IGF-1 DES

Origin and structure

IGF-1 DES, written in the scientific literature as des(1-3)IGF-1, is insulin-like growth factor 1 (IGF-1) without its first three amino acids. Natural IGF-1, the growth factor that the liver and other tissues release in response to growth hormone, is a single chain of 70 amino acids that starts with glycine, proline and glutamic acid (Gly-Pro-Glu). Take those three away and 67 remain, otherwise identical to human IGF-1. "Des" is not a brand or a code: it is the chemical prefix for a part that has been removed.

Unlike most IGF-1 variants, it was found before it was made. In 1986 a Swedish group isolated a form of IGF-1 with a shortened front end from human fetal brain and from adult brain. In 1988 Francis, Ballard and colleagues at the CSIRO Division of Human Nutrition in Adelaide, Australia, published the full sequence of the form they had purified from bovine colostrum, the first milk after calving, and showed that it lacked exactly Gly-Pro-Glu. A US group later found it in pig uterus. The Adelaide team, who went on to build IGF-1 LR3 around the same insight, used both variants to show that IGF-1 is held back by its binding proteins.

The three amino acids that are cut off have a life of their own. The tripeptide Gly-Pro-Glu, or GPE, has effects of its own on brain tissue in laboratory studies, and a modified version of it, trofinetide, became a medicine for Rett syndrome, approved in the US in 2023 and authorised in the EU in August 2026. IGF-1 DES itself was never developed into a medicine. It is sold as a laboratory reagent for cell culture, and outside the lab it circulates on the black market as a bodybuilding drug.

How it is thought to work

IGF-1 DES acts on the same target as IGF-1: the type 1 IGF receptor, found on muscle, bone, gut and most other cells, which drives cell growth and division and, like insulin, moves glucose into tissues. Losing the first three amino acids barely changes its grip on that receptor. On rat muscle cells, half of the receptor binding was displaced by 14 ng/ml of IGF-1 DES and 20 ng/ml of IGF-1.

What changes is its contact with the IGF-binding proteins, which hold most IGF-1 in blood and tissues and decide how much of it reaches the receptor. The glutamic acid at position 3, the same residue that IGF-1 LR3 swaps for arginine, is key to that binding. Binding proteins made by cultured rat muscle cells held on to IGF-1 at least 60 times better than to IGF-1 DES, so more of it stayed free: half the maximal effect on protein synthesis in those cells took 1.5 ng/ml of IGF-1 DES against 13 ng/ml of IGF-1. Three is the sweet spot: removing four amino acids still beat IGF-1 but was weaker than IGF-1 DES, because that variant binds the receptor less well, and removing five made it about 90 times less potent than IGF-1.

In the body the advantage shrinks. In rats wasting on a steroid it was about 2.5 times as potent as IGF-1, not ten times. It also leaves the blood quickly, because little of it is held in the binding-protein complex: in rats its clearance was nearly four times that of IGF-1 (4.59 against 1.20 ml/min per kg), and more of it reached the gut, skin, adrenal glands and brain. Rats are a poor guide to people on this point. In a comparison of five species the variants bound very weakly in rat plasma but clearly in human plasma, and IGF-1 DES bound the binding proteins more than IGF-1 LR3 did. Those were test-tube measurements: how it behaves in the blood of a person who receives it has never been studied.

Is IGF-1 DES approved?

No. No medicines regulator has authorised IGF-1 DES for use in people, it is not an ingredient of any licensed medicine, and no trial in people has been published or registered on ClinicalTrials.gov. In the Netherlands it is not a registered medicine, so it may not be sold or promoted for use in people. Selling it as research material is a different status. In 2021 the French anti-doping laboratory described IGF-1 DES, IGF-1 LR3 and R3-IGF-1 as never approved for human use but readily available as black-market products for bodybuilding.

The approved form of IGF-1 is mecasermin, sold as Increlex: recombinant IGF-1 with the full natural sequence of 70 amino acids, including the three that IGF-1 DES lacks. Its approvals cover that molecule only.

• EU: Increlex was authorised on 3 August 2007, under exceptional circumstances because the disease is too rare for complete data to be collected, for the long-term treatment of growth failure in children and adolescents aged 2 to 18 with severe primary IGF-1 deficiency. It is a medicine on restricted prescription, in the Netherlands as elsewhere in the EU; the marketing authorisation is held by Esteve Pharmaceuticals.
• US: Increlex has been approved since 2005; the label covers children from 2 years with severe primary IGF-1 deficiency or with a growth-hormone gene deletion and neutralising antibodies to growth hormone. IGF-1 DES has no FDA approval.
• Sport: the WADA Prohibited List names "insulin-like growth factor 1 (IGF-1, mecasermin) and its analogues" in class S2.3, growth factors, prohibited in and out of competition. The Netherlands publishes the list in the Tractatenblad; the 2026 list appeared as Tractatenblad 2026, no. 25. Doping laboratories can detect IGF-1 DES: with the French laboratory's method, the unchanged peptide was still detectable 24 hours after a single injection into the muscle of rats.

What the research shows

There are no human data on IGF-1 DES. No clinical trial has been published, none is registered on ClinicalTrials.gov, and no study has measured how the body handles it in people. Everything below comes from cells and animals, most of it from the Adelaide group that characterised it, and most of the animal studies used sick or wasting animals. None of it tests muscle growth in healthy, well-fed adults.

• Muscle cells (Francis et al., 1988; Bagley et al., 1989): in rat muscle cells it was about ten times as potent as IGF-1 at raising protein synthesis and slowing protein breakdown, because the binding proteins the cells release did not hold it back.
• Steroid-treated rats (Tomas et al., 1992): in rats losing weight on the steroid dexamethasone, IGF-1 partly reversed the losses, and IGF-1 DES and IGF-1 LR3 did so at about 2.5 times lower doses, with more muscle protein synthesis and less breakdown. IGF-1, and the variants even more, also made the gut heavier, by up to 45%.
• Acute kidney injury (Clark et al., Genentech, 1994): in rats whose kidneys had been cut off from their blood supply for 60 minutes, a week of IGF-1 DES under the skin brought kidney function back sooner and more completely; 6% of treated rats died, against 28% of untreated rats.
• Marmosets and pigs (Tomas et al., 1997): single injections lowered blood sugar 2 to 3 times more potently than IGF-1, IGF-1 DES most strongly of the variants tested, and the variants kept it down for longer, with 4 to 8 times more lowering in total over four hours.
• Transgenic mice (Hadsell et al., 2000): mice engineered to make human IGF-1 DES in their mammary glands developed precancerous lesions, and by 23 months 53% had breast cancer (adenocarcinoma), a tumour rate 2 to 3 times that of normal mice. This tested lifelong production in the gland, not injections.

IGF-1 DES versus IGF-1 LR3 and mecasermin

All three act on the same receptor. Mecasermin is natural IGF-1, an approved medicine with two decades of clinical use. IGF-1 DES and IGF-1 LR3 both came out of one Adelaide laboratory's work on a single question: what happens when IGF-1 escapes its binding proteins? LR3 swaps the glutamic acid at position 3 for arginine and adds a 13-amino-acid extension at the front; DES simply lacks the first three amino acids. In cell culture the two were about equally potent, and in steroid-treated rats both were about 2.5 times as potent as IGF-1. DES still binds the binding proteins more than LR3 does, and unlike LR3 it is a form the body makes itself. Neither has been tested in people.

What carries over from mecasermin are the effects of the receptor itself. Across 413 trial patients, the EU product information for Increlex reports headache in 44%, low blood sugar in 28%, vomiting in 26%, thickening at injection sites in 17% and ear infections in 17%. It rules the medicine out in active or suspected cancer and warns of an increased risk of benign and malignant tumours, because IGF-1 plays a role in how tumours start and grow. The animal data on IGF-1 DES point the same way: the strongest blood-sugar lowering of the IGF-1 variants tested in marmosets and pigs, and more breast cancer in mice that made it.

What does not carry over is the dose or the benefit. Increlex is dosed per kilogram in children who cannot make enough IGF-1, and its benefit is height. IGF-1 DES was 2.5 to 10 times as potent as IGF-1 in rats and cells and behaves differently in blood, so mecasermin doses say nothing about it. In adults, natural IGF-1 has also not shown the muscle effect that IGF-1 DES is sold for; our article on IGF-1 LR3 describes those trials.

Frequently asked questions

What is the difference between IGF-1 DES and IGF-1 LR3?

Both are IGF-1 variants that dodge the binding proteins restraining IGF-1, and both were studied by the same Australian group. IGF-1 DES is natural IGF-1 minus its first three amino acids, 67 in total, and also occurs in the body. IGF-1 LR3 has 83 amino acids, arginine at position 3 and an extra 13 at the front, and is purely man-made. In steroid-treated rats both were about 2.5 times as potent as IGF-1. Neither has been tested in people, and both are banned in sport.

Is IGF-1 DES legal in the Netherlands?

It is not a registered medicine in the Netherlands or anywhere else in the EU, so it may not be sold or advertised for use in people; any IGF-1 DES on the market is offered only as research material, and we do not sell it. The IGF-1 medicine authorised in the EU, Increlex, is a different molecule on restricted prescription, licensed only for children with a rare growth disorder. In sport it is prohibited at all times.

Is IGF-1 DES banned in sport?

Yes, in and out of competition. The WADA Prohibited List names IGF-1, including mecasermin, and its analogues in class S2.3, growth factors, and IGF-1 DES is such an analogue. In the Netherlands the list is published in the Tractatenblad; the 2026 version is Tractatenblad 2026, no. 25. A French doping laboratory has published a validated test for it.

How long does IGF-1 DES stay in the body?

In people, nobody knows: it has never been measured. In rats it was cleared from the blood nearly four times faster than IGF-1, because little of it shelters in the binding-protein complex, yet in marmosets and pigs its blood-sugar lowering lasted longer than that of IGF-1, and in rats a doping test still found it 24 hours after a single injection into muscle. Half-lives quoted online have no human measurement behind them. For comparison, the half-life of mecasermin in children with IGF-1 deficiency is about 5.8 hours.

Does IGF-1 DES build muscle?

That has never been tested in people. In rats wasting on a steroid it limited the loss of weight and muscle protein at lower doses than IGF-1, but those were sick animals, and the clearest growth was in the gut, which became up to 45% heavier. No study has measured its effect on muscle size or strength in people, and the claim that it acts mainly where it is injected has never been tested in people.

Does IGF-1 DES occur naturally?

Yes. It was isolated from human fetal and adult brain in 1986, fully sequenced from bovine colostrum in 1988 and later found in pig uterus. The Adelaide group that studied it concluded that it probably arises when ordinary IGF-1 is clipped after it has been made. The synthetic peptide sold as IGF-1 DES has the same 67-amino-acid sequence as this natural form.

Storage and handling

Store according to product-label instructions and batch handling notes. Lyophilized research peptides are commonly kept dry, protected from light, and handled with clean laboratory technique.

References

Checked against these sources on 28 October 2026.

Related peptides