Research onlyGrowth hormoneSubcutaneousEvidence 2/5

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.

IGF-1 DES
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
Evidence 2/5

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.

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Research & educational purposes only

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