Plate Nº 82 · recorded October 8, 2026
Health & Medicine ResearchReported finding
Epilepsy Drug Lacosamide May Reverse Osteoarthritis Cartilage Damage
Yale researchers found that the epilepsy drug lacosamide, delivered via a heat-activated hydrogel, reduced pain and reversed cartilage damage in preclinical osteoarthritis studies.
By Marcus Bennett5 min read917 words
In brief
- Yale researchers reported on October 8, 2026 that lacosamide, an FDA-approved epilepsy drug, reduced pain and reversed cartilage damage in preclinical osteoarthritis studies.
- One hydrogel injection every four weeks prevented cartilage loss more effectively than a daily oral dose in preclinical testing.
- The drug blocks Nav1.7, a sodium channel protein active in both pain signaling and cartilage breakdown.
- The study was published in the journal Bioactive Materials (2026, vol. 61).
- No FDA-approved drug currently both stops osteoarthritis pain and prevents structural cartilage breakdown.
An FDA-approved epilepsy drug reduced joint pain and reversed cartilage damage in preclinical studies of osteoarthritis, researchers at Yale School of Medicine reported on October 8, 2026. One injection of the drug lacosamide, held in place by a temperature-sensitive hydrogel, prevented cartilage loss more effectively than a daily oral dose — and a single injection kept working for a month or longer.
The study, published in the journal Bioactive Materials, points toward a treatment that could do something no currently approved medicine can: relieve osteoarthritis pain while also stopping, and potentially reversing, the structural breakdown of cartilage itself.
Why current osteoarthritis treatments fall short
Roughly put, osteoarthritis is often described as a wear-and-tear condition. That framing misses much of the biology.
Healthy joints rely on cells called chondrocytes, which maintain cartilage by balancing the creation of new tissue against the removal of old material. Osteoarthritis disrupts that balance. Cartilage breaks down faster than the body can replace it, and eventually bones begin rubbing against one another. Advanced cases can require total knee replacement.
Today's options — over-the-counter painkillers and steroid injections — may ease symptoms for a while, but they do nothing to slow the underlying joint damage.
"There is a major unmet need in osteoarthritis," says the study's principal investigator, Chuan-Ju Liu, PhD, the Charles W. Ohse Professor of Orthopaedics & Rehabilitation at Yale. "We need therapies that don't just mask pain but actually change how the disease progresses."
What does the protein Nav1.7 do?
The research centers on Nav1.7, a protein that acts as a sodium channel — a microscopic gate in cell membranes that helps control electrical signaling.
Scientists long believed Nav1.7 worked mainly in nerve cells that transmit pain signals to the brain. But earlier work by Liu's team showed the protein is also highly active in chondrocytes, the cartilage-maintaining cells. In healthy joints, Nav1.7 stays relatively quiet. In osteoarthritis, its activity rises sharply, amplifying pain while pushing chondrocytes to break down the very tissue they normally preserve.
That dual role makes it an unusual target. "When Nav1.7 becomes dysregulated, it contributes to both joint degeneration and pain," Liu says. "By blocking this single protein, we can potentially quiet the pain nerves and tell the cartilage cells to not only stop breaking down but start repairing as well."
How did the drug perform?
Rather than building a new molecule from scratch, Liu's team screened existing sodium-channel blockers. Lacosamide, already prescribed for epilepsy, stood out: it produced strong biological effects at considerably lower concentrations than older drugs in its class and offered a better safety profile.
Dose mattered enormously. At an ideal low concentration, lacosamide prompted cells to produce cartilage-building proteins while suppressing tissue breakdown. When the dose drifted too high or too low, those benefits faded.
"This tells us the system is finely tuned," Liu notes. "There is an optimal range where the drug helps restore balance without overcorrecting. What stood out was not just its effectiveness, but how little of a dose was needed."
The drug also changed how cells communicate. Lacosamide stimulated the release of two beneficial signaling proteins: HSP70, which helps cells respond to stress and supports tissue repair, and midkine, which helps regulate inflammation and protect joint tissue from degeneration.
"These proteins create a supportive environment for cartilage maintenance," Liu explains. "They allow the effects of the drug to extend beyond individual cells and influence the entire tissue."
Why inject the drug into the joint?
Oral lacosamide worked in preclinical testing, but pills circulate through the entire body, raising the risk of side effects elsewhere. So the researchers tested intra-articular injection — placing the medication directly inside the affected joint.
One obstacle remained. "The knee joint, which is also the most common location for osteoarthritis, naturally acts like a leaky bucket," Liu says. "The body's drainage system can clear out liquids injected into the knee within hours."
The solution was a hydrogel made from Collagen II. The material stays liquid inside a cool syringe, then firms into a jelly-like substance at body temperature. Once inside the joint, the gel acts as a reservoir, concentrating the drug where it is needed and releasing it gradually over several weeks.
"It transforms a daily pill into a long-lasting, local treatment that stays active for a month or longer," Liu says.
What happens next?
Because regulators have already approved lacosamide for epilepsy, testing it in osteoarthritis patients could move faster than developing an entirely new drug. The medication has also been tested in humans with nerve-related pain conditions caused by Nav1.7 mutations, giving the researchers added confidence that laboratory results might translate into real pain relief.
Important caveats remain. The findings come from preclinical studies, not human trials, and no one yet knows whether the cartilage repair seen in the lab will hold up in patients.
Still, the work reflects a broader trend in medicine: pairing existing drugs with advanced biomaterials to control exactly where and how treatments act. If the approach succeeds in people, it could reduce the number of procedures patients need, limit side effects, and provide longer-lasting protection against structural joint damage.
"We are not just developing a treatment," Liu concludes. "We are developing a system that allows the medicine to work more effectively where it matters most. Our goal is to move beyond symptom control and towards true disease modification. This effort brings us closer to that reality."
via medicine.yale.edu (Original)
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