PF-562271 | CAS:717907-75-0

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Name:PF-562271; 
Cat. No. :CS-0039
CAS No. :717907-75-0
Formula:C21H20F3N7O3S
M. Wt. : 507.49
Solubility:DMSO: ≥ 48 mg/mL

PF-562271 is a potent ATP-competitive, reversible inhibitor of FAK and Pyk2 kinase, with IC50 of 1.5 nM and 13 nM, respectively. IC50 & Target: IC50: 1.5 nM (FAK), 13 nM (Pyk2), 30 nM (CDK2), 47 nM (CDK3), 58 nM (CDK1), 97 nM (CDK7), 97 nM (Flt3)[1]In Vitro: PF-562271 is shown to be a 30- to 120-nM inhibitor of CDK2/E, CDK5/p35, CDK1/B, and CDK3/E in recombinant enzyme assays, in cell-based assays evaluating the role of CDKs, a 48-hour exposure of 3.3 μM PF-562271 is required to alter cell cycle progression. PF-562271 is potent in an inducible cell-based assay measuring phospho-FAK with a IC50 of 5 nM[1]. PF-562271, a selective inhibitor of both FAK and proline-rich tyrosine kinase 2 (PYK2), a FAK-related family member, on cell growth and colony formation in Ewing sarcoma cell lines. Seven cell lines are treated for 5 days with PF-562271 across a range of concentrations using 2-fold serial dilutions. Treatment with PF-562271 impaires cell viability in all cell lines, with an average IC50 of 2.4 μM after 3 days of treatment. TC32 and A673 are the 2 most sensitive cell lines, with IC50 concentrations of 2.1 and 1.7 μM, respectively[2].In Vivo: PF-562271 inhibits FAK phosphorylation in vivo in a dose-dependent fashion (calculated EC50 of 93 ng/mL, total) after p.o. administration to tumor-bearing mice[1]. Rats that receive PF-562271 demonstrate a decrease in tumor growth after 2 weeks of treatment with signs of bone healing as evidenced by the deposition of new bone (cortical and cancellous) at sites previously damaged by the tumor[3].

Roberts WG, et al. Antitumor activity and pharmacology of a selective focal adhesion kinase inhibitor, PF-562,271. Cancer Res, 2008, 68(6), 1935-1944. Bagi CM, et al. Dual focal adhesion kinase/Pyk2 inhibitor has positive effects on bone tumors: implications for bone metastases. Cancer. 2008 May 15;112(10):2313-21. Crompton BD, et al. High-throughput tyrosine kinase activity profiling identifies FAK as a candidate therapeutic target in Ewing sarcoma. Cancer Res. 2013 May 1;73(9):2873-83.