Also known as REGN2477 · Pasatru · garetosmab-grts
An anti-activin-A antibody (Regeneron) — the first drug on the whole activin/myostatin axis to reach FDA approval (as Pasatru, for the rare bone disease FOP), and the activin-A leg of obesity muscle-preservation combinations.
Research refreshed
Garetosmab is a monoclonal antibody from Regeneron that neutralizes activin A — a TGF-β-superfamily ligand that, like myostatin, signals through the activin type II receptors. Blocking activin A widens the axis beyond myostatin alone, and garetosmab plays two roles in this catalog: in August 2026 it became the first agent on the entire activin/ActRII axis to win FDA approval (as Pasatru, for fibrodysplasia ossificans progressiva), and it is the third leg of the triple obesity combination.
Garetosmab’s lead indication is fibrodysplasia ossificans progressiva (FOP) — an ultra-rare disease in which soft tissue turns to bone, driven by activin A. Its Phase 3 OPTIMA trial was positive (roughly 90–94% reduction in new heterotopic bone lesions), and on August 19, 2026 the FDA approved it as Pasatru (garetosmab-grts) — the first and only approved FOP therapy shown to reduce both new bone lesions and flare-ups, and the first drug of the activin/myostatin axis to reach the market at all.
That approval is for a rare bone disease, not for obesity; its metabolic use remains investigational. In that setting garetosmab is the activin-A arm of the semaglutide + trevogrumab + garetosmab triple combination, which produced the best body-composition profile in the Phase 2 COURAGE trial — preserving roughly 80% of the lean mass that semaglutide alone would have cost, though the triplet carried more tolerability-driven discontinuations. As an anti-activin-A antibody (~150 kDa), it illustrates that the "myostatin axis" is really a broader activin/ActRII network with multiple blockable nodes.
Binds and neutralizes activin A, blocking its signaling through ActRII. In bone disease this prevents activin-A-driven abnormal ossification; in the metabolic setting, adding activin-A blockade to myostatin blockade and incretin therapy further shifts body composition toward fat loss with preserved muscle.
Behind every vial of Garetosmab is the same exacting pipeline every research peptide runs — but the chemistry plays out differently for this molecule. Here is how Garetosmab, specifically, is brought into being.
On paper, Garetosmab weighs in at roughly 150,000 daltons. Before a single bond is made, the target sequence, salt form, and purity threshold are written down as the contract the finished material must meet.
Garetosmab is assembled by solid-phase peptide synthesis — the chain grows one protected residue at a time on resin, and what you fail to build cleanly here you pay to remove later.
The crude mixture — Garetosmab plus its deletions and side products — is then separated on preparative HPLC, and where the cut is taken decides the difference between a genuinely pure peptide and a barely-passable one.
A real batch of Garetosmab proves itself: identity confirmed by mass spectrometry against its ~150,000 Da, purity read directly off an analytical HPLC trace, water and counterion content measured. That batch-specific certificate of analysis is the only honest way to know what is actually in a vial of Garetosmab — and a short, cold, accountable chain of custody is how that purity survives the trip to your bench.
Garetosmab is a recombinant monoclonal antibody (~150 kDa) produced in mammalian cell culture, characterized with antibody-grade analytics (glycan/charge-variant profiling, mass spectrometry, binding/potency bioassay) — not a synthetic peptide.
Don't judge a vial by its cake. A fluffy, good-looking lyophilized powder reflects bulking agents and freeze-drying parameters — not purity. Insist on a batch-specific certificate of analysis.
Recent clinical trials and publications mentioning Garetosmab, pulled automatically from ClinicalTrials.gov and PubMed and refreshed daily. Listings are unfiltered search results, not curated endorsements.
A Regeneron monoclonal antibody that neutralizes activin A. It is FDA-approved as Pasatru (garetosmab-grts) for the rare bone disease FOP, and it is also studied as a component of an obesity triple-combination aimed at preserving muscle.
Yes — for fibrodysplasia ossificans progressiva (FOP). The FDA approved it as Pasatru on August 19, 2026, making it the first drug of the activin/myostatin axis to reach the market. Its use in obesity or muscle preservation is investigational and not approved.
Activin A signals through the same ActRII receptors as myostatin. Blocking it both prevents abnormal bone formation in FOP and, combined with myostatin blockade and a GLP-1 drug, shifts weight loss toward fat while sparing muscle.
No — this is a research and educational reference. Garetosmab is FDA-approved for FOP only; its obesity and muscle-preservation uses are investigational.
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ViewDual GIP / GLP-1 receptor agonist with industry-leading weight-loss endpoints.
ViewDosing protocols, mechanism, comparisons, and the latest trials — citation-backed answers grounded in PubMed, PubChem, and ClinicalTrials.gov.