Research Cluster
Performance & Body Composition Peptides
This cluster is where the gap between community use and human evidence is the most dramatic on this site. The IGF-1 analogs and MGF variants documented here are among the most actively used compounds in performance and bodybuilding communities worldwide. Every one of them has zero published human clinical trials for any indication. The community evidence base for these compounds consists entirely of anecdotal reports, extrapolation from rodent and cell data, and forum pharmacology. That gap is documented here without judgment—but without softening it either.
For context: recombinant human IGF-1 (mecasermin, Increlex) is FDA-approved for severe primary IGF-1 deficiency in children, with an established human safety and pharmacology record. The IGF-1 analogs in this cluster—LR3, DES, and MGF variants—are structurally modified research compounds distinct from the approved form, with different receptor kinetics, tissue selectivity profiles, and substantially different pharmacological behavior. They are not the same compound as Increlex, and the Increlex safety record does not transfer to them.
Cluster at a Glance
8 compounds • 0 FDA-approved therapeutics in this cluster • 2 Phase I/II clinical programs • 5 preclinical only • All WADA-prohibited
Clinical Trials
Preclinical Only
⚠ WADA Status: All compounds in this cluster are prohibited in-competition and out-of-competition under the World Anti-Doping Agency Prohibited List, Category S2 (Peptide Hormones, Growth Factors, Related Substances and Mimetics). Athletes subject to anti-doping rules should treat every compound on this page as prohibited regardless of source or formulation.
Editorial note: Preclinical data in rodent muscle injury and hypertrophy models is real data—it describes genuine biological mechanisms. It is not human data. Rodent IGF-1 axis pharmacology does not map directly to human physiology in ways that make rodent dosing, response magnitude, or safety profiles predictive of human outcomes. This distinction matters for every compound in the preclinical tier of this cluster.
AOD-9604: The Growth Hormone Fragment That Failed Its Only Clinical Trial
hGH fragment 176-191. Phase IIb oral trial (n=300) failed primary endpoint—no significant weight loss vs placebo. GRAS for food ingredient use is not drug approval.
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WADA
Follistatin: Myostatin Inhibition, Muscle Growth, and the Gene Therapy Gap
Glycoprotein neutralizing myostatin. AAV-follistatin gene therapy has Phase I/II human data (Mendell, Nationwide Children's). Peptide injection has zero clinical validation.
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WADA
IGF-1 DES: The Truncated High-Potency IGF-1 Variant
Truncated IGF-1 missing first 3 amino acids. High-potency local paracrine signaling. WADA prohibited (S2). No human trials. Short half-life limits systemic exposure.
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WADA
IGF-1 LR3: The Extended Half-Life IGF-1 Analog
Half-life-extended IGF-1 analog with Arg3 substitution reducing IGFBP binding. WADA prohibited (S2). Zero human clinical trials. Widely used in performance communities.
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WADA
MGF and PEG-MGF: Mechano Growth Factor and Its Pegylated Analog
IGF-1 splice variant E-peptides targeting satellite cell activation. PEG-MGF extends half-life via pegylation. WADA prohibited (S2). No human clinical data.
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MOTS-c: The Mitochondrial Peptide That Tells Your Cells to Burn
Mitochondrial-derived peptide activating AMPK-mediated metabolic regulation. Exercise mimetic in rodent models. No human clinical trials for exogenous use.
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How These Compounds Relate
Five of the eight compounds in this cluster address the IGF-1 axis from different angles. IGF-1 LR3 is a half-life–extended analog of IGF-1 designed to maximize systemic availability. IGF-1 DES is a high-potency truncated form that acts as a local paracrine signal. MGF and PEG-MGF are derived from the IGF-1 gene via alternative splicing—the E-peptide extension produced by the IGF-1Ea splice variant is proposed to have satellite cell activation activity independent of the IGF-1 receptor. Follistatin acts upstream of the IGF-1 axis by neutralizing myostatin—removing the inhibitory brake on muscle growth rather than pressing the accelerator. MOTS-c and AOD-9604 operate through entirely different mechanisms: AMPK-mediated mitochondrial metabolic regulation and hGH C-terminal lipolytic fragment activity, respectively.
LR3 and DES are often discussed as though they are interchangeable IGF-1 forms with different potencies. They are not. LR3’s pharmacological premise is extended half-life through IGFBP displacement—a sustained systemic signal. DES’s premise is high-affinity local receptor activation at sites of injury or injection—a brief, potent local signal. The community practice of combining them in the same protocol treats the IGF-1 axis as a lever to push in one direction; the actual pharmacology is more specific than that, and the interaction between sustained systemic LR3 exposure and high-potency local DES receptor activation has not been studied in humans.
The follistatin story is the cluster’s most scientifically grounded mechanism—myostatin as a negative regulator of muscle mass is not disputed, the myostatin–follistatin axis is well-characterized, and the gene therapy data in dystrophy patients is real. The gap is between that biology and the exogenous peptide application: follistatin peptide is large, glycosylated, and subject to rapid protease degradation in a way that makes the pharmacokinetics of subcutaneous injection substantially different from the sustained expression achieved by AAV-follistatin gene delivery.
AOD-9604’s Phase IIb failure is the most consequential data point in this cluster for evidence calibration purposes. It is the compound with the only controlled human trial data, and the controlled human trial data showed no significant effect on its primary endpoint. Community use of AOD-9604 continues. The disconnect between Phase IIb results and community adoption is part of the broader pattern this cluster illustrates: human trial data rarely terminates community use of performance compounds once the compounds have entered circulation.