| CAT # |
Product Name |
Description |
| CPDD0995 |
Bardoxolone methyl;RTA 402;NSC 713200;TP155;CDDOMe |
The synthetic oleanane triterpenoid CDDO (Item No. 81035) is a Nrf2 activator that inhibits proliferation and induces differentiation and apoptosis in various cancer cells. |
| CPD0854 |
Sotagliflozin;LX-4211 |
Sotagliflozin (LX-4211) is an SGLT1/2 inhibitor and an anti diabetes agent. |
| CPD1111 |
MAK683; EED inhibitor 1 |
MAK683 is an inhibitor of embryonic ectoderm development (EED) |
| CPD107768 |
Icotinib HCl；BPI2009 |
Icotinib Hydrochloride (BPI-2009) is an effective and selective EGFR inhibitor |
| CPD2809 |
AMG-510 |
AMG-510 is a potent KRAS G12C covalent inhibitor. AMG-510 selectively targets the KRAS p.G12C mutant, at either the DNA, RNA or protein level, and prevents, through an as of yet not elucidated manner, expression of and/or tumor cell signaling through the KRAS p.G12C mutant. This may inhibit growth in KRAS p.G12C-expressing tumor cells |
| CPD100230 |
JBJ-04-125-02 R-isomer |
|
| CPD102300 |
S-55746 |
|
| CPD101235 |
diABZI STING agonist-1 trihydrochloride |
diABZI STING agonist-1 (trihydrochloride) is a selective stimulator of interferon genes (STING) receptor agonist, with EC50s of 130, 186 nM for human and mouse, respectively. |
| CPD101234 |
diABZI STING agonist-1 (Tautomerism) |
diABZI STING agonist-1 Tautomerism (compound 3) is a selective stimulator of interferon genes (STING) receptor agonist, with EC50s of 130, 186 nM for human and mouse, respectively. |
| CPD101233 |
diABZI STING agonist-1 |
diABZI STING agonist-1 is a selective stimulator of interferon genes (STING) receptor agonist, with EC50s of 130, 186 nM for human and mouse, respectively. |
| CPD101232 |
STING agonist-4 |
STING agonist-4 is an stimulator of Interferon Genes (STING) receptor agonist with an apparent inhibitory constant (IC50) of 20 nM. STING agonist-4 is a two symmetry-related amidobenzimidazole (ABZI)-based compound to create linked ABZIs (diABZIs) with enhanced binding to STING and cellular function |
| CPD101231 |
STING agonist-3 |
STING agonist-3, extracted from patent WO2017175147A1 (example 10), is a selective and non-nucleotide small-molecule STING agonist with a pEC50 and pIC50 of 7.5 and 9.5, respectively. STING agonist-3 has durable anti-tumor effect and tremendous potential to improve treatment of cancer |
| CPD100904 |
Voruciclib |
Voruciclib, also known as P1446A-05, is a protein kinase inhibitor specific for the cyclin-dependent kinase 4 (CDK4) with potential antineoplastic activity. CDK4 inhibitor P1446A-05 specifically inhibits CDK4-mediated G1-S phase transition, arresting cell cycling and inhibiting cancer cell growth. The serine/threonine kinase CDK4 is found in a complex with D-type G1 cyclins and is the first kinase to become activated upon mitogenic stimulation, releasing cells from a quiescent stage into the G1/S growth cycling stage; CDK-cyclin complexes have been shown to phosphorylate the retinoblastoma (Rb) transcription factor in early G1, displacing histone deacetylase (HDAC) and blocking transcriptional repression. |
| CPD100905 |
Alvocidib |
Alvocidib is a synthetic N-methylpiperidinyl chlorophenyl flavone compound. As an inhibitor of cyclin-dependent kinase, alvocidib induces cell cycle arrest by preventing phosphorylation of cyclin-dependent kinases (CDKs) and by down-regulating cyclin D1 and D3 expression, resulting in G1 cell cycle arrest and apoptosis. This agent is also a competitive inhibitor of adenosine triphosphate activity. Check for active clinical trials or closed clinical trials using this agent. |
| CPD100906 |
BS-181 |
BS-181 is a highly selective CDK inhibitor for CDK7 with an IC(50) of 21 nmol/L. Testing of other CDKs as well as another 69 kinases showed that BS-181 only inhibited CDK2 at concentrations lower than 1 micromol/L, with CDK2 being inhibited 35-fold less potently (IC(50) 880 nmol/L) than CDK7. In MCF-7 cells, BS-181 inhibited the phosphorylation of CDK7 substrates, promoted cell cycle arrest and apoptosis to inhibit the growth of cancer cell lines, and showed antitumor effects in vivo. |
| CPD100907 |
Riviciclib |
Riviciclib, also known as P276-00 , is a flavone and cyclin dependent kinase (CDK) inhibitor with potential antineoplastic activity. P276-00 selectively binds to and inhibits Cdk4/cyclin D1, Cdk1/cyclin B and Cdk9/cyclin T1, serine/threonine kinases that play key roles in the regulation of the cell cycle and cellular proliferation. Inhibition of these kinases leads to cell cycle arrest during the G1/S transition, thereby leading to an induction of apoptosis, and inhibition of tumor cell proliferation. |
| CPD100908 |
MC180295 |
MC180295 is a highly selective CDK9 inhibitor (IC50 = 5 nM). (MC180295 has broad anti-cancer activity in vitro and is effective in in vivo cancer models. Additionally, CDK9 inhibition sensitizes to the immune checkpoint inhibitor α-PD-1 in vivo, making it an excellent target for epigenetic therapy of cancer. |
| 1073485-20-7 |
LDC000067 |
LDC000067 is a potent and selective CDK9 inhibitor. LDC000067 inhibited in vitro transcription in an ATP-competitive and dose-dependent manner. Gene expression profiling of cells treated with LDC000067 demonstrated a selective reduction of short-lived mRNAs, including important regulators of proliferation and apoptosis. Analysis of de novo RNA synthesis suggested a wide ranging positive role of CDK9. At the molecular and cellular level, LDC000067 reproduced effects characteristic of CDK9 inhibition such as enhanced pausing of RNA polymerase II on genes and, most importantly, induction of apoptosis in cancer cells. LDC000067 inhibits P-TEFb-dependent in vitro transcription. Induces apoptosis in vitro and in vivo in combination with BI 894999. |
| CPD100910 |
SEL120-34A |
SEL120-34A is a potent and selective CDK8 inhibitor active in AML cells with high levels of serine phosphorylation of STAT1 and STAT5 transactivation domains. EL120-34A inhibits phosphorylation of STAT1 S727 and STAT5 S726 in cancer cells in vitro. Consistently, regulation of STATs- and NUP98-HOXA9- dependent transcription has been observed as a dominant mechanism of action in vivo. |
| CPD100501 |
UNC2541 |
UNC2541 is a potent and MerTK-specific inhibitor that exhibits sub-micromolar inhibitory activity in the cell-based ELISA. In addition, an X-ray structure of MerTK protein in complex with 11 was resolved to show that these macrocycles bind in the MerTK ATP pocket. UNC2541 showed IC50 MerTH=4.4 nM; IC50 AXL = 120 nM; IC50 TYRO3 = 220 nM; IC50 FLT3 = 320 nM. |
| CPD100745 |
RU-302 |
RU-302 is a novel pan-tam inhibitor, blocking the interface between tam ig1 ectodomain and gas6 lg domain, potently inhibiting axl reporter cell lines and native tam receptors cancer cell lines |
| CPD100744 |
R916562 |
|
| CPD100743 |
Ningetinib-Tosylate |
CT-053, also known as DE-120, is a VEGF and PDGF inhibitor potentially for the treatment of wet age-related macular degeneration. |
| CPD100742 |
SGI-7079 |
SGI-7079 is a potent and selective Axl inhibitor with potential anticancer activity. SGI-7079 effectively inhibited Axl activation in the presence of exogenous Gas6 ligand. SGI-7079 inhibited tumor growth in a dose dependent manner. Axl is a potential therapeutic target for overcoming EGFR inhibitor resistance. |
| CPD100741 |
2-D08 |
2-D08 is a synthetic flavone that inhibits sumoylation. 2-D08 showed anti-aggregatory and neuroprotective effect |
| CPD100740 |
Dubermatinib |
Dubermatinib, also known as TP-0903, is a potent and selective AXL inhibitor. TP-0903 induces massive apoptosis in CLL B cells with LD50 values of nanomolar ranges. Combination of TP-0903 with BTK inhibitors augments CLL B-cell apoptosis AXL overexpression is a reoccurring theme observed in multiple tumor types that have acquired resistance to various agents. Treatment of cancer cells with TP-0903 reverses the mesenchymal phenotype in multiple models and sensitizes cancer cells to treatment with other targeted agents. Administration of TP-0903 either as a single agent or in combination with BTK inhibitors may be effective in treating patients with CLL. |
| CPD100739 |
NPS-1034 |
NPS-1034 is a novel MET inhibitor, which inhibits the activated MET receptor and its constitutively active mutants. NPS-1034, inhibits various constitutively active mutant forms of MET as well as HGF-activated wild-type MET. NPS-1034 inhibited the proliferation of cells expressing activated MET and promoted the regression of tumors formed from such cells in a mouse xenograft model through anti-angiogenic and pro-apoptotic actions. NPS-1034 also inhibited HGF-stimulated activation of MET signaling in the presence or absence of serum. Notably, NPS-1034 inhibited three MET variants that are resistant to the MET inhibitors SU11274, NVP-BVU972, and PHA665752. |
| CPD100738 |
Glesatinib |
Glesatinib, also known as MGCD-265, is an orally bioavailable, small-molecule, multitargeted tyrosine kinase inhibitor with potential antineoplastic activity. MGCD265 binds to and inhibits the phosphorylation of several receptor tyrosine kinases (RTKs), including the c-Met receptor (hepatocyte growth factor receptor); the Tek/Tie-2 receptor; vascular endothelial growth factor receptor (VEGFR) types 1, 2, and 3; and the macrophage-stimulating 1 receptor (MST1R or RON). |
| CPD100737 |
CEP-40783 |
CEP-40783, also known as RXDX-106, is a potent, selective and orally available inhibitor of AXL and c-Met with IC50 values of 7 nM and 12 nM, respectively for use in breast, non-small cell lung (NSCLC), and pancreatic cancers. |
| CPD1725 |
Bemcentinib |
BGB-324, also known as R428 or Bemcentinib, is a selective small molecule inhibitor of Axl kinase, which showed activity to blocks tumor spread and prolongs survival in models of metastatic breast cancer. The receptor tyrosine kinase Axl may play an important role in cancer progression, invasion, metastasis, drug resistance, and patient mortality. R428 inhibits Axl with low nanomolar activity and blocked Axl-dependent events, including Akt phosphorylation, breast cancer cell invasion, and proinflammatory cytokine production. |
| CPD3545 |
Gilteritinib |
Gilteritinib, also known as ASP2215, is a potent FLT3/AXL inhibitor, which showed potent antileukemic activity against AML with either or both FLT3-ITD and FLT3-D835 mutations. In invitro, among the 78 tyrosine kinases tested, ASP2215 inhibited FLT3, LTK, ALK, and AXL kinases by over 50% at 1 nM with an IC50 value of 0.29 nM for FLT3, approximately 800-fold more potent than for c-KIT, the inhibition of which is linked to a potential risk of myelosuppression. ASP2215 inhibited the growth of MV4-11 cells, which harbor FLT3-ITD, with an IC50 value of 0.92 nM, accompanied with inhibition of pFLT3, pAKT, pSTAT5, pERK, and pS6. ASP2215 decreased tumor burden in bone marrow and prolonged the survival of mice intravenously transplanted with MV4-11 cells. ASP2215 may have potential use in treating AML. |
| CPD100734 |
UNC2881 |
UNC2881 is a potent Mer kinase inhibitor. UNC2281 inhibits steady-state Mer kinase phosphorylation with an IC50 value of 22 nM. Treatment with UNC2281 is also sufficient to block EGF-mediated stimulation of a chimeric receptor containing the intracellular domain of Mer fused to the extracellular domain of EGFR. In addition, UNC2881 potently inhibits collagen-induced platelet aggregation, suggesting that this class of inhibitors may have utility for prevention and/or treatment of pathologic thrombosis. |
| CPD100733 |
UNC2250 |
UNC2250 is a potent and selective Mer Kinase inhibitor. When applied to live cells, UNC2250 inhibited steady-state phosphorylation of endogenous Mer with an IC50 of 9.8 nM and blocked ligand-stimulated activation of a chimeric EGFR-Mer protein. Treatment with UNC2250 also resulted in decreased colony-forming potential in rhabdoid and NSCLC tumor cells, thereby demonstrating functional antitumor activity. The results provide a rationale for further investigation of UNC2250 for therapeutic application in patients with cancer. |
| CPD100732 |
LDC1267 |
LDC1267 is a potent and selective TAM kinase inhibitor. LDC1267 displays lower activity against Met, Aurora B, Lck, Src, and CDK8. LDC1267 markedly reduced murine mammary cancer and melanoma metastases dependent on NK cells. The TAM tyrosine kinase receptors Tyro3, Axl and Mer (also known as Mertk) were identified as ubiquitylation substrates for Cbl-b. Treatment of wild-type NK cells with a newly developed small molecule TAM kinase inhibitor conferred therapeutic potential, efficiently enhancing anti-metastatic NK cell activity in vivo. |
| CPD100731 |
BMS-777607 |
BMS-777607, also known as BMS-817378 and ASLAN-002, a Met tyrosine kinase inhibitor, is an inhibitor of MET tyrosine kinase with potential antineoplastic activity. MET tyrosine kinase inhibitor BMS-777607 binds to c-Met protein, or hepatocyte growth factor receptor (HGFR), preventing binding of hepatocyte growth factor (HGF) and disrupting the MET signaling pathway; this agent may induce cell death in tumor cells expressing c-Met. c-Met, a receptor tyrosine kinase overexpressed or mutated in many tumor cell types, plays an important role in tumor cell proliferation, survival, invasion, and metastasis, and in tumor angiogenesis. |
| CPD100730 |
Cabozantinib |
Cabozantinib, also known as XL-184 or BMS-907351, is an orally bioavailable, small molecule receptor tyrosine kinase (RTK) inhibitor with potential antineoplastic activity. Cabozantinib strongly binds to and inhibits several tyrosine receptor kinases. Specifically, cabozantinib appears to have a strong affinity for the hepatocyte growth factor receptor (Met) and vascular endothelial growth factor receptor 2 (VEGFR2), which may result in inhibition of tumor growth and angiogenesis, and tumor regression. Cabozantinib was approved by the U.S. FDA in November 2012 for the treatment of medullary thyroid cancer. |
| CPD100654 |
PD-169316 |
PD-169316 is a selective inhibitor of p38 MAPK. It inhibits p38 MAPK with an IC50 of 89 nM. PD169316, inhibits transforming growth factor beta-induced Smad signaling in human ovarian cancer cells. |
| CPD100653 |
LDN-193189 |
LDN193189 is a highly potent small molecule BMP inhibitor with IC50 of 5 and 30 nM for ALK2 and ALK3, respectively. LDN193189 also inhibits BMP type I receptors ALK6 (TGFβ1/BMP signaling) and subsequent SMAD phosphorylation. |
| CPD100652 |
K02288 |
K02288 is a potent inhibitor of BMP signaling. K02288 has in vitro activity against ALK2 at low nanomolar concentrations similar to the current lead compound LDN-193189. K02288 specifically inhibited the BMP-induced Smad pathway without affecting TGF-β signaling and induced dorsalization of zebrafish embryos |
| CPD100650 |
SB-431542 |
SB-431542 is a novel small molecule inhibitor of the type I TGF-beta receptor, on a panel of human malignant glioma cell lines. SB-431542 blocked the phosphorylation and nuclear translocation of the SMADs, intracellular mediators of TGF-beta signaling, with decreased TGF-beta-mediated transcription. Furthermore, SB-431542 inhibited the expression of two critical effectors of TGF-beta-vascular endothelial growth factor and plasminogen activator inhibitor-1. |
| CPD100649 |
GW788388 |
GW788388 is a new TGF-beta type I receptor inhibitor with a much improved pharmacokinetic profile compared with SB431542. We studied its effect in vitro and found that it inhibited both the TGF-beta type I and type II receptor kinase activities, but not that of the related bone morphogenic protein type II receptor. Further, it blocked TGF-beta-induced Smad activation and target gene expression, while decreasing epithelial-mesenchymal transitions and fibrogenesis. |
| CPD100648 |
SB-525334 |
SB525334 is a potent and selective inhibitor of the transforming growth factor-beta1 (TGF-beta1) receptor, activin receptor-like kinase (ALK5). SB525334 inhibited ALK5 kinase activity with an IC(50) of 14.3 nM and was approximately 4-fold less potent as an inhibitor of ALK4 (IC(50) = 58.5 nM). SB-525334 was inactive as an inhibitor of ALK2, ALK3, and ALK6 (IC(50) > 10,000 nM). In cell-based assays, SB-525334 (1 microM) blocked TGF-beta1-induced phosphorylation and nuclear translocation of Smad2/3 in renal proximal tubule cells and inhibited TGF-beta1-induced increases in plasminogen activator inhibitor-1 (PAI-1) and procollagen alpha1(I) mRNA expression in A498 renal epithelial carcinoma cells. |
| CPD100647 |
BIBF0775 |
BIBF0775 is an inhibitor of the transforming growth factor β receptor I (TGFβRI). X-ray structure analysis showed that BIBF0775 soaked into the kinase domain of TGFβRI |
| CPD100646 |
LY3023414 |
LY3023414 is a small molecule that has been shown in vitro to be a selective ATP-competitive inhibitor of PI3Kα and mTOR, DNA-PK, and other class I PI3K family members. In vitro, LY3023414 has demonstrated inhibitory activity against PI3K and mTOR in tumor cells, as well as antiproliferative activity and cell cycle effects. In addition, in vitro, LY3023414 inhibits the ability of PI3K and mTOR to phosphorylate substrates in the PI3K/mTOR pathway. LY3023414 is being investigated in a phase I clinical trial. |
| CPD100645 |
Onatasertib |
CC-223 is an orally available inhibitor of the mammalian target of rapamycin (mTOR) with potential antineoplastic activity. mTOR kinase inhibitor CC-223 inhibits the activity of mTOR, which may result in the induction of tumor cell apoptosis and a decrease in tumor cell proliferation. mTOR, a serine/threonine kinase that is upregulated in a variety of tumors, plays an important role downstream in the PI3K/AKT/mTOR signaling pathway, which is frequently dysregulated in human cancers. |
| CPD100644 |
Bimiralisib |
Bimiralisib, also known as PQR309, is an orally bioavailable pan inhibitor of phosphoinositide-3-kinases (PI3K) and inhibitor of the mammalian target of rapamycin (mTOR), with potential antineoplastic activity. PI3K/mTOR kinase inhibitor PQR309 inhibits the PI3K kinase isoforms alpha, beta, gamma and delta and, to a lesser extent, mTOR kinase, which may result in tumor cell apoptosis and growth inhibition in cells overexpressing PI3K/mTOR. Activation of the PI3K/mTOR pathway promotes cell growth, survival, and resistance to both chemotherapy and radiotherapy. |
| CPD100643 |
CZ415 |
CZ415 is a potent ATP-competitive mTOR inhibitor with unprecedented selectivity over any other kinase (IC50 = 14.5 nM IC50 for pS6RP and 14.8 nM for pAKT) with very good cell permeability (Kd app = 6.9 nM). Pharmacokinetic properties of moderate clearance and good oral bioavailability showed suitability of CZ415 for progression to in vivo studies. CZ415 represents an ideal molecule for the pharmacological investigation of mTOR pathophysiological role in vivo. |
| CPD100642 |
GDC-0084 |
GDC-0084, also known as RG7666 and Paxalisib, is a phosphatidylinositol 3-kinase (PI3K) inhibitor with potential antineoplastic activity. PI3K inhibitor GDC-0084 specifically inhibits PI3K in the PI3K/AKT kinase (or protein kinase B) signaling pathway, thereby inhibiting the activation of the PI3K signaling pathway. This may result in the inhibition of both cell growth and survival in susceptible tumor cell populations. Activation of the PI3K signaling pathway is frequently associated with tumorigenesis. |
| CPD100641 |
CC-115 |
CC-115 is a dual inhibitor of DNA-dependent protein kinase (DNA-PK) and mammalian target of rapamycin (mTOR), with potential antineoplastic activity. CC-115 binds to and inhibits the activity of DNA-PK and both raptor-mTOR (TOR complex 1 or TORC1) and rictor-mTOR (TOR complex 2 or TORC2), which may lead to a reduction in cellular proliferation of cancer cells expressing DNA-PK and TOR. DNA-PK, a serine/threonine kinase and a member of the PI3K-related kinase subfamily of protein kinases, is activated upon DNA damage and plays a key role in repairing double-stranded DNA breaks via the DNA nonhomologous end joining (NHEJ) pathway. |
| CPD100640 |
XL388 |
XL388 is a Novel Class of Highly Potent, Selective, ATP-Competitive, and Orally Bioavailable Inhibitors of the Mammalian Target of Rapamycin (mTOR). XL388 inhibited cellular phosphorylation of mTOR complex 1 (p-p70S6K, pS6, and p-4E-BP1) and mTOR complex 2 (pAKT (S473)) substrates. XL388 displayed good pharmacokinetics and oral exposure in multiple species with moderate bioavailability. Oral administration of XL388 to athymic nude mice implanted with human tumor xenografts afforded significant and dose-dependent antitumor activity. |
