by AICAR or C13 alone, and it is dose dependently increased when coincubations are carried out with EX229. EX229 also dose dependently (0.01 and 0.1 μM) inhibits lipogenesis (34% and 63%, respectively), which is further reduced when it is coincubated with a low dose of AICAR (0.03 mM) or C13 (1 μM). Treatment with EX229 promotes dose-dependent increases in ACC and RAPTOR phosphorylation. Similar to the observations in hepatocytes[2].

Name: LY2452473, CAS: 1029692-15-6, stock 8.7g, assay 98.1%, MWt: 374.44, Formula: C22H22N4O2, Solubility: DMSO : 62.5 mg/mL (166.92 mM; Need ultrasonic), Clinical_Informat: Phase 2, Pathway: Others, Target: Androgen Receptor, Biological_Activity: LY2452473 is an orally bioavailable, selective androgen receptor modulator (SARM).
IC50 & Target: Androgen receptor[1]
In Vivo: LY2452473 is a selective androgen receptor modulator being developed for the treatment of disorders related to hypogonadism. LY2452473 is absorbed rapidly (time to reach maximum plasma concentration for both LY2452473 and total radioactivity is 2-3 h) and cleared slowly (plasma terminal t1/2 of 27 h for LY2452473 and 51 h for the total radioactivity)[1].

Name: Glumetinib SCC244, CAS: 1642581-63-2, stock 37.8g, assay 98.2%, MWt: 459.48, Formula: C21H17N9O2S, Solubility: DMSO : 41.67 mg/mL (90.69 mM; Need ultrasonic), Clinical_Informat: Phase 1, Pathway: Protein Tyrosine Kinase/RTK, Target: c-Met/HGFR, Biological_Activity: Glumetinib (SCC244) is a potent and highly selective c-Met kinase inhibitor with an IC50 of 0.42 nM. Glumetinib shows antitumor activity and a superior safety margin[1].
IC50 & Target: IC50: 0.42 nM (c-Met kinase)[1]

Name: RMC-4550, CAS: 2172651-73-7, stock 19.7g, assay 98.6%, MWt: 437.36, Formula: C21H26Cl2N4O2, Solubility: DMSO : 125 mg/mL (285.81 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Phosphatase, Biological_Activity: RMC-4550 is a potent, selective and allosteric inhibitor of SHP2, with an IC50 of 0.583 nM.
IC50 & Target: IC50:0.583 nM (SHP2)[1].
In Vitro: RMC-4550 is an allosteric inhibitor of SHP2 and stabilizes the auto-inhibited conformation of wild-type SHP2 enzyme, with a mode of inhibition similar to SHP099. Consistent with an allosteric mode of inhibition, RMC-4550 inhibits the activity of full-length wild-type SHP2 enzyme activated by a di-phosphotyrosine peptide, but lacks activity against the free catalytic domain of SHP2[1].

Name: Oleandomycin, CAS: 3922-90-5, stock 31.3g, assay 98.3%, MWt: 687.86, Formula: C35H61NO12, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Anti-infection, Target: Bacterial, Biological_Activity: Oleandomycin is a macrolide antibiotic structurally closely related to Erythromycin. Oleandomycin is similar to Erythromycin with antimicrobial activity.

Name: Lerociclib dihydrochloride G1T38 dihydrochloride, CAS: 2097938-59-3, stock 0.7g, assay 98.8%, MWt: 547.52, Formula: C26H36Cl2N8O, Solubility: H2O : 4 mg/mL (7.31 mM; Need ultrasonic), Clinical_Informat: Phase 2, Pathway: Cell Cycle/DNA Damage, Target: CDK, Biological_Activity: Lerociclib dihydrochloride (G1T38 dihydrochloride) is a potent and selective inhibitor of CDK4/CDK6, with IC50s of 1 nM and 2 nM for CDK4/CyclinD1 and CDK6/CyclinD3, respectively.
In Vitro: Within the CDK family, Lerocyclib is least selective against CDK9/cyclin T, ~30 fold between CDK4/cyclin D1 and CDK9/ cyclin T at the biochemical IC50. Lerociclib produces a robust and sustained G1 arrest in CDK4/6 dependent cells with an EC50 of ~20 nM. A dose dependent increase of cells in the G1 phase of the cell cycle is observed when CDK4/6 dependent WM2664 cells are treated with G1T38 for 24 hours. This arrest is maintained through 300 nM, more than 300x the biochemical IC50. WM2664 cells treated with 30-1000 nM of Lerociclib for 24 hours exhibits a complete inhibition of RB phosphorylation compared to vehicle controls. Treatment with G1T38 reduces RB phosphorylation within 1 hour post-treatment and generates near complete inhibition of RB phosphorylation by 16 hours post-treatment. G1T38 produces a robust inhibition of proliferation in a diverse array of tumor cell lines including breast, melanoma, leukemia and lymphoma with EC50 concentrations as low as 23 nM[1].
In Vivo: In this HER2+ breast cancer model, Mice treated with Lerociclib elicits 8% tumor regression after 21 days of treatment while control animals have a 577% increase in tumor burden over the same treatment period. Compared to the vehicle-treated mice, daily treatment with 100 mg/kg of Lerociclib or palbociclib shows tumor regression within 10 days in the MCF7 xenograft model. After 27 days of treatment, tumor growth inhibition is observed in the 10, 50, and 100 mg/kg Lerociclib cohorts (approximately 12%, 74%, and 90% inhibition, respectively). Daily oral palbociclib treatment causes an 18%, 66%, and 87% tumor growth inhibition in the 10, 50, and 100 mg/kg dosage cohorts, respectively. Interestingly, at 50 mg/kg, Lerociclib is significantly more efficaciou than palbociclib. Similar results are seen in the ER+ ZR-75-1 breast cancer xenograft model when comparing Lerocyclib and palbociclib at the 50 mg/kg dose. Lerociclib treated mice exhibits 77% TGI with an overall 60% tumor growth delay demonstrating Lerociclib alone is highly efficacious in this NSCLC tumor model[1].

Name: Etilevodopa L-DOPA ethyl ester;Levodopa ethyl ester, CAS: 37178-37-3, stock 19.4g, assay 98.4%, MWt: 225.24, Formula: C11H15NO4, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Drug Metabolite, Biological_Activity: Etilevodopa (L-Dopa ethyl ester), an ethyl-ester prodrug of Levodopa, is rapidly hydrolyzed to Levodopa and ethanol by nonspecific esterases in the gastrointestinal tract. Etilevodopa is used for the treatment of Parkinson disease (PD). Levodopa is the direct precursor of dopamine and is a suitable prodrug as it facilitates CNS penetration and delivers dopamine[1][2][3].
In Vitro: Etilevodopa (L-Dopa ethyl ester) passes unchanged through the stomach to the duodenum, where it is rapidly hydrolyzed by local esterases to Levodopa and ethanol, and is subsequently absorbed into the blood stream as Levodopa[1]. 
Compared with standard Levodopa, Etilevodopa has greater solubility in the stomach, faster passage to the small intestine, and a shortened time to maximum Levodopa concentration[2].

Name: PF-4191834 PF-04191834, CAS: 1029317-21-2, stock 27.7g, assay 98.3%, MWt: 393.50, Formula: C22H23N3O2S, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Lipoxygenase, Biological_Activity: PF-4191834 (PF-04191834) is an orally active, noniron chelating, and non-redox inhibitor of the 5-Lipoxygenase (5-LOX) (IC50=229 nM), displays ~300-fold selectivity for 5-LOX over 12-LOX and 15-LOX, shows no activity toward the cyclooxygenase enzymes, and is effective in inflammation and pain[1].
IC50 & Target: IC50: 229 nM (5-LOX), 130 nM (human 5-LOX)[1]
In Vitro: PF-4191834 (PF-04191834) inhibits the synthesis of the 5-LOX products 5-HETE, 5-oxo-ETE, LTB4, and LTE4 with estimated IC50 values between 100 and 190 nM and do not inhibit significantly the COX-1/2 enzymes or the 12- or 15-LOX enzymes at concentrations up to 30 μM[1]. 
PF-4191834 (PF-04191834) exerts a concentration-dependent inhibition of human 5-LOX, with an IC50 value of 130 nM and an IC80 value of 370 nM[1].

Name: L-Lysine thioctate, CAS: 20902-53-8, stock 0.9g, assay 98.3%, MWt: 352.51, Formula: C14H28N2O4S2, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: L-Lysine thioctate is a substrate of lipoamidase[1].

Name: Dabuzalgron Ro 115-1240, CAS: 219311-44-1, stock 1.9g, assay 98.2%, MWt: 317.79, Formula: C12H16ClN3O3S, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: GPCR/G Protein;Neuronal Signaling, Target: Adrenergic Receptor;Adrenergic Receptor, Biological_Activity: Dabuzalgron (Ro 115-1240) is an orally active and selective α-1A adrenergic receptor agonist for the treatment of urinary incontinence. Dabuzalgron protects against Doxorubicin-induced cardiotoxicity by preserving mitochondrial function[1].
IC50 & Target: α-1A adrenergic receptor[1]
In Vitro: Dabuzalgron treatment increases ERK phosphorylation in a dose-dependent fashion with an EC50 of 4.8 μM. ERK1/2 activation contributes to the cardioprotective effects of Dabuzalgron[1]. 
Dabuzalgron (10 μM; 4 hours) protects NRVMs from cell death due to Doxorubicin (DOX)[1]. 
Activation of the α1A-AR with Dabuzalgron (10 μM; 4 hours) mitigates the detrimental effects of DOX on mitochondrial membrane potential and abrogates the activation of important elements of the apoptotic response to mitochondrial damage[1].
In Vivo: Dabuzalgron (10 μg/kg; oral gavage; twice daily; for 7 days; C57Bl6J wild-type or α1A-AR knockout mice) treatment protects against DOX cardiotoxicity by activating the α1A-AR. Dabuzalgron protects against the reduction in transcripts related to mitochondrial function, up-regulates PGC1α, preserves ATP content, and reduces oxidative stress in the hearts of mice treated with DOX[1].

Name: Isocryptotanshinone, CAS: 22550-15-8, stock 29.5g, assay 98.9%, MWt: 296.36, Formula: C19H20O3, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: JAK/STAT Signaling;Stem Cell/Wnt;Metabolic Enzyme/Protease, Target: STAT;STAT;Phosphatase, Biological_Activity: Isocryptotanshinone is a potent signal transducer and activator of transcription 3 (STAT3) and protein tyrosine phosphatase 1B PTP1B inhibitor, with an IC50 of 56.1 μM for PTP1B.
IC50 & Target: IC50: STAT3[1], 56.1 μM (PTP1B)[2].
In Vitro: It is showed that tanshinones significantly inhibited A549 proliferation and Isocryptotanshinone (ICTS) exhibits the strongest activity. Isocryptotanshinone inhibits the constitutive STAT3 and p-STAT3 (Y705) expression in concentration and time-dependent manners. Isocryptotanshinone dramatically inhibits the IL-6-stimulated expression of p-STAT3 (Y705) in a time-dependent manner[1].

Name: JI051, CAS: 2234281-75-3, stock 4.4g, assay 98.9%, MWt: 364.44, Formula: C22H24N2O3, Solubility: DMSO : 125 mg/mL (342.99 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Stem Cell/Wnt;Neuronal Signaling, Target: Notch;Notch, Biological_Activity: JI051 is a stabilizer for the Hes1-PHB2 interaction, interacts with a cancer-associated protein chaperone prohibitin 2 (PHB2), induces cell-cycle arrest by inhibiting the Notch downstream effector gene Hes1. Anti-cancer activity[1].
In Vitro: JI051 causes G2/M cell-cycle arrest[1]. 
JI051 (0.1-10 µM, 24 hours) significantly inhibits cell proliferation of HEK293 cells, with an EC50 of 0.3 μM[1].

Name: BN82002, CAS: 396073-89-5, stock 16.7g, assay 98.6%, MWt: 359.42, Formula: C19H25N3O4, Solubility: DMSO : ≥ 150 mg/mL (417.34 mM), Clinical_Informat: No Development Reported, Pathway: Metabolic Enzyme/Protease, Target: Phosphatase, Biological_Activity: BN82002 is a potent, selective and irreversible inhibitor of CDC25 phosphatase family. BN82002 inhibits CDC25A, CDC25B2, CDC25B3, CDC25C CDC25A, and 25C-cat with IC50 values of 2.4, 3.9, 6.3, 5.4, and 4.6 µM, respectively. BN82002 displays ~20-fold greater selectivity over CD45 tyrosine phosphatase[1].
IC50 & Target: IC50: 2.4 μM (CDC25A), 3.9 μM (CDC25B2), 6.3 μM (CDC25B3), 5.4 μM (CDC25C), 4.6 μM (CDC25C-cat)[1].
In Vitro: The effect of BN82002 on cell proliferation is evaluated in vitro on several human tumor cell lines. Menadione, which has been reported to inhibit cell proliferation, is used as a control. All of the examined cell lines are sensitive to BN82002 and Menadione in a concentration-dependent manner in the low micromolar range. The most sensitive is the pancreatic cancer cell line MIA PaCa-2 with an IC50 of 7.2 μM, and the less sensitive cell line is the colon cancer HT-29 with an IC50 of 32.6 μM. The range of activity is very similar to the one observed with menadione (5-15 μM). It is also showed that 50 μM BN82002 is a concentration that fully inhibits cell proliferation, the cell cycle distribution is only modestly affected with a slight decrease in S phase and an increase in cells containing both a G1 and a G2 DNA content, suggesting that the cells treated with BN82002 are arrested at various stages of the cell cycle[1].

Name: Kinesore, CAS: 363571-83-9, stock 1.1g, assay 98.2%, MWt: 536.17, Formula: C20H16Br2N4O4, Solubility: DMSO : 125 mg/mL (233.14 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Kinesore is an inhibitor of the KLC2-SKIP Interaction.
IC50 & Target: KLC2-SKIP[1].
In Vitro: Remarkably, in kinesore-treated cells, the microtubule network is entirely reorganized into a series of loops and bundles. In addition, the lysosomal compartment accumulates in a juxtanuclear position, where there are relatively few microtubules. At 50 μM kinesore, this phenotype is highly penetrant, with 95±2.4% (n=3, total of 200 cells) of cells exhibiting a reorganized nonradial microtubule network. In titration experiments, in cells treated for 1 h, this phenotype becomes apparent at a concentration of 25 μM kinesore, with relatively little effect at or below concentrations of 12.5 μM. The effect is reversible because a 2-h washout of kinesore from cells treated for 1 h led to the reestablishment of the radial microtubule array. This kinesore-induced reorganization of the microtubule network is observed in a panel of mammalian normal and cancer cell lines. In wild-type cells, 50 μM kinesore induces the remodeling of the microtubule network and the formation of extensive microtubule-rich projections. This phenotype is strongly suppressed in Kif5B knockout cells, confirming that microtubule remodeling induced by kinesore is dependent upon the presence of kinesin-1[1].

Name: NFAT Transcription Factor Regulator-1, CAS: 245747-71-1, stock 24.9g, assay 98.4%, MWt: 416.28, Formula: C17H10F6N4O2, Solubility: H2O : < 0.1 mg/mL (insoluble); DMSO : ≥ 150 mg/mL (360.33 mM), Clinical_Informat: No Development Reported, Pathway: Immunology/Inflammation, Target: Interleukin Related, Biological_Activity: NFAT Transcription Factor Regulator-1 is an IL-2 synthesis inhibitor with an IC50 of 182 nM.
IC50 & Target: IC50: 182 nM (IL-2 synthesis)[1]
In Vitro: NFAT Transcription Factor Regulator-1 (compound example 19) inhibits IL-2 synthesis with an IC50 of 182 nM. NFAT Transcription Factor Regulator-1 inhibits human and rat PBMC proliferation with IC50s of 82 and 146 nM, respectively. NFAT Transcription Factor Regulator-1 is able to inhibit IL-4 and IL-5 production in human T-cell lines with similar potency to its effects on IL-2 release[1].
In Vivo: NFAT Transcription Factor Regulator-1 is found to have an inhibitory potency approximately 10-fold better than that of cyclosporine. Comparable inhibitory effects on T-cell IL-2 production are obtained with NFAT Transcription Factor Regulator-1 and cyclosporine at doses of 3.0 and 30 mg/kg, po, respectively. The efficacies achieved in monkeys in vivo for blocking T-cell cytokine production suggest that NFAT Transcription Factor Regulator-1 has potential similar to that of cyclosporine for use in transplantation[1].

Name: Pertussis Toxin, CAS: 70323-44-3, stock 26.8g, assay 98.4%, MWt: 1000, Formula: N/A, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: Pertussis Toxin is a protein-based AB5-type exotoxin produced by the bacterium Bordetella pertussis, which causes whooping cough.
In Vitro: Pertussis toxin is a secreted protein exotoxin and an important virulence factor produced exclusively by B. pertussis.

Name: Everolimus RAD001;SDZ-RAD, CAS: 159351-69-6, stock 8.2g, assay 98.7%, MWt: 958.22, Formula: C53H83NO14, Solubility: DMSO : ≥ 54 mg/mL (56.35 mM); H2O : < 0.1 mg/mL (insoluble), Clinical_Informat: Launched, Pathway: PI3K/Akt/mTOR;Autophagy;Immunology/Inflammation;Apoptosis;Autophagy, Target: mTOR;Autophagy;FKBP;FKBP;FKBP, Biological_Activity: Everolimus is a targeted, highly specific agent with an IC50 for binding to isolated FKBP-12, or FKBP-12 complexed to mTOR of 5 to 6 nM, and no significant activity against other protein kinases.
IC50 & Target: IC50: 5 to 6 nM (mTOR)[1]
In Vitro: Everolimus (RAD001) is an orally active derivative of rapamycin that inhibits the Ser/Thr kinase, mTOR[1]. In both the sensitive murine B16/BL6 melanoma (IC50, 0.7 nM) and the insensitive human cervical KB-31 (IC50, 1,778 nM), antiproliferative concentrations of Everolimus results in total dephosphorylation of S6K1 and the substrate S6 and a shift in the mobility of 4E-BP1, which is indicative of a reduced phosphorylation status[2]. Everolimus exhibits a dose-dependent inhibition in both the total cells and the stem cells from the BT474 cell line and the primary breast cancer cells, albeit with different degrees of growth inhibition. Compare with the total cells, Everolimus is less effective in growth inhibition in the stem cells at all tested concentrations (P<0.001). The IC50 values of Everolimus for BT474 and the primary CSCs are 2,054 and 3,227 nM, or 29 times and 21 times greater than the IC50 values for their corresponding total cells, respectively[3].
In Vivo: Everolimus is orally active in both mice and rats, producing an antitumor effect that is characterized by dramatic reduction in tumor growth rates as opposed to producing tumor regressions. In the rat CA20498 model, daily treatment with Everolimus (0.5 or 2.5 mg/kg) dose-dependently inhibits growth, and intermittent dosing using a higher dose of 5 mg/kg (once or twice per week) also shows similar antitumor efficacy. Inhibition by Everolimus is characterized by sustained suppression rather than regression and is not associated with any body weight loss[1]. The effect of Everolimus treatment (0.1-10 mg/kg/d) is selective and differ from the effects of PTK/ZK (100 mg/kg). With either growth factor, Everolimus dose-dependently increases the hemoglobin content (convert to blood equivalents and indicative of the number of vessels as well as vascular leakiness) but reduces the Tie-2 content (number of endothelial cells indicative of the number of vessels) and this is significant for VEGF stimulation but not bFGF stimulation. The pharmacokinetics of Everolimus in mice shows that maximum levels of only 0.1 μM are achieved in a human tumor xenograft following a single administration, whereas plasma levels reach 1 to 3 μM for ~4 h[2].

Name: GW7604, CAS: 195611-82-6, stock 19.7g, assay 98%, MWt: 370.44, Formula: C25H22O3, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: Others, Target: Estrogen Receptor/ERR, Biological_Activity: GW7604 is an antiestrogen. GW7604 is the metabolite of GW5638, which is a high affinity estrogen receptor (ER) antagonist[1].
In Vitro: GW7604 is the presumed metabolite of GW5638 in breast (MCF-7) and endometrial (ECC-1) cell lines. GW7604 (0.1 nM-1 μM; 24 hours) inhibits both Estradiol (1 nM) and 4-hydroxytamoxifen (4-OHT; 10 and 100 nM) induction of TGF-alpha in a concentration related manner (1-1000 nM) in MDA-MB-231 cells[1].

Name: INH154, CAS: 1587705-63-2, stock 10.5g, assay 98.3%, MWt: 392.52, Formula: C22H24N4OS, Solubility: DMSO : 62.5 mg/mL (159.23 mM; Need ultrasonic); H2O : < 0.1 mg/mL (insoluble), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: INH154 is a highly potent inhibitor for Nek2 and Hec1 binding (INH), with IC50s of 200 nM and 120 nM for INH in Hela and MB468 cells.
IC50 & Target: IC50: 200 nM (INH in Hela cells), 120 nM (INH in MB468 cells)[1].
In Vitro: INH154 is highly potent in treating breast tumors with co-elevated expression of Hec1 and Nek2. INH154 is the most potent inhibitor of tumor cell growth. The IC50 values of INH154 in HeLa and MDA-MB-468 cancer cells are 0.20 and 0.12 μM, respectively. INH154 also suppresses the growth of leukemia, osteosarcoma, and glioblastoma cells[1].
In Vivo: Tumor growth rates in mice treated with INH154 are evidently slower than those in control animals in a dose-dependent manner. In agreement with the tumor-growth data, the tumor proliferation index, determined by measuring BrdU staining, is clearly reduced in residual tumors treated with INH154 in comparison with vehicle alone. The expression levels of Nek2 and Hec1 S165 phosphorylation are also substantially reduced in INH154-treated tumors than in vehicle-treated tumors. On the other hand, mice body weights are measured during the 6.5 weeks treatment period and show little difference among treated and control groups. In addition, the toxicity of INHs by treating normal BALB/c ByJNarl mice with high dosage of INH154 (20 mg/kg) shows no significant difference of body weights, blood chemistry, and complete blood count (CBC) analysis among these groups of animals[1].

Name: PKI-166, CAS: 187724-61-4, stock 3.7g, assay 98.9%, MWt: 330.38, Formula: C20H18N4O, Solubility: 10 mM in DMSO, Clinical_Informat: No Development Reported, Pathway: JAK/STAT Signaling;Protein Tyrosine Kinase/RTK, Target: EGFR;EGFR, Biological_Activity: PKI-166 is a potent, selective and orally bioavailable EGFR tyrosine kinase inhibitor, with an IC50 of 0.7 nM[1].
IC50 & Target: IC50: 0.7 nM (EGFR tyrosine kinase)[1]
In Vitro: Pretreatment with PKI-166 (0–0.5 μM; 1 hour) inhibits EGFR autophosphorylation in human pancreatic cancer cells[1]. 
PKI-166 (0.03μ M; 6 days) enhanced the cytotoxicity mediated by gemcitabine[1]. 
In Vivo: PKI-166 (100 mg/kg; p.o.; daily; day 7-day 35 after xenograft) inhibits of pancreatic cancer growth[1].

Name: KI696 isomer, CAS: 1799974-69-8, stock 23.8g, assay 98.2%, MWt: 550.63, Formula: C28H30N4O6S, Solubility: H2O : < 0.1 mg/mL (insoluble); DMSO : 125 mg/mL (227.01 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: NF-κB, Target: Keap1-Nrf2, Biological_Activity: KI696 isomer is the less active isomer of KI696. KI696 is a high affinity probe that disrupts the Keap1/NRF2 interaction.

Name: Retro-2 cycl RN 1-001, CAS: 1429192-00-6, stock 36.1g, assay 98.5%, MWt: 320.41, Formula: C19H16N2OS, Solubility: DMSO : ≥ 125 mg/mL (390.13 mM); H2O : < 0.1 mg/mL (insoluble), Clinical_Informat: No Development Reported, Pathway: Anti-infection;Anti-infection, Target: Arenavirus;Virus Protease, Biological_Activity: Retro-2 cycl (RN 1-001) is a dihydroquinazolinone (DHQZ) inhibitor of retrograde trafficking. Retro-2 cycl (RN 1-001) inhibits JCPyV and HPV16 pseudovirus with IC50s of 54 μM and 160 μM, respectively[1]. Antiviral agent[1].

Name: Eslicarbazepine BIA 2-194, CAS: 104746-04-5, stock 8.6g, assay 98.5%, MWt: 254.28, Formula: C15H14N2O2, Solubility: 10 mM in DMSO, Clinical_Informat: Launched, Pathway: Others, Target: Others, Biological_Activity: Eslicarbazepine is an oral anticonvulsant indicated for the adjunctive treatment of partial seizures.
In Vivo: Eslicarbazepine is an anti-epileptic drug, chemically related to carbamazepine but with a more favorable safety profile. Eslicarbazepine acetate is a prodrug for eslicarbazepine (S-licarbazepine), which is a dual a dual Inhibitor of β-Secretase and voltage-gated sodium channel[1][2].

Name: VTX-27, CAS: 1321924-70-2, stock 17.3g, assay 98.5%, MWt: 418.90, Formula: C20H24ClFN6O, Solubility: DMSO : 125 mg/mL (298.40 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: TGF-beta/Smad;Epigenetics, Target: PKC;PKC, Biological_Activity: VTX-27 is a selective protein kinase C θ (PKC θ) inhibitor, with Kis of 0.08 nM and 16 nM for PKC θ and PKC δ.
IC50 & Target: Ki: 0.08 nM (PKC θ), 16 nM (PKC δ)[1].
In Vitro: VTX-27 (Compound 27) possesses excellent overall characteristics. Good selectivity of VTX-27 is also seen against other PKC family members, particularly classical isoforms (>1000-fold except PKCβ I, 200-fold) and atypical isoforms (>10000-fold). As anticipated, attaining selectivity over the more closely related novel PKC family members is more challenging, with a good 200-fold being achieved over PKC δ[1].
In Vivo: VTX-27 shows the best PK profile with a low clearance (7 mL min-1 kg-1), long half-life (4.7 h), and good oral bioavailability (65%). A single dose of VTX-27 is administered orally at 6.25, 12.5, 25, and 50 mg/kg (e.g., at 25 mg/kg Cmax concentration 700 ng/mL) and demonstrates potent dose dependent inhibition of IL-2 production[1].

Name: SJ572403 SJ403, CAS: 19970-45-7, stock 18.4g, assay 98.3%, MWt: 275.31, Formula: C13H17N5O2, Solubility: DMSO : 13.89 mg/mL (50.45 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Others, Target: Others, Biological_Activity: SJ572403 (SJ403) is an inhibitor of disordered protein p27(Kip1). p27(Kip1) is a regulator of the CDKs that control eukaryotic cell division[1].
IC50 & Target: p27Kip1[1]

Name: Picaridin Lcaridin, CAS: 119515-38-7, stock 11.2g, assay 98.8%, MWt: 229.32, Formula: C12H23NO3, Solubility: DMSO : 250 mg/mL (1090.18 mM; Need ultrasonic), Clinical_Informat: No Development Reported, Pathway: Anti-infection, Target: Parasite, Biological_Activity: Picaridin (Lcaridin) is a topical insect repellent[1].

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