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Herbimycin A, an Inhibitor of Tyrosine Kinase, Prolongs Survival of Mice Inoculated with Myeloid Leukemia C1 Cells with High Expression of v-abl Tyrosine Kinase¹

Department of Chemotherapy, Saitama Cancer Center Research Institute, Saitama 362 [Y. H., J. O-K., T. K., M. H.], Department of Anatomy, Ohu University School of Dentistry, Koriyama 963 [H. K.], and Department of Hematology, Jichi Medical School, Tochigi 329-04 [S. K., T. S., Y. M.], Japan

Herbimycin A, a benzoquinonoid ansamycin antibiotic, reduces intracellular phosphorylation by some tyrosine kinases, including v-abl. The mouse megakaryoblastic cell line C1 expresses v-abl protein at high levels. Herbimycin A at about 20 ng/ml caused 50% inhibition of growth of C1 cells but at 100 ng/ml scarcely affected the growth of another mouse leukemia cell line, M1 cells, or of normal bone marrow cells.

Injection of 10⁶ C1 cells into nude mice resulted in death of all the mice within 30 days. Administration of herbimycin A significantly enhanced the survival of mice inoculated with C1 cells but scarcely affected the survival of mice inoculated with M1 cells. These results suggest that herbimycin A and/or related compounds may be useful for treatment of some types of leukemia in which tyrosine kinase activity is implicated as a determinant of the oncogenic state.

¹ This work was supported in part by Grants for Cancer Research from the Ministry of Education, Science, and Culture and a Grant for a Comprehensive 10-year Strategy for Cancer Control, Japan, from the Ministry of Health and Welfare.

² To whom requests for reprints should be addressed, at Department of Chemotherapy, Saitama Cancer Center Research Institute, Ina, Saitama-362, Japan.

Received 1/27/92. Accepted 5/ 5/92.