Servier to Acquire Edgewise Muscular Dystrophy Unit for Up to $2.65 Billion
Servier will acquire Edgewise Therapeutics' muscular dystrophy business, including the drug sevasemten, for up to $2.65 billion. Sevasemten recently faced an FDA rejection for accelerated approval in Becker muscular dystrophy but is advancing to a Phase 3 trial in 2026. The drug has received multiple FDA and EMA designations for both Becker and Duchenne muscular dystrophy.
Servier has agreed to acquire Edgewise Therapeutics' muscular dystrophy business for up to $2.65 billion, a deal that includes the investigational drug sevasemten, which recently saw the FDA decline accelerated approval for Becker muscular dystrophy but is progressing toward a Phase 3 trial in 2026.
The transaction is valued at $1.55 billion upfront, with an additional $1.1 billion in potential milestone payments. The acquisition encompasses sevasemten, an oral myosin ATPase inhibitor designed to protect against contraction-induced muscle damage in rare muscular dystrophies. The deal has been approved by both companies' governance bodies and is expected to close in the third quarter of 2026, subject to regulatory clearance and customary closing conditions.
Sevasemten is currently in Phase 2 development for both Becker muscular dystrophy (BMD) and Duchenne muscular dystrophy (DMD). The FDA recently declined to grant accelerated approval for sevasemten in BMD, but the company has outlined plans to begin a Phase 3 trial in 2026. The drug has secured several regulatory milestones, including FDA Orphan Drug Designation for both Becker and Duchenne, Rare Pediatric Disease Designation for Duchenne, and Fast Track designations for both indications. It also holds EMA Orphan Drug Designations for Becker and Duchenne.
Clinical data presented at the 2026 Muscular Dystrophy Association (MDA) Clinical and Scientific Conference highlighted long-term functional stabilization. A poster session reported that sevasemten prevented functional decline for up to 3.5 years in the MESA open-label extension trial for Becker muscular dystrophy. Another presentation examined the effects of sevasemten on left ventricular ejection fraction and NT-proBNP levels in adults with Becker muscular dystrophy from the CANYON trial. Early clinical results have shown decreased serum biomarkers associated with muscle damage, and preclinical studies demonstrated functional improvements in dystrophin-deficient mice.
Sevasemten is described as the only small molecule in advanced clinical development for Becker muscular dystrophy and one of just a few in development for Duchenne. The drug's novel mechanism of action selectively limits the exaggerated muscle damage caused by the absence or loss of functional dystrophin. If approved, sevasemten could become the first approved treatment for Becker muscular dystrophy.