IGF-1 LR3

IGF-1 LR3 (Long R3 Insulin-like Growth Factor 1) is an 83-residue synthetic analog of native IGF-1 with an N-terminal 13-residue extension and an arginine substitution at position 3. The modifications reduce binding to IGF-binding-proteins (IGFBPs), extending plasma half-life dramatically.

Native IGF-1 is rapidly cleared due to high-affinity binding by IGFBP-3 and other IGFBPs. The Arg-substitution at position 3 in LR3 significantly reduces IGFBP binding, leaving more free IGF-1 available for receptor engagement. Half-life extends from ~10 minutes (native) to ~6 hours (LR3).

No. LR3 is a research-grade compound. The FDA has approved mecasermin (Increlex) — recombinant native IGF-1 — for severe primary IGF-1 deficiency. LR3 is a distinct molecule and is not approved.

Yes. IGF-1 and its analogs are prohibited at all times under WADA Section S2 (Peptide Hormones, Growth Factors, Related Substances and Mimetics).

Growth hormone (GH) is the upstream pituitary hormone. IGF-1 is the downstream effector produced primarily by the liver in response to GH. LR3-IGF-1 bypasses the GH-axis and directly engages the IGF-1 receptor — producing IGF-1-receptor effects without the broader pleiotropic GH effects.

Hypoglycemia is the most acute concern — at higher doses LR3 binds the insulin receptor with sufficient affinity to lower blood glucose. Theoretical concerns with chronic high-dose use include organ enlargement and exacerbation of active malignancy via IGF-1 axis growth signaling.

Lyophilized at 2–8 °C for 12+ months. Reconstituted at 2–8 °C, use within 14 days. Protein peptides this large are more sensitive to repeated freeze-thaw than smaller peptides; aliquot-freeze for long storage.

Both are modified IGF-1 analogs. LR3 has an N-terminal extension that reduces IGFBP binding (long half-life). DES has the opposite — a tripeptide deletion at the N-terminus that also reduces IGFBP binding but with different receptor-affinity profile and shorter half-life. They are distinct compounds.