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Compound record / IGF & growth factors

IGF-1 DES

A truncated IGF-1 variant missing the first three residues, roughly ten times more potent than native IGF-1 but very short-acting.

Animal models only Research use only Banned in sport
Written by Lindy Health editorial Updated 2026-10-18 Also known as DES(1-3) IGF-1, Des-IGF
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IGF-1 DES · molecular diagram awaiting verified source

What is IGF-1 DES?

IGF-1 DES, also written des(1-3)IGF-1, is a shortened form of insulin-like growth factor 1 (IGF-1). IGF-1 is the hormone the liver and other tissues make in response to growth hormone. It drives much of growth hormone's effect on muscle, bone and other tissue. IGF-1 DES is the same molecule with its first three amino acids removed.

The truncated form occurs naturally. It was isolated in the 1980s from bovine colostrum and has been reported in human brain tissue. Since then it has mainly served as a laboratory tool. Scientists use it because it barely binds the proteins that normally hold IGF-1 in check, which lets them separate the hormone's direct effects from the effects of those binding proteins.4 Today it is also sold online as a research chemical, marketed to bodybuilders for localized muscle growth. It has never been tested in a human clinical trial.

  1. Anecdotal only
  2. In vitro only
  3. Animal models only
  4. Preliminary human
  5. Clinical trials
  6. Regulator approved
No published human trials. Evidence level describes the literature, not a recommendation.
US statusNot FDA approved
Half-life~20-30 minutes
RoutesSubcutaneous, Intramuscular
Reported range50-150 mcg
Banned in sportYes (WADA)

How IGF-1 DES works

Most IGF-1 in the blood does not float freely. It is bound to a family of IGF binding proteins that act like a holding tank. They extend IGF-1's life in the blood but limit how much reaches cells at any moment.

Removing the first three amino acids changes the shape of IGF-1 just enough that the binding proteins can no longer grip it well. The receptor on cells still recognizes it. So a larger share of the dose is free to act, which is why it looks much more potent in lab dishes. The flip side is that free IGF-1 is cleared quickly, so its effect is short.

In more precise terms, des(1-3)IGF-1 keeps its affinity for the type 1 IGF receptor but has weak affinity for most IGF binding proteins.3 In human myeloid cell lines, IGFBP-3 blocked the growth effect of normal IGF-1 but not of des-IGF-1.5 The picture is not simple, though. IGFBP-3 can still dampen receptor activation by des(1-3)IGF-1 through a separate mechanism that does not depend on binding the hormone.3 The missing tripeptide, glycine-proline-glutamate, has its own biology: a synthetic analog of it, trofinetide, is an FDA-approved treatment for Rett syndrome.

The growth hormone axis
Hypothalamus GHRH (+) Somatostatin (−) Pituitary releases GH in pulses Ghrelin receptor(GHS-R) GH Liver IGF-1 Muscle, bone, fat growth, repair, fat use IGF-1 feeds back to slow GHRH and GH release, which is why the axisself-limits.

IGF-1 analogues act at the end of the axis, directly on tissues, bypassing the pituitary and the liver.

What the research shows on IGF-1 DES

All the evidence on IGF-1 DES comes from cells and animals. No human trial has tested it for muscle growth, recovery or any other outcome.

In cell culture, des(1-3)IGF-1 is an effective growth signal. It increased DNA synthesis in human myeloid cells.5 Researchers have used it to switch on myogenin, a key gene in muscle cell development, in mouse muscle cells.7 In cultured human fat cells, it changed the expression of genes linked to insulin sensitivity.6 These studies used it as a tool to study IGF signaling. They were not designed to test it as a treatment.

Lower binding-protein affinity is not always an advantage. In a model of brain injury, IGF-1 improved nerve cell survival but des(1-3)IGF-1 was ineffective, which suggests binding proteins help deliver IGF-1 to where it is needed.2

The most relevant animal safety data are concerning. Mice engineered to make IGF-1 DES in prostate tissue all developed hyperplastic lesions, meaning abnormal overgrowth of cells, although these did not progress to cancer within a year.8 The same paper notes that higher blood IGF levels are a risk factor for prostate and other cancers.8 In prostate cell studies, des(1-3)IGF-1 is used as a known growth promoter of prostate cells.1

The often-quoted figure of roughly ten times the potency of native IGF-1 comes from lab systems where binding proteins are present. It describes how much of the dose escapes those proteins in a dish, not what happens in a living person. The main limit is obvious. Lab potency does not show that injecting it builds muscle in people, and there are no human data on dose, safety or effect.

Studied for: Localised hypertrophy research, Satellite cell studies.

IGF-1 DES reference data

Molecular weight7,371 Da
FDA statusNot approved for any indication.
Prohibited in sportYes, under the WADA prohibited list

IGF-1 DES dosage in published research

Read this first These figures describe ranges reported in published research and in practitioner protocols. They are a reference, not a recommendation, and this page is not a prescription. Dosing for any compound should be set by a licensed clinician.
Reported range50-150 mcg
FrequencyOnce daily, peri-workout
Typical cycle4 weeks
Typical schedule in published protocols
M●
T●
W●
T●
F●
S●
S●

Once daily, peri-workout · usually run for about 4 weeks. A reference pattern, not a prescription.

Reconstitution1 mg vial + 1 mL bacteriostatic water = 1.0 mg/mL
On a 100-unit syringe50 mcg = 5.0 units · 150 mcg = 15.0 units

Open this in the dosage calculator ↗

How IGF-1 DES is used in practice

IGF-1 DES has no approved medical use, and legitimate telehealth services and compounding pharmacies do not offer it. In practice it is bought online as a "research use only" powder and injected, often into a specific muscle shortly after training. The idea is that its short life keeps the effect local. That idea has not been tested in humans.

Product quality is a major problem. IGF-1 DES is a protein of about 67 amino acids that has to fold correctly to work. Research-chemical sellers do not make it to pharmaceutical standards, and buyers cannot verify identity, potency, sterility or endotoxin content. Some vials may contain little active protein. IGF-1 and its analogs are prohibited in sport.

IGF-1 DES risks and side effects

IGF-1 acts partly like insulin, so low blood sugar is the most predictable acute risk. Symptoms include shakiness, sweating, confusion and, if severe, seizures or loss of consciousness. The risk is higher in anyone also using insulin or other diabetes drugs. Injection-site reactions and headache are also reported.

The larger concern is growth of the wrong tissue. IGF-1 signaling promotes cell growth and survival, and the prostate data above show that local IGF-1 DES can drive abnormal overgrowth.8 Anyone with active or suspected cancer should avoid it. It should not be used in pregnancy or by people with diabetes.

There are no data on long-term effects, safe doses or interactions in humans. Non-sterile products add the risk of infection and immune reactions.

Reported side effects

HypoglycaemiaInjection-site reactionsHeadache
ContraindicationsActive or suspected malignancy, Diabetes, Pregnancy
InteractionsAdditive hypoglycaemia with insulin

Alternatives to IGF-1 DES

For muscle growth, progressive resistance training with enough protein and calories has by far the strongest evidence. For people with diagnosed hormone deficiencies, approved treatments exist. Testosterone treats confirmed male hypogonadism. Recombinant growth hormone (somatropin) treats growth hormone deficiency. Mecasermin (Increlex), a recombinant form of IGF-1, is approved for children with severe primary IGF-1 deficiency, and it requires close monitoring for low blood sugar.

For recovery between sessions, sleep, nutrition and sensible training volume have far better support than any injected growth factor. Among unapproved peptides, IGF-1 LR3 is the long-acting relative, but it has no human trial data either and is not a safer choice.

The bottom line on IGF-1 DES

IGF-1 DES is a useful lab tool for studying how IGF-1 and its binding proteins work. It is not a tested human treatment. There are no human trials, the most predictable risks are low blood sugar and unwanted tissue growth, and grey-market products are of unknown quality. The case for injecting it is weak.

Questions for a clinician

  • What evidence applies to my situation, and at what level?
  • What established alternatives should I consider first?
  • What monitoring would be necessary, and how often?
  • Can this be prescribed at all where I live, or only sold for research?

IGF-1 DES FAQ

What is IGF-1 DES?

A truncated IGF-1 variant missing the first three residues, roughly ten times more potent than native IGF-1 but very short-acting. It is classed as IGF & growth factors.

Is IGF-1 DES FDA approved?

No. IGF-1 DES is not approved by the FDA for any indication. Material sold online is labelled for research use only.

Is IGF-1 DES legal in the US?

IGF-1 DES is not FDA approved and is not on FDA’s 503A bulks list. US compounding pharmacies cannot routinely prepare it.

What dose of IGF-1 DES is used in research?

Published research and practitioner protocols report 50-150 mcg, once daily, peri-workout, typically for 4 weeks. This is a reference range, not a recommendation; dosing should be set by a licensed clinician.

How is IGF-1 DES reconstituted?

A 1 mg vial mixed with 1 mL of bacteriostatic water gives 1.0 mg/mL. At that concentration 50 mcg is 5.0 units on a 100-unit insulin syringe.

What are the side effects of IGF-1 DES?

Reported side effects include hypoglycaemia, injection-site reactions, headache. Contraindications: active or suspected malignancy, diabetes, pregnancy.

What is the half-life of IGF-1 DES?

The reported half-life of IGF-1 DES is ~20-30 minutes.

Is IGF-1 DES banned in sport?

Yes. IGF-1 DES falls under the World Anti-Doping Agency prohibited list.

References

Regulatory and primary sources

  1. FDA: Bulk drug substances that may present significant safety risks (Category 2 and withdrawn nominations) ↗ · content current as of April 22, 2026; checked October 18, 2026
  2. FDA: Bulk drug substances used in compounding under section 503A ↗ · how the 503A categories work
  3. WADA Prohibited List ↗ · current year
  4. FDA: Unapproved drugs and "research use only" products ↗ · regulatory status of non-approved products

Published literature

  1. Espinosa G, Esposito R, Kazzazi A, et al.. Vitamin D and benign prostatic hyperplasia -- a review.Can J Urol 2013.PubMed 23930605
  2. Werther GA, Russo V, Baker N, et al.. The role of the insulin-like growth factor system in the developing brain.Horm Res 1998.PubMed 9554468 · doi:10.1159/000053066
  3. Ricort JM, Binoux M. Insulin-like growth factor (IGF) binding protein-3 inhibits type 1 IGF receptor activation independently of its IGF binding affinity.Endocrinology 2001.PubMed 11145572 · doi:10.1210/endo.142.1.7915
  4. Forbes B, Szabo L, Baxter RC, et al.. Classification of the insulin-like growth factor binding proteins into three distinct categories according to their binding specificities.Biochem Biophys Res Commun 1988.PubMed 2973786 · doi:10.1016/s0006-291x(88)80032-9
  5. Li YM, Schacher DH, Liu Q, et al.. Regulation of myeloid growth and differentiation by the insulin-like growth factor I receptor.Endocrinology 1997.PubMed 8977425 · doi:10.1210/endo.138.1.4847
  6. Pamuklar ZN, Chen J, Muehlbauer M, et al.. Necdin-E2F4 interaction provides insulin-sensitizing effect after weight loss induced by gastric bypass surgery.Surg Obes Relat Dis 2013.PubMed 22138333 · doi:10.1016/j.soard.2011.10.014
  7. Viñals F, Ventura F. Myogenin protein stability is decreased by BMP-2 through a mechanism implicating Id1.J Biol Chem 2004.PubMed 15322112 · doi:10.1074/jbc.M408059200
  8. Kaplan-Lefko PJ, Sutherland BW, Evangelou AI, et al.. Enforced epithelial expression of IGF-1 causes hyperplastic prostate growth while negative selection is requisite for spontaneous metastogenesis.Oncogene 2008.PubMed 18026134 · doi:10.1038/sj.onc.1210943

Literature retrieved from PubMed on October 16, 2026, favouring human studies and reviews. Numbered markers in the text show which paper supports which statement; uncited entries are background reading.

A useful next read.