In patients with metastatic melanoma, standard cytotoxic drugs such as dacarbazine have no proven impact on survival. Vemurafenib is the first BRAF protein inhibitor to be approved for the treatment of melanoma. In about half of patients with melanoma, this protein, important for cell growth, is dysregulated owing to a mutation (V600) in the gene that encodes it. An unblinded clinical trial that included 675 patients with metastatic melanoma harbouring a V600 BRAF mutation compared oral vemurafenib with intravenous dacarbazine. An interim analysis showed a statistically significant increase in the median overall survival time of about 1.5 months with vemurafenib (9.2 versus 7.7 months). These results are too preliminary to determine the survival advantage, if any, conferred by vemurafenib. About 20% of patients treated with vemurafenib developed skin cancer. The most common adverse effects were skin rash (37%), photosensitivity (33%), diarrhoea (28%), and arthralgia (54%). Vemurafenib also causes ocular disorders, including uveitis, and prolongs the QT interval in a dose-dependent manner. The potential for pharmacokinetic interactions is high: vemurafenib inhibits P-glycoprotein and CYP 1A2, and induces CYP 3A4. In practice, vemurafenib should only be used in rigorous clinical trials, on a case-by-case basis.