The current read
ISEMBYLD establishes myostatin inhibition as a clinically relevant mechanism in SMA, where patients already have substantial functional muscle deficit. We are considerably less convinced that this translates into a broad obesity opportunity.
- Apitegromab clearly preserves lean mass during GLP-1-induced weight loss, but EMBRAZE has not established that preserved tissue produces meaningful functional benefit, and the drug does not add meaningful fat or total weight loss. Regeneron’s COURAGE data strengthen the underlying muscle-preservation biology and suggest the effect may be more relevant in patients starting with low lean mass, but they do not yet close the mass-to-function gap.
- Our base case therefore treats obesity as a narrower sarcopenic/frailty opportunity until prospective data demonstrate that preserving muscle improves something patients, physicians or payers value beyond body composition.