FLT3-IN-32 hydrochloride is a potent, orally active FLT3 inhibitor with IC50 values of 0.29 nM for FLT3-ITD, 0.77 nM for FLT3-D835Y, and 2.07 nM for FLT3-N676K. It induces apoptosis in FLT3-mutant Ba/F3 cells by reducing the phosphorylation of FLT3 and its downstream signaling molecules (STAT5, MAPK, AKT). In MV4-11 xenograft models, it demonstrates significant antitumor effects. This compound is suitable for research in acute myeloid leukemia (AML).

FLT3-IN-32 hydrochloride (Compound 29c) at concentrations between 0-100 nM for 72 hours exhibits no cytotoxicity towards HepG2 liver cells, NCI-H460 lung cancer cells, or HMEC-1 endothelial cells. It specifically inhibits Ba/F3 pMIY cells expressing various resistant FLT3 mutations (ITD-mutation NPOS, TKD-mutation D835Y, ITD-mutation NPOS and TKD-mutation D835Y, ITD-mutation NPOS and TKD-mutation N676K). Furthermore, FLT3-IN-32 hydrochloride at 1-500 nM for 4-48 hours induces apoptosis in Ba/F3 pMIY cells by reducing FLT3 phosphorylation.

20(R)-Ginsenoside Rh2, administered at 20-75 mg/kg either orally (p.o.) or intraperitoneally (i.p.) once daily for 4-5 days, demonstrates antitumor efficacy and good tolerability in the MV4-11 xenograft mouse model.