Structurally distinct from the anthracyclines, Actinomycin D binds strongly to DNA by intercalation and inhibits synthesis of RNA and proteins. In pre-clinical models, reduced cellular uptake is associated with resistance to Actinomycin D; it also appears to be a substrate for the Pgp pump.
Actinomycin D is especially active against childhood tumours and is used in combination therapy for:
The dose-limiting toxicity is myelosuppression, maximal around 10 days after treatment. Actinomycin D can also cause:
♦ Nausea and vomiting
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