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[Cancer Research 56, 100-104, January 1, 1996]
© 1996 American Association for Cancer Research
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Inhibition of the Abl Protein-Tyrosine Kinase in Vitro and in Vivo by a 2-Phenylaminopyrimidine Derivative

Elisabeth Buchdunger1, Jürg Zimmermann, Helmut Mett, Thomas Meyer, Marcel Müller, Brian J. Druker and Nicholas B. Lydon

Ciba Pharmaceuticals Division, Oncology Research Department, Ciba-Geigy Limited, CH-4002 Basel, Switzerland [E. B., J. Z., H. M., T. M., M. M., N. B. L.], and Division of Hematology and Medical Oncology, Oregon Health Sciences University, Portland, Oregon 97201 [B. J. D.]

Oncogenic activation of Abl proteins due to structural modifications can occur as a result of viral transduction or chromosomal translocation. The tyrosine protein kinase activity of oncogenic Abl proteins is known to be essential for their transforming activity. Therefore, we have attempted to identify selective inhibitors of the Abl tyrosine protein kinase. Herein we describe an inhibitor (CGP 57148) of the Abl and platelet-derived growth factor (PDGF) receptor protein-tyrosine kinases from the 2-phenylaminopyrimidine class, which is highly active in vitro and in vivo. Submicromolar concentrations of the compound inhibited both v-Abl and PDGF receptor autophosphorylation and PDGF-induced c-fos mRNA expression selectively in intact cells. In contrast, ligand-induced growth factor receptor autophosphorylation in response to epidermal growth factor (EGF), insulin-like growth factor-I, and insulin showed no or weak inhibition by high concentrations of CGP 57148. c-fos mRNA expression induced by EGF, fibroblast growth factor, or phorbol ester was also insensitive to inhibition by CGP 57148. In antiproliferative assays, the compound was more than 30–100-fold more potent in inhibiting growth of v-abl-transformed PB-3c cells and v-sis-transformed BALB/c 3T3 cells relative to inhibition of EGF-dependent BALB/MK cells, interleukin-3-dependent FDC-P1 cells, and the T24 bladder carcinoma line. Furthermore, anchorage-independent growth of v-abl- and v-sis-transformed BALB/c 3T3 cells was inhibited potently by CGP 57148. When tested in vivo, CGP 57148 showed antitumor activity at tolerated doses against tumorigenic v-abl- and v-sis-transformed BALB/c 3T3 cells. In contrast, CGP 57148 had no antitumor activity when tested using src-transformed BALB/c 3T3 cells. These findings suggest that CGP 57148 may have therapeutic potential for the treatment of diseases that involve abnormal cellular proliferation induced by Abl protein-tyrosine kinase deregulation or PDGF receptor activation.

1 To whom requests for reprints should be addressed, at Ciba Pharmaceuticals Division, Research Department, Ciba-Geigy Limited, CH-4002 Basel, Switzerland. Phone: 061/6962853 or 061/6964498; Fax: 061/6963835.

Received 7/31/95. Accepted 10/31/95.




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