Preclinical study points to cancer drugs as possible treatments for chronic nerve pain

by University of Texas MD Anderson Cancer Center

edited by Sadie Harley, reviewed by Robert Egan

Sadie Harley

Scientific Editor

Meet our editorial team
Behind our editorial process

Robert Egan

Senior Editor

Meet our editorial team
Behind our editorial process Editors' notes

This article has been reviewed according to Science X's editorial process and policies. Editors have highlighted the following attributes while ensuring the content's credibility:

fact-checked

peer-reviewed publication

trusted source

proofread

The GIST Add as preferred source

Researchers at The University of Texas MD Anderson Cancer Center have found new evidence that BRAF, a protein commonly involved in cancer, plays a key role in developing, amplifying and maintaining chronic pain caused by nerve damage. BRAF inhibitors reduced pain sensitivity in preclinical models, suggesting the therapeutic potential of this approach for treating chronic nerve pain.

The study, published in Science Signaling, 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.

"Our findings identify the cancer-promoting protein BRAF as a key driver of pathological pain signaling following nerve injury," Pan said. "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."

How nerve injury causes chronic pain

Chronic nerve pain, or neuropathic pain, can result from injury, disease or even life-saving cancer treatments. This pain can be intense and persistent, and it responds poorly to conventional pain medications, negatively affecting patient quality of life.

Protein channels in the brain and spinal cord, known as NMDA receptors, help nerve cells communicate. After nerve injury, these NMDA receptors can become hyperactive, amplifying pain signals. To identify potential mechanisms, the researchers explored the role of BRAF in NMDA receptor activity.

Key findings

Using preclinical models of nerve injury, the researchers discovered that BRAF moved from peripheral sensory nerve cells to their terminals inside the spinal cord, where it activated molecular signals to increase NMDA receptor activity. They also found a correlation between BRAF signaling proteins and NMDA receptors in human spinal cord samples.

These initial results suggested that targeting BRAF could help reduce activity in the NMDA receptors to reduce pain.

Does targeting BRAF reduce pain?

In the preclinical models, the BRAF inhibitor vemurafenib and the MEK inhibitor selumetinib reduced sensitivity to touch, pressure and heat but did not change normal responses in models without nerve injury.

Deleting the Braf gene also resulted in less persistent pain sensitivity. Conversely, activating BRAF directly caused pain sensitivity in models that did not have nerve injury, highlighting the key role of BRAF in starting and maintaining neuropathic pain.

What this means for patients who have nerve injury and chronic pain

These results are preclinical, and researchers will need to further examine the appropriate dosing, delivery methods and possible side effects of BRAF inhibitors before clinical trials in humans. The researchers also hope to understand how nerve injury triggers the translocation of BRAF from the nerves to the spinal cord.

However, these results suggest that BRAF signaling is associated with NMDA receptor activation in the spinal cord and that currently available BRAF inhibitors have therapeutic potential to treat neuropathic pain.

Publication details

Daozhong Jin et al, BRAF recruitment to spinal sensory synapses promotes neuropathic pain by potentiating transsynaptic NMDA receptor activity, Science Signaling (2026). DOI: 10.1126/scisignal.aeh6852

Journal information: Science Signaling

Key medical concepts

Neuropathic PainReceptors, N-Methyl-D-AspartateVemurafenib

Clinical categories

AnesthesiologyNeurology Provided by University of Texas MD Anderson Cancer Center Who's behind this story?

Sadie Harley

BSc Life Sciences & Ecology. Microbiology lab background with pharmaceutical news experience in oil, gas, and renewable industries. Full profile →

Robert Egan

Bachelor's in mathematical biology, Master's in creative writing. Well-traveled with unique perspectives on science and language. Full profile →

Citation: Preclinical study points to cancer drugs as possible treatments for chronic nerve pain (2026, August 29) retrieved 30 August 2026 from https://medicalxpress.com/news/2026-08-preclinical-cancer-drugs-treatments-chronic.html This document is subject to copyright. Apart from any fair dealing for the purpose of private study or research, no part may be reproduced without the written permission. The content is provided for information purposes only.