FLT3 Inhibitor

SR-2890 is a highly selective, ATP-competitive inhibitor of casein kinase CK1δ and CK1ε, with IC₅₀ values ​​of 4 nM and 44 nM, respectively, and a K_i of 14 nM for CK1δ. SR-2890 exhibits antiproliferative effects. SR-2890 blocks the serine/threonine kinase activity of CK1δ and weakly inhibits a few off-target kinases such as FLT3, CDK4. SR-2890 has an oral bioavailability of 10% and a blood-brain barrier penetration rate of <1%. SR-2890 demonstrates stable in vitro metabolism and favorable in vivo pharmacokinetic properties, effectively inhibiting the growth of human A375 melanoma cells. SR-2890 can be used in melanoma research and is also a useful compound for studying CK1δ/ε-related diseases such as Alzheimer's disease.

3-Hydroxy Midostaurin-d₅ is a deuterium labeled 3-Hydroxy Midostaurin. 3-Hydroxy Midostaurin is a metabolite of PKC412, which effectively inhibits FMS-like tyrosine kinase-3 (FLT3) autophosphorylation with IC₅₀s of approximately 132 nM and 9.8 μM in culture medium and plasma, respectively.

HPK1-IN-2 TFA is an orally active HPK1 inhibitor (IC₅₀ < 0.05 µM) with antitumor activity. HPK1-IN-2 TFA inhibits the activity of Lck (IC₅₀ <0.05 µM) and Flt3 (IC₅₀ < 0.05 µM) kinases.

YTB53 is a MNK1 and MNK2 inhibitor with IC₅₀s of 37 nM and 9 nM, respectively. YTB53 inhibits PDGFRα, TRKB and FLT3 in leukemia cells. YTB53 induces cell cycle arrest, apoptosis, pyroptosis, and mitochondrial dysfunction. YTB53 exhibits antiangiogenic effects. YTB53 can be used for the study of acute myeloid leukemia (AML).

FLT3/IRAK4-IN-1 is a selective FLT3/IRAK4 inhibitor with the remarkable activity towards FLT3-WT (IC₅₀ = 1.95 nM), FLT3-D835Y (IC₅₀ = 3.22 nM) and IRAK4 (IC₅₀ = 53.72 nM). LT3/IRAK4-IN-1 has relatively low toxicity to normal bone marrow cells, can effectively promote cell apoptosis, and has the potential to overcome drug resistance. FLT3/IRAK4-IN-1 can be used for research on acute myeloid leukemia (AML).

BTK-IN-48 is a BTK inhibitor with an IC₅₀ of 1.14 μM. BTK-IN-48 inhibits recombinant BTK and c-Src, and exerts moderate inhibitory effects on LCK, BMX/ETK, FLT3 and PIM1. BTK-IN-48 can be used in the research of B-cell malignancies and autoimmune diseases.

FLT3-IN-33 (Compound 7r) is a FLT3 inhibitor with an IC₅₀ of 7.82  nM. FLT3-IN-33 has superior anticancer activities against acute myeloid leukemia (AML) cells, such as MV4-11 and MOLM-13 cells. FLT3-IN-33 significantly induces cell apoptosis and inhibits phosphorylation of FLT3 pathways. FLT3-IN-33 can be used for AML and other cancers research.

FLT3-IN-23 (compound 15) is an inhibitor of JFMS-like tyrosine kinase 3 (FLT3) with an IC₅₀ of 7.42 nM. FLT3-IN-23 has antiproliferative activities against BaF3 cells carrying various FLT3-TKD and FLT3-ITD-TKD mutations.

LY2457546 is a potent and orally active multi-targeted anti-angiogenic tyrosine kinases inhibitor. LY2457546 demonstrates potent activity against targets that include VEGFR2, PDGFRβ, FLT-3, Tie-2 and members of the Eph family of receptors. LY2457546 can be used for the research of cancer, such as leukemia.

JI6 is a potent, selective and orally active FLT3 inhibitor, with IC₅₀s of ～40, 8, and 4 nM for FLT3-WT, FLT3-D835Y, and FLT3-D835H, respectively. JI6 also inhibits JAK3 and c-Kit, with IC₅₀s of ～250 and ～500 nM, respectively. JI6 can be used for the research of acute myeloid leukemia.

FW-1 is a type I inhibitor for FLT3 with IC₅₀ of ca. 1 μM. FW-1 exhibits cytotoxicity in FLT3 mutated AML cell. FW-1 arrests the cell cycle at G0/G1 phase, and induces apoptosis in cell MV4-11 and MOLM-13.

FLT3-IN-32 hydrochloride is a potent and orally active FLT3 inhibitor with an IC₅₀s of 0.29 nM, 0.77 nM and 2.07 nM against FLT3-ITD, FLT3-D835Y and FLT-N676K. FLT3-IN-32 hydrochloride reduces the phosphorylation of FLT3 and its downstream signaling molecules (STAT5, MAPK, AKT) to induce FLT3-mutated Ba/F3 cells apoptosis. FLT3-IN-32 hydrochloride shows significant anti-tumor efficacy in n the MV4-11 xenograft model. FLT3-IN-32 hydrochloride can be used for the study of acute myeloid leukemia (AML).

TRK II-IN-1 is a potent type II TRK inhibitor, with IC₅₀s of 3.3, 6.4, 4.3 and 9.4 nM, for TRKA/B/C and TRKA^G667C, respectively. TRK II-IN-1 also inhibits FLT3, RET, and VEGFR2 with IC₅₀s of 1.3, 9.9, and 71.1 nM, respectively. TRK II-IN-1 can be used for the research of TRK driven cancers.

FLT3/D835Y-IN-1 (compound 13a) is a orally active, potent and selective FLT3 and FLT3/D835Y inhibitor, with IC₅₀ values of 0.26 nM and 0.18 nM, respectively. FLT3/D835Y-IN-1 also blocks tumor growth, has anticancer efficacy, and can be used to research for AML (acute myeloid leukemia).

FLT3-IN-14 is a potent FLT3 inhibitor with IC₅₀s of 5.6 nM and 1.4 nM for FLT3-WT and FLT3-ITD. FLT3-IN-14 reduces the phosphorylation of FLT3 (Y591), induces cell cycle arrest at G1 phase and apoptosis. FLT3-IN-14 significantly reduces the tumor growth in an MV4-11 xenograft mouse model.

FLT3-IN-25 (compound 17) is a potent inhibitor of FLT3, with IC₅₀s of 1.2 nM, 1.4 nM and 1.1 nM for FLT3-WT, FLT3-D835Y and FLT3-ITD, respectively. FLT3-IN-25 plays an important role in acute myeloid leukemia (AML).

FLT3-IN-43 is an orally active inhibitor of tubulin and FLT3 kinase, with an IC₅₀ of 3.6 μM against tubulin and an IC₅₀ of 58.6 nM against human FLT3 kinase. FLT3-IN-43 binds to the colchicine-binding site on tubulin to inhibit microtubule polymerization. FLT3-IN-43 suppresses FLT3 kinase activity. FLT3-IN-43 disrupts the cellular microtubule network. Tubulin-IN-69 induces cell cycle arrest. Tubulin-IN-69 induces tumor cell apoptosis. FLT3-IN-43 is used for research on acute myeloid leukemia and solid tumors including colorectal cancer, lung adenocarcinoma, and breast cancer.

CHEMBL4444839 is an inhibitor of FLT3 and can be used in the research of acute myeloid leukemia (AML).

FLT3/HDAC-IN-2 is (compound 25h) a FLT3/HDAC dual inhibitor. FLT3/HDAC-IN-2 has antiproliferative activity against MOLM-13 cells. FLT3/HDAC-IN-2 can be used in acute myeloid leukemia research.

VEGFR2-IN-84 is an orally active, multi-targeted tyrosine kinase inhibitor based on a naphthalene ring scaffold. VEGFR2-IN-84 inhibits VEGFR2 with sub-nanomolar affinity and broadly targets kinases including Kit, FGFR, PDGFR, and Ret. By competitively binding to the ATP-binding pocket, VEGFR2-IN-84 blocks the phosphorylation of VEGFR2 and its downstream AKT/ERK signaling pathway, thereby significantly inhibiting endothelial cell proliferation, migration, and tumor angiogenesis. VEGFR2-IN-84 exhibits broad-spectrum antiproliferative activity against various solid tumors such as liver cancer, lung cancer, and renal cancer, shows weak toxicity to normal cells, and has superior potency to Lenvatinib (HY-10981). VEGFR2-IN-84 possesses favorable pharmacokinetic properties and high safety (LD₅₀>2000 mg/kg), and can be used in related studies of various malignant tumors.