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Bimagrumab (BYM338) — anti-activin type II receptor (ActRII) monoclonal antibody
An investigational monoclonal antibody that blocks the activin type II receptor (ActRII) — the receptor through which myostatin and activin restrain muscle — producing a striking body recomposition (fat DOWN, lean muscle UP) but NO proven functional benefit. In a phase 2 trial in adults with type 2 diabetes and obesity, bimagrumab caused a large loss of fat mass and a real gain in lean mass over 48 weeks, which is why it is now being developed as a metabolic / obesity drug. But the muscle-disease story is a cautionary one: its pivotal phase 2b trial in inclusion-body myositis (RESILIENT) added muscle yet FAILED its primary walking endpoint, and a 2025 systematic review concluded it had no effect on disease progression. It is NOT an approved drug, NOT a dietary supplement, and NOT a longevity drug — gaining muscle on a scan is not the same as moving or living better. This entry exists to inform, not to recommend.
Prescription medication — not a dietary supplement
Bimagrumab is a prescription (or investigational) drug, not a supplement. It is included here for reference because people research and discuss it (often used off-label) — not as a recommendation. Take it only under a qualified clinician's supervision and only as prescribed; do not source it from grey-market vendors, where identity, purity, and dosing are unverified. The evidence below reflects its clinical trials.
What the evidence says
Most Bimagrumab studies are mechanism or observational rather than RCTs that measure a clinical effect — keep findings provisional.
Most evidence is from high-quality meta-analyses and randomised trials published 2014–2026 with a typical study size of 507 participants.
Based on 23 studies · 2 meta-analyses · 14 RCTs · 507 total participants
Confidence
High confidenceBy outcome
Bimagrumab has a real, replicated pharmacodynamic effect — striking body recomposition (fat loss + lean gain) in a phase 2 metabolic trial and consistent muscle-mass gains in muscle-disease trials — but its pivotal phase 2b trial in inclusion-body myositis FAILED to improve function, a systematic review found no effect on disease progression, and it is an unapproved investigational biologic, so its clinical value stays emerging.
17 rigorous studies
14 randomized trials · 3 meta-analyses · 2 systematic reviews
Our evidence rating for Bimagrumab is accountable to this entire body of rigorous research indexed in PubMed — not a hand-picked subset.
PubMed · as of Jul 2026
2 trials ongoing or recruiting · 13 completed on ClinicalTrials.gov
10 of the completed trials have posted results
Registered trials show research momentum for Bimagrumab, not proof of effect — a registration is a plan, and posted results are sponsor-reported, not peer-reviewed. They are never counted toward the evidence rating above.
Browse these trials on ClinicalTrials.govClinicalTrials.gov · as of Aug 2026
Bimagrumab (development code BYM338) is a fully human monoclonal antibody, originally developed by Novartis, that binds and blocks the activin type II receptors (ActRIIA and ActRIIB) — the shared receptor through which myostatin (GDF-8), activin A, and related TGF-β-family ligands signal to hold skeletal-muscle mass in check.
By occupying the receptor, bimagrumab prevents those negative regulators from delivering their growth-restraining signal, releasing the brake on muscle and driving hypertrophy.
Mechanistically it sits alongside the myostatin/activin 'trap' biologics like ACE-031, but it is an antibody against the receptor rather than a ligand decoy, and it has progressed further in human trials. The early human signal in muscle disease was genuinely encouraging.
In a pilot randomized trial in sporadic inclusion-body myositis (sIBM), a single dose of bimagrumab increased thigh-muscle volume by ~6.5% and lean body mass by ~5.7% versus placebo at 8 weeks, with a transient improvement in 6-minute walking distance — Class I evidence that ActRII blockade builds muscle in humans (Amato 2014).
But the load-bearing result came next: the pivotal phase 2b RESILIENT trial (251 patients across 38 sites) randomized sIBM patients to three bimagrumab doses or placebo and measured 6-minute walking distance at 52 weeks.
Despite added muscle, bimagrumab did NOT improve walking distance over placebo at any dose (10 mg/kg treatment difference 17.6 m, p=0.22) — the trial FAILED its primary functional endpoint, and a 2025 systematic review of IBM drug treatments concluded bimagrumab had no effect on disease progression (Hanna 2019; Santos 2025).
This is the honest core of bimagrumab's muscle-disease story: muscle gain on imaging did not translate into functional benefit. The drug's second act is metabolic.
In a phase 2 trial in 75 adults with type 2 diabetes and obesity, monthly intravenous bimagrumab over 48 weeks produced a striking body recomposition — a large loss of total body fat mass (~20.5% relative reduction), a gain in lean mass (~3.6%), reduced waist circumference and body weight, and improved HbA1c versus placebo (Heymsfield 2021).
That fat-loss-plus-muscle-gain profile is unusual and is why bimagrumab is now being pursued as an obesity / metabolic agent (later acquired and advanced by Versanis/Eli Lilly), including in combination with GLP-1 drugs.
Because ActRII also binds activins that act on the pituitary, bimagrumab transiently alters neurohormonal signalling — it reversibly raised FSH-axis activity in women in a dedicated endocrine study, an on-target reminder that this antibody does more than act on muscle (Garito 2018).
The tolerability signal across trials is consistent: muscle spasms (reported in roughly half of treated IBM patients), diarrhoea, and mild acne are the characteristic adverse events.
Bottom line: bimagrumab is an investigational ActRII-blocking antibody with a real, reproducible body-recomposition effect (fat down, lean up) that makes it a serious metabolic-drug candidate — but it is NOT approved, its muscle-disease trials failed to improve function, and added muscle mass is not proven to improve strength, mobility, or any hard health outcome.
It is a prescription-grade investigational biologic given by infusion under medical supervision, not a dietary supplement and not a longevity drug.
The score reflects a genuine, multiply-replicated pharmacodynamic effect on body composition set against unproven functional/clinical benefit and a failed pivotal muscle-disease trial, and it is sandboxed out of all goal- and stack-based recommendations.
Bimagrumab is a human monoclonal antibody that binds ActRIIA/ActRIIB, the shared receptor through which myostatin (GDF-8), activin A and related TGF-β-family ligands signal to restrain muscle. By occupying the receptor it prevents those negative regulators from binding — removing the brake on muscle growth. Demonstrated by SMAD2/3-signalling and body-composition changes in humans.
With ActRII signalling blocked, skeletal muscle grows: thigh-muscle volume and lean mass rose in human trials. Distinctively, ActRII blockade also drives a loss of fat mass and improves insulin sensitivity, producing a fat-down/lean-up body recomposition seen in the type-2-diabetes/obesity trial.
Because ActRII also binds activins acting on the pituitary, bimagrumab transiently shifts neurohormonal signalling — it reversibly raised FSH-axis activity in women in a dedicated endocrine study. The same broad receptor blockade that drives the muscle/fat effect also touches reproductive-hormone signalling and underlies side effects such as muscle spasms and diarrhoea.
How Bimagrumab works — from molecular targets to health outcomes. Click an edge to see supporting research.This visualization is in beta — pathways are being refined and expanded.
Avoid outside a clinical trial — bimagrumab is investigational, not approved, has no quality-controlled self-administered product, and its added muscle did not improve function in the pivotal muscle-disease trial.
Avoid — bimagrumab reversibly alters activin/FSH-axis signalling and interactions are unstudied.
Avoid entirely — unstudied, and the antibody affects reproductive-hormone signalling.
Bimagrumab blocks ActRII, through which activins act on the pituitary; it reversibly altered the FSH/LH axis in women in a dedicated endocrine study. Combining it with fertility or hormone treatments could perturb that axis and has not been studied.
Bimagrumab is being investigated in combination with GLP-1 drugs for body recomposition, but combination safety and efficacy are still investigational and unproven outside trials; do not combine outside medical supervision.
There are no controlled human drug-interaction data for self-administered bimagrumab. As a broad ActRII-ligand blocker with metabolic and neurohormonal effects, interactions cannot be reliably predicted.
Tip: The most characteristic adverse event — reported in roughly half of treated inclusion-body-myositis patients and in the pilot trial; thought to be an on-target effect of ActRII blockade. No validated self-use mitigation outside medical supervision.
Tip: Frequently reported across bimagrumab trials (around 40-50% of treated IBM patients); a consistent gastrointestinal effect of the drug.
Tip: Reported in the sIBM pilot trial alongside muscle contractions; usually mild.
Tip: Reversible with drug clearance; reflects ActRII/activin blockade at the pituitary. Relevant for anyone with fertility or hormonal concerns.
Bimagrumab has an evidence score of 3.9/10 — emerging evidence based on 9 indexed studies, including 1 meta-analysis. An investigational monoclonal antibody that blocks the activin type II receptor (ActRII) — the receptor through which myostatin and activin restrain muscle — producing a striking body recomposition (fat DOWN, lean muscle UP) but NO proven functional benefit. In a phase 2 trial in adults with type 2 diabetes and obesity, bimagrumab caused a large loss of fat mass and a real gain in lean mass over 48 weeks, which is why it is now being developed as a metabolic / obesity drug. But the muscle-disease story is a cautionary one: its pivotal phase 2b trial in inclusion-body myositis (RESILIENT) added muscle yet FAILED its primary walking endpoint, and a 2025 systematic review concluded it had no effect on disease progression. It is NOT an approved drug, NOT a dietary supplement, and NOT a longevity drug — gaining muscle on a scan is not the same as moving or living better. This entry exists to inform, not to recommend. Representative study: PMID 39843353.
The commonly studied dose of Bimagrumab is No approved or recommended dose — bimagrumab is an investigational monoclonal antibody, not an approved medicine or a supplement. We do NOT provide a dosing protocol. In trials it was given by INTRAVENOUS infusion every 4 weeks (10 mg/kg, up to ~1200 mg, in the type-2-diabetes/obesity study; 1, 3, or 10 mg/kg in the inclusion-body-myositis trials). Some early studies dosed subcutaneously, but the pivotal trials used IV infusion. These were monitored clinical-trial regimens, not a recommendation for any self-use.. Individual needs vary — start at the lower end of the range and adjust based on how you respond.
Timing is flexible for Bimagrumab — consistent daily use matters more than the time of day. There is no validated self-administration schedule.
Bimagrumab should be used with caution — talk to a healthcare provider before taking it. The most commonly reported side effects are muscle spasms / involuntary muscle contractions, diarrhoea, acne (mild). Use caution if any of these apply to you: Not an approved medicine and not a dietary supplement — investigational biologic; do not self-source; No established self-administration safety data; given only by infusion in monitored trials; Pregnancy and breastfeeding (unstudied; bimagrumab transiently alters reproductive-hormone/FSH-axis signalling).
Caffeine
Likely helpsBlocks adenosine receptors to boost alertness, reaction time, and endurance — one of the most proven ergogenic aids.
Berberine
Likely helpsActivates AMPK to regulate blood sugar, improve insulin sensitivity, and support lipid metabolism — comparable to metformin in some trials.
Epicatechin
Probably helpsDark chocolate flavanol with consistent human evidence for improved endothelial function and modest blood pressure reduction. Muscle-building claims are not supported in humans.
Orlistat
Mostly mechanism / observationalA gastrointestinal lipase inhibitor that blocks roughly 30% of dietary fat from being absorbed. It is the only weight-loss drug sold both on prescription (Xenical 120 mg) and over the counter (Alli 60 mg). The evidence base is large and old: across 16 long-term randomised trials it produces about 2.9 kg more weight loss than placebo, and in the 4-year XENDOS trial it cut new type 2 diabetes from 9.0% to 6.2%, though exploratory analysis found the effect was detectable ONLY in the ~21% of participants who already had impaired glucose tolerance. The trade-off is that the unabsorbed fat leaves in the stool — oily spotting, faecal urgency and steatorrhoea — and it measurably impairs fat-soluble vitamin absorption, which is what drives its real drug interactions (warfarin, levothyroxine, ciclosporin). Modest, unglamorous, and hard to stay on.
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Reviewed by Dr. Baher Al Hakim · Last reviewed June 2026 · evidence from 23 studies · how we score · editorial policy
This information is for educational purposes only. It is not a substitute for professional medical advice. Always consult a qualified healthcare provider before starting, stopping, or changing any supplement or medication.
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