Peptide library
Your guide to this compound.
Binding-protein differences in laboratory and animal studies may alter activity. They do not establish local muscle growth in people. Mecasermin labeling is related safety context, not approval or PK evidence for DES.
Existing source snapshot critically reassessed.
Based on the selected source scope described in this profile, often an indexed abstract. Full methods and clinician sign-off remain pending; no systematic-review claim.
Editorial assessment · 2026-09-07
Source 1 · pubmed.ncbi.nlm.nih.gov
Source 2 · pubmed.ncbi.nlm.nih.gov
Laboratory systems and rats; human tissue assays are not human dosing trials.
Experimental activity varies with binding proteins and the model. This does not establish clinical physique, recovery or site-specific growth benefits.
US: the cited INCRELEX label concerns mecasermin, not this modified IGF-1. Its authorization cannot be assigned to this derivative. A complete derivative-specific jurisdictional review remains outstanding.
Selected abstracts and a related medicine label reviewed. No derivative-matched human dosing, efficacy, PK, long-term safety or stability was verified; this is not an exhaustive clinical review.
Truncated IGF-1 with altered binding-protein interactions; cell potency is not a clinical benefit estimate.
In cell experiments, des(1–3)IGF-I interacted weakly with certain IGF-binding proteins. This reduced sequestration helped explain increased activity in those systems; it does not imply a universal increase in receptor affinity.
Binding-protein effects vary with assay.
The catalog primarily cites laboratory or animal research. Human benefit, a safe dose and long-term risks cannot be inferred from those findings.
Related mecasermin risks support precaution only; not derivative-specific rates.
The catalog primarily cites laboratory or animal research. Human benefit, a safe dose and long-term risks cannot be inferred from those findings.
Source 1 · pubmed.ncbi.nlm.nih.gov
Source 2 · pubmed.ncbi.nlm.nih.gov
IGF-1 DES is an IGF-1 derivative lacking the first three N-terminal residues, Gly-Pro-Glu. The studied truncated molecule is distinct from intact IGF-1 and from LR3; its name does not establish a site-specific muscle-growth effect.
Missing Gly-Pro-Glu; no local-growth inference.
In cell experiments, des(1–3)IGF-I interacted weakly with certain IGF-binding proteins. This reduced sequestration helped explain increased activity in those systems; it does not imply a universal increase in receptor affinity.
Binding-protein effects vary with assay.
Laboratory studies reported stronger activity in selected binding and cell-growth assays than intact IGF-1. Human physique or recovery benefits were not established in this pass.
Tissue/cell activity, not treated-human benefit.
The related mecasermin medicine label warns about severe hypoglycemia and neoplasia. This supports caution about IGF-pathway effects, but does not supply adverse-event rates for this derivative.
Related mecasermin risks support precaution only; not derivative-specific rates.
Carlsson-Skwirut C, Lake M, Hartmanis M, Hall K, Sara VR. A comparison of the biological activity of the recombinant intact and truncated insulin-like growth factor 1 (IGF-1). 1989.
PMID: 2469478
Ross M, Francis GL, Szabo L, Wallace JC, Ballard FJ. Insulin-like growth factor (IGF)-binding proteins inhibit the biological activities of IGF-1 and IGF-2 but not des-(1-3)-IGF-1. 1989.
PMID: 2539101
Gillespie CM, Hazel SJ, Walton PE, Martin AA. Effects of chronic renal failure on plasma clearance of insulin-like growth factor I, des-(1-3)IGF-I, and LR3IGF-I. 1996.
PMID: 8897852
DailyMed. INCRELEX (mecasermin), US prescribing information, revised October 2025. Related medicine only; not an LR3 or DES label. Checked September 7, 2026.
Catalog review date: Sep 7, 2026. This date alone does not establish independent clinical review.