OncoPharm Carboplatin
Oct 31, 2019
Discover the ins and outs of carboplatin, its unique mechanism compared to cisplatin, and the intentional design to minimize kidney toxicity. Explore its versatile applications in treating various cancers and learn about the innovative AUC dosing strategy. Delve into the Calvert equation for calculating doses influenced by GFR, and understand the implications of creatinine variations. Plus, gain insights on managing toxicities, desensitization protocols, and why personalized dosing leads to better patient outcomes.
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Carboplatin’s Slower Activation
- Carboplatin forms DNA adducts like cisplatin but is chemically much more stable and activates ~100x slower.
- Its stability was designed to reduce nephrotoxicity compared to cisplatin.
History And Dose-Limiting Toxicity
- Carboplatin was FDA-approved in 1989 after trials beginning in 1980.
- Early dose-limiting toxicity identified was myelosuppression, especially thrombocytopenia.
Broad Oncology Uses
- Carboplatin is widely used across tumor types including lung, germ cell, ovarian, bladder, and breast cancers.
- It’s rarely used in leukemias but is a backbone in many solid-tumor regimens.