Evidence Grade D — Primarily preclinical. 10 published studies, mostly animal models. 0 registered clinical trials.
Medically reviewed by a licensed medical professional
IGF-1 LR3 is a modified version of insulin-like growth factor 1, specifically engineered to bypass the body's natural regulation system. It was developed as a laboratory research tool and cell culture supplement — not as a therapeutic. By evading the binding proteins that normally control IGF-1 activity, it is significantly more potent and less predictable than natural IGF-1. It has no approval for human use.
IGF-1 LR3 is also known by these brand and alternate names:
10 published studies: 2 human, 8 animal, 4 in-vitro, 0 reviews
IGF-1 LR3 has no marketing authorisation for human use. It was developed as a research reagent and cell culture media supplement. No human clinical trials have been conducted. Animal studies characterised its increased potency relative to native IGF-1.
The compound's design specifically circumvents the body's natural IGF-1 regulation — the binding proteins that normally control IGF-1 activity. This means standard IGF-1 safety data cannot be extrapolated to LR3. Products available through unregulated channels lack pharmaceutical quality assurance. Unregulated IGF-1 receptor activation carries theoretical risks including hypoglycaemia.
Research indicates IGF-1 LR3 activates the IGF-1 receptor with the same potency as native IGF-1, but its modifications prevent it from being captured by the binding proteins that normally regulate IGF-1 activity in the body. This means a much higher proportion remains biologically active. The modifications that make it a useful laboratory tool also make it pharmacologically unpredictable for human use — it bypasses the body's normal IGF-1 regulatory mechanisms.
Research in animal models shows IGF-1 LR3 causes significant organ effects — gut weight increased by up to 45% in one study — and promoted tumour growth in tumour-bearing rats. The PI3K/Akt/mTOR pathway it activates is strongly linked to cancer biology. No human pharmacokinetic data, clinical trials, or long-term safety data exist. The compound was designed as a cell culture reagent, and its pharmacological profile reflects this origin — it bypasses the body's normal IGF-1 regulatory mechanisms in ways that create unpredictable effects. Products from unregulated channels lack pharmaceutical quality assurance.
PeptideTrace tracks 0 registered clinical trials for IGF-1 LR3 sourced from ClinicalTrials.gov.
No trials registered on ClinicalTrials.gov for this compound.
IGF-1 LR3 (Long-Arg3-IGF-1) is a recombinant 83 amino acid polypeptide with two critical modifications to native IGF-1 (70 amino acids): a Glu-to-Arg substitution at position 3 and a 13 amino acid N-terminal extension (sequence: MFPAMPLSSLFVN). Molecular weight is approximately 9,111-9,200 Da (CAS: 946870-92-4). These modifications dramatically reduce binding to IGF binding proteins (IGFBPs), resulting in much higher bioavailability compared to native IGF-1, which is >99% IGFBP-bound in circulation. The half-life is approximately 20-30 hours versus approximately 12-15 hours for native IGF-1. The compound was originally designed as a cell culture supplement for biopharmaceutical manufacturing. Research administration routes include subcutaneous injection, intramuscular injection, and continuous infusion via osmotic minipumps.
IGF-1 LR3 retains full agonist activity at the IGF-1 receptor (IGF-1R), a receptor tyrosine kinase. Binding triggers autophosphorylation and activation of two major downstream cascades: the PI3K/Akt/mTOR pathway (promoting protein synthesis via p70S6K1, inhibiting protein degradation via FoxO suppression of MuRF1/MAFbx, enhancing glucose uptake via GLUT4 translocation, and providing anti-apoptotic signaling) and the MAPK/ERK pathway (driving cell proliferation and differentiation). Because virtually all administered LR3 exists as free, unbound peptide, it produces sustained receptor activation far exceeding that of equivalent doses of native IGF-1. Research suggests it is approximately 3x more potent than native IGF-1 in vivo (Tomas et al., 1992).
The landmark study by Tomas et al. (1992, Biochem J) in dexamethasone-treated rats demonstrated that LR3-IGF-I was approximately 2.5-fold more potent than native IGF-I at promoting weight gain and reducing muscle breakdown markers (3-methylhistidine excretion decreased from 83.5 +/- 4.2 to 65.1 +/- 2.2 umol/kg over 7 days). The same study showed gut weight increases of up to 45%, a notable safety signal. Additional animal studies have shown plaque-stabilizing effects in atherosclerosis models and protection of dystrophic muscle from contraction-mediated damage. Cell culture bioassays show activity at concentrations < 2 ng/mL. No human clinical trials have been conducted for IGF-1 LR3. The compound is not approved by any regulatory agency and is classified as a prohibited substance by WADA.
The information on this page is provided for educational and research reference purposes only. This is not medical advice. Always consult a qualified healthcare professional before making any health-related decisions.
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This content is for informational purposes only and does not constitute medical advice. Always consult a qualified healthcare professional before making decisions about your health.
