CAT # Product Name Description
CPD100534 AZD4573 AZD-4573 is a selective, short-acting inhibitor of the serine/threonine cyclin-dependent kinase 9 (CDK9), the catalytic subunit of the RNA polymerase II (RNA Pol II) elongation factor positive transcription elongation factor b (PTEF-b; PTEFb), with potential antineoplastic activity. Upon intravenous administration, AZD4573 binds to and blocks the phosphorylation and kinase activity of CDK9, thereby preventing PTEFb-mediated activation of RNA Pol II, leading to the inhibition of gene transcription of various anti-apoptotic proteins.
CPD100029 Pemigatinib Pemigatinib, also known as INCB054828, is an orally bioavailable inhibitor of the fibroblast growth factor receptor (FGFR) types 1, 2, and 3 (FGFR1/2/3), with potential antineoplastic activity. FGFR inhibitor INCB054828 binds to and inhibits FGFR1/2/3, which may result in the inhibition of FGFR1/2/3-related signal transduction pathways. This inhibits proliferation in FGFR1/2/3-overexpressing tumor cells.
CPD100502 UNC4203 UNC4203 is a potent and selective MERTK Inhibitor. UNC4203 showed IC50 MerTK=2.4 nM (Ki=0.42 nM); IC50 Axl = 80 nM (Ki=40.22 nM); IC50 Tyro3 = 9.1 nM (Ki=3.87 nM). IC50 FLT3 = 39 nM *Ki=16.14 nM). T1/2 = 3.0 h; %F=15. UNC4203 may be a potential candidate for cancer treatment
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.
CPD100500 UNC-2025 UNC-2025 is a novel potent and highly orally bioavailable Mer/FLT3 dual inhibitor, capable of inhibiting Mer phosphorylation in vivo, following oral dosing as demonstrated by pharmaco-dynamic (PD) studies examining phospho-Mer in leukemic blasts from mouse bone marrow. Kinome profiling versus more than 300 kinases in vitro and cellular selectivity assessments demonstrate that UNC-2025 has similar subnanomolar activity against Flt3, an additional important target in acute myelogenous leukemia (AML), with pharmacologically useful selectivity versus other kinases examined.
CPD100418 CPD100418
CPD100417 CPD100417
CPD100464 Erdafitinib Erdafitinib, also known as JNJ-42756493, is a potent and selective orally bioavailable, pan fibroblast growth factor receptor (FGFR) inhibitor with potential antineoplastic activity. Upon oral administration, JNJ-42756493 binds to and inhibits FGFR, which may result in the inhibition of FGFR-related signal transduction pathways and thus the inhibition of tumor cell proliferation and tumor cell death in FGFR-overexpressing tumor cells. FGFR, upregulated in many tumor cell types, is a receptor tyrosine kinase essential to tumor cell proliferation, differentiation and survival.
CPD100395 BI-3802
CPD100394 AZD1390
CPD100393 AZD0156
CPD100392 ATM Inhibitor-1
CPD100391 SHP394
CPD100390 SHP389 (free base)
CPD100377 BAY-677
CPD100375 MLT-747
CPD100374 MLT-748
CPD100099 BMS-986165 BMS-986165 is a Highly Potent and Selective Allosteric Inhibitor of TYK2. BMS-986165 Blocks Il-12, IL-23 and type I Interferon Signaling and Provides for Robust Efficacy in Preclinical Models of Inflammatory Bowel Disease. MS-986165 potently binds to the Tyk2 pseudokinase domain (Ki = 0.02 nM), and is highly selective against a panel of 265 kinases and pseudokinases. The compound potently inhibited IL-23-, IL-12-, and Type I interferon-driven cellular signaling and transcriptional responses (IC50 range 2-14 nM).
CPD10000 BI-3406 BI-3406 is Potent & Selective SOS1::KRAS Inhibitor (IC50=5 nM), which Opens a New Approach for Treating KRAS-Driven Tumours. BI 3406 selectively binds to SOS1 and blocks the interaction with KRAS, irrespective of the KRAS mutation. BI 3406 causes RAS GTP and pERK reduction and inhibits cell growth of KRAS mutated cell lines, carrying most of the typical KRAS mutations (i.e. G12D, G12V, G13D and others). BI 3406, when administered orally to tumour bearing mice, causes a dose dependent tumour static effect that can be converted into regressions when combined with MEK1 inhibition
CPDD1551 CPDD1551
CPDD1622 CPDD1622
CPDD2025 CPDD2025

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