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How does the cancer drug Keytruda work? And how is it different to chemo?

Monoclonal antibody drugs like Keytruda attack cancer cells in a different way to chemotherapy drugs.

Keytruda, or pembrolizumab, is a cancer treatment that functions differently from traditional chemotherapy drugs. While chemotherapy drugs from the 1950s to 1990s were small molecules that targeted cancer cells broadly, Keytruda is a protein-based drug from a family of medicines called monoclonal antibodies. Monoclonal antibodies like Keytruda are highly specific to cancer cells, causing less damage to healthy cells and thus milder side effects.

Keytruda works by targeting a protein called PD-1, which is the body's immune system brake that prevents it from attacking healthy cells. Some cancers have another protein called PD-L1 on their surface that interferes with PD-1, allowing the cancer to escape the immune system. Keytruda blocks this interaction, reactivating the immune system to fight the cancer.

Previously approved in 2014 for advanced melanoma, Keytruda significantly increased the five-year survival rate from less than 10% to over 55%. Its use has since expanded to treat cervical, renal cell carcinoma, triple negative breast cancer, squamous cell carcinoma of the pharynx, larynx, and mouth, bile duct, ovarian, and Merkel cell cancers.

For advanced bile duct and ovarian cancers, treatment with Keytruda has increased the five-year survival rate from 5% and 10-40% respectively to over 16% and 50%. For Merkel cell carcinomas, it has increased the survival rate from 34% to 43%.

In Australia, while cancer treatment is mostly free for patients, Keytruda can still incur out-of-pocket costs. However, the introduction of a Pharmaceutical Benefit Scheme (PBS) listing for these new cancers will save patients significant money, providing much-needed financial relief during their treatment.

Written by urgent.news from The Conversation AU's reporting — not their text. Machine-written — may contain errors; check the original before relying on it.

Read the original at theconversation.com →

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