Ipilimumab
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A lab-made antibody that releases a different immune brake (CTLA-4), helping the immune system recognize and attack cancer.
How it works
T cells are the immune system's attack cells, but the body keeps built-in brakes on them so they don't overreact and damage healthy tissue. CTLA-4 is one such brake, switched on early when T cells are first being activated. Ipilimumab attaches to CTLA-4 and blocks it, so T cells can activate and multiply more freely, giving the immune system a stronger shot at recognizing and destroying cancer cells.
What it’s used for
Used to treat several advanced or hard-to-treat cancers, most often paired with another immunotherapy drug for a stronger combined effect, including melanoma, kidney cancer, certain colorectal cancers, liver cancer, lung cancer, mesothelioma, and esophageal cancer.
- Mechanism
- CTLA-4 checkpoint inhibitor (mAb)
- Drug class
- Monoclonal antibody
- Therapeutic area
- Oncology
The drug that proved the immune system itself could be a cancer treatment
Cancer cells often survive by tricking the immune system into leaving them alone, using built-in "off switches" on immune cells. Ipilimumab was the first drug ever approved that works by disabling one of those switches (CTLA-4) rather than attacking the tumor directly — it frees the immune system to recognize and fight the cancer itself. It was the first drug of any kind shown to help people with advanced melanoma live longer in a randomized trial, and it proved that unleashing the immune system was a viable cancer treatment strategy, opening the door to later checkpoint drugs like pembrolizumab and nivolumab, also on this site, which target a related but distinct brake called PD-1.
Pivotal trial
A randomized phase 3 trial in previously treated, unresectable stage III/IV melanoma comparing ipilimumab, a gp100 peptide vaccine, or both; ipilimumab-containing arms showed significantly improved overall survival versus the vaccine alone.