In mice, a single injection of the antibody SRK-015 increases muscle mass by 17.5% and stops muscle loss caused by dexamethasone without reducing muscle quality.
See the scientific wording
In mice, a single dose of the monoclonal antibody SRK-015, which inhibits the proteolytic activation of myostatin precursor forms, increases gastrocnemius muscle mass by 17.5% and prevents dexamethasone-induced muscle atrophy without impairing muscle quality.
Correlational — new studies may shift this
Randomized trialsOne low-scoring study links this claim to the outcome, but causation is not established.
What the research says
1 study reviewedSupporting (1)
Blocking extracellular activation of myostatin as a strategy for treating muscle wasting
Randomized Controlled TrialAnimal2018
Scientists gave mice a special antibody that stops a protein called myostatin from becoming active, and the mice grew bigger, stronger muscles without any harm. It also stopped muscle loss caused by a steroid drug.
Contradicting (0)
No contradicting studies found yet
That doesn't mean it's settled — it just means no study has tested the opposite.
Quality-weighted scoring: we follow the GRADE framework — each study is rated High, Moderate, Low, or Very Low based on study design, methodology rigor, and risk of bias. A single high-quality RCT can outweigh several weaker observational studies.
Scores reflect study quality, not just count.
A special antibody binds to inactive myostatin before it can be activated, preventing the release of the active growth factor. Without active myostatin, muscle cells stop breaking down proteins and start building more muscle, leading to larger muscles and protection against muscle loss.
Score breakdown, mechanism chain, raw evidence, ideal studies needed & 1 supporting study
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In mice, a single injection of the antibody SRK-015 increases muscle mass by 17.5% and stops muscle loss caused by dexamethasone without reducing muscle quality.
Mechanism
1 studyA targeted antibody locks myostatin in its inactive form before it can turn on, so muscles stop breaking down and start growing bigger. This same block stops muscle loss caused by steroids, without harming muscle strength or function.
A special antibody binds to inactive myostatin before it can be activated, preventing the release of the active growth factor. Without active myostatin, muscle cells stop breaking down proteins and start building more muscle, leading to larger muscles and protection against muscle loss.
Pro-myostatin and latent myostatin accumulate in the extracellular matrix surrounding muscle fibers
A monoclonal antibody binds specifically to pro-myostatin and latent myostatin, preventing access by tolloid proteases
Tolloid protease cleavage of the myostatin prodomain is blocked, preventing release of mature myostatin
Mature myostatin does not bind to ActRIIb receptors on muscle cell membranes
SMAD2/3 signaling is reduced in muscle cells, decreasing transcription of atrophy-related genes such as MuRF1 and Atrogin-1
Muscle protein degradation is suppressed and protein synthesis is favored, leading to increased fiber cross-sectional area and muscle mass
Evidence from Studies
Supporting (1)
Community contributions welcome
Blocking extracellular activation of myostatin as a strategy for treating muscle wasting
Scientists gave mice a special antibody that stops a protein called myostatin from becoming active, and the mice grew bigger, stronger muscles without any harm. It also stopped muscle loss caused by a steroid drug.
Contradicting (0)
Community contributions welcome
Score Breakdown
No multi-axis breakdown available yet. The overall Pro / Against score above is the best signal.
- No clinical evidence is available; the score reflects mechanistic plausibility only.
What Would Prove This
Per GRADE and EBM methodology, here is what ideal scientific evidence would look like to definitively prove or disprove this claim, ordered from strongest to weakest.
Systematic Review of Monoclonal Antibodies Targeting Myostatin Activation in Animal Models of Muscle Wasting
Population: Mice with induced muscle atrophy; Intervention: Single dose of SRK-015; Comparator: Placebo or control antibody; Outcome: Gastrocnemius muscle mass change, atrophy prevention, muscle quality metrics; Duration: Single-dose observation period
Double-Blind, Placebo-Controlled Trial of SRK-015 in Mice with Dexamethasone-Induced Muscle Atrophy
Population: Mice with dexamethasone-induced atrophy; Intervention: Single intravenous dose of SRK-015; Comparator: Saline placebo; Outcome: Gastrocnemius muscle mass, atrophy markers, muscle fiber quality; Duration: 7–14 days post-dose
Longitudinal Cohort Study of SRK-015 Effects on Muscle Mass and Quality in Mice Exposed to Dexamethasone
Population: Mice exposed to dexamethasone; Intervention: Single SRK-015 dose; Comparator: Untreated dexamethasone-exposed mice; Outcome: Muscle mass, atrophy progression, quality metrics over 28 days; Duration: 28 days
In Vitro Analysis of SRK-015 Inhibition of Myostatin Proteolytic Activation in Murine Skeletal Muscle Cells
Population: Murine skeletal muscle cell lines; Intervention: SRK-015 exposure; Comparator: Control antibody or buffer; Outcome: Myostatin precursor cleavage rate, downstream signaling markers; Duration: 24–72 hours
Single-Dose SRK-015 Study in Mice Assessing Muscle Mass, Atrophy Prevention, and Muscle Quality
Population: C57BL/6 mice; Intervention: Single SRK-015 injection; Comparator: Vehicle control; Outcome: Gastrocnemius muscle mass, dexamethasone-induced atrophy, histological muscle quality; Duration: 7 days