Cancer Drug May Treat Chronic Nerve Pain
A preclinical study from MD Anderson Cancer Center suggests existing BRAF inhibitor cancer drugs could be repurposed to treat chronic nerve pain by
Researchers at The University of Texas MD Anderson Cancer Center have identified a cancer protein as a key driver of chronic nerve pain. Their study, published in Science Signaling on August 29, 2026, found that BRAF inhibitors reduced pain sensitivity in preclinical models of nerve injury.
According to the source, chronic nerve pain, or neuropathic pain, can result from injury, disease, or cancer treatments. This pain is often intense, persistent, and responds poorly to conventional medications. The study was co-led by Shao-Rui Chen, M.D., professor of Anesthesiology and Perioperative Medicine, and Hui-Lin Pan, M.D., Ph.D., endowed chair of Anesthesiology and Perioperative Medicine.
How BRAF Drives Pain Signaling
The research explored the role of the protein BRAF, commonly involved in cancer, in pain pathways. The team discovered that after nerve injury, BRAF moves from peripheral sensory nerve cells to their terminals inside the spinal cord. There, it activates molecular signals that increase the activity of NMDA receptors, protein channels that help nerve cells communicate. Hyperactive NMDA receptors are known to amplify pain signals. The researchers also reported a correlation between BRAF signaling proteins and NMDA receptors in human spinal cord samples.
Testing BRAF Inhibition in Models
In preclinical models of nerve injury, the researchers tested the effect of inhibiting the BRAF pathway. They used two specific drugs: the BRAF inhibitor vemurafenib and the MEK inhibitor selumetinib. The study found these inhibitors reduced sensitivity to touch, pressure, and heat in the injured models but did not alter normal pain responses in models without nerve injury.
Further genetic manipulation supported these findings. Deleting the Braf gene resulted in less persistent pain sensitivity. Conversely, directly activating BRAF caused pain sensitivity in models that did not have a nerve injury, underscoring BRAF's role in both initiating and maintaining neuropathic pain.
Potential for Rapid Drug Repurposing
Hui-Lin Pan stated the findings identify BRAF as a key driver of pathological pain signaling. "Because BRAF inhibitors are already approved for cancer treatment, this discovery raises the possibility of rapidly repurposing existing therapies to reduce the level of pain signals entering the spinal cord and improve patient quality of life," Pan said, according to the source.
The results are preclinical. The researchers note that appropriate dosing, delivery methods, and possible side effects of BRAF inhibitors for pain would need further examination before human clinical trials. They also aim to understand how nerve injury triggers BRAF's movement to the spinal cord. The study concludes that BRAF signaling is associated with NMDA receptor activation and that available BRAF inhibitors have therapeutic potential for neuropathic pain.
