FLT3-IN-36 

FLT3-IN-36 is a potent FLT3 inhibitor. FLT3-IN-36 exhibits antitumor activity against FLT3-mutated acute myeloid leukemia (AML) cells. FLT3-IN-36 induces cell cycle arrest, reduces mitochondrial membrane potential, and induces apoptosis, downregulating FLT3 and downstream protein expression (including AKT, ERK, PI3K, and STAT5). FLT3-IN-36 can be used for AML research^[1].

FLT3-IN-36 (compound 8h) (24 h) exhibits selective antiproliferative activity against FLT3 mutant AML cells, with IC₅₀s of 2.04 (MV4-11) and 3.25 μM (MOLM-13), while showing significantly weaker effects on FLT3 wild-type cells such as THP-1, U937, and OCI-AML2 (IC₅₀ = 19.59, 91.49, and 55.38 μM)^[1].
FLT3-IN-36 (0.1-100 μM, 24 h) inhibits MV4-11 cell growth in a time- and dose-dependent manner, while showing low cytotoxicity in normal HK-2 and HepRG cells^[1].
FLT3-IN-36 (1-10 μM, 24 h) induces apoptosis, G2/M phase cell cycle arrest and a reduction of mitochondrial membrane potential in MV4-11 cells in a dose-dependent manner^[1].
FLT3-IN-36 (0-10 μM, 24 h) inhibits the growth of MV4-11 cells by by downregulating FLT3 protein levels and inactivating its downstream signaling pathway, including key effectors such as AKT, ERK, PI3K, and STAT5^[1].
FLT3-IN-36 fits well to the ATP binding pocket of FLT3 and only interacts with the residues Glu692 and Cys694 in the hinge region of the active conformation^[1].
FLT3-IN-36 (1-10 μM) directly targets FLT3 kinase, exhibiting 58% inhibition of FLT3-ITD kinase activity at 10 μM^[1].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

331.36

C₂₁H₁₇NO₃

O=C(C1CC1)C2=CC(C(C3=C(C(C)=O)C=CC=C3)=O)=C4C=CC=CN42

Room temperature in continental US; may vary elsewhere.

Please store the product under the recommended conditions in the Certificate of Analysis.

• [1]. Xing Q, et al. Development and bio-evaluation of novel indolizine derivatives in FLT3 mutant acute myeloid leukemia cells. Bioorg Med Chem Lett. 2025 Oct 4;130:130429.