IGF-1 DES

What it is

IGF-1 is the growth factor that mediates a large part of the effect of growth hormone. IGF-1 DES is a short form of it: at the front end of the chain, the three amino acids glycine, proline and glutamic acid are missing – DES stands for the missing positions 1 to 3.

This form was not invented in the laboratory. It was isolated from human brain tissue in 1986, later also described from bovine colostrum, and is most likely produced by cleavage of the first three building blocks from mature IGF-1. Incidentally, the cleaved three-piece fragment has had a career of its own: an analogue of it has been approved in the US since March 2023 for Rett syndrome in children aged 2 and over.

In the peptide scene, IGF-1 DES is treated as a relative of IGF-1 LR3. Both evade the binding proteins, but in different ways: LR3 is an engineered construct with an additional extension and a substitution at position 3, DES the short form that occurs in the body. Both have the same gap: no study in humans.

How it is supposed to work

The key lies in the IGF binding proteins. In the blood, the vast majority of IGF-1 is bound to such transport proteins and thus inactive for the time being. This brake barely applies to IGF-1 DES, and a single building block is responsible: the missing glutamic acid at position 3.

The consequence in cell culture: about 10 times stronger stimuli on cell growth and cell division. In the living animal, part of this extra potency is retained. In the circulation, the substance behaves differently from IGF-1: in the rat experiment it left the blood markedly faster; plasma clearance was 4.59 versus 1.20 milliliters per minute and kilogram, the volume of distribution 461 versus 167 milliliters per kilogram. The authors concluded that it is precisely the variants that disappear quickly from the blood that have more effect in tissue.

This contradicts a widespread narrative: IGF-1 DES does not stay in the blood longer, but shorter. What lasted longer was the effect on blood sugar.

What happened in animals

The key studies were done in disease models, not in healthy animals building muscle. In rats of 150 grams that were put into a catabolic state with dexamethasone, IGF-1 reversed part of this over 7 days: plus 6 grams of body weight at the highest study dose, while the comparison group lost 19 grams. IGF-1 DES and LR3 were about 2.5 times more potent than IGF-1.

In diabetic rats of 160 grams, the peptides restored growth, the variants 2.5 to 3 times more potent than IGF-1; muscle protein synthesis and RNA content rose by up to 50 percent. The comparison with insulin is remarkable: the insulin group gained the most, at 64.5 grams per 7 days, but the extra gain was fat, whereas the gain under the IGF peptides was protein.

The gut responds more strongly than the muscle

One finding is rarely cited by the scene, although it is well documented: in these experiments, the most sensitive target tissue was the gut. Under the highest IGF-1 study dose, total gut weight rose by up to 60 percent, as a share of body weight by up to 32 percent, and the variants were more potent here too. The researchers logically saw a possible application in inflammatory bowel disease – for muscle there is no comparably clear response.

Why it never became a medicine

The 1996 review by the discovering group stated that clinical possibilities had not yet been investigated – a statement that has not been superseded since. The axis made it into the clinic only in another form: mecasermin, body-identical IGF-1, has been approved in the EU since August 3, 2007, for children and adolescents aged 2 to 18 with severe primary IGF-1 deficiency.

Two findings show what the likely reasons were: blood sugar, which IGF-1 DES lowered in marmosets and pigs more than any other IGF-1 variant tested, and cell growth – mice that permanently produced IGF-1 DES in the mammary gland developed mammary carcinomas in 53 percent of cases by the age of 23 months. This is a genetic model and not an injection study, but as a signal for the growth question it is the most concrete work there is.

What the studies show

Anabolic in a catabolic state (Tomas, Biochem J 1992)

Male rats of 150 grams were put into a catabolic state with dexamethasone and treated for 7 days via osmotic pumps with IGF-1 or one of the two variants. The highest IGF-1 study dose produced plus 6 grams of body weight; the group without peptide lost 19 grams, and the pair-fed control gained 18 grams. IGF-1 DES and LR3 were about 2.5 times more potent than IGF-1, and gut weight rose by up to 45 percent.

Blood sugar in monkey and pig (Tomas, J Endocrinol 1997)

Marmosets and pigs received a single injection of IGF-1 or one of the variants, with blood samples up to 4 hours afterwards. The maximum reduction was 4.8 millimoles per liter in the pig, 3.7 in the conscious and 2.5 in the anesthetized marmoset. The variants were 2 to 3 times more potent than IGF-1, the cumulative reduction over four hours 4 to 8 times greater, and IGF-1 DES was at the top of the ranking. The authors were thinking of a supplement to insulin treatment, not of muscle building.

Tumors in the overexpression model (Hadsell, Oncogene 2000)

Mice with permanent production of IGF-1 DES in the mammary gland showed precursor lesions; by the age of 23 months, 53 percent developed mammary carcinomas, and tumor frequency was 2 to 3 times higher than in unmodified animals. When a mutated p53 was added, the tumor appeared 8 months earlier.

Where the data stop

The decisive limit is quickly named: there is no study in humans. A search in Europe PMC on September 27, 2026, returned 247 papers on this substance, none of them with injected IGF-1 DES in humans; ClinicalTrials.gov lists no matching entry. A 2026 review of the peptides of this axis assigns the substances to levels of evidence down to the complete absence of human data – IGF-1 DES belongs in the lower level.

Even in animals, the endpoint of muscle building was never tested. What was measured was body weight, nitrogen balance, organ weights and blood sugar, in models of cortisone administration, diabetes and bowel surgery. And what is traded as IGF-1 DES is unknown goods: in a doping analysis study from 2021, black-market products showed clear signs of inferior quality and oxidized peptide forms.

Status, approval and legal

IGF-1 DES is neither an approved medicine nor a dietary supplement in Germany and the EU; it is sold as a research substance. The scientific literature notes that it was never approved for use in humans and is nevertheless available as a black-market product for strength sports. In sport, IGF-1 and its analogues are prohibited, and Des(1-3)-IGF-I is covered by name; a detection method from blood has been validated and was effective in rats up to 24 hours after a single dose. The only approved product on this axis is body-identical IGF-1 as mecasermin, since August 3, 2007, in the EU, for children and adolescents aged 2 to 18 with severe primary IGF-1 deficiency. We do not state dosages for unapproved substances; quantities mentioned are study figures from animal experiments.

Safety

The leading risk is hypoglycemia. In animals, IGF-1 DES was the most strongly blood sugar-lowering IGF-1 variant of all, 2 to 3 times more potent than IGF-1 and cumulatively 4 to 8 times stronger over four hours. With the approved mecasermin, hypoglycemia occurs in more than 1 in 10 patients. The second point is the growth question: mecasermin must not be used in active or suspected neoplasia, and more tumors occurred in the mouse model with permanent overexpression. Added to this is tissue growth in unwanted places: gut weight up to plus 60 percent in animals, heavier kidneys. With self-use of peptides of this axis, the scientific literature reports disturbances of glucose metabolism, fluid retention, muscle and joint pain and injection-site reactions. For people with a history of cancer or with diabetes, there is no data basis.

Sources

• Ballard FJ et al., Int J Biochem Cell Biol 1996 – review of des(1-3)IGF-I
• Sara VR et al., PNAS 1986 – isolation of the truncated IGF-1 variant from fetal brain tissue
• Carlsson-Skwirut C et al., FEBS Lett 1986 – variant in adult brain tissue
• Tomas FM et al., Biochem J 1992 – anabolic in rats on dexamethasone
• Tomas FM et al., Biochem J 1993 – growth in diabetic rats
• Read LC et al., J Endocrinol 1992 – gut growth
• Ballard FJ et al., J Endocrinol 1991 – clearance and tissue distribution
• Tomas FM et al., J Endocrinol 1997 – blood sugar reduction in pig and marmoset
• Hadsell DL et al., Oncogene 2000 – tumors in the overexpression model
• Mongongu C et al., Drug Test Anal 2021 – detection of IGF-1 analogues, black-market products