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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. It is described here 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
Bimagrumab doesn't have enough studies with structured effect-size data yet to pool a verdict. Browse the studies below for individual findings.
Most evidence is from high-quality meta-analyses and randomised trials published 2014–2026.
Based on 25 studies · 3 meta-analyses · 15 RCTs
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.
15 randomised trials
93% were about Bimagrumab in an audit of 15 of them
Every randomised or controlled trial of Bimagrumab indexed in PubMed, not a hand-picked subset. Meta-analyses and systematic reviews are deliberately excluded from this count: most of them cover many compounds at once, so counting them would inflate it.
PubMed · as of Sep 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 Nov 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. This interaction is awaiting review by a qualified pharmacist and has not been assigned a severity. It is shown so you can raise it, not because its risk has been established. Ask a pharmacist or prescriber before combining, and do not stop or change prescribed medicines based on this notice.
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 25 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. It is described here to inform, not to recommend. Representative study: PMID 39843353.
Dosing for Bimagrumab: SupStack does not provide a self-directed dosing protocol for Bimagrumab. A dose used in a clinical trial does not establish a safe consumer dose. 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.
Timing is flexible for Bimagrumab — consistent daily use matters more than the time of day. There is no validated self-administration schedule.
No consumer dose of Bimagrumab is endorsed, so there is no dose at which it can be called safe. Talk to a healthcare provider before taking it. Reported side effects include muscle spasms / involuntary muscle contractions, transient changes in reproductive-hormone (FSH/LH) signalling, diarrhoea. How often they occur is not established for all of them. 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
Probably helpsBlocks adenosine receptors to boost alertness, reaction time, and endurance — an umbrella review of 21 meta-analyses found it ergogenic for endurance, strength and power.
Berberine
Likely helpsActivates AMPK to regulate blood sugar, improve insulin sensitivity, and support lipid metabolism. Its only head-to-head trial with metformin cited here was a 36-person pilot, which does not show it can replace metformin.
Epicatechin
Mixed evidenceDark 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 25 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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