Bimagrumab

Bimagrumab is a lab-made antibody, not a peptide. Antibodies are much larger molecules, and they are given by a drip into a vein rather than as a small injection under the skin. It works by blocking a docking point on muscle cells that normally receives signals telling muscle to stop growing. With that docking point blocked, the brake comes off: muscle tissue grows, and in the studies done so far fat tissue also went down. It is still experimental everywhere in the world — no regulator has approved it for anything.

In a study of adults who had type 2 diabetes along with overweight or obesity, people given bimagrumab lost body fat and gained lean tissue over about a year, while those given a placebo did neither. A later and much larger study tested it in adults with obesity, on its own and alongside an existing weight-loss medicine, and the combination brought about more weight loss than either one used alone. Muscle spasms, diarrhoea and acne were the side effects that came up most often with it. Its biggest test was in a rare muscle-wasting disease, where the main thing the trial set out to measure — how far people could walk in six minutes — did not improve compared with placebo at any dose. It has never been approved for sale, and all the weight-related work so far has been mid-stage.

Not a peptide — a monoclonal antibody. Not FDA-approved, and not approved by any regulator anywhere; it has been investigational throughout its development. Originated at Novartis as BYM338 and now studied by Eli Lilly as LY3985863. Its largest and best-powered programme — a phase 2b trial in sporadic inclusion body myositis — did not improve its primary endpoint. Current weight-management work is phase 2; no phase 3 weight-management trial exists. WADA status: Prohibited at all times. The 2026 WADA Prohibited List names bimagrumab by name under S4.3, "Agents Preventing Activin Receptor IIB Activation", as an example of an anti-activin receptor IIB antibody. Per the S4 section header, S4.3 substances are non-Specified Substances. Not DEA-scheduled.

Bimagrumab is investigational and is not approved anywhere, so it is not available by prescription and nothing sold as it has been reviewed by a regulator. Muscle spasms, diarrhoea and acne were the side effects reported most often in its studies. It is banned in drug-tested sport, where it is named directly on the banned list. VialWise is a research and educational reference, not medical advice — consult a licensed professional.

⚠️ Bimagrumab is an investigational compound not approved by any regulator for any indication. Information in this entry is informational, not medical advice.

⚠️ This is a monoclonal antibody, not a peptide. Bimagrumab is a fully human monoclonal antibody[¹] — a large immunoglobulin protein of roughly 150 kDa, given by intravenous infusion. It is not a lyophilized research peptide, it is not reconstituted with bacteriostatic water, and it is not injected subcutaneously. The library carries non-peptide compounds deliberately; a reader mistaking an antibody for a peptide is a different matter, because every handling, preparation, and dosing convention used elsewhere in this library is wrong for it.

⚠️ Investigational everywhere. Not approved, not withdrawn — never approved. Bimagrumab has been in clinical development since at least 2011 without an approval in any jurisdiction. FDA labeling and application records return no result for it (checked 2026-09-10), and the 2026 Nature Medicine report describes it in its own opening sentence as "an investigational antibody".[³]

⚠️ The muscle-preservation story is the most hype-adjacent claim in this space. Read the populations. Every efficacy figure below belongs to a specific trial in a specific population at a specific dose, and none of them generalises. The body-composition findings come from phase 2 trials of 75 and 507 participants; the combination finding excludes people with diabetes; and the compound's largest trial — in a muscle-wasting disease — missed its primary endpoint entirely.[¹] A phase 2 body-composition result is not a general claim that bimagrumab preserves muscle.

⚠️ WADA-banned, named explicitly. The 2026 WADA Prohibited List names bimagrumab under S4.3, "Agents Preventing Activin Receptor IIB Activation", verbatim as "Anti-activin receptor IIB antibodies (e.g. bimagrumab)".[⁵] Per the S4 section header, "Prohibited substances in classes S4.1 and S4.2 are Specified Substances. Those in classes S4.3 and S4.4 are non-Specified Substances."[⁵] Non-Specified status carries a stricter sanction range. Prohibited at all times, in and out of competition. This is the same S4.3 cluster as [follistatin.md](./follistatin.md) and [ace-031.md](./ace-031.md).

Bimagrumab (development codes BYM338 at Novartis, LY3985863 at Eli Lilly) is a fully human monoclonal antibody that binds the activin type II receptors.[¹][²] Antibody blockade of ActRII signalling stimulates skeletal muscle growth, and the 2021 trial report notes that earlier clinical work had also suggested it promotes loss of excess adipose tissue and improves insulin resistance.[²]

Mechanism, stated at the level the sources support. The receptor is the point of blockade. Myostatin and the activins signal through ActRII to restrain muscle growth; an antibody occupying the receptor prevents that signalling regardless of which ligand is present.[²] This is mechanistically adjacent to, but not the same as, the two other myostatin-pathway compounds in this library: [ace-031.md](./ace-031.md) is a soluble decoy receptor that mops up ligands, and [follistatin.md](./follistatin.md) is a binding protein that sequesters myostatin and activins. A naming caution worth carrying: the WADA List files bimagrumab under anti-activin receptor IIB antibodies,[⁵] while the trial literature describes its target as the activin type II receptors more generally.[²][³] Both descriptions are reproduced here as their sources give them; this entry does not assert a receptor-subtype selectivity figure [ADD].

Sporadic inclusion body myositis — the largest programme, and it failed. RESILIENT was a multicentre, double-blind, placebo-controlled phase 2b trial at 38 academic sites across Australia, Europe, Japan and the USA, enrolling 251 participants aged 36–85 randomised 1:1:1:1 to bimagrumab 10, 3 or or placebo, infused every 4 weeks for at least 48 weeks.[¹] The primary outcome was 6-minute walking distance at week 52, analysed by intention-to-treat.[¹] At week 52, 6MWD change from baseline did not differ between any bimagrumab dose and placebo — the least-squares mean treatment differences were 17·6 m (SE 14·3; 99% CI −19·6 to 54·8; p=0·22) for, 18·6 m (14·2; −18·2 to 55·4; p=0·19) for, and −1·3 m (14·1; −38·0 to 35·4; p=0·93) for.[¹] The authors' own conclusion is that bimagrumab "showed a good safety profile, relative to placebo, in individuals with inclusion body myositis but did not improve 6MWD."[¹] The study was funded by Novartis Pharma.[¹] A long-term extension reported progressive deterioration in 6MWD from weeks 24 to 104 in all treatment groups, including those receiving bimagrumab.[⁶]

Type 2 diabetes with overweight or obesity. A 48-week, double-masked, placebo-controlled phase 2 randomised trial at 9 US and UK sites enrolled adults with type 2 diabetes, BMI 28–40 and HbA1c 6.5–10.0%.[²] 75 patients were randomised (bimagrumab n=37, placebo n=38) and 58 (77.3%) completed; the published analysis included only participants who completed the full treatment regimen.[²] At week 48, changes for bimagrumab versus placebo were: fat mass −20.5% (−7.5 kg; 80% CI −8.3 to −6.6) versus −0.5% (−0.18 kg; 80% CI −0.99 to 0.63), P<.001; lean mass +3.6% (+1.70 kg; 80% CI 1.1 to 2.3) versus −0.8% (−0.4 kg; 80% CI −1.0 to 0.1), P<.001; waist circumference −9.0 cm versus +0.5 cm, P<.001; HbA1c −0.76 percentage points versus −0.04, P=.005; and body weight −6.5% (−5.9 kg) versus −0.8% (−0.8 kg), P<.001.[²] Three design facts travel with those numbers: the trial had 75 participants, the analysis was restricted to completers, and the intervals reported are 80% confidence intervals, not the conventional 95%.[²]

Obesity, with and without semaglutide. The 2026 Nature Medicine report is the largest weight-related trial: a double-blind, placebo-controlled phase 2 trial randomising 507 adults with obesity (BMI ≥30, or ≥27 with at least one obesity-associated complication, excluding diabetes) 1:1:1:1:1:1:1:1:1 across nine groups for 48 weeks — placebo, bimagrumab 10 or intravenously every 12 weeks, semaglutide 1.0 or subcutaneously once weekly, and combinations — followed by an open-label extension to week 72.[³] The primary endpoint was absolute change from baseline in body weight at week 48.[³] Least-squares mean absolute body-weight changes at week 48 were −9.3 kg (bimagrumab), −14.2 kg (semaglutide) and −17.8 kg (bimagrumab plus semaglutide), versus −3.3 kg for placebo (all P<0.001 versus placebo).[³] Common adverse events for bimagrumab were muscle spasms, diarrhoea and acne; semaglutide was associated with nausea, diarrhoea, constipation and fatigue.[³]

On the body-composition question this trial is best known for: the published abstract reports body weight, and does not report the fat-mass and lean-mass split. This entry therefore attributes lean-mass gain only to the 2021 type 2 diabetes trial, which measured and reported it,[²] and makes no claim about lean-mass preservation in the semaglutide combination.

Sarcopenia. A 24-week randomised, double-blind, placebo-controlled parallel-arm phase 2 proof-of-concept study at five US centres enrolled 40 community-dwelling adults aged 65 and over with gait speed 0.4–1.0 m/s and low appendicular skeletal muscle index, randomised to intravenous bimagrumab (n=19) or placebo (n=21).[⁴] Thigh muscle volume increased by week 2 and remained above baseline at study end in the bimagrumab group with no change on placebo (week 24: 4.80±5.81% versus −1.01±4.43%, P=.002).[⁴] Participants with slower baseline walking speed who received bimagrumab had greater improvements in gait speed (mean 0.15 m/s, P=.009) and 6-minute walk distance (mean 82 m, P=.022) than placebo at week 16 — a subgroup finding in a 40-person study, and framed as such here.[⁴]

Development status (checked against ClinicalTrials.gov, 2026-09-10). The registry record shows the programme moving from Novartis to Eli Lilly. The furthest any bimagrumab trial has been registered is phase 2/phase 3, in sporadic inclusion body myositis — the programme that missed its endpoint. Every registered weight-management trial is phase 2, including the completed 507-participant semaglutide combination study (NCT05616013) and an active phase 2 weight-management study of 252 participants (NCT06643728). A registered bimagrumab-plus-tirzepatide study (NCT06901349) is listed as withdrawn with zero enrolment.

Regulatory status (US). Not FDA-approved. Searches of FDA labeling and application records return no result for bimagrumab (checked 2026-09-10). Consistent with a compound that has never held an approval, there is nothing to be withdrawn or discontinued. Not DEA-scheduled.

Regulatory status (sport — WADA). Prohibited at all times, named explicitly. See the callout above for the verbatim S4.3 listing and the non-Specified Substance framework note.[⁵]

Commonly reported

• Muscle spasms — the most characteristic bimagrumab adverse event. In RESILIENT, reported in 51%, 68% and 40% of participants versus 21% on placebo.[¹] Also common in the 2026 obesity trial.[³]
• Diarrhoea — 52%, 44% and 32% across the RESILIENT bimagrumab arms versus 18% on placebo.[¹] Also common in the obesity trial.[³]
• Acne — reported as a common bimagrumab adverse event in the 2026 obesity trial.[³]

No approved product exists anywhere. Anything sold as bimagrumab outside a clinical trial is outside any regulatory system for identity, purity, or sterility, and is not the trial material any figure in this entry describes.

The route is intravenous infusion under clinical supervision. Nothing in this entry supports self-administration by any route.

Drug-tested athletes: prohibited at all times and named on the list. S4.3 substances are non-Specified, carrying a stricter sanction range.[⁵]

Class-level caution from the pathway. The ACE-031 phase 2 programme in Duchenne muscular dystrophy was stopped for epistaxis and telangiectasias — vascular adverse events attributed to inhibition of TGF-β-superfamily ligands beyond myostatin. See [ace-031.md](./ace-031.md) and [follistatin.md](./follistatin.md). Whether that concern extends to receptor-level blockade by bimagrumab is not established in the trials cited here.

Pregnancy and lactation: no data presented here. Default to contraindicated.

Monoclonal antibody

A large lab-made protein designed to stick to one specific target in the body. Much bigger than a peptide, and usually given by a drip.

Activin type II receptor

A docking point on muscle cells. Signals arriving there tell muscle to limit its own growth.

Myostatin

A natural signal that acts as a brake on muscle growth. Blocking its docking point releases that brake.

Lean mass

The weight of everything in the body that is not fat — muscle, organs, bone and water.

Investigational

Still being studied and not approved by regulators for general use.

1. Hanna MG, Badrising UA, Benveniste O, Lloyd TE, Needham M, Chinoy H, Aoki M, Machado PM, et al. (2019). Safety and efficacy of intravenous bimagrumab in inclusion body myositis (RESILIENT): a randomised, double-blind, placebo-controlled phase 2b trial. The Lancet Neurology, 18(9):834–844.(PMID 31397289 · NCT01925209)
2. Heymsfield SB, Coleman LA, Miller R, Rooks DS, Laurent D, Petricoul O, Praestgaard J, Swan T, et al. (2021). Effect of Bimagrumab vs Placebo on Body Fat Mass Among Adults With Type 2 Diabetes and Obesity: A Phase 2 Randomized Clinical Trial. JAMA Network Open, 4(1):e2033457.(PMID 33439265 · NCT03005288)
3. Heymsfield SB, Aronne LJ, Montgomery P, Klickstein LB, Coleman LA, Dole K, Mindeholm L, Spruill S, et al. (2026). Bimagrumab plus semaglutide alone or in combination for the treatment of obesity: a randomized phase 2 trial. Nature Medicine, 32(3):869–882.(PMID 41772149 · NCT05616013)
4. Rooks D, Praestgaard J, Hariry S, Laurent D, Petricoul O, Perry RG, Lach-Trifilieff E, Roubenoff R. (2017). Treatment of Sarcopenia with Bimagrumab: Results from a Phase II, Randomized, Controlled, Proof-of-Concept Study. Journal of the American Geriatrics Society, 65(9):1988–1995.(PMID 28653345)
5. World Anti-Doping Agency. The 2026 Prohibited List, International Standard (effective 1 January 2026). Canonical PDF: wada-ama.org; local archival copy at docs/legal/wada-2026-prohibited-list.pdf.
6. Amato AA, Hanna MG, Machado PM, Badrising UA, Chinoy H, Benveniste O, Karanam AK, Wu M, et al. (2021). Efficacy and Safety of Bimagrumab in Sporadic Inclusion Body Myositis: Long-term Extension of RESILIENT. Neurology, 96(12):e1595–e1607.(PMID 33597289 · NCT02573467)

• Semaglutide — discussed together in this entry's stacks section
• Tirzepatide — discussed together in this entry's stacks section
• Adipotide — same mechanism class
• Follistatin — same mechanism class
• FOXO4-DRI — same mechanism class
• PNC-27 — same mechanism class