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Protein kinase inhibitors (PKI) have become prominent agents in cancer therapeutics. However, the specificity for target kinase inhibition can be poor and unwanted effects can emerge in combination regimens. The PKI emodin, for instance, can produce mixed results when combined with cisplatin, and we have sought a biochemical pharmacologic explanation for the negative cytotoxic effects.

cancer chemotherapy and pharmacology

Protein kinase inhibitors emodin and dichloro-ribofuranosylbenzimidazole modulate the cellular accumulation and cytotoxicity of cisplatin in a schedule-dependent manner