Lestaurtinib

Lestaurtinib (CEP-701) is an orally active and selective RPTKs (receptor protein tyrosine kinase) inhibitor, competitively inhibits ATP binding to the TrkA/B/C domain. Lestaurtinib inhibits RPTKs phosphorylation, with IC₅₀s of 2, 25 and 0.9 nM for FLT3, TrkA and JAK2, respectively. Lestaurtinib induces apoptosis and cycle arrest, also can inhibit growth of tumor^{[1][2][3][4][5][6]}. In Vitro: Lestaurtinib (0.01-10 µM; 72 h) inhibits growth of ATC cells, with IC₅₀s of 0.21, 0.41 and 2.35 µM for KMH2, CAL62 and THJ-21T cells, respectively^[1].
Lestaurtinib (0.125-4 µM; 24 h) decreases STAT5 phosphorylation in a concentration-dependent manner, and completely inhibits expression of pSTAT5 at 4 μM^[1].
Lestaurtinib (0.5 µM; 24 h) shows antiproliferative effect on WI-38, CAL62 and KMH2 cells^[1].
Lestaurtinib (4 μM; 24 h) induces cell cycle arrest in the G2/M phase in CAL62 and KMH2 cells^[1].
Lestaurtinib (30-300 nM; 48 h) induces apoptosis in a dose-dependent manner in HL (hodgkin lymphoma) cell lines^[2].
Lestaurtinib (30, 100, 300 nM; 1 h) inhibits JAK2, STAT5 and STAT3 phosphorylation when at 300 nM^[2]. In Vivo: Lestaurtinib (20 mg/kg; s.c.; twice daily (monday to friday) and once daily (saturday and sunday); 3 weeks) significantly inhibits growth of tumor in vivo^[3].