Carl read the papersWhat it actually is
IGF-1 DES is des(1-3)IGF-1: the full IGF-1 molecule with the N-terminal tripeptide glycine-proline-glutamate clipped off. It is not a designer invention. It was purified from bovine colostrum in the 1980s and has also been found in human brain and porcine uterus, so it occurs naturally as a cleavage product.
Most circulating IGF-1 is bound to IGF binding proteins, which act as a brake and a reservoir. Removing that tripeptide, specifically losing the glutamate at position 3, greatly reduces binding protein affinity. Less restraint means more free molecule reaching receptors, which is where the extra potency comes from. The receptor itself is not the thing that changed.
How it’s thought to work
- Escaping the binding proteins — The 1996 review in Int J Biochem Cell Biol summarises it: des(1-3)IGF-1 is generally about tenfold more potent than IGF-1 at stimulating hypertrophy and proliferation of cultured cells, as a consequence of much reduced binding to IGF binding proteins.
- Same receptor — It acts through the IGF-1 receptor like IGF-1 does. Nothing exotic in the signalling, just less of a brake on getting there.
- Short-lived by design — Lower binding protein affinity also means faster clearance from the circulation, which is why the in-dish potency does not translate one-for-one in a living animal.
- Insulin-like effects — IGF-1 receptors and insulin receptors are structurally related, and the variants that dodge the binding proteins lower blood glucose more strongly and for longer than IGF-1 does. That is the dominant acute effect, not the anabolic one.
What the research says
Unusually deep for this shelf, and almost all of it is animal work from one era. In 1991 an Adelaide group infused des(1-3)IGF-1 into diabetic rats for seven days and reported improved weight gain, nitrogen retention and muscle protein synthesis, with the truncated form at least as potent as full-length IGF-1 at the same dose. The 1996 review of this work notes the extra potency is partly kept in living animals, with the anabolic effect most obvious in gut tissue. The most relevant study for anyone considering it is a 1997 paper in J Endocrinol in pigs and marmoset monkeys: the binding-protein-dodging variants were two to threefold more potent than IGF-1 at lowering blood glucose, and suppressed glucose over a much longer period, with des(1-3)IGF-1 the most potent of the lot. The authors proposed it as a possible adjunct to insulin treatment, which tells you what its strongest documented action actually is. What does not exist is a clinical trial of des(1-3)IGF-1 in humans. The human-sample literature is doping control: a 2017 method paper detects it, alongside LongR3 and R3 IGF-1, in plasma.
- Isolated from bovine colostrum, human brain and porcine uterus, so it is a naturally occurring cleavage product rather than a synthetic novelty.
- About tenfold more potent than IGF-1 in cultured cells, driven by much reduced IGF binding protein affinity.
- In pigs and marmosets, two to threefold more potent than IGF-1 at lowering blood glucose, with a longer-lasting effect.
- In diabetic rats, infused des(1-3)IGF-1 improved weight gain, nitrogen retention and muscle protein synthesis, and was at least as potent as full-length IGF-1.
- No human clinical trial of des(1-3)IGF-1. Human-sample work is anti-doping detection chemistry.
Reported protocols
These are the doses the peptide community actually reports running (Reddit & forums), alongside published research — logged for education, not as a recommendation to use.
| Parameter | Commonly reported range |
|---|---|
| Human dose | Not established. There is no clinical trial of des(1-3)IGF-1 in people, so no dose, interval or ceiling exists to quote. |
| The closest approved reference | A full-length recombinant IGF-1 medicine does exist, mecasermin (INCRELEX), prescribed for growth failure in children aged 2 and over with severe primary IGF-1 deficiency, or with a growth hormone gene deletion and antibodies to growth hormone. Its label starts at 0.04 to 0.08 mg/kg twice daily by subcutaneous injection and allows 0.04 mg/kg steps up to a maximum of 0.12 mg/kg twice daily, given shortly before or after a meal, with preprandial glucose monitoring until a tolerated dose is found. That is a different molecule, a different population and a prescription medicine under specialist supervision, and it is not a template for anything else. |
| Why the DES number cannot be borrowed | Des(1-3)IGF-1 is roughly tenfold more active in cells and clears faster. Scaling a label dose across a potency difference and a pharmacokinetic difference, in a different age group, for a different purpose, is not arithmetic. It is guessing. |
| Animal doses | The rodent, pig and marmoset studies used infusions or single injections at microgram to milligram per kilogram amounts under laboratory conditions. Those designs do not convert into a human protocol. |
| Reported online | People do post about using it, usually in the tens of micrograms, injected into the muscle they have just trained. One user described a bad hypoglycaemic episode after taking more than usual and needing sugar to come right, which is the same effect the animal data predicts. Self-reports, no study, and the risk they describe is real. |
| Carl's position | The one thing the animal work establishes clearly is a strong and prolonged glucose-lowering effect. That makes an invented dose more dangerous here than in most entries, not less. |
Common use cases
| Goal | Community protocol notes |
|---|---|
| Reading the IGF binding protein literature | the clearest worked example of what the binding proteins actually do |
| Understanding the IGF-1 variant family | DES, R3 and LongR3 are all binding-protein escapes, built the same way for the same reason |
| Sport eligibility | IGF-1 and its analogues are named on the WADA list and are detectable in plasma by published methods |
Mixing it (reconstitution)
Freeze-dried peptides must be reconstituted with bacteriostatic water before they can be measured. Carl’s calculator turns “mg in the vial + ml of water + target dose” into “units on the syringe” — and tells you how long the vial lasts.
→ Open the Reconstitution Calculator
Injection & handling
No administration guide on this page. The reason is specific rather than generic: the best-characterised acute effect of this molecule in living animals is lowering blood glucose, harder and for longer than IGF-1 itself. The approved full-length IGF-1 medicine carries a warning for severe hypoglycaemia leading to hypoglycaemic seizures, requires dosing shortly before or after a meal, within twenty minutes either way, and requires glucose monitoring while a tolerated dose is found. None of that supervision exists around a research vial, and des(1-3)IGF-1 is the more potent molecule of the two in exactly that respect. The same label is contraindicated in patients with malignant neoplasia or a history of malignancy, and lists several cases of malignant neoplasia observed on treatment, which is the other reason this is a prescription medicine and not a supplement.
Stacks it appears in
- With IGF-1 LR3 — the two most common IGF-1 variants, sold as short-acting and long-acting halves of a pair. Both escape the binding proteins, so stacking them stacks the same glucose risk twice.
- With MGF or PEG-MGF — the proliferate-then-grow theory again. Those have no human evidence at all, so adding them adds unknowns rather than support.
- With insulin — this combination appears in the same circles and it is the most dangerous thing on this page. Two glucose-lowering agents with different time courses and no monitoring is how people end up in an emergency department.
Sources
- Ballard FJ et al. 1996, Int J Biochem Cell Biol. Des(1-3)IGF-I: a truncated form of insulin-like growth factor-I (PMID 8930132)
- Francis GL et al. 1988, Biochem J. Insulin-like growth factors 1 and 2 in bovine colostrum, sequences and biological activities compared with a potent truncated form (PMID 3390164)
- Ballard FJ et al. 1987, Biochem Biophys Res Commun. Natural and synthetic IGF-1 and the potent derivative destripeptide IGF-1 (PMID 2962574)
- Tomas FM et al. 1997, J Endocrinol. IGF-I variants which bind poorly to IGF-binding proteins show more potent and prolonged hypoglycaemic action in pigs and marmoset monkeys (PMID 9415072)
- Tomas FM et al. 1991, Biochem J. Increased weight gain, nitrogen retention and muscle protein synthesis in diabetic rats treated with IGF-I and des(1-3)IGF-I (PMID 1710892)
- Carlsson-Skwirut C et al. 1989, Biochim Biophys Acta. Comparison of recombinant intact and truncated IGF-1 (PMID 2469478)
- Sara VR et al. 1989, Biochem Biophys Res Commun. Identification of Gly-Pro-Glu (GPE), the aminoterminal tripeptide of IGF-1 truncated in brain, as a novel neuroactive peptide (PMID 2574573)
- Keam SJ 2023, Drugs. Trofinetide: First Approval (PMID 37191913)
- Thomas A et al. 2017, Growth Horm IGF Res. Determination of LongR3-IGF-I, R3-IGF-I, Des1-3 IGF-I and their metabolites in human plasma by LC-MS (PMID 28668757)
- INCRELEX (mecasermin) prescribing information, DailyMed / openFDA
- WADA 2026 Prohibited List, S2.3 growth factors
- SAHPRA, Peptide Products: Public Information (May 2026)
- ClinicalTrials.gov search: des(1-3)IGF-1 / IGF-1 DES
