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[Cancer Research 57, 4838-4848, November 1, 1997]
© 1997 American Association for Cancer Research
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Induction of Apoptosis and Cell Cycle Arrest by CP-358,774, an Inhibitor of Epidermal Growth Factor Receptor Tyrosine Kinase

James D. Moyer1, Elsa G. Barbacci, Kenneth K. Iwata, Lee Arnold, Bruce Boman, Ann Cunningham, Catherine DiOrio, Jonathan Doty, Michael J. Morin, Mikel P. Moyer, Mark Neveu, Vincent A. Pollack, Leslie R. Pustilnik, Margaret M. Reynolds, Don Sloan, April Theleman and Penny Miller

Pfizer Central Research, Groton, Connecticut 06340 [J. D. M., E. G. B., L. A., A. C., C. D., J. D., M. J. M., M. P. M., M. N., V. A. P., L. R. P., D. S., P. M.]; Oncogene Science Inc., Uniondale, New York 11553 [K. K. I., M. M. R., A. T.]; and Storz Cancer Institute, Omata, Nebraska 68105 [B. B.]

The epidermal growth factor receptor (EGFR) is overexpressed in a significant percentage of carcinomas and contributes to the malignant phenotype. CP-358,774 is a directly acting inhibitor of human EGFR tyrosine kinase with an IC50 of 2 nM and reduces EGFR autophosphorylation in intact tumor cells with an IC50 of 20 nM. This inhibition is selective for EGFR tyrosine kinase relative to other tyrosine kinases we have examined, both in assays of isolated kinases and whole cells. At doses of 100 mg/kg, CP-358,774 completely prevents EGF-induced autophosphorylation of EGFR in human HN5 tumors growing as xenografts in athymic mice and of the hepatic EGFR of the treated mice. CP-358,774 inhibits the proliferation of DiFi human colon tumor cells at submicromolar concentrations in cell culture and blocks cell cycle progression at the G1 phase. This inhibitor produces a marked accumulation of retinoblastoma protein in its underphosphorylated form and accumulation of p27KIP1 in DiFi cells, which may contribute to the cell cycle block. Inhibition of the EGFR also triggers apoptosis in these cells as determined by formation of DNA fragments and other criteria. These results indicate that CP-358,774 has potential for the treatment of tumors that are dependent on the EGFR pathway for proliferation or survival.

1 To whom requests for reprints should be addressed, at Pfizer Central Research, Eastern Point Road, Groton, CT 06340. E-mail: james_d_moyer@groton.pfizer.com.

Received 6/26/97. Accepted 9/19/97.




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