IGF-1 DES
Also known as: DES(1-3) IGF-1
Removal of the N-terminal tripeptide sharply lowers IGF-binding-protein affinity while preserving IGF-1 receptor binding, leaving more free peptide to activate IGF-1R.
This page is a structured profile. Narrative evidence, dosing context and FAQs live on the research guide — not duplicated here as a second full article.
- Drug class
- Truncated IGF-1 analog
- Primary targets
- IGF-1R
- Dose reference
- No established human dose; research-only
- Half-life
- Very short; minutes in animal studies
- Developer / origin
- Sara, Carlsson-Skwirut et al. (Karolinska Institutet)
- Reference year
- 1986
- Evidence score
- 2/5 - Preclinical only
Preclinical only
IGF-1 DES has a clear mechanism but evidence is limited to cell-culture and rodent studies, with no human therapeutic approval, validated dose, or human safety data.
Mostly animal, ex vivo, cell, or indirect evidence.
Evidence basis
- Removal of N-terminal tripeptide reduces IGFBP affinity to ~1% of native IGF-1
- ~10-fold greater mitogenic potency in binding-protein-containing cultures
- Rat studies show improved nitrogen retention and muscle protein synthesis
- No human trials, approval, or validated dosing
How to read this entry
Dose references and half-life values are pulled from trial protocols, labels, reviews, or published summaries where available. They are context for research and comparison, not a personal dosing recommendation.
Status matters: approved drugs have regulated indications; investigational compounds are still being studied; research-only peptides do not have established human dosing, safety, or efficacy for consumer use.
IGF-1 DES guides
Read the matching guide or adjacent research pages for more context.
Peptide calculators
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Compare with related peptides
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IGF-1 LR3
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A modified IGF-1 that binds IGF binding proteins far more weakly than native IGF-1, leaving it free to act as a potent, long-acting agonist at the IGF-1 receptor.
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