Landogrozumab
Landogrozumab (LY2495655), anti-myostatin monoclonal antibody
Written by Aaron CuhaReviewed Sep 2026
Also known as: LY2495655, LY anti-myostatin antibody
The clearest test in the whole field. In 201 older adults who had fallen, it added 0.43 kg of lean mass at p below 0.0001 and moved two of about seven physical performance measures.
Overview
This is the trial to read if you want to understand what myostatin inhibition actually delivers, because it was run in exactly the population the idea is meant to help: older adults who were weak and who had fallen.
The body composition result is unambiguous. Appendicular lean body mass went the wrong way on placebo, down 0.12 kg, and up 0.30 kg on the drug, a between-group difference of 0.43 kg with a p value below 0.0001. That is about as clean as a body composition finding gets.
The function result is the interesting half. Of the physical performance measures tested, the twelve-step stair climb improved significantly. Chair rise with arms and fast gait speed came in at p values of 0.054 and 0.088 against a prespecified threshold of 0.1 for these tests, which the trial had loosened in advance precisely because it expected small effects. Everything else was null. The drug added tissue and the people it was given to did not become meaningfully more capable.
Mechanism of action
A humanised monoclonal antibody neutralising myostatin, blocking its signalling through activin type II receptors and the SMAD2/3 pathway that suppresses muscle protein synthesis. Same target as stamulumab, engineered for higher potency.
Human evidence
The best-designed test of myostatin inhibition in the population the concept targets. Strongly positive on body composition, largely null on function, and honest about both in its own abstract.
- 201 older weak fallers randomised, 24 weeks, monthly injection. Completion 86% on placebo and 80% on drug.
- Appendicular lean body mass difference 0.43 kg favouring the antibody (95% CI 0.192 to 0.660, p < 0.0001).
- Twelve-step stair climb improved by 1.28 seconds (p = 0.011). This is the one clearly positive functional result.
- Chair rise with arms (p = 0.054) and fast gait speed (p = 0.088) were borderline against a prespecified alpha of 0.1 that had been loosened in advance for performance tests. Four-step stair climb was null at p = 0.093.
- No effect detected on the remaining performance-based measures.
- Injection site reactions affected 30% on drug against 9% on placebo, generally mild, causing two discontinuations.
- The authors' own wording is careful: treatment increases lean mass and might improve functional measures of muscle power, and additional studies are needed.
What this does not tell you: A 24-week proof-of-concept trial in 201 people, reporting many functional endpoints at a relaxed significance threshold, which is the design most likely to produce a scattered set of borderline results. It measured no falls, no fractures and no hospitalisations, so the outcome the whole rationale points at was never tested. Lilly did not advance the programme, which is itself informative even though the reason is not published.
Reading the research record
Read the myostatin field as a set and one result repeats. Blocking myostatin reliably adds lean mass, by roughly a quarter to half a kilogram in the trials that measured it properly, and reliably fails to improve what a person can actually do. Stamulumab found no improvement in strength or function. Domagrozumab missed its primary endpoint and every secondary clinical endpoint. Landogrozumab added 0.43 kg of appendicular lean mass at p < 0.0001 and moved two of roughly seven physical performance measures. Bimagrumab, which this site covers separately, produced the largest body composition change in the class and did not deliver a matching functional gain either. The tissue appears. The capability does not follow.
The evidence, charted
Fig. 1 · evidence composition
4of 4 citations (100%) are in people
Every citation cited here is Human work; no other study type is cited on this page. This count is of our own citation list and understates any literature larger than the sources we cite.
Fig. 2 · evidence over time
Citations here span just two years, 2014 and 2015.
Too few distinct publication years on this page to plot as a timeline. The newest citation on file is from 2015, more than five years ago; the published record may have gone quiet.
Fig. 3 · legal status at a glance
US
Not approved
UK
Approved
AU
Not approved
CA
Not approved
Approved in 1 of 4, prescription route in 0, not approved in 3. A jurisdiction's classification is a regulatory fact, not a verdict on the science; see Legal status below for the full text and any notes.
Key studies & citations
- Human2015
Myostatin antibody (LY2495655) in older weak fallers: a proof-of-concept, randomised, phase 2 trial
201 older adults randomised, 99 to placebo and 102 to the antibody, from 365 screened. At 24 weeks appendicular lean body mass changed by minus 0.123 kg on placebo and plus 0.303 kg on drug, a difference of 0.43 kg (95% CI 0.192 to 0.660, p < 0.0001). On function: twelve-step stair climb minus 1.28 s (p = 0.011), four-step stair climb minus 0.46 s (p = 0.093), chair rise with arms minus 4.15 s (p = 0.054), fast gait speed plus 0.05 m/s (p = 0.088), tested against a prespecified two-sided alpha of 0.1 for performance tests. No effect on other performance measures. Injection site reactions in 30% on drug against 9% on placebo (p < 0.0001). Funded by Eli Lilly.
Lancet Diabetes and Endocrinology - Human2015
A study of LY2495655 in older participants who have fallen
The registry record for the falls trial above.
ClinicalTrials.gov - Human2014
A study of LY2495655 in participants undergoing elective total hip arthroplasty
A separate randomised trial in hip replacement, a setting where rapid muscle loss around surgery is predictable and measurable. Listed because the programme tested the idea in more than one population.
ClinicalTrials.gov - Human2015
A study of LY2495655 in participants with pancreatic cancer
Cancer cachexia, the third population tested. Wasting from cancer is a different mechanism from disuse or ageing.
ClinicalTrials.gov
Frequently asked questions
Did it actually build muscle?
Yes, and the result is clean: 0.43 kg more appendicular lean mass than placebo at 24 weeks, with a p value below 0.0001. The placebo group lost lean mass over the same period, which is what you would expect in weak older adults, so part of the effect is preventing loss rather than adding tissue.
Did the people get stronger or steadier?
Barely. One measure, the twelve-step stair climb, improved by 1.28 seconds. Two more were borderline against a threshold that had been deliberately loosened for these tests. The rest showed nothing. And no falls were counted, even though preventing falls was the entire rationale.
Why does that gap keep appearing?
Nobody has established the reason, and the leading explanations are worth knowing. Lean mass on a DXA scan includes water, and an antibody that changes muscle fibre size may not change the neural drive, tendon stiffness or coordination that strength actually depends on. Strength is also lost several times faster than mass with age, which suggests mass was never the limiting factor.
Could it help someone losing muscle on a GLP-1 drug?
That is the open question and it has not been tested with this antibody. The population is different in a way that might matter: a person losing lean mass rapidly during weight loss is not the same as an older adult with long-standing weakness. GYM329 is the antibody now being tested in that setting, including alongside tirzepatide.