||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.
||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.
||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.
||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
||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
||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.
||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.
|| 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.
||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.
||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.
||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.
||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.
||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.
||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
||CT-053, also known as DE-120, is a VEGF and PDGF inhibitor potentially for the treatment of wet age-related macular degeneration.
||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.
||2-D08 is a synthetic flavone that inhibits sumoylation. 2-D08 showed anti-aggregatory and neuroprotective effect
||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.
||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.
||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).
|| 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.
||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.
||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.