Taldefgrobep alfa

Taldefgrobep alfa is an investigational injected protein, not a classic peptide, that blocks myostatin, a signal that holds muscle growth back. Bristol Myers Squibb developed it, and Biohaven is testing it in a 150-person phase 2b obesity study at 100 mg weekly and 150 mg every four weeks, per a Biohaven poster. A phase 3 trial in spinal muscular atrophy did not reach statistical significance. No obesity results exist, and topline data are now expected in the second half of 2027.

Research snapshot

Peptide category	Engineered fusion protein (a small binding protein joined to an antibody Fc fragment). Not a classic peptide. Myostatin-pathway inhibitor.
Primary research interest	Body composition and weight in adults with overweight or obesity; earlier work in spinal muscular atrophy (SMA)
Highest available evidence	Company-reported phase 3 topline results in SMA; registered phase 2b obesity trial with no results
Human research available	Yes. A 269-person phase 3 SMA trial (RESILIENT) and a 150-person phase 2b obesity trial. Biohaven says more than 700 people have been studied across its trials. No peer-reviewed obesity result was identified.
Development status	Phase 2b obesity study fully enrolled; a GLP-1 combination cohort is being added; topline data expected in the second half of 2027
Regulatory status	Not approved anywhere

Technical identity

Primary name	Taldefgrobep alfa (INN, USAN)
Alternative names	BMS-986089, RO7239361, talditercept alfa, anti-GDF8 adnectin Fc fusion
Peptide sequence	Not publicly available as a complete sequence. The FDA substance record lists component segments only.
Amino-acid length	Not reliably established
Molecular formula	Not reliably established
Molecular weight	Not reliably established
CAS Registry Number	1580555-26-5 (FDA Global Substance Registration System)
PubChem CID	Not reliably established
UNII	766C38JSAR
DrugBank ID	Not reliably established
Chemical modifications	Anti-myostatin adnectin (fibronectin type III scaffold) fused to a human IgG1 Fc fragment through a synthetic linker; described by the FDA record as a dimer
Peptide class	Adnectin-Fc fusion protein (a protein therapeutic, not a classic peptide)
Primary biological target	Myostatin (GDF8); Biohaven says it also affects related activin signaling
Developer or originator	Bristol Myers Squibb (as BMS-986089); licensed to Biohaven
Development status	Phase 2b obesity (active, not recruiting); phase 3 SMA trial reported without a statistically significant result in the broad population

Not a classic peptide: why it is on this site

Taldefgrobep alfa is a fusion protein, much larger than a peptide such as semaglutide. It sits here because it belongs to the same conversation: drugs tested alongside peptide weight-loss medicines to keep muscle during weight loss. The wider field is mapped in our guide to GLP-1 muscle loss and the drugs aimed at it.

What is taldefgrobep alfa?

Taldefgrobep alfa is an engineered protein built from two parts. The first is an adnectin, a small binding protein made from a fibronectin scaffold, designed to grab myostatin. The second is the Fc tail of a human antibody, which the body treats like a familiar part of its own immune system and which tends to make a drug last longer in the bloodstream. The two are joined by a short linker, and the finished molecule is a dimer (two copies paired up).

Bristol Myers Squibb created it under the code BMS-986089 and tested it in early human studies, including in people without obesity. Biohaven licensed it and moved it into a phase 3 trial called RESILIENT in children and young adults with spinal muscular atrophy (SMA), a genetic disease that weakens muscle. In November 2024 the company reported that the trial did not show a statistically significant benefit over placebo in the broad population on its main motor-function score, while describing better numbers in some prespecified subgroups. Subgroup findings of that kind are hypothesis-generating and should be read with caution.

Biohaven then turned to obesity. The idea is simple: weight-loss drugs such as GLP-1 medicines remove fat, but also some lean mass, and a drug that blocks myostatin might tilt that balance toward keeping muscle. In a phase 2b study registered as NCT07281495, Biohaven is randomizing 150 adults with overweight or obesity (without diabetes) to taldefgrobep alfa or placebo for 24 weeks, followed by a 24-week open-label extension. Enrollment finished in the first quarter of 2026. On October 29, 2026, the company said it is amending the study to add a cohort that pairs the drug with a GLP-1-based therapy, and it moved expected topline data to the second half of 2027. The release did not name the GLP-1 drug or the size of the new cohort. Biohaven has not published any human obesity efficacy or safety numbers.

Why researchers care: the muscle-preservation question is now one of the busiest areas in obesity medicine. Lilly’s bimagrumab, Scholar Rock’s apitegromab and Regeneron’s trevogrumab are all being tested for the same goal. Taldefgrobep alfa is the newest entrant with no obesity data yet.

How does it work?

Plain-English explanation

Muscle cells are held in check by signaling proteins. Myostatin is the best known: it tells muscle to stop growing. Taldefgrobep alfa is designed to bind myostatin so it cannot deliver that message. In theory, when someone is losing weight fast, less myostatin signaling could mean less muscle lost along with the fat. That is a hypothesis, and for this drug in people with obesity it has not been tested publicly yet.

Technical explanation

The adnectin domain binds free myostatin (GDF8), preventing it from engaging activin type II receptors on muscle cells. Biohaven describes the drug as a myostatin-activin pathway inhibitor, meaning it also influences related activin signaling; the original mechanism data behind that wording are the company’s. The Fc fragment extends circulating time. In Biohaven’s pharmacokinetic and pharmacodynamic model, presented at the American Diabetes Association meeting in 2026, 100 mg weekly was predicted to suppress free myostatin by about 94.6 percent at week 12 and 150 mg every four weeks by about 59.9 percent. Those are simulation outputs, not measured results, although the company says interim data from about 30 percent of participants at week 12 showed robust suppression of free myostatin with both regimens, without giving numbers.

Potential benefits and research applications

Preserving lean mass during weight loss (investigational)

What is being investigated: whether blocking myostatin changes how much lean mass, fat mass and total weight people lose. In the obesity study, the registered primary outcome is percent change in body weight at week 24, with fat mass, lean mass and safety as secondary outcomes.

Evidence: none disclosed for obesity. Biohaven’s poster describes obese-mouse findings of lower body weight and fat with higher lean mass, and says non-obese human groups showed reductions in fat mass and increases in lean mass, with no numbers given. These are company descriptions of animal and early human work, so treat them as Tier 3 to Tier 6 claims. The registry’s body-composition outcomes measure total lean mass, not skeletal muscle volume or strength, so even a good lean-mass result would leave the function question open.

Spinal muscular atrophy (earlier indication)

What was investigated: whether adding taldefgrobep alfa to an approved SMA therapy improves motor function. RESILIENT enrolled 269 participants aged 4 to 21 and used the 32-item Motor Function Measure (MFM-32) at week 48 as its primary outcome.

Evidence: the company reported on November 25, 2024 that the trial did not reach statistical significance in the broad population. It reported numerically better results in a prespecified subgroup and in people with measurable baseline myostatin. Full peer-reviewed results were not identified in the sources reviewed. This history matters for obesity because it shows that biological activity against myostatin does not guarantee a clinical benefit.

What dosage information circulates?

Figures in this section summarize amounts and schedules reported in published research or circulating online. Their inclusion documents what is reported and does not establish that a regimen is verified, safe, effective, or appropriate. The only specific obesity amounts come from one company poster. The registry lists no amounts, and no results have been disclosed.

Reported use or research objective	Route reported	Amount reported	Frequency reported	Reported duration	Evidence or source category
Weight, fat mass and lean mass in adults with overweight or obesity (NCT07281495)	Subcutaneous, self-administered autoinjector	100 mg per administration	Once weekly	24-week double-blind period, then 24-week open-label extension	Registered human trial without results; dose from company poster
Same study, second regimen	Subcutaneous, self-administered autoinjector	150 mg per administration	Once every 4 weeks (monthly)	24-week double-blind period, then 24-week open-label extension	Registered human trial without results; dose from company poster
Motor function in spinal muscular atrophy (RESILIENT, NCT05337553)	Subcutaneous	Weight-based; amount not stated in sources reviewed	Once weekly	48-week double-blind phase, then 48-week open-label extension	Company-reported (trade press); registered trial without posted results
Any use outside registered trials (community or practitioner)	Not consistently reported	No established or reliably sourced dosing information was identified.	Not consistently reported	Not consistently reported	None identified

Explanation of the reported figures

The 100 mg weekly and 150 mg every-four-weeks figures appear in Biohaven’s 2026 ADA poster, which also gives the randomization (2:2:1:1 across the two active arms and two matching placebo arms, about 50, 50, 25 and 25 people). The registry entry confirms a randomized, double-blind, placebo-controlled, multiple-dose design but lists no amounts. Biohaven’s March 2026 release describes weekly and monthly subcutaneous dosing, which matches the poster. Nothing here has been independently replicated, and no peer-reviewed paper reports these doses.

There are no community or practitioner protocols with an identifiable source, and the drug is not available outside clinical trials. We have not converted animal amounts into human amounts. The GLP-1 combination cohort has no disclosed dose. Unknowns: the doses used with a GLP-1 drug, how many people stay on treatment, and whether either regimen changes lean mass in a measurable way.

Amounts studied in human research

Research objective	Amount studied	Frequency	Duration	Route	Study population	Source
Weight and body composition	100 mg	Weekly	24 weeks plus 24-week extension	Subcutaneous	About 150 adults with overweight or obesity, no diabetes (phase 2b)	Biohaven ADA 2026 poster; ClinicalTrials.gov NCT07281495
Weight and body composition	150 mg	Every 4 weeks	24 weeks plus 24-week extension	Subcutaneous	Same study	Biohaven ADA 2026 poster; ClinicalTrials.gov NCT07281495
Motor function in SMA	Weight-based; amount not stated	Weekly	48 weeks plus 48-week extension	Subcutaneous	269 people aged 4 to 21 with SMA on an approved therapy (phase 3)	Pharmaceutical Executive report; ClinicalTrials.gov NCT05337553

Amounts studied in animal research

Biohaven describes obese-mouse data showing lower body weight and fat and higher lean mass, but the poster gives no species details beyond that, no amounts and no schedule. No reliable animal dosing information was identified.

Practitioner and community-reported protocols

No established or reliably sourced dosing information was identified.

Conflicts and unanswered questions

The poster’s two regimens are the only amounts on record, and they are sponsor-reported. The registry omits doses, and the new GLP-1 cohort has no disclosed design. Whether the same doses will be used with a GLP-1 drug, and how they compare with the doses of other myostatin-pathway drugs, is unknown.

Important published research

RESILIENT phase 3 SMA trial (2024, company-reported). 269 participants aged 4 to 21, randomized to weekly subcutaneous taldefgrobep alfa or placebo on top of an approved SMA therapy, for 48 weeks. The primary outcome was change in MFM-32 total score. The company reported no statistically significant benefit in the broad population and pointed to subgroup signals. Limits: results came through company announcements and trade press; no peer-reviewed paper was identified. Meaning: the drug was active enough to be tested at scale, but did not clearly improve function in SMA.

Phase 2b obesity study (NCT07281495, design only). 150 adults aged 18 to 65, BMI above 30 and below 42, or 27 to under 30 with a weight-related condition; people with diabetes were excluded. Primary outcome is percent change in body weight at week 24. Limits: no results; the study is being amended to add a GLP-1 combination cohort.

Timing, duration, and research variables

The two obesity regimens differ in how often the drug is given, which is a research variable in its own right: weekly dosing gives steadier exposure, while monthly dosing is more convenient. The poster’s model predicts deeper myostatin suppression with the weekly schedule at week 12. Beyond that, no evidence on timing or on whether effects last after stopping has been disclosed. We do not suggest an ideal schedule.

Combinations and related research

Formally studied combinations

The GLP-1 combination cohort in NCT07281495 is planned but not yet registered or described. Its design and drug have not been disclosed.

Mechanistically plausible combinations

Because GLP-1 medicines are the most common weight-loss treatment, a myostatin blocker added to one is the natural test. Other myostatin and activin programs have been tested this way, for example bimagrumab with semaglutide and trevogrumab with semaglutide. Their results do not transfer to taldefgrobep alfa.

Practitioner and community combinations

None identified.

Side effects, risks, and limitations

Biohaven’s 2026 poster calls the drug’s safety profile favorable across more than 700 trial participants, but gives no adverse-event figures, and no obesity-study safety data have been released. For context, other drugs that block the myostatin-activin route have shown muscle spasms and other tolerability issues, especially with broader blockade; whether this molecule shares those effects is not known. Anti-drug antibodies, a standard concern with protein drugs, have not been reported in the sources reviewed. Because the drug is only available in trials, product-quality questions such as mislabeling or contamination do not apply to approved supply, and any unlabeled product sold online as this compound would be unverifiable.

Limitations of the evidence: one failed-primary-endpoint phase 3 trial in a different disease, one unreported phase 2b trial, company-only sources, and a measure (lean mass) that is not the same as strength or function. For the same reasons, claims of benefit in obesity should be treated as unproven.

Regulatory and developmental status

Taldefgrobep alfa is not approved by the FDA, the European Medicines Agency or any other regulator, for any use. It is investigational. The phase 2b obesity study is active, not recruiting, with a registry primary completion date of September 2026 that does not reflect the amendment announced on October 29, 2026; topline data are now guided to the second half of 2027. The RESILIENT SMA trial remains listed as active, not recruiting, with a registry completion date of December 2027. Status verified from the sources listed below.

Frequently asked questions

What is taldefgrobep alfa?

An investigational fusion protein that blocks myostatin, a signal that limits muscle growth. It was created by Bristol Myers Squibb as BMS-986089 and is being developed by Biohaven.

Is taldefgrobep alfa a peptide?

Not in the classic sense. It is a larger engineered protein (an adnectin fused to an antibody Fc fragment). It is covered here because it is being tested alongside peptide weight-loss drugs.

How does taldefgrobep alfa work?

It is designed to bind myostatin so the signal cannot reach muscle cells. Biohaven also says it affects related activin signaling. Whether that preserves muscle in people losing weight is not yet known.

What dosage of taldefgrobep alfa has been studied?

Per a Biohaven poster, the obesity study uses 100 mg weekly and 150 mg every four weeks, given by subcutaneous autoinjector, against placebo. The SMA phase 3 used weekly weight-based dosing with no amount stated in the sources reviewed.

What dosage commonly circulates online?

No established or reliably sourced dosing information was identified outside the trials. The drug is not available outside clinical studies.

Has taldefgrobep alfa been studied in humans?

Yes. A 269-person phase 3 trial in spinal muscular atrophy did not reach statistical significance in the broad population, and a 150-person phase 2b obesity trial has no results yet.

Why did Biohaven move the data to 2027?

On October 29, 2026, the company said it is adding a GLP-1 combination cohort and now expects topline data from both portions in the second half of 2027. It gave no results and no reason, so the delay says nothing about whether the drug works.

Is taldefgrobep alfa approved?

No. It is not approved anywhere for any use.

What remains unknown?

Whether it changes weight, fat or lean mass in people with obesity, whether it helps on top of a GLP-1 drug, its tolerability in that setting, and whether any lean-mass change improves strength or function.

Bottom line

Taldefgrobep alfa is interesting because it targets the same muscle-preservation goal as better-studied antibodies, but with a different structure and a different dosing format. The strongest published-style evidence is negative or inconclusive: a phase 3 SMA trial that did not reach significance in the broad population. The only dose figures, 100 mg weekly and 150 mg every four weeks, come from a company poster for a trial with no results. Everything about weight, fat and lean mass in people with obesity remains speculative until Biohaven reports in the second half of 2027. The drug is not approved anywhere. Compare it with bimagrumab, apitegromab and trevogrumab, or see the clinical trial tracker.