IGF-1 DES(1-3)

Mechanism of action

Binds IGF-1R with similar affinity to native IGF-1 but with ~10-fold reduced binding to IGFBP-3, the dominant serum IGFBP. In IGFBP-rich environments — which is essentially all extracellular human biology — DES(1-3) is therefore substantially more bioavailable at the receptor. Downstream signaling (PI3K/Akt/mTOR and MAPK) is identical to native IGF-1.

Primary uses

• Research reagent for IGF-1 bioavailability studies
• Cell culture growth media
• Community bodybuilding use (unapproved, no safety data)

Typical dosing

Regulatory status

Not approved. Research reagent only. Unlike LR3, DES(1-3) occurs endogenously in small quantities and was not deliberately engineered.

Status as of this entry's last review, October 4, 2026. Approvals, compounding rules and sport rules change; the regulatory tracker is checked more often.

What we checked

IGF-1 DES(1-3) is a natural, truncated form of IGF-1 studied in the laboratory since the late 1980s and never developed as a medicine. This section adds what can be checked.

Identity, computed

It is IGF-1 without its first three residues, Gly-Pro-Glu. The calculator gives C319H495N91O96S7 at 7,365.43 g/mol with three disulfide bonds; an earlier version of this entry gave 7,372, which matched no form of the sequence, and was corrected on October 4, 2026.

Regulatory status, read October 5, 2026

Drugs@FDA: 2 records for “mecasermin”. EMA medicines list: 2 records for “IGF-1”. Run for semaglutide, the same queries return 6 and 5 records (and the registry search 84 trials), so a zero here is an absence, not a broken search. WADA 2026: section S2.3; WADA 2027: section S2.3.

Those Drugs@FDA and EMA records are for mecasermin (Increlex), the approved full-length IGF-1, not for this truncated form, which has no record of its own.

What the maker or sellers claim

Claim, from research-chemical and bodybuilding sellers: DES IGF-1 builds muscle locally when injected. It was never approved for human use, and black-market vials analysed by anti-doping laboratories contained degraded forms.

What the literature shows

Losing the glutamate at position 3 sharply reduces binding to IGF-binding proteins, which normally hold IGF-1 inactive, so in cell culture DES(1-3) is about ten times more potent than IGF-1; part of that advantage survives in animals, with selective effects on gut tissue (Ballard et al., 1996). It is prohibited in sport, and a 2021 doping-control method detected it and two other IGF-1 analogues after injection in rats, noting abundant oxidised and lower-quality forms in black-market products (Mongongu et al., 2021).

What we looked for and did not find

No human trial, no registry record and no human dose from a controlled study.

References

1. [pubmed] Ballard FJ, et al. "Des(1-3)IGF-I: a truncated form of insulin-like growth factor-I." Int J Biochem Cell Biol, 1996;28:1085-1087. PMID: 8930132.
2. [pubmed] Francis GL, et al. "Insulin-like growth factor (IGF)-I and IGF-II which partially lack N-terminal amino acids have reduced affinity for IGF-binding proteins." J Mol Endocrinol, 1992;8:213-223.
3. [pubmed] Mongongu C, et al. "Detection of LongR(3) -IGF-I, Des(1-3)-IGF-I, and R(3) -IGF-I using immunopurification and high resolution mass spectrometry for antidoping purposes." Drug Test Anal, 2021;13(7):1256-1269. PMID: 33587816.

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