Epilepsy Drug Lacosamide Paired With Hydrogel Shows Potential to Reverse Osteoarthritis Damage in Preclinical Study
New research from Yale University published in Bioactive Materials indicates that the FDA-approved epilepsy medication lacosamide, when delivered directly into joints via a specialized temperature-sensitive hydrogel, can both reduce joint pain and reverse cartilage damage in osteoarthritis. Led by principal investigator Chuan-Ju Liu, the study identifies the protein Nav1.7 as a dual-acting target that influences both pain signaling and the physical breakdown of joint tissue. Preclinical testing showed that a single intra-articular injection every four weeks prevented cartilage loss more effectively than daily oral dosing, offering a promising potential treatment pathway that avoids addictive opioids.
Key points
- Yale researchers found that the epilepsy drug lacosamide can reduce joint pain and reverse cartilage damage in osteoarthritis.
- The treatment uses a specialized temperature-responsive hydrogel made from Collagen II to keep the drug concentrated inside the joint.
- The target protein Nav1.7 is highly active in chondrocytes during osteoarthritis, driving both pain and tissue degradation.
- Preclinical tests demonstrated that one injection of the gel every four weeks prevented cartilage loss more effectively than daily oral doses.
What Happened
Researchers at Yale published a study in Bioactive Materials revealing that the FDA-approved epilepsy medication lacosamide can serve a dual purpose in treating osteoarthritis by reducing joint pain while simultaneously reversing cartilage damage. The therapeutic effects were significantly enhanced when the medication was paired with a specialized, temperature-sensitive hydrogel designed to deliver the drug directly into the affected joint.
Osteoarthritis disrupts the natural balance maintained by chondrocytes, causing cartilage to break down faster than it can be replaced. According to the study's principal investigator, Chuan-Ju Liu, current approved medications only mask symptoms without stopping the underlying structural progression of the disease.
Context and Mechanism
The research centers on Nav1.7, a protein functioning as a sodium channel. While previously thought to operate primarily in nerve cells transmitting pain, Liu's team discovered the protein is also highly active in cartilage-maintaining chondrocytes during osteoarthritis. In diseased joints, heightened Nav1.7 activity intensifies pain signaling and pushes chondrocytes to break down cartilage.
Lacosamide inhibits sodium channels at low concentrations, encouraging cells to build cartilage while suppressing tissue breakdown. To overcome the body's natural tendency to clear out joint injections quickly, the team developed a Collagen II hydrogel that remains liquid in a syringe but forms a firm reservoir at body temperature, slowly releasing lacosamide over a month or longer.
What's Next
Because lacosamide is already approved for human use in treating epilepsy and has undergone testing for nerve-related pain conditions, the researchers suggest the compound could move toward clinical studies in osteoarthritis patients more quickly than entirely new chemical entities. If successful in human trials, the approach could reduce the frequency of medical procedures, limit systemic side effects, and provide long-lasting disease modification.
