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IGF-1 DES(1-3)

Also known as des(1-3)IGF-1, DES(1-3)IGF-I, IGF-1 DES, brain IGF-1

A naturally occurring truncated IGF-1 that escapes its binding proteins; no human studies exist.

preclinical Growth hormone research chemical

At a glance

Category
Growth hormone
Status
research chemical
Made from
recombinant Recombinant protein expressed in Escherichia coli and supplied as a cell culture reagent, despite occurring naturally as a proteolytic fragment in human and bovine tissue.
Route
subcutaneous or intramuscular in non-medical use; there is no established route because there is no established use
Half-life
Not established. There is no human pharmacokinetic study. Because it barely binds the IGF-binding proteins that normally buffer IGF-1 in the circulation, its plasma residence is expected to be considerably shorter than native IGF-1's, not longer — the same correction that applies to IGF-1 LR3
Onset
unknown
Molecular weight
approximately 7.4 kDa
Sequence
The 70-amino-acid human IGF-1 sequence with the first three N-terminal residues (Gly-Pro-Glu) removed, leaving 67 amino acids. It is otherwise identical to native IGF-1

Not approved for human use anywhere and never entered clinical development. It occurs naturally in small amounts in human and bovine tissue as a proteolytic fragment of IGF-1, and is used commercially as a cell culture growth supplement. Material sold to individuals is labelled for laboratory research use only and is not manufactured or released to injectable-medicine standards.

Doping status: Prohibited at all times (WADA S2, growth factors)

Checked against the WADA 2026 Prohibited List. For a specific product and country, Global DRO is the lookup athletes are expected to use — the List names substances, not brand names.

This is a short entry. There is little or no published research on this compound, so there is correspondingly little to report. Empty dosing or reconstitution sections mean no credible figures exist — not that they were left out.

Mechanism of action

IGF-1 DES(1-3) is native IGF-1 missing its first three residues. The tripeptide Gly-Pro-Glu that is removed is not incidental: it is a substantial part of the surface through which IGF-1 binds the IGF-binding proteins. Removing it cuts affinity for IGFBP-3 by roughly 25-fold while leaving affinity for the IGF-1 receptor essentially intact.

The consequence is a much larger free fraction available at the receptor, and correspondingly greater potency in systems where IGFBPs are present — reported at roughly ten-fold in vivo, and around twenty-fold in the rat pituitary cell system where the half-maximal inhibitory concentrations were approximately 20 mcg/l for IGF-1 and 1 mcg/l for des(1-3)IGF-1 1. Once bound, it activates the same IGF-1 receptor and the same downstream pathways as native IGF-1: PI3K/Akt/mTOR for protein synthesis and survival, Ras/MAPK for proliferation. It cross-reacts with the insulin receptor at supraphysiological concentrations, which is the direct basis of the hypoglycaemia risk.

The commonly repeated claim that DES(1-3) is a 'local, short-acting' IGF-1 that acts only near the injection site is an inference from the loss of IGFBP binding, not a finding from any study. Escaping the binding proteins increases potency and shortens plasma residence; it does not confer tissue selectivity. No study has demonstrated site-restricted action in a living animal, let alone in a human.

What the research shows

There is no published human study of IGF-1 DES(1-3) — no pharmacokinetics, no safety data, no efficacy data for any outcome. The compound is real and its in vitro pharmacology is genuinely well characterised, but that characterisation comes from cell culture and rodent work done in the late 1980s and early 1990s, mostly as part of basic research into how IGFBPs regulate IGF action. Nothing about human use follows from it.

Research in humans

No published human studies. DES(1-3)IGF-1 occurs endogenously as a minor IGF-1 fragment in human tissue, but it has never been administered to humans in a published trial for any purpose. The nearest approved comparator is mecasermin (Increlex), native recombinant human IGF-1, approved for severe primary IGF-1 deficiency — a different molecule that deliberately retains IGFBP binding, and whose label is dominated by hypoglycaemia warnings.

Animal and lab research

The Ballard, Francis and Read group in Adelaide characterised the analogue in rats, showing roughly ten-fold greater in vivo potency than native IGF-1 for growth and nitrogen retention. A 1991 study in cultured rat anterior pituitary cells found DES(1-3)IGF-1 approximately twenty-fold more potent than IGF-1 at suppressing GH secretion, and attributed the difference specifically to reduced binding by pituitary IGFBPs 1 — a useful demonstration of the mechanism, and also a reminder that IGF-1 analogues feed back onto and suppress the GH axis rather than stimulating it. There is extensive in vitro use as a cell proliferation reagent. There is no toxicology or carcinogenicity programme of the kind required for a medicine.

Caveats. The entire evidence base is preclinical and decades old, and was generated to answer questions about IGFBP biology rather than about therapeutic use. Half-life figures circulating in the trade (commonly quoted as 20-30 minutes) cannot be traced to any published human measurement. Because IGFBP buffering is what normally prevents free IGF-1 from acting on the insulin receptor, removing that buffering plausibly increases hypoglycaemia risk rather than reducing it — but this has not been quantified in humans either. Material sold under this name is not identity- or purity-verified to any medicinal standard, and IGF-1 analogues are difficult to distinguish from one another without proper analysis.

What it is used for

  • Research: as a high-potency IGF-1 receptor agonist in cell culture and in rodent studies of IGFBP function
  • Commercial: as a growth supplement in serum-free cell culture media
  • Non-medical: used for muscle growth and localised tissue effects on the basis of the 'local action' claim described above, which no study supports and which no human data addresses

Dosing

Route
subcutaneous or intramuscular in non-medical use
  • There is no established dose. No dose-finding study exists in humans, and none exists in animals for a therapeutic purpose either.
  • Figures circulating on forums and vendor sites are copied from IGF-1 LR3 protocols, which are themselves not derived from any study. They are not data about this compound.
  • For the approved native IGF-1 product, dosing within 20 minutes either side of a meal or snack is mandatory because of hypoglycaemia, and the dose is withheld if the patient cannot eat 2. No equivalent protocol exists here, and the loss of IGFBP buffering makes the risk plausibly greater rather than smaller.
  • The studied-dose fields are left empty deliberately, because no human study exists. The section below records what bodybuilders actually do, as a social fact and not as a validated schedule.
  • Doses are in micrograms (tens to low hundreds) while vials are usually labelled in milligrams, so the familiar decimal trap applies. More important here is the hypoglycaemia risk: unlike the GH fragments, an IGF-1 receptor agonist can drop blood glucose, and the loss of IGFBP buffering plausibly makes DES(1-3) worse in this respect, not better.

These figures describe what the literature and published protocols report. They are not advice and not a dosing instruction.

Protocols

Post-workout site-injection pattern, borrowed from IGF-1 LR3 (user-reported)

user protocol — not validated

Source: Bodybuilding forums, which reuse IGF-1 LR3 figures

This is not a validated schedule. It is a pattern that circulates among users and sellers, reproduced because it is what people actually follow — not because it has been tested. No trial established these doses, this interval or this duration, and nobody is checking what is in the vial. Treat every number below as an assertion, not a finding.

Reported per-dose amountroughly 50-150 mcg, occasionally up to 200 mcg
Reported timing and siteinjected immediately after training, frequently split bilaterally into the muscle just worked, on the belief that the short-acting analogue drives localised growth
Reported cycle lengthshort runs of about 4 to 6 weeks, on training days only, justified by a belief in receptor downregulation

These numbers are lifted wholesale from IGF-1 LR3 protocols, which are themselves not derived from any study, and they carry a specific internal contradiction: LR3 is engineered to be long-acting while DES(1-3) is short-acting, yet users dose the two identically and then time DES around the workout precisely because they assume a brief, local action. No study has ever demonstrated site-restricted action in a living animal, let alone a human, and the '20-30 minute half-life' quoted in the trade traces to no published human measurement. The 'local growth from injecting the worked muscle' belief is the central claim and it is unsupported. Reports are badly confounded, since IGF-1 analogues are almost always run alongside anabolic steroids, growth hormone or insulin; hypoglycaemia is the foreseeable acute harm and mirrors the meal-timing warnings on the approved native IGF-1 product, which must be taken with food and withheld if the user cannot eat 2. No safety data exist for this compound in humans.

Schedules are reproduced as their source states them. Units, IU and milligrams explains why the figures are not interchangeable between products.

Reconstitution

Solvent
bacteriostatic water is what suppliers commonly specify; some specify dilute acetic acid because of solubility, and the disagreement between suppliers is itself informative
Storage
Lyophilised powder frozen and protected from light; reconstituted solution refrigerated. Shelf-life claims for reconstituted material are supplier statements, not the output of stability testing.

No reconstitution example is given because no credible dose exists to calculate one from.

Safety

Side effects

  • Hypoglycaemia is the foreseeable primary risk. IGF-1 activates the insulin receptor at high concentrations, and DES(1-3) does not bind the IGFBPs that normally buffer that action. On the label of the approved native rhIGF-1 product, severe hypoglycaemia leading to hypoglycaemic seizures has been observed, which is why that product must be given within 20 minutes either side of a meal or snack and withheld if the patient cannot eat 2
  • Suppression of endogenous growth hormone through IGF-1 negative feedback on the pituitary and hypothalamus — demonstrated directly in the rat pituitary cell work 1
  • Effects known from the approved rhIGF-1 product and reasonably expected here, though not documented for this compound: tonsillar hypertrophy, which occurred in 15 per cent of subjects in the first 1 to 2 years of the mecasermin trials with snoring, sleep apnoea and middle-ear effusion, seven of whom needed surgery; intracranial hypertension with papilloedema, visual changes, headache, nausea and vomiting; and slipped capital femoral epiphysis with or without osteonecrosis during growth 2. Fluid retention and injection site reactions likewise
  • Soft tissue and organ overgrowth under sustained supraphysiological IGF-1 signalling
  • No systematic safety data of any kind exists in humans

Do not use if

  • Active or suspected malignancy — IGF-1 is mitogenic and anti-apoptotic, and malignant neoplasia is one of only three contraindications on the approved rhIGF-1 product's label, alongside known hypersensitivity to mecasermin and closed epiphyses 2. Circulating IGF-1 is positively associated with prostate cancer risk in pooled individual-participant data, and acromegaly, with its chronic IGF-1 elevation, carries increased colorectal neoplasia risk. This does not prove that an exogenous IGF-1 analogue causes cancer, but the direction of evidence is consistent
  • Diabetes mellitus, particularly on insulin or sulfonylureas, without strict glucose monitoring
  • Closed epiphyses is itself a contraindication on the approved IGF-1 product's label 2; conversely, open epiphyses raise the risk of slipped capital femoral epiphysis
  • Intravenous administration
  • Pregnancy and breastfeeding: no data
  • Competitive athletes under the WADA code: prohibited at all times
  • In general: no human safety data exists, so no informed risk assessment is possible

Interactions

Not systematically studied for this compound. By mechanism, additive hypoglycaemia is expected with insulin, sulfonylureas and meglitinides; the approved rhIGF-1 label notes that insulin and other antidiabetic medications may need dose adjustment because of its blood-glucose-lowering effect 2. Concurrent growth hormone or GH secretagogues raise IGF-1 further and would compound both the hypoglycaemia and the overgrowth risk. IGF-1 analogues suppress endogenous GH secretion through negative feedback, so they work against, not with, the GHRH analogues and secretagogues in this category. These inferences come from the approved native rhIGF-1 product; no interaction study has been done on DES(1-3) itself.

Sources