Des(1-3) Insulin-like Growth Factor-1
A truncated variant of IGF-1 lacking the first 3 amino acids, resulting in reduced binding to IGF binding proteins (IGFBPs) and approximately 10-fold increased potency at the IGF-1 receptor compared to full-length IGF-1 (Ballard et al., PMID 8930132). No human clinical trials exist and no FDA product match has been identified.
Last updated: 2026-03-10
Human safety data specific to Des(1-3) IGF-1 were not identified in the source set. All side effect information is derived from vendor/community reports and extrapolation from general IGF-1 biology, not from controlled clinical safety studies. Hypoglycemia is the primary acute concern due to IGF-1 pathway effects on glucose metabolism, reported across multiple sources. Hand cramping and stiffness was reported in a single online communities 90-day review that included a GH stack, so attribution to Des(1-3) specifically is uncertain. Organ growth is a theoretical extrapolation from GH/IGF-1 excess biology (acromegaly), listed by vendor sources but with no case reports specific to Des(1-3) IGF-1. Theoretical long-term cancer promotion risk exists due to IGF-1's well-established role in cell proliferation and anti-apoptosis (PMC7564605; PMID 12466191).
reported (frequency unknown)
reported (frequency unknown)
reported (frequency unknown)
reported at higher doses (frequency unknown)
reported (single user, frequency unknown)
theoretical (no case reports specific to Des(1-3) IGF-1)
IGF-1 pathway promotes cell proliferation, angiogenesis, and inhibits apoptosis. IGF-regulated pathways are linked to cell cycle control, apoptosis, and cancer biology (Firth et al. 2002, PMID 12466191; PMC7564605). Exogenous IGF-1 variants could theoretically accelerate growth of existing tumors. While no Des(1-3)-specific contraindication study was identified, the biological principle is well-established.
Des(1-3) IGF-1 has reported hypoglycemic effects that would compound with diabetes medications, creating risk of severe hypoglycemia. No direct Des(1-3) interaction study was identified in the source set.
No safety data exists. Growth factor effects on fetal development are unpredictable. Standard precautionary principle for untested growth factors.
Before considering IGF-1 DES, discuss it with your healthcare provider. Ask about potential interactions with your current medications, whether it is appropriate for your health conditions, and what monitoring may be needed.
Sources: [1-7]
Tier 5: Animal/in vitro only. No human clinical trials exist for Des(1-3) IGF-1 specifically. The ClinicalTrials.gov database returned no intervention entries, FDA product databases returned no match, and the peptideprotocolwiki.com source explicitly states the complete absence of human safety data. The preclinical evidence consists of well-characterized biochemistry (Ballard et al. 1996, PMID 8930132), general IGFBP biology (Firth et al. 2002, PMID 12466191), and animal anabolic studies (Tomas et al. 1992, PMID 1371669). Full-length recombinant IGF-1 (mecasermin) has clinical data, but the truncated Des(1-3) variant has never been tested in a formal human clinical trial. All human usage data comes from anecdotal community reports.
Ballard FJ et al. - Int J Biochem Cell Biol (1996) - review - N/A (review article)
Comprehensive review characterizing Des(1-3) IGF-1 as a truncated form of IGF-1 with markedly reduced affinity for IGF binding proteins, resulting in substantially increased bioactivity compared to intact IGF-1. Established the approximately 10-fold potency enhancement. Primary scientific source for Des(1-3) IGF-1 characterization.
Limitations: Review article, not primary experimental data. Published in 1996; field has advanced since then.
Tomas FM et al. - Biochem J (1992) - animal study - Rat study (sample size not specified in available source data)
Demonstrated that IGF-1 variants including Des(1-3) IGF-1 exhibit enhanced anabolic effects compared to native IGF-1 in dexamethasone-treated rats, showing superior nitrogen retention and muscle-sparing properties in a catabolic state.
Limitations: Animal study only. Dexamethasone-induced catabolic model may not directly translate to healthy human physiology.
Firth SM, Baxter RC - Endocrine Reviews (2002) - review - N/A (narrative review)
IGFBPs can sequester IGFs away from the type I IGF receptor or concentrate them near receptors, providing the fundamental biological context for why reduced IGFBP binding (as in Des(1-3) IGF-1) would increase IGF bioavailability.
Limitations: Not a Des(1-3) IGF-1 study specifically. General IGFBP biology review.
Not fully specified in source extract - Cells (MDPI) (2020) - review - N/A (review article)
Comprehensive review of IGF-1 signaling in skeletal muscle covering PI3K/Akt and MAPK/ERK pathways, satellite cell activation, protein synthesis regulation, and the role of IGF binding proteins. Notes that IGF-1 extends satellite cell replicative lifespan via PI3K/Akt signaling.
Limitations: Covers general IGF-1 biology, not Des(1-3) IGF-1 specifically. Review article synthesizing preclinical data.
Guan J, Gluckman PD - Br J Pharmacol (2009) - review - N/A (review article)
Provided evidence that the bioactivity of IGF-1 is mediated via different modes of action through its two cleavage products, including the N-terminal tripeptide GPE (Gly-Pro-Glu) and the Des(1-3) fragment. Confirms Des(1-3) IGF-1 as a naturally occurring cleavage product in brain tissue.
Limitations: Review focused on neuroprotection, not muscle growth. Primarily covers preclinical data.
Bailes J, Soloviev M - Biomolecules (2021) - review - N/A (narrative review)
Comprehensive review of IGF-1 biology, monitoring, and misuse detection. Discusses detection of IGF-1 misuse in athletes including biochemical markers for rhIGF-1 administration. Provides sports anti-doping context relevant to Des(1-3) IGF-1.
Limitations: Review article. IGF-1 DES is mentioned contextually but is not the primary focus. Only metadata was available in the permitted source set.
Esteve Pharmaceuticals, S.A. - ClinicalTrials.gov (2009) - registry - Not stated in provided excerpt
Comparator context only. Tracks mecasermin (Increlex) at 40-120 mcg/kg twice daily in severe primary IGF-1 deficiency. Demonstrates that human IGF-1 therapeutics exist but involve a different drug from Des(1-3) IGF-1.
Limitations: NOT a Des(1-3) IGF-1 trial. Manufacturer-sponsored registry for a different compound.