MA191

MA191 (10-100 nM; 24-72 h) significantly induces apoptosis and inhibits cell growth in MV4-11 and MOLM-13 cells, with an IC₅₀ range of 9.6-11 nM after 72 h of treatment^[1].
MA191 (10-50; 6-24 h) degrades FLT3-ITD (with a DC₅₀ of 10 nM after 24 h), inhibits FLT3 autophosphorylation and the phosphorylation of downstream ERK1/2, STAT5 and AKT, downregulates HSP110, and activates caspase-3 in MV4-11 and MOLM-13 cells^[1].
MA191 (50 nM; 24-72 h) weakly degrades wild-type FLT3 in RS4-11 cells, and does not activate STAT5 or induce apoptosis^[1].
MA191 (50-100 nM; 24-72 h) slightly induces apoptosis in HMC-1.1 cells, inhibits c-KIT phosphorylation but does not degrade c-KIT^[1].
MA191 (50 nM; 48-72 h) significantly induces cell apoptosis, degrades FLT3-ITD and FLT3-ITD/TKD, inhibits STAT5 phosphorylation, and triggers caspase-3 cleavage in MOLM-13, LM-13-RES and MOLM-13-RES-AC cells^[1].
MA191 (50 nM; 48 h) significantly induces apoptosis in AML cells in MOLM-13 and MV4-11 cells co-cultured with HS-5 bone marrow stromal cells, while exhibiting no toxicity to HS-5 cells^[1].
MA191 (72 h) reduces cell viability in primary FLT3-ITD⁺ AML cells (with an IC₅₀ range of 0.015-0.883 µM), while it exerts toxic effects on normal human bone marrow cells only at 50 μM.
MA191 (20-100 nM; 24-48 h) does not affect cell viability in normal human peripheral blood mononuclear cells (PBMCs) and murine SCA-1⁺/c-KIT⁺ hematopoietic stem cells^[1].
MA191 (20-50 nM; 24 h) induces the collapse of mitochondrial membrane potential in MV4-11 cells^[1].
MA191 (50-100 nM; 7 days) does not affect cell differentiation and the expression of functional surface markers (such as CD86) in mouse bone marrow-derived macrophages and dendritic cells^[1].

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