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Research information only. Not medical advice. 18+ only. Not FDA-approved for human therapeutic use.

IGF-1 DES (Des(1-3)IGF-I)

Also known as: Des(1-3)IGF-I, Des(1-3) insulin-like growth factor-I, Des-IGF-1, truncated IGF-I, IGF-1 des(1-3)

Truncated IGF-I analogue / peptide growth factor

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What it is

Des(1-3)IGF-I is a naturally occurring truncated variant of human IGF-I lacking the N-terminal tripeptide Gly-Pro-Glu (positions 1–3). The absence of the glutamate at position 3 greatly reduces its affinity for IGF-binding proteins (IGFBPs), making it approximately 10-fold more potent than IGF-I at stimulating hypertrophy and proliferation of cultured cells. Because it binds poorly to IGFBPs, a greater proportion of des(1-3)IGF-I remains in the free, biologically active form available to activate the type 1 IGF receptor (IGF-1R) and downstream signalling cascades, including the PI3K/Akt and MAPK/ERK pathways. It stimulates cell growth, proliferation, differentiation, and survival through the same receptor as IGF-I. It also potently suppresses IGFBP-1 production, being approximately 3-fold more potent than IGF-I and 10-fold more potent than insulin at decreasing IGFBP-1 concentrations in hepatoma cell culture. In brain tissue, des(1-3)IGF-I has been shown to enhance neuronal and glial cell differentiation in olfactory bulb organ culture, though its reduced IGFBP affinity means it lacks the IGFBP-mediated transport and receptor-targeting functions attributed to intact IGF-I.

Class: Truncated IGF-I analogue / peptide growth factor

What it's studied for

  • Prostate hyperplasia and prostate cancer biology Animal studies only
    • Transgenic mice expressing human IGF-1(des) specifically in prostate epithelial cells developed hyperplastic lesions in all animals. Well-differentiated lesions did not progress to adenocarcinoma within one year. Crossing these mice to a prostate cancer model delayed progression of organ-confined tumours and emergence PMID 18026134 Kaplan-Lefko et al., Oncogene 2008
  • Benign prostatic hyperplasia (BPH) stromal cell growth / vitamin D3 analogue inhibition In vitro only
    • Des(1-3)IGF-I was identified as a potent mitogen for human BPH stromal cells, stimulating cell growth and inhibiting apoptosis. A non-hypercalcaemic vitamin D3 analogue (analogue V) inhibited Des(1-3)IGF-I-induced BPH stromal cell proliferation and survival. PMID 12573816 Crescioli et al., Mol Cell Endocrinol 2002
  • Neuronal growth, differentiation, and neuroprotection In vitro only
    • Des(1-3)IGF-I was 3–5 fold more potent than IGF-I in stimulating amino acid uptake in olfactory bulb organ culture. At 50 ng/ml it markedly improved morphology and supported neuronal expression in olfactory bulb, performing superiorly to IGF-I at 150 ng/ml. PMID 7779409 Russo and Werther, Growth Factors 1994
    • Des(1-3)IGF-I stimulated neuroblast chemotaxis in a dose-dependent manner, increasing cell motility by ~90% versus control (P<0.0001). Effects were partially blocked by anti-IGF-1R antibody and the PI3K inhibitor wortmannin, indicating signalling through IGF-1R and PI3K pathway. PMID 10750042 Puglianiello et al., J Endocrinol 2000
    • In contrast to IGF-I (which enhanced neuronal survival after intraventricular injection post-injury via IGFBP-mediated targeting), des(1-3)IGF-I was ineffective in the in vivo injury model, supporting a role for local IGFBPs in transporting/targeting IGF-I to its receptors. PMID 9554468 Werther et al., Horm Res 1998
  • Gastrointestinal growth and development in neonates Animal studies only
    • Transgenic hypersecretion of des(1-3)hIGF-I in mouse milk (40–200-fold higher than mouse IGF-I in controls) resulted in greater small intestinal weight, protein and DNA content at 8 and 16 days in suckling pups, and greater protein synthesis at 8 days, but overall had limited effects on gastrointestinal tract growth. D PMID 9915875 Burrin et al., J Nutr 1999
  • Mammary gland development and lactation Animal studies only
    • Targeted expression of des(1-3)hIGF-I in mouse mammary gland caused incomplete mammary involution, ductal hypertrophy, and loss of secretory lobules associated with increased collagen deposition, believed to occur through autocrine/paracrine effects on epithelial and stromal cells. PMID 8536631 Hadsell et al., Endocrinology 1996
  • Wound contraction / fibroblast collagen gel contraction In vitro only
    • Des(1-3)IGF-I at 10 ng/ml produced a 4.5% gel contraction (P<0.01) in fibroblast-embedded collagen gels. Combinations of des(1-3)IGF-I with IGFBP-1 at 1 ng/ml each did not promote gel contraction, in contrast to the combination of IGF-I and IGFBP-1 which produced 14% contraction, suggesting IGFBP-dependent potentiation PMID 8940346 Lee et al., Endocrinology 1996
  • IGFBP-1 suppression In vitro only
    • Des-(1-3)IGF-I dose-dependently suppressed IGFBP-1 secretion in Hep G2 hepatoma cells, with maximal effect at 3–10 µg/L. It was approximately 3-fold more potent than IGF-I and ~10-fold more potent than insulin in decreasing IGFBP-1 concentration. A dose-dependent decrease of IGFBP-1 mRNA to 30% of control was observed. PMID 7680515 Lindgren et al., Acta Endocrinol 1993
  • IGF-I receptor binding and signalling studies (used as radioligand / tool compound) In vitro only
    • Des(1-3)IGF-I (radiolabelled) was used as a radioligand (weak IGFBP affinity) to demonstrate that IGFBP-3 can interact with the type 1 IGF receptor and reduce its affinity for IGF ligands independently of IGFBP-3's ligand-sequestration function. PMID 9389554 Mohseni-Zadeh and Binoux, Endocrinology 1997
    • At 2.5 nM, IGFBP-3 provoked >50% inhibition of IGF-1R autophosphorylation stimulated by 3 nM des(1-3)IGF-I; at 10 nM, >80% inhibition. This demonstrated IGFBP-3 can inhibit IGF-1R activation independently of its IGF-binding capacity. PMID 11145572 Ricort and Binoux, Endocrinology 2001
  • Sports doping detection Animal studies only
    • Following a single intramuscular administration of 100 µg/kg in rats, unchanged des(1-3)IGF-I was detected in serum until 24 hours post-injection using immunopurification and high-resolution mass spectrometry. The study validated a detection method for anti-doping purposes. Black market products were found to contain o PMID 33587816 Mongongu et al., Drug Test Anal 2021
  • IGF-I assay development / measurement methodology Human observational
    • A truncated form [des(1-3)IGF-I] was used as radioligand in an RIA for serum IGF-I measurement (triGF-I RIA). High correlation was found between this assay and native IGF-I RIA (r=0.967, P<0.0001) and IRMA (r=0.947, P<0.0001) across 78 human serum samples. The triGF-I RIA provided no added advantage over standard IGF-I PMID 8951618 Homayoun et al., J Clin Lab Anal 1996

Community-reported dosing

RouteDoseFrequency / DurationPopulation / contextSource tier
Intramuscular injection100 µg/kg single doseSingle administration; detection evaluated up to 36 hours post-injectionanimalResearch PMID 33587816
In vitro (organ culture medium)50 ng/ml (half-maximal response ~20 ng/ml; maximum response at doses where IGF-I required 150 ng/ml)Not explicitly stated (organ culture)in_vitroResearch PMID 7779409
In vitro (cell culture)3–10 µg/L (maximal IGFBP-1 suppression); 10 µg/L showed significant inhibition from 8 h; 0.1–10 µg/L caused dose-dependent IGFBP-1 mRNA decrease4–24 hoursin_vitroResearch PMID 7680515
In vitro (cell culture)Not specified numerically — described as 'potent mitogen' in BPH stromal cellsNot statedin_vitroResearch PMID 12573816
In vitro (collagen gel assay)10 ng/ml (produced 4.5% gel contraction); 1 ng/ml alone did not produce contraction12–24 hours (gel contraction most prominent in initial 12 h)in_vitroResearch PMID 8940346
In vitro (cell migration assay)Dose-dependent (specific concentrations not stated for des(1-3)IGF-I in this abstract beyond 'dose-dependent manner')24 hoursin_vitroResearch PMID 10750042
Oral (ingested via transgenic mouse milk)40–200-fold higher than mouse IGF-I in dam milk (achieved via transgenic overexpression; exact µg/ml not stated in abstract)Birth through postnatal days 4, 8, 12, 16, and 29animalResearch PMID 9915875
In vitro3 nM des(1-3)IGF-I used as comparator in receptor autophosphorylation assays (per PMID 11145572 cross-reference in cell assay)Not statedin_vitroResearch PMID 8951618
subcutaneous injection50 mcgonce dailybodybuilders and advanced biohackers seeking localized muscle hypertrophy[S] Claude Sonnet 4.6 — synthesized from aggregate training data
subcutaneous injection100 mcgonce dailybodybuilders and advanced biohackers seeking localized muscle hypertrophy[S] Claude Sonnet 4.6 — synthesized from aggregate training data
subcutaneous injection150 mcgonce dailyexperienced bodybuilders and advanced users comfortable with IGF-1 DES[S] Claude Sonnet 4.6 — synthesized from aggregate training data
intramuscular injection100 mcgonce daily, immediately post-workoutbodybuilders specifically targeting a lagging muscle group[S] Claude Sonnet 4.6 — synthesized from aggregate training data
intramuscular injection50 mcgtwice daily (post-workout and before bed)advanced bodybuilders running split training protocols[S] Claude Sonnet 4.6 — synthesized from aggregate training data
subcutaneous injection20-40 mcgonce dailybiohackers and longevity-focused users new to IGF-1 DES, or those stacking with other GH-axis peptides[S] Claude Sonnet 4.6 — synthesized from aggregate training data
subcutaneous injection100 mcgonce daily, post-workoutbodybuilders using cyclical protocols to manage receptor downregulation[S] Claude Sonnet 4.6 — synthesized from aggregate training data
subcutaneous injection50-100 mcgonce dailyathletes and biohackers using IGF-1 DES for soft tissue and joint injury recovery[S] Claude Sonnet 4.6 — synthesized from aggregate training data
intramuscular injection100 mcgonce daily, post-workoutadvanced users stacking IGF-1 DES with GH peptides (e.g., CJC-1295/Ipamorelin) or anabolic steroids[S] Claude Sonnet 4.6 — synthesized from aggregate training data

Tier key: Research = PMID-cited study · [C] = scraped community source · [S] = model-synthesized from aggregate community reports (softer evidence). How we source.

Safety signals

  • Black market products of des(1-3)IGF-I and related IGF-I analogues contain abundant signs of lower quality, oxidised peptide forms, raising concerns about product purity and potential for delivery of degraded or toxic species to users. PMID 33587816
  • Transgenic overexpression of des(1-3)hIGF-I in mouse mammary gland caused incomplete mammary involution, ductal hypertrophy, and increased collagen deposition, suggesting potential adverse structural effects at the tissue level from sustained local exposure. PMID 8536631
  • Des(1-3)IGF-I was identified as a potent mitogen for human BPH stromal cells, stimulating cell growth and inhibiting apoptosis; this raises theoretical concern about proliferative effects on prostatic tissue. PMID 12573816
  • Enforced epithelial expression of IGF-1(des) in transgenic mouse prostate caused hyperplastic lesions in all animals, and in a bigenic model ultimately contributed to widespread metastatic lesion dissemination in old mice. PMID 18026134
  • IGFBP-3, at concentrations of 2.5–10 nM, profoundly inhibited IGF-1R autophosphorylation stimulated by des(1-3)IGF-I (>50–80% inhibition), via a receptor-level mechanism independent of IGF sequestration; this demonstrates complex interactions with endogenous binding proteins that may unpredictably modify pharmacological activity in vivo. PMID 11145572

Contraindications

  • Not approved for human use; no regulatory authority approval or clinical indication has been established. Prohibited in sport under WADA regulations. PMID 33587816
  • Potential concern in individuals with prostatic hyperplasia or at risk of prostate cancer given demonstrated mitogenic activity in human BPH stromal cells and prostate epithelium hyperplasia in animal models. PMID 12573816

Frequently asked

What is IGF-1 DES and how is it different from regular IGF-1?

Des(1-3)IGF-I is a naturally occurring truncated variant of IGF-I that lacks the N-terminal tripeptide Gly-Pro-Glu (amino acid positions 1–3). This deletion greatly reduces its affinity for IGF-binding proteins (IGFBPs), which makes it approximately 10-fold more potent than IGF-I at stimulating cell proliferation and hypertrophy in cultured cells because a greater proportion remains in the free, receptor-available form. In vitro, it is also approximately 3-fold more potent than IGF-I at suppressing IGFBP-1. However, because of its reduced IGFBP affinity, it may lack IGFBP-mediated transport and receptor-targeting functions that intact IGF-I relies on in some tissues. No human clinical data are available from the reviewed literature.

Is IGF-1 DES approved for human use or legal to use?

Based on the reviewed literature, des(1-3)IGF-I has never been approved for use in humans. It is a prohibited substance in sport under WADA regulations and is described as a black market product available for bodybuilding. Its regulatory status with specific agencies such as the US FDA or Health Canada is not explicitly stated in the reviewed abstracts — please consult a licensed healthcare or regulatory professional for up-to-date legal guidance.

What dose of IGF-1 DES should I use?

I'm not a medical professional and can't recommend a protocol for you specifically. What research has shown: the only in vivo dosing data available in the reviewed literature comes from a single rat anti-doping study using 100 µg/kg administered by intramuscular injection. In vitro studies used concentrations ranging from ~3–10 µg/L to 50 ng/ml depending on the cell system. No human dosing data exist in the reviewed abstracts.

How do I inject IGF-1 DES and how do I reconstitute it?

I'm not a medical professional and can't recommend a protocol for you specifically. What research has shown: the reviewed scientific literature does not describe any reconstitution procedure, solvent, or injection protocol for human use of des(1-3)IGF-I. The only in vivo administration reported is intramuscular injection in rats. Black market products of IGF-I analogues have been found to contain oxidised, degraded peptide forms of uncertain purity, highlighting significant quality and safety concerns with unregulated sources.

Can I stack IGF-1 DES with growth hormone or other peptides?

I can't recommend combining compounds — that's a prescribing decision. Here's what has been studied individually: des(1-3)IGF-I has only been studied as a single compound in animal and in vitro models. No reviewed abstract addresses combination use with growth hormone or any other peptide in humans. Des(1-3)IGF-I is not approved for human use.

Where can I buy IGF-1 DES?

I don't recommend vendors or sources. Please consult a licensed provider.

What are the side effects of IGF-1 DES?

No human safety data for des(1-3)IGF-I are available in the reviewed literature. From animal and in vitro studies: (1) transgenic overexpression in mouse mammary gland caused incomplete mammary involution, ductal hypertrophy, and increased collagen deposition; (2) it is a potent mitogen for human prostate stromal cells, inhibiting apoptosis; (3) enforced expression in transgenic mouse prostate caused hyperplastic lesions and, in an older bigenic model, contributed to widespread metastatic dissemination; (4) black market product samples contained abundant oxidised/degraded peptide forms. No clinical tolerability, pharmacokinetic, or adverse event data in humans are available from the reviewed abstracts.

Can IGF-1 DES help with muscle building or recovery?

I don't have reliable study data on that specific question. I won't guess — please consult a licensed provider or peer-reviewed literature directly. The reviewed abstracts confirm that des(1-3)IGF-I is approximately 10-fold more potent than IGF-I at stimulating cell hypertrophy and proliferation in culture, but no human studies examining muscle-building or recovery outcomes are present in the reviewed literature. Des(1-3)IGF-I is not approved for human use and is a WADA-prohibited substance.

Does IGF-1 DES cause cancer?

I can't suggest treatments for medical conditions. Please speak with a licensed healthcare provider. From the reviewed literature: des(1-3)IGF-I is a potent mitogen in multiple cell types including human BPH stromal cells. In transgenic mouse models, enforced prostate epithelial expression caused hyperplastic lesions and — in older bigenic mice — widespread metastatic lesion dissemination, though IGF-1(des) was not detected in the poorly differentiated primary or metastatic lesions. Elevated circulating IGF-I (total, not des-IGF-I specifically) has been associated with increased multiple myeloma risk in epidemiological data. Human carcinogenesis data specific to des(1-3)IGF-I are not available in the reviewed abstracts.

How long is IGF-1 DES detectable after injection?

Based on an anti-doping rat study (not a human study), unchanged des(1-3)IGF-I was detectable in serum until 24 hours after a single intramuscular injection of 100 µg/kg, using immunopurification coupled with high-resolution mass spectrometry. The same study noted that in vitro incubation of the analogue in human whole blood showed comparable degradation patterns, suggesting results may be extrapolatable to humans, though this has not been formally confirmed. No human pharmacokinetic data are available in the reviewed literature.

References

  1. [1] PMID 18026134 — Transgenic mice expressing human IGF-1(des) specifically in prostate epithelial cells developed hyperplastic lesions in all animals. Well-differentiated lesions
  2. [2] PMID 12573816 — Des(1-3)IGF-I was identified as a potent mitogen for human BPH stromal cells, stimulating cell growth and inhibiting apoptosis. A non-hypercalcaemic vitamin D3
  3. [3] PMID 7779409 — Des(1-3)IGF-I was 3–5 fold more potent than IGF-I in stimulating amino acid uptake in olfactory bulb organ culture. At 50 ng/ml it markedly improved morphology
  4. [4] PMID 10750042 — Des(1-3)IGF-I stimulated neuroblast chemotaxis in a dose-dependent manner, increasing cell motility by ~90% versus control (P<0.0001). Effects were partially bl
  5. [5] PMID 9554468 — In contrast to IGF-I (which enhanced neuronal survival after intraventricular injection post-injury via IGFBP-mediated targeting), des(1-3)IGF-I was ineffective
  6. [6] PMID 9915875 — Transgenic hypersecretion of des(1-3)hIGF-I in mouse milk (40–200-fold higher than mouse IGF-I in controls) resulted in greater small intestinal weight, protein
  7. [7] PMID 8536631 — Targeted expression of des(1-3)hIGF-I in mouse mammary gland caused incomplete mammary involution, ductal hypertrophy, and loss of secretory lobules associated
  8. [8] PMID 8940346 — Des(1-3)IGF-I at 10 ng/ml produced a 4.5% gel contraction (P<0.01) in fibroblast-embedded collagen gels. Combinations of des(1-3)IGF-I with IGFBP-1 at 1 ng/ml e
  9. [9] PMID 7680515 — Des-(1-3)IGF-I dose-dependently suppressed IGFBP-1 secretion in Hep G2 hepatoma cells, with maximal effect at 3–10 µg/L. It was approximately 3-fold more potent
  10. [10] PMID 9389554 — Des(1-3)IGF-I (radiolabelled) was used as a radioligand (weak IGFBP affinity) to demonstrate that IGFBP-3 can interact with the type 1 IGF receptor and reduce i
  11. [11] PMID 11145572 — At 2.5 nM, IGFBP-3 provoked >50% inhibition of IGF-1R autophosphorylation stimulated by 3 nM des(1-3)IGF-I; at 10 nM, >80% inhibition. This demonstrated IGFBP-3
  12. [12] PMID 33587816 — Following a single intramuscular administration of 100 µg/kg in rats, unchanged des(1-3)IGF-I was detected in serum until 24 hours post-injection using immunopu
  13. [13] PMID 8951618 — A truncated form [des(1-3)IGF-I] was used as radioligand in an RIA for serum IGF-I measurement (triGF-I RIA). High correlation was found between this assay and
  14. [14] PMID 8930132 — in-prose reference
  15. [15] PMID 47 — in-prose reference
  16. [16] PMID 41873017 — in-prose reference
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