IGF-1 DES(1-3)

des(1-3)IGF-I, des-IGF-1, truncated IGF-1, DES IGF

Growth hormone axis

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Summary

Class: Naturally occurring 67-amino-acid variant of IGF-1 (which has 70) lacking the first three amino acids (Gly-Pro-Glu); the research product is a recombinant copy
Mechanism: Activates the IGF-1 receptor like IGF-1 but binds far more weakly to IGF-binding proteins, so more of it is free and active — roughly 10 times as potent as IGF-1 in cell culture
Routes studied: Infusion and injection in rodents; cell culture; oral in some animal gut studies; subcutaneous and intramuscular (community)
Dose range reported: Animal: tens to hundreds of µg/kg/day by infusion. Community: 20–100 µg per injection, often injected into a trained muscle immediately after exercise, with very short cycles. No human dose has ever been studied
Half-life: Very short — reported as roughly 20–30 minutes, because it is not protected by binding proteins. (IGF-1 LR3, by contrast, is estimated at 20+ hours.)
Storage: Lyophilised: refrigerate or freeze, protect from light. Reconstituted: refrigerate; growth factors are fragile — community practice is use within 2–4 weeks and avoid any agitation
Regulatory status: Not approved anywhere

Doses are as reported in studies or by the community — never recommendations.

1What it is

IGF-1 (insulin-like growth factor 1) is the hormone the liver produces in response to growth hormone and the main mediator of GH's growth effects. Des(1-3)IGF-1 is IGF-1 missing its first three amino acids. Unlike most compounds on this site, it is a natural molecule: it was discovered independently in the mid-1980s in human brain tissue (Sara 1986, PNAS) and in bovine colostrum (Francis 1986–1988, Biochem J). The clipped-off tripeptide, Gly-Pro-Glu (GPE), has a research history of its own as a neuroprotective fragment.

The missing glutamate at position 3 is critical for IGF-1's binding to the IGF-binding proteins (IGFBPs) that carry more than 99% of IGF-1 in blood in an inactive form. Without it, des(1-3)IGF-1 is largely free, which makes it much more potent in culture and much shorter-lived in the body. An Australian company (GroPep) developed recombinant des(1-3)IGF-1 and the related long-acting analogue IGF-1 LR3 as research reagents in the 1990s, and the two have circulated as research compounds ever since. IGF-1 itself, as mecasermin, is an approved medicine for severe primary IGF-1 deficiency; des(1-3)IGF-1 is not.

2How it's thought to work

Des(1-3)IGF-1 activates the IGF-1 receptor (and, more weakly, the insulin receptor), switching on the PI3K/Akt/mTOR pathway that drives protein synthesis and cell survival, and the MAPK pathway that drives proliferation. In muscle, IGF-1 signalling promotes satellite-cell activation and fibre growth, and reduces protein breakdown. Because des(1-3)IGF-1 escapes the IGFBPs, a given dose delivers more receptor activation than the same dose of IGF-1 — but for a much shorter time, and with more acute hypoglycaemia risk, since free IGF-1 lowers blood glucose.

The community rationale for injecting it into a trained muscle is that the short keeps the effect local. There is no human evidence that locally injected IGF-1 variants produce local growth, and animal infusion studies were systemic.

IGF-1 missing its first three amino acids, which is where the binding proteins attach. Free of them it is far more potent locally, and cleared far faster.Schematic — not to scale

3What the research shows

Potency and binding-protein escape

In cell-culture assays des(1-3)IGF-1 was roughly 10-fold more potent than IGF-1 at stimulating protein synthesis and DNA synthesis, an effect attributable to its weak IGFBP binding rather than higher receptor affinity (Ballard 1987, Biochem Biophys Res Commun; Francis 1988, Biochem J). [2][3]

Anabolic effects in animals

In rats, including dexamethasone-treated catabolic rats and gut-resection models, infused des(1-3)IGF-1 improved nitrogen balance, body weight and organ or muscle protein more than equimolar IGF-1 (Tomas 1991, Biochem J; Tomas 1992, Biochem J; Lemmey 1991, Am J Physiol — gut growth). Doses were continuous infusions of tens to hundreds of µg/kg/day; the design (continuous) does not resemble community bolus injection. [4][5]

Gut and wound healing in animals

Rodent and pig studies report increased intestinal growth and improved healing after resection or injury; this was the main therapeutic direction explored in the 1990s (reviewed in Ballard 1996, Int J Biochem Cell Biol). [6]

Neuroprotection

Rat studies after hypoxic-ischaemic brain injury reported neuroprotection with centrally administered des(1-3)IGF-1 and GPE; this line of work shifted to the GPE fragment and its analogues.

Human muscle growth, fat loss, recovery

No published human studies of any kind. Community use rests entirely on cell and rodent data plus anecdote.

4Reported side effects and interactions

Literature-reported

no human data. In animals, hypoglycaemia at higher doses is the predictable effect; organ growth (kidney, spleen, gut) is documented with sustained infusion.

Community-reported

hypoglycaemia symptoms (shakiness, sweating, hunger, confusion) within 20–60 minutes of injection — the most consistent and the most dangerous; injection-site pain and local swelling; headache; fatigue. Reports of "localised growth" are anecdotal and unverifiable.

Theoretical. IGF-1 receptor signalling promotes cell proliferation and survival, and higher circulating IGF-1 is epidemiologically associated with several cancers; a potent, binding-protein-free IGF-1 variant is the form of this concern with the least reassurance available. Sustained IGF-1 excess also causes organomegaly and may worsen diabetic retinopathy. Mecasermin's label (for IGF-1 itself) warns of hypoglycaemia, intracranial hypertension, tonsillar hypertrophy, slipped capital femoral epiphysis and malignancy.

Interactions. additive hypoglycaemia with insulin, sulfonylureas and GLP-1 ; co-use with insulin in bodybuilding contexts is a documented cause of severe hypoglycaemia. GH and GH raise endogenous IGF-1 and IGFBP-3 on top.

Markers researchers commonly monitor

Based on IGF-1 physiology and the mecasermin label; nothing is established for this variant:

Marker	Why it's watched
Fasting and post-injection glucose (fingerstick)	hypoglycaemia is the acute risk; a glucose meter is the single most relevant tool.
IGF-1 (serum)	note that standard immunoassays may detect des(1-3)IGF-1 variably, so a "normal" result does not mean low exposure; endogenous IGF-1 may fall through feedback.
HbA1c and fasting insulin	longer-term glucose handling.
CBC and CMP	general baseline; kidney and liver values given organ-growth effects in animals.
Blood pressure	fluid retention is reported with IGF-1 therapy.
Age-appropriate cancer screening and any existing tumour marker	because of the proliferative mechanism; a clinician conversation, not a self-test.

Free for everyone. Safety information is never behind a paywall.

5Reconstitution and handling

Usually supplied as 1 mg vials, sometimes with acetic acid rather than as the recommended because IGF-1 variants are more stable at low pH — check what the vial requires. slowly against the vial wall, never shake, and keep cold; doses are in tens of micrograms, so volumes are tiny. Food containing carbohydrate around dosing is standard community practice because of hypoglycaemia.

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6Commonly studied alongside

IGF-1 LR3 (the long-acting sibling; see that page), mecasermin (approved IGF-1), GH / somatropin and GH secretagogues (which raise endogenous IGF-1), insulin (community; dangerous combination). In animal research, often compared head-to-head with IGF-1.

Informational cross-links. Not stack recommendations.

7Regulatory status by region

Region	Status (checked —)
United States	Not FDA-approved. Not named individually in the FDA's 2023 Category 2 compounding list †
European Union	Not authorised
United Kingdom	Not licensed
Australia	Not approved; IGF-1 and analogues are prescription-only (Schedule 4) †
South Africa	Not registered
Sport	Prohibited by WADA (S2 — IGF-1 and its analogues are named)

8Open questions

Any human pharmacokinetics — none published.
Whether local injection produces local effects in humans, or simply a systemic bolus with hypoglycaemia.
Long-term cancer risk from intermittent exposure to a binding-protein-free IGF-1.
How much community product is intact, correctly folded protein; growth factors are harder to manufacture than short peptides.

9References

1Sara VR et al. (1986). Identification of Gly-Pro-Glu (GPE), the aminoterminal tripeptide of insulin-like growth factor 1 which is truncated in brain, as a novel neuroactive peptide. Proc Natl Acad Sci USA (and related Sara 1986 PNAS report of truncated IGF-1 in brain). PubMed
2Francis GL et al. (1988). Insulin-like growth factors 1 and 2 in bovine colostrum: sequences and biological activities compared with those of a potent truncated form. Biochem J. PubMed · DOI
3Ballard FJ et al. (1987). Des(1-3)IGF-I: a truncated form of insulin-like growth factor-I with enhanced biological potency. Biochem Biophys Res Commun [verify exact title]. PubMed
4Tomas FM et al. (1991). Insulin-like growth factor-I (IGF-I) and especially IGF-I variants are anabolic in dexamethasone-treated rats. Biochem J. PubMed · DOI
5Tomas FM et al. (1992). Anabolic effects of insulin-like growth factor-I (IGF-I) and an IGF-I variant in normal female rats. J Endocrinol [verify journal]. PubMed · DOI
6Ballard FJ, Wallace JC, Francis GL, Read LC, Tomas FM (1996). Des(1-3)IGF-I: a truncated form of insulin-like growth factor-I. Int J Biochem Cell Biol. PubMed · DOI
7Ipsen. Increlex (mecasermin) prescribing information (current label) — for class warnings. PubMed

References are being resolved to PubMed/DOI identifiers; links search PubMed for the citation until then.

† Being confirmed by our reviewers against current sources.

10Community

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11Page history

26 Oct 2026Profile published — awaiting medical review

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