IGF-1 DES
Aliases: Des(1-3)IGF-1 · Des1-3 IGF-1
Last verified: 2026-09-24
The short version
IGF-1 DES is technically the most interesting 'muscle peptide' on the gray market: molecularly it is superior to IGF-1 in vitro — weaker carrier binding, freer, more potent. But the same property that impresses in a dish (independence from IGFBPs) makes it less predictable in the body: controlled IGF-1 transport is a biological feature, not a bug. Add to this the real concern about cardiac effects and growth of IGF-receptor-bearing cells under chronic stimulation, and the fact that every 'local injection' into muscle is still a systemic dose. This is a hormonal axis, not a supplement: playing with it without measuring IGF-1, glucose and blood pressure is flying without instruments.
Identity & type
- Molecular type
- truncated hormone
- Sequence / structure
- des(1-3) IGF-1 (67 aa)
- Molecular weight
- ~7.3 kDa
- Origin
- Occurs naturally as a product of IGF-1 proteolysis in circulation; gray supply is a synthetic/recombinant analog.
Mechanism of action
A truncated form of IGF-1 lacking the first three amino acids; it binds IGF-binding proteins (IGFBPs) much more weakly, so the free fraction is larger and theoretically more potent in vitro; it acts on the IGF-1 receptor with the same affinity but a shorter circulating half-life.
not confirmed in humans
Dosing & routes
Official / clinical context
No official context exists; IGF-1 as a class has strict regulatory and anti-doping frameworks.
Regulator-approved labeling and published study designs — never a recommendation.
Community-reported practice
The standard 'site enhancement' narrative: 50–100 µg locally post-workout, 4–6 weeks; reports include pump, water retention and hunger — the last is consistent with its pharmacology. Nobody systematically measures glucose or cycle length.
Unverified self-reports. Not medical advice. Not endorsement.
Protocol — official vs community
Official / label
No approved protocol exists — investigational agent. IGF-1 DES (des(1-3)IGF-1) is preclinical; its weaker IGFBP binding and short half-life are biochemical facts, not clinical findings.
Duration: —
WADA-prohibited (S2). The unbound-fraction pharmacology is real in vitro; the human outcome data is nonexistent.
Community (anecdotal)
50–100 mcg SC 1–3× daily, frequently injected locally into the trained muscle post-workout. Approximate and unvalidated — every regimen is forum empiricism.
- Cycle:
- 4–6 weeks.
- Break:
- 4+ weeks off between cycles.
Dose-fractionation logic (short half-life → split dosing → local injection) is internally consistent but entirely untested in humans. The classic IGF-1 risk set — hypoglycemia, tissue growth where you didn't want it — applies with less predictability, not more.
Human evidence
None for the DES form in healthy/muscle contexts. Decades of IGF-1 data exist in therapeutic contexts (e.g. Laron syndrome), but that is not an argument for DES.
Preclinical evidence
Good molecular characterization without clinically relevant interventional studies: a larger free fraction in vitro does not guarantee a better therapeutic ratio in vivo — reduced IGFBP binding also shortens half-life and clearance.
Known risks
- Hypoglycemia (especially at higher doses in healthy athletes)characterized
- Internal-organ hypertrophy and heart failure under chronic stimulationtheoretical
- Proliferative effect on cells bearing IGF-1 receptorstheoretical
Teal: characterized in clinical/labeling contexts. Amber: theoretical or reported outside controlled settings.
Unknowns & evidence gaps
- True bioavailability and free/bound ratio in human circulation
- Long-term cardiac effect of cyclic use
Frequently asked questions
References
- Ballard FJ et al. — des(1-3)IGF-1 characterization (IGFBP affinity literature)
- WADA Prohibited List — S2 Peptide Hormones, Growth Factors