PF15 TFA

PF15 TFA potently and selectively inhibits FLT3 kinase with an IC₅₀ of 36 nM, and its inhibitory potency against c-Kit kinase is over 35-fold lower; it exhibits high selectivity for FLT3 among a panel of 93 tumor-related kinases^[1].
PF15 (1-2000 nM; 1-24 h) TFA induces proteasome-dependent degradation of FLT3 protein in BaF3-FLT3-ITD cells, with a DC₅₀ of 76.7 nM, and prolonged incubation achieves complete degradation of the protein^[1].
PF15 (10-1000 nM; 2 h) TFA upregulates FLT3 mRNA levels in BaF3-FLT3-ITD cells at low concentrations (10 nM, 30 nM)^[1].
PF15 (72 h) TFA potently inhibits the proliferation of MV4-11 FLT3-ITD-positive AML cells with an IC₅₀ of 4.83 nM; potently inhibits the proliferation of Molm-13 FLT3-ITD-positive AML cells with an IC₅₀ of 4.01 nM; potently inhibits the proliferation of BaF3-FLT3-ITD transformed cells with an IC₅₀ of 7.85 nM; inhibits the proliferation of drug-resistant BaF3-FLT3-ITD-D835V transformed cells with an IC₅₀ of 120.1 nM; inhibits the proliferation of drug-resistant BaF3-FLT3-ITD-F691L transformed cells with an IC₅₀ of 116.6 nM; and exhibits only extremely low antiproliferative activity against FLT3 wild-type cancer cells (THP-1, K562, Daudi, HEL, Jurkat, RS4;11)^[1].
PF15 (10-1000 nM; 6 h) TFA downregulates the phosphorylation levels of FLT3 and STAT5 in BaF3-FLT3-ITD, BaF3-FLT3-ITD-D835V, and BaF3-FLT3-ITD-F691L cells at a concentration of 100 nM after 6 h of treatment, whereas a higher concentration is required for FLT3 degradation^[1].

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