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Research-onlyVendors pendingFacts verified · 2026-05-25

IGF-1 DES (1-3)

Also known as des(1-3)igf-1, igf-1(4–70), des igf-1 · Wikipedia

IGF-1 DES (1-3), also written des(1-3)IGF-1 or IGF-1(4-70), is a 67-amino-acid truncated analog of native human insulin-like growth factor 1 in which the N-terminal tripeptide glycine-proline-glutamate has been removed. The deletion dramatically reduces affinity for IGF binding proteins (Szabo et al., 1988), substantially increasing the free, bioactive fraction at the IGF-1 receptor in cell-culture and short-term in vivo models. It is studied primarily as a local-acting anabolic growth factor at the injection site, used in research to drive site-specific hypertrophy. There are no published human clinical trials. WADA classifies all IGF-1 analogs as prohibited substances.

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Mechanism of action

IGF-1 DES(1-3) is a 67-amino-acid truncated analog of native IGF-1 missing the N-terminal tripeptide glycine-proline-glutamate (GPE). Removal of this tripeptide reduces binding to IGF binding proteins (IGFBPs) by roughly an order of magnitude or more (Szabo et al.

IGF-1 DES(1-3) is a 67-amino-acid truncated analog of native IGF-1 missing the N-terminal tripeptide glycine-proline-glutamate (GPE). Removal of this tripeptide reduces binding to IGF binding proteins (IGFBPs) by roughly an order of magnitude or more (Szabo et al., 1988), leaving a much greater free, bioactive fraction available to the IGF-1 receptor (IGF-1R). DES preserves full agonism at IGF-1R, signalling through PI3K/Akt/mTOR (anabolic, protein-synthesis) and Ras/MAPK/ERK (proliferative) pathways. Because its systemic plasma half-life is very short, DES acts predominantly in an autocrine/paracrine manner at the site of injection, supporting local satellite-cell activation, myofiber protein accretion, and local hyperplastic signalling. Cell-culture studies report it is 5-10x more potent than native IGF-1 in certain tissues; in-vivo human data are absent.

Pharmacokinetic properties

Half-life

~20-30 minutes (some sources cite <5 min); much shorter than LR3

Routes

intramuscular · subcutaneous

Bioavailability

Effectively a local-acting agent due to its short systemic half-life. Injected directly into target muscle for site-specific hypertrophy effect.

Amino-acid sequence

(67 aa) IGF-1 lacking the N-terminal tripeptide (Gly-Pro-Glu)

Use & research dosing

StrengthHypertrophyRecovery

There is no approved therapeutic dose and no published human clinical trials. Self-experimentation protocols commonly report 50-150 mcg per injection delivered intramuscularly into the target muscle post-workout on training days only, on the rationale that the very short systemic half-life confines effect to the injection site. Preclinical rodent studies have used variable parenteral doses for short-term anabolic and metabolic endpoints. These doses are not derived from controlled human PK studies and the IGFBP-evasion phenotype creates a higher per-mole biological exposure than native IGF-1.

Research-use framing only. SavePeptides sells nothing for human consumption. Doses above reflect reported research / self-experimentation ranges, not clinical recommendations.

Editorial perspective

DES(1-3) IGF-1 differs from IGF-1 LR3 in route of action: DES is essentially a local injection for site-specific effect because of its short systemic half-life, whereas LR3 is a long-acting, systemic anabolic. The 5-10x potency claim derives from cell-culture studies and should not be extrapolated as a clean in-vivo human dose multiplier. All IGF-1 analogs are WADA-prohibited (S2) at all times. There is no IND-stage clinical program.

— SavePeptides editorial desk · last updated 2026-05-25

Cautions & contraindications

Before researching this compound, note:

  • Not FDA-approved; no published human clinical trials
  • Hypoglycaemia risk (lower than IGF-1 LR3 because of shorter half-life, but still present, especially with co-administered insulin)
  • Avoid in active or suspected malignancy - potent local mitogen; IGFBP-evasion increases free bioactive fraction
  • Avoid in pregnancy and breastfeeding (no safety data)
  • Avoid in proliferative retinopathy and any IGF-driven proliferative disorder
  • Repeated same-site dosing risks focal/asymmetric hypertrophy, scar tissue, and fibrotic remodelling
  • WADA-banned at all times under S2 (peptide hormones, growth factors)
  • Vendor material identity, purity, and sequence verification highly variable in the gray market
  • Theoretical risk of acromegalic-type changes with chronic systemic exposure

Research foundation

The papers behind the page.

  1. [01]https://pubmed.ncbi.nlm.nih.gov/2450535/
  2. [02]https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7913862/

Facts verified

2026-05-25

Confidence

low

What this means

  • no human clinical trials
  • WADA prohibited (S2)
  • potency multiplier claims derive from cell culture, not in-vivo human data
  • vendor identity/purity highly variable

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