Although the RAS family of proteins was discovered nearly four decades ago there has not been a viable drug therapy developed to effectively blocks mutant RAS dysfunction. Targeting RAS directly is difficult because of the absence of known allosteric regulatory sites, as well as the fact that it has picomolar affinity to GTP/GDP (3). Alternative drugs have been developed to target Farnesyl transferase and downstream MEK targets, but these have failed for various reasons (reviewed in (1, 2)). Recently, a drug that targets mutant RAS G12C specifically has shown promising clinical results and is now the first FDA approved RAS-targeting drug for the treatment of NSCLC, read on for a summary of this drugs journey from discovery to approval, and roadblocks that still lie ahead.
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