Roche announced today that the pivotal Phase III study (FENhance 1) of fenebrutinib in RMS met its primary endpoint, showing clinically meaningful and statistically significant results.

The study demonstrated that fenebrutinib, an investigational Bruton’s tyrosine kinase (BTK) inhibitor, markedly reduced the annualised relapse rate (ARR) by 51% compared to teriflunomide over a period of at least 96 weeks of treatment, consistent with FENhance 2 results showing a 59% reduction in ARR. Together, these results equate to approximately one relapse every 17 years.

Secondary endpoints in both RMS studies show statistically significant and clinically meaningful reductions in brain lesions. Additionally, all progression endpoints show favorable trends for fenebrutinib.

Full data from the FENhance 1 and 2 studies will be shared at the American Academy of Neurology (AAN) Annual Meeting 2026 and submitted to regulatory authorities together with data from the FENtrepid study.

“These pivotal results, together with the earlier data,  provide convincing evidence that fenebrutinib can become the first high-efficacy oral treatment for RMS and PPMS,” said Levi Garraway, M.D., Ph.D., Roche’s Chief Medical Officer and Head of Global Product Development. “Building on a decade of transforming MS treatment, we are committed to advancing innovation to one day allow people with MS to live a life without disability.”

The positive FENhance 1 study follows positive results for FENhance 2 in RMS and for FENtrepid in PPMS, which were both announced in November. The collective positive results across all three pivotal studies demonstrate that fenebrutinib consistently shows a profound benefit on relapsing and progressive disease biology.

In both RMS studies, liver transaminase elevations were comparable with teriflunomide. In the FENhance 1 study, there was one Hy’s Law case in the fenebrutinib arm and one in the teriflunomide arm. Both cases were asymptomatic and resolved after study drug discontinuation. There were no additional Hy's Law cases across all of the fenebrutinib clinical development programme in MS or in other autoimmune diseases.

In the FENhance 1 and 2 studies in RMS, 1 fatal case was reported in the teriflunomide arm and 8 fatal cases with various causes and at different points in treatment in the fenebrutinib arms. Further analyses are ongoing to better understand these findings.

Fenebrutinib targets cells in the immune system known as B cells and microglia. Targeting B cells helps control the acute inflammation that causes relapses, while targeting microglia inside the brain addresses the chronic damage that is thought to drive long-term disability progression. Fenebrutinib, a non-covalent BTK inhibitor, is designed to have high potency, selectivity and reversibility. This design allows it to act throughout the body, and also to cross the blood-brain barrier into the central nervous system (CNS) targeting chronic inflammation.