Growth ⏱ Half-life: Approximately 20-30 minutes. Ultrashort — designed for local, immediate action. Preclinical

IGF-1 DES

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

Updated March 15, 2026

Evidence at a Glance

Regulatory statusPreclinical
Truncated DES(1-3) IGF-1 analog; in vitro and limited animal data only, no human trials, not FDA-approved
Human evidenceNone
Animal evidenceLimited

IGF-1 DES is a truncated IGF-1 variant that is more potent than native IGF-1 in cell-proliferation assays, but its evidence is almost entirely in vitro with only limited animal work and zero human trials.

What the research does not support

  • No human clinical trials of any kind have been conducted, so muscle or recovery claims are unproven in people.
  • It is not FDA-approved and is not a GRAS or compoundable substance for human use.
  • Greater in-vitro potency than IGF-1 does not translate to demonstrated human benefit or safety.
  • As an IGF-1 analog it is prohibited in sport under WADA rules.
Half-Life
Approximately 20-30 minutes. Ultrashort — designed for local, immediate action.
Mol. Weight
7365 g/mol

What is IGF-1 DES?

IGF-1 DES is the most potent naturally occurring form of IGF-1, created by removal of the first three amino acids. This small modification eliminates most binding protein interactions, freeing the peptide to act immediately and powerfully at IGF-1 receptors — but only briefly.

Research Applications

Local tissue growth signaling, site-specific muscle research, wound healing, and IGF-1 receptor pharmacology studies.

Dosage Information (Research Use)

Research protocols: 50-150 mcg injected locally into target tissue, pre- or post-training. Very short window of activity. Research use only.

Reconstitution & Handling

Reconstitute with BAC water or 0.6% acetic acid. Use promptly — less stable than LR3 variant.

Half-Life & Pharmacokinetics

Approximately 20-30 minutes. Ultrashort — designed for local, immediate action.

Reported Observations in Literature

Hypoglycemia risk (potent insulin-like activity). Local injection site reactions. Systemic effects minimal due to short half-life.

Key Research References

  • Francis GL, et al. “Novel recombinant fusion protein analogues of insulin-like growth factor (IGF)-I indicate the relative importance of IGF-binding protein and receptor binding.” J Mol Endocrinol. 1992

How IGF-1 DES Works

IGF-1 DES is a naturally occurring truncated form of IGF-1 missing the first three N-terminal amino acids. This deletion dramatically reduces binding to IGF-binding proteins (IGFBPs), resulting in approximately 10x greater potency than native IGF-1 at the receptor level. The ultrashort half-life (20-30 minutes) makes it primarily useful for local, site-specific injection where concentrated growth signaling is desired without prolonged systemic exposure.

Research Findings

Found naturally in brain tissue and bovine colostrum. The combination of extreme potency and ultrashort duration makes it suited for targeted local administration. Often used in research for site-specific muscle or tissue effects.

Dosage & Administration

Research protocols: 50-150 mcg injected locally into target tissue, pre- or post-training. Very short window of activity. Research use only.

Safety & Side Effects

Hypoglycemia risk (potent insulin-like activity). Local injection site reactions. Systemic effects minimal due to short half-life.

Important: All safety information is derived from published research, primarily animal studies. No controlled human clinical trial data exists unless explicitly noted. This compound is sold for research purposes only.

Quick Facts

Sequence IGF-1 minus first 3 N-terminal amino acids (Gly-Pro-Glu)
Molecular Weight 7365 g/mol
Half-Life Approximately 20-30 minutes. Ultrashort — designed for local, immediate action.
Available Sizes 1mg
Storage Lyophilized: -20°C. Reconstituted: 2-8°C, use within 14 days.

Key Research References

  • Francis GL, et al. "Novel recombinant fusion protein analogues of insulin-like growth factor (IGF)-I indicate the relative importance of IGF-binding protein and receptor binding." J Mol Endocrinol. 1992

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