IGF-1 LR3

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Long R3 IGF-1 — ~3x more potent than native IGF-1 with an extended 20–30 hour half-life for muscle-growth research.

A 83-residue analog of insulin-like growth factor 1 with an N-terminal 13-residue extension and an Arg³ substitution characterised in the primary literature as reducing binding to IGF-binding proteins while retaining IGF-1 receptor activity in in-vitro assays. For laboratory characterisation only.

IGF-1 LR3 is a synthetic 83-amino-acid IGF-1 analog with an Arg3 substitution and 13-aa N-terminal extension that reduces IGFBP binding, extending half-life from ~15 min to 20-30 hours. Activates PI3K/Akt/mTOR pathway for protein synthesis while suppressing FoxO-mediated ubiquitin-proteasome degradation via GSK3β inhibition.

In-vitro autophosphorylation assays on isolated IGF-1 receptor report full agonism by LR3-IGF-1 with potency comparable to native IGF-1.

The Arg³ substitution is described in the primary literature as reducing affinity for IGFBP-1, -2, -3, and -5 relative to native IGF-1, extending in-vitro receptor availability.

In-vitro / preclinical characterisation only — no clinical or therapeutic claim is expressed or implied. Research use only.

IGF-1 LR3 is a synthetic 83-amino-acid IGF-1 analog with an Arg3 substitution and 13-aa N-terminal extension that reduces IGFBP binding, extending half-life from ~15 min to 20-30 hours. Activates PI3K/Akt/mTOR pathway for protein synthesis while suppressing FoxO-mediated ubiquitin-proteasome degradation via GSK3β inhibition. It has a molecular formula C400H625N111O115S9, mass 9111.2 Da. Common synonyms in the literature include Long R3 IGF-1, Long arginine 3-IGF-1, and LR3-IGF-1.

Investigation of IGF-1 LR3 to date is primarily preclinical, with the majority of citations concentrated in animal models and in-vitro assays rather than randomized controlled human trials. Published work referencing IGF-1 LR3 spans Cell culture applications: IGF-1 LR3 is widely used in research cell culture media as a growth factor supplement. Its extended stability and higher bioactivity compared to native IGF-1 make it valuable for maintaining cells in serum-free or reduced-serum conditions, Skeletal muscle research: Animal studies have examined IGF-1 LR3's effects on muscle protein synthesis, satellite cell activation, and muscle hypertrophy. Research demonstrates activation of PI3K/Akt/mTOR pathways leading to increased protein synthesis and reduced protein degradation, and IGFBP binding studies: Structural research has characterized IGF-1 LR3's dramatically reduced affinity for all six IGF-binding proteins. This allows investigation of IGF-1R signaling without the confounding effects of IGFBP-mediated regulation. Proposed mechanisms in the literature include IGF-1R activation: binds IGF-1 receptor tyrosine kinase, triggering autophosphorylation and IRS-1 recruitment and PI3K/Akt cascade: activates protein synthesis via mTOR, S6K1, 4E-BP1; increases ribosome biogenesis. None of this material describes therapeutic outcomes in humans, and No vendor listed here provides dosing guidance for IGF-1 LR3 outside laboratory research.

For the full mechanistic profile, published references, and constraint notes on IGF-1 LR3, see the IGF-1 LR3 research page. All references cited on that page are peer-reviewed primary literature.

Binding and functional-assay data for IGF-1 LR3, from peer-reviewed in-vitro pharmacology publications. Values are receptor activity parameters — not clinical outcomes.

Study designs referencing this compound in the published literature. Descriptions cover framework only — phase, participant count, duration, and citation — not outcomes. Click a card to review the source directly.