IGF-1 DES (des(1-3)IGF-1): what it is, how it compares with LR3 and what the research shows

Insulin-like growth factor-1 is a 70-amino-acid hormone made mainly by the liver in response to growth hormone. Most of it circulates bound to IGF-binding proteins (IGFBPs), which limit how much free hormone reaches tissues. IGF-1 DES is the same hormone with its first three amino acids, glycine, proline and glutamic acid, missing, leaving 67 amino acids ^{[1] [2]}. The name is short for des(1-3)IGF-1, which means “IGF-1 without residues 1 to 3”. Unlike IGF-1 LR3, which was designed in a laboratory, IGF-1 DES is a natural variant.

It was found in 1986 by researchers in Stockholm, who purified a form of IGF-1 from human fetal brain that was truncated at its N-terminal end and stimulated DNA synthesis in fetal brain cells ^[3], and then found the same variant in adult human brain, where they suggested it acts as a neuropeptide ^[4]. In 1988 a group in Adelaide sequenced it from bovine colostrum, the first milk of cows, and found the variant lacked the tripeptide Gly-Pro-Glu and was about ten times more potent than IGF-1 in rat muscle cells ^[1]. It has also been isolated from pig uterus, and probably arises when an enzyme clips the end off ordinary IGF-1 after it is made ^[2].

The IGF-1 DES sold by research peptide vendors is a recombinant protein with the same 67-amino-acid sequence. Vendors write the name many ways, including IGF1 DES, IGF-DES, DES(1-3)IGF-1 and des 1-3 IGF-1, and often describe it as a “short-acting IGF-1” to be injected into a trained muscle. See what research peptides are for how such products reach the market.

IGF-1 DES acts on the same type 1 IGF receptor as native IGF-1. Its difference lies in the binding proteins. The glutamic acid at position 3 of IGF-1 is important for binding to IGFBPs, and removing it, along with the two amino acids before it, leaves a hormone that IGFBPs hold only weakly ^[2]. In cell cultures that secrete binding proteins, this makes IGF-1 DES roughly ten times more potent than IGF-1 at stimulating growth and protein synthesis, even though its affinity for the receptor is not higher ^{[1] [2]}. In the 1992 Adelaide experiments that also produced IGF-1 LR3, the two analogues were about equally potent in binding-protein-secreting cells, ranking LR3 ≈ des(1-3) > Long Gly3 > Long IGF-1 > IGF-1 ^[5].

The same property carries into animals, where it has an unexpected consequence. Binding proteins do not only restrain IGF-1; they also carry it to where it is needed. In rats with hypoxic-ischaemic brain injury, IGF-1 given into the brain ventricle reduced neuronal loss, but IGF-1 DES at the same dose, and at a tenth of it, did not, with only a trend at a much higher dose. The authors concluded that binding proteins help target IGF-1’s protective action ^[6]. Escaping the binding proteins is therefore not simply a gain in potency.

Because so little of it is bound, more IGF-1 DES is free to act on the insulin receptor as well as the IGF receptor, which is why its most consistent effect in animals is a fall in blood sugar ^[7].

IGF-1 DES vs LR3 is the most common question about this compound. Both were studied side by side by the same Adelaide group. IGF-1 DES is IGF-1 shortened by three amino acids; LR3 is the full chain with arginine in place of glutamic acid at position 3 and a 13-amino-acid extension at the start, giving 83 amino acids against 67 ^[5]. Both changes achieve the same end, weak binding to IGFBPs, and in cells and in dexamethasone-treated rats the two were similarly potent, about 2.5 times as anabolic as IGF-1 ^[8]. In pigs, IGF-1 DES was slightly the more potent at lowering blood sugar, with the order IGF-1 < Long IGF-1 < R3IGF-1 ≈ LR3IGF-1 < des(1-3)IGF-1 ^[7].

The difference sellers emphasise, that IGF-1 DES is short-acting and LR3 long-acting, has no published human measurement behind it for either molecule. In rats, LR3 was actually cleared from the blood faster than native IGF-1 ^[20], and neither analogue has human pharmacokinetics. What is documented is that the analogues’ effects on blood sugar last longer than IGF-1’s in animals because more of the hormone is free ^[7]. Our IGF-1 LR3 guide covers that compound in full; anti-doping laboratories screen for both as prohibited substances ^{[9] [10]}.

The claimed IGF-1 DES benefits online are localised muscle growth, faster recovery and fat loss. The animal research was designed to answer different questions, mostly about catabolic states and the gut. In rats made catabolic with dexamethasone, seven days of infused IGF-1 DES or LR3 improved weight gain and nitrogen retention about 2.5 times more potently than IGF-1, and both analogues increased gut weight by up to 45% ^[8]. In a companion study, the analogues increased total gut weight by up to 60%, with thicker rather than longer intestine, leading the authors to call the gut one of the most sensitive IGF-1 target tissues ^[11].

In rats that had 80% of their small intestine removed, 0.96 mg/kg per day of IGF-1 DES produced the same weight gain and nitrogen balance as 2.4 mg/kg per day of IGF-1, and both were better than vehicle; the kidneys were heavier in all treated groups and the thymus after IGF-1 DES ^[12]. A 1996 review summarised the animal evidence as showing selective anabolic effects, particularly in gut tissues, and noted that clinical opportunities, perhaps in catabolic illness or inflammatory bowel disease, had not been evaluated ^[2].

Blood sugar is the best-documented effect. In pigs and marmoset monkeys, IGF-1 DES and related analogues lowered plasma glucose two to three times more potently than IGF-1 and kept it down for much longer, with a four- to eight-fold greater cumulative hypoglycaemic effect over four hours ^[7]. No published study has tested whether IGF-1 DES injected into a muscle makes that muscle grow, in any species. The site-specific growth claim rests on the idea that a hormone with a short life will act where it is injected, which has not been examined.

We found no published clinical trial of IGF-1 DES in humans, no case series, no pharmacokinetic study and no registered trial on ClinicalTrials.gov. This is a natural human variant, found in the brain ^{[3] [4]}, but no one has reported giving it to people. The 1996 review by the Adelaide group that discovered its potency stated plainly that its clinical opportunities had not been evaluated ^[2], and nothing published since changes that.

The human evidence that does exist comes from anti-doping science. Laboratories have developed methods to detect IGF-1 DES, LR3 and R3-IGF-1 in plasma ^[9] and, using immunopurification and high-resolution mass spectrometry, in doping-control samples ^[10]. These methods exist because the analogues are sold and used, not because their effects have been studied. A 2026 clinical review grouped IGF-1 analogues sold as research compounds in the tier with no human studies, and listed dysglycaemia, fluid retention and joint and muscle pain among adverse effects reported across the class ^[13].

The licensed medicine closest to IGF-1 DES is mecasermin (Increlex), which is recombinant native 70-amino-acid IGF-1 given to children with severe primary IGF-1 deficiency ^[14]. Its trial data describe a different molecule that is held by binding proteins in the normal way, and cannot be transferred to a variant that escapes them.

Sellers usually quote an IGF-1 DES half-life of 20 to 30 minutes. We could not find a published human or animal measurement to support it. What is known is indirect: native IGF-1 is protected in the circulation by its binding proteins, and a variant that does not bind them would be expected to be cleared faster, but its effects on blood sugar in pigs and marmosets lasted longer than IGF-1’s, not shorter, because more of the hormone was free to act ^[7]. For comparison, mecasermin has a mean half-life of about 5.8 hours after a subcutaneous dose in children with severe IGF-1 deficiency ^[14].

So how long does IGF-1 DES take to work? There is no human answer. In animals, the effects on blood sugar appeared within an hour of a bolus dose ^[7], and the anabolic and gut effects were measured after seven days of continuous infusion ^{[8] [11] [12]}. None of this describes a person injecting the protein into a muscle after training.

All published doses are from animals. Continuous infusion of 0.96 mg/kg per day by osmotic pump in rats after gut resection ^[12]; seven-day infusions in dexamethasone-treated rats, where the analogues were about 2.5 times as potent as IGF-1 given at up to 695 µg per day ^[8]; single bolus injections of 20 and 50 µg/kg in pigs and of 42 to 270 µg/kg in marmosets for blood-sugar studies ^[7]; and 2, 20 and 150 µg into the brain ventricle of rats ^[6]. No human dose has been established, and animal doses cannot be converted into human doses.

There is no evidence-based IGF-1 DES dosage for people. The IGF-1 DES bodybuilding protocols found on forums, typically 50 to 150 µg injected into a trained muscle immediately after a workout, are not drawn from any study. IGF-1 DES is sold by weight, usually in 1 mg vials. For the arithmetic only, 1 mg mixed with 1 mL of bacteriostatic water gives 1 mg per mL, so each unit on a U-100 insulin syringe holds 10 µg; the peptide calculator and the IGF-1 DES calculator page handle other volumes. These are calculations, not recommendations, and the only IGF-1 dose on a medicine label is for the different drug mecasermin, given under specialist supervision within 20 minutes of a meal because of the risk of low blood sugar ^[14].

IGF-1 DES is sold as a freeze-dried recombinant protein for injection, usually in 1 mg vials, and is typically marketed for injection into the muscle being trained. In the animal studies it was given by continuous subcutaneous infusion, intravenous bolus or injection into the brain ^{[6] [7] [8] [12]}; none injected it into a muscle to see whether that muscle grew. We found no study of oral, nasal or transdermal IGF-1 DES, and as a 67-amino-acid protein it would not be expected to survive the gut.

Because it is a protein made by recombinant expression rather than a short synthetic peptide, the product is only as good as the expression and purification behind it. Anti-doping analysis of the related IGF-1 LR3 has found a black-market version carrying a His-tag, a purification label used in laboratory reagents ^[21], so identity should not be assumed from a label.

The best-documented risk is low blood sugar. IGF-1 DES was the most potent of the IGF-1 variants at lowering plasma glucose in pigs, and the variants kept glucose suppressed for far longer than native IGF-1 ^[7]. The licensed native IGF-1, mecasermin, carries prominent warnings: hypoglycaemia was reported by 42% of children in its trials, some with seizures or loss of consciousness, and patients are told to avoid high-risk activities for two to three hours after a dose ^[14]. A variant that escapes binding proteins cannot be assumed to carry less of this risk.

IGF-1 signalling promotes cell growth. A Lancet meta-analysis found that people with higher circulating IGF-1 had a modestly higher risk of prostate cancer and of premenopausal breast cancer ^[15], mecasermin is contraindicated in anyone with active or suspected cancer ^[14], and a 2026 review described mitogenic concerns about IGF-1 analogues as biologically plausible but unproven ^[13]. The gut growth seen in every rat study, with intestinal weight rising by up to 60% ^{[8] [11]}, and the heavier kidneys and thymus after IGF-1 DES ^[12], are reminders that a free IGF-1 acts on many tissues, not just muscle. There are no controlled human safety data, so whether IGF-1 DES is safe cannot be answered from evidence.

IGF-1 DES is not approved as a medicine anywhere. For sport, the 2026 WADA Prohibited List names insulin-like growth factor 1 and its analogues under section S2.3, growth factors, prohibited at all times, and anti-doping laboratories specifically screen for des(1-3)IGF-1 ^{[9] [10] [16]}. UK Anti-Doping applies the same list ^[17].

In the UK, IGF-1 DES has no marketing authorisation, and regulation 46 of the Human Medicines Regulations 2012 makes it an offence to sell or supply an unauthorised medicinal product ^[18]. It is not a controlled drug: Class C of the Misuse of Drugs Act 1971 names somatropin and chorionic gonadotrophin but not IGF-1 or its analogues ^[19]. It is a protein hormone, not a steroid. See our UK legal status page, the US page and the legal status overview for other countries.

IGF-1 DES is supplied as a freeze-dried protein. Proteins of this size are sensitive to heat, repeated freezing and thawing, and vigorous shaking, which can cause them to unfold or aggregate. Keep it cold, dry and dark, reconstitute gently, and refrigerate once mixed. See how to store peptides.

PepFinder does not sell IGF-1 DES. You can compare IGF-1 DES prices, including UK listings and US listings, and filter for third-party tested suppliers.

For a recombinant protein, the certificate of analysis should show more than an HPLC purity figure: a mass spectrum consistent with a 67-amino-acid protein, evidence of the correct sequence, and results for endotoxin and host-cell contaminants, since the material is made in cells. Read how to read a COA, third-party peptide testing and how to spot a fake peptide supplier. If muscle growth is the aim, our peptides for muscle growth page sets IGF-1 DES beside HGH, MGF and GDF-8 (myostatin) pathway proteins.