Tandutinib is an effective antagonist for FLT3, platelet-derived growth factor receptor (PDGFR), and c-Kit. Tandutinib potently inhibited the activity of FLT3, PDGFR, and c-Kit (IC50: ~200 nM).

Tandutinib showed no significant effects on other tyrosine or serine/threonine kinases. In Ba/F3 cells expressing different FLT3-ITD mutants, Tandutinib inhibited IL-3-independent cell growth and FLT3-ITD autophosphorylation (IC50: 10–100 nM). In human FLT3-ITD-positive AML cell lines, Tandutinib induced apoptosis and inhibited FLT3-ITD phosphorylation, cellular proliferation, and signaling through the MAP kinase and PI3 kinase pathways. Tandutinib inhibited phosphorylation of c-Kit, Akt, mTOR, and p70S6 kinase. Tandutinib significantly inhibited the proliferation and colony formation ability of colon cancer cell lines. Tandutinib decreased the expression level of COX-2, VEGF, and interleukin-8. Intraperitoneal administration of Tandutinib significantly suppressed the growth of colon cancer tumor xenografts. Tandutinib inhibited the expression of cancer-promoting genes COX-2 and VEGF and suppressed the activation of Akt/mTOR signaling proteins in the xenograft tissues [1][2].