Researchers at MD Anderson Cancer Center discovered that the cancer-linked protein BRAF initiates and sustains chronic nerve pain by increasing NMDA receptor activity in the spinal cord.
Preclinical trials published in Science Signaling on August 25 showed that existing cancer drugs, specifically vemurafenib and selumetinib, successfully reduced pain sensitivity in nerve-damaged models.
While the findings are currently preclinical, the study suggests that repurposing these FDA-approved cancer inhibitors could provide a new therapeutic pathway for treating neuropathic pain in humans.