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Max-Planck Society, Research Group "Growth Factor Signal Transduction," Medical Faculty, Friedrich-Schiller University, Drackendorfer Str. 1, D 07747 Jena, Germany [M. K., F-D. B.]; The Alexander Silberman Institute of Life Sciences, The Hebrew University of Jerusalem, Givat Ram, Jerusalem 91904, Israel [A. G., A. L.]; Institute of Biochemistry, Medical Faculty, Friedrich-Schiller University, Löbderstr. 3, D 07743 Jena, Germany [A. B.]; Ludwig Institute for Cancer Research, Uppsala Branch, Box 595, S-75124 Uppsala, Sweden [C. R., L. R., C-H. H.]; and Department of Medicine II, Ulm University Medical Center, D 89081 Ulm, Germany [J. W.]
A novel class of tyrosine kinase blockers represented by the tyrphostins AG1295 and AG1296 is described. These compounds inhibit selectively the platelet-derived growth factor (PDGF) receptor kinase and the PDGF-dependent DNA synthesis in Swiss 3T3 cells and in porcine aorta endothelial cells with 50% inhibitory concentrations below 5 and 1 µM, respectively. The PDGF receptor blockers have no effect on epidermal growth factor receptor autophosphorylation; weak effects on DNA synthesis stimulated by insulin, by epidermal growth factor, or by a combination of both; and over an order of magnitude weaker blocking effect on fibroblast growth factor-dependent DNA synthesis. AG1296 potently inhibits signaling of human PDGF 
- and ß-receptors as well as of the related stem cell factor receptor (c-Kit) but has no effect on autophosphorylation of the vascular endothelial growth factor receptor KDR or on DNA synthesis induced by vascular endothelial growth factor in porcine aortic endothelial cells. Treatment by AG1296 reverses the transformed phenotype of sis-transfected NIH 3T3 cells but has no effect on src-transformed NIH 3T3 cells or on the activity of the kinase p60c-src(F527) immunoprecipitated from these cells. These potent and selective compounds represent leads for the development of novel agents to combat tumors driven by PDGF or to inhibit PDGF action in other diseases in which PDGF plays a key role, such as restenosis.
1 Part of this work was supported by Research Scholarship Bo 1043/1-1 to F-D. B. and by a grant from SUGEN, Inc. (Redwood City, CA) to A. L.
2 The two first authors contributed equally to the study.
3 To whom correspondence regarding the functional studies should be addressed.
4 To whom requests for reprints and correspondence regarding the chemical aspects should be addressed.
Received 7/ 5/94. Accepted 9/28/94.
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