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Strategies of targeting KRAS, challenging drug target.

In the developed world, cancer is the most common cause of death. Among the 36 human genes of the RAS family, KRAS, NRAS, and HRAS play a prominent role in human cancer. KRAS belongs to the Rassuperfamily of proteins and is a small GTPase signal transduction protein. Among the RAS isoform, KRAS is the dominant mutant that induced approximately 86% of the RAS mutations. The most frequently mutated KRAS isoform is KRAS4B, about 90% of pancreatic cancer, 30-40% of colon cancer, and 15 to 20% of lung cancers are caused by mutations KRAS4B isoform. Liver cancer, bladder cancer, breast cancer, and myeloid leukaemia are also caused by mutations in KRAS but are rare. Currently, no FDA-approved drugs are available for KRAS-driven cancer. As the RAS proteins lack a right pocket accessible to the chemical inhibitors, the cancer-causing mutant proteins are almost identical to their essential wild-type counterparts. Therefore, it was considered undruggable. The structure and function of new insights in RAS have changed this understanding and encouraged the development of many drug candidates. This review provides information about the different strategies of targeting KRAS, a challenging drug target that might be valuable for the scientific community.