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IGF-1 LR3

Modified insulin-like growth factor 1 analogue

Also known as Long R3 IGF-1, Mecasermin analogue (unapproved)

A cell-culture reagent, engineered to evade the binding proteins that regulate IGF-1 in the body. That modification is exactly why it should not be administered to people.

Guide updated Sep 2, 2026Literature checked Sep 2, 20261 curated study15 literature recordsBaseline editorial

This entry is preclinical

There is no completed human trial reporting results for this compound. Everything below describes what has been observed in animals or in cell culture, and the transfer rate from those findings to humans is poor. Read the limitations on each study, not just the findings.

Overview

In shortA modified version of IGF-1 designed as a lab reagent for cells in a dish. The modifications stop it being caught by the proteins that normally hold IGF-1 in check, so a predictable amount reaches the cells. That design goal is the entire safety problem: those proteins are how your body keeps free IGF-1 in a narrow range, and this was built to escape them.

IGF-1 LR3 is a modified IGF-1 with an arginine substitution and a 13-residue N-terminal extension. It was designed as a cell culture reagent: the modifications reduce binding to IGF binding proteins so that a predictable concentration reaches cells in a dish.

That design goal is the entire safety problem. IGF binding proteins are how the body keeps free IGF-1 within a narrow range, and a molecule engineered to escape them is engineered to escape the regulation. Nothing about it was designed for administration to a person, and no regulator has ever evaluated it for that.

Approved IGF-1 therapy exists, as mecasermin, for severe primary IGF-1 deficiency. It is administered under close supervision with glucose monitoring, and it is a different molecule.

Mechanism

In shortIGF-1 tells cells to grow, multiply and survive, and it also acts on the insulin receptor, which is why it can drop blood sugar. Normally 98% or more of what circulates in you is bound up by carrier proteins that limit how much is available. The modifications here largely remove that limit, producing something longer-acting and far less regulated.

IGF-1 signals through the IGF-1 receptor, driving cell growth, proliferation and survival, and has meaningful affinity for the insulin receptor, which is the source of its hypoglycaemic effect.

Normally 98% or more of circulating IGF-1 is bound to IGFBPs, which buffer availability and extend half-life. The LR3 modifications substantially reduce that binding, producing a longer-acting and less regulated agonist.

Evidence

In shortA lab reagent only. There is no human trial of it for anything and there is not going to be one. Evidence about the approved IGF-1 medicine, which is a different molecule given under close supervision with blood sugar monitoring, is not evidence about this one, and that substitution is made constantly.

Preclinical only, in the specific sense that it is a laboratory reagent rather than a candidate. There is no human trial of IGF-1 LR3 for any indication and there is not going to be one.

Evidence about approved mecasermin in IGF-1 deficiency is not evidence about this molecule, and the substitution is made constantly.

Safety

In shortThis is the section that matters. The immediate risk is dangerously low blood sugar, because it also acts on the insulin receptor, and escaping the carrier proteins widens the window in which that can happen. The long-term risk is cell growth: higher IGF-1 has repeatedly been linked to several cancers. This is a known mechanism pointed in a bad direction.

This is the section that matters.

Hypoglycaemia is the acute risk, through insulin receptor cross-reactivity, and it can be severe. The reduced binding protein interaction extends the window in which it can occur.

Mitogenicity is the chronic one. IGF-1 signalling promotes cell proliferation and inhibits apoptosis, and epidemiological work has repeatedly associated higher circulating IGF-1 with increased risk of several cancers. Deliberately raising unbound IGF-1 signalling for a sustained period is not a neutral unknown; it is a known mechanism pointed in a bad direction.

Reagent-grade material carries no sterility, endotoxin or identity assurance for human use, because it was never intended for it. Prohibited in sport under WADA's S2 category.

Regulatory status

In shortNever approved for human use anywhere, and not a candidate for approval. Sold as a laboratory reagent. Banned in sport.

Never approved for human use anywhere and not a candidate for approval. Sold as a laboratory reagent. Prohibited in sport.

The literature

1 study indexed. Findings and limitations get equal weight, on purpose.

Always check the primary source

Members area

The IGF-1 LR3 literature needs an account

Everything above is free to read. What an account opens is the evidence underneath it: 1 study with their limitations, and the regimen each trial actually reported.

  • Every study, with what it found and what it cannot show
  • The limitations, given the same weight as the findings
  • The dose each named trial administered, where recorded
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The wider literature

15 indexed papers and 0 registered trials mentioning IGF-1 LR3, straight from PubMed and ClinicalTrials.gov. These have not been read by us. Unlike the studies above, they carry no findings and no limitations written by anyone here, because writing either would mean claiming a reading nobody has done. They are a starting point for yours.

Papers (15)

  1. The emerging landscape of performance-enhancing peptides modulating GH-IGF1 axis: bridging the gap between clinical evidence and patient self-administration.

    Dominikowski A, et al.Frontiers in endocrinology2026PMID 42395176

    journal articlereview

  2. IGF-1 LR3 does not promote growth in late-gestation growth-restricted fetal sheep.

    White A, et al.American journal of physiology. Endocrinology and metabolism2025PMID 39679943

    journal article

  3. Revolutionary decellularized Alstroemeria stem-based nerve conduit integrated with GelMA and controlled IGF-1 LR3 release for enhanced rat sciatic nerve regeneration.

    Yavuz E, et al.International journal of biological macromolecules2025PMID 41015370

    journal article

  4. Intranasal long R3 insulin-like growth factor-1 treatment promotes amyloid plaque remodeling in cerebral cortex but fails to preserve cognitive function in male 5XFAD mice.

    Engel MG, et al.Journal of Alzheimer's disease : JAD2025PMID 39610283

    journal articleresearch support, non-u.s. gov'tresearch support, n.i.h., extramural

  5. Attenuated glucose-stimulated insulin secretion during an acute IGF-1 LR3 infusion into fetal sheep does not persist in isolated islets.

    White A, et al.Journal of developmental origins of health and disease2023PMID 37114757

    journal articleresearch support, n.i.h., extramural

  6. Recombinant expression of IGF-1 and LR3 IGF-1 fused with xylanase in Pichia pastoris.

    Lu Z, et al.Applied microbiology and biotechnology2023PMID 37261455

    journal article

  7. N-Linked Glycosylation in Chinese Hamster Ovary Cells Is Critical for Insulin-like Growth Factor 1 Signaling.

    Salvi R, et al.International journal of molecular sciences2022PMID 36499281

    journal article

  8. IGF-1 infusion to fetal sheep increases organ growth but not by stimulating nutrient transfer to the fetus.

    Stremming J, et al.American journal of physiology. Endocrinology and metabolism2021PMID 33427051

    journal articleresearch support, n.i.h., extramural

  9. Reduced glucose-stimulated insulin secretion following a 1-wk IGF-1 infusion in late gestation fetal sheep is due to an intrinsic islet defect.

    White A, et al.American journal of physiology. Endocrinology and metabolism2021PMID 33938236

    journal articleresearch support, n.i.h., extramural

  10. Coronary vascular growth matches IGF-1-stimulated cardiac growth in fetal sheep.

    Jonker SS, et al.FASEB journal : official publication of the Federation of American Societies for Experimental Biology2020PMID 32573852

    journal articleresearch support, n.i.h., extramural

  11. IGF-1 has plaque-stabilizing effects in atherosclerosis by altering vascular smooth muscle cell phenotype.

    von der Thüsen JH, et al.The American journal of pathology2011PMID 21281823

    journal articleresearch support, non-u.s. gov't

  12. Novel insulin-like growth factor-methotrexate covalent conjugate inhibits tumor growth in vivo at lower dosage than methotrexate alone.

    McTavish H, et al.Translational research : the journal of laboratory and clinical medicine2009PMID 19446281

    journal articleresearch support, non-u.s. gov't

  13. Extracellular signal-regulated kinase and phosphoinositol-3 kinase mediate IGF-1 induced proliferation of fetal sheep cardiomyocytes.

    Sundgren NC, et al.American journal of physiology. Regulatory, integrative and comparative physiology2003PMID 12947030

    journal articleresearch support, non-u.s. gov'tresearch support, u.s. gov't, p.h.s.

  14. Action of long(R3)-insulin-like growth factor-1 on protein metabolism in beef heifers.

    Hill RA, et al.Domestic animal endocrinology1999PMID 10370861

    journal articleresearch support, non-u.s. gov't

  15. Insulin-like growth factor-1 (IGF-1) receptor-insulin receptor substrate complexes in the uterus. Altered signaling response to estradiol in the IGF-1(m/m) mouse.

    Richards RG, et al.The Journal of biological chemistry1998PMID 9565625

    journal article

Discussion

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For Research & Educational Discussion Only. Not Medical Advice

This guide is educational reference material compiled from published literature. It is not medical advice, not a recommendation, and not a substitute for a clinician who knows your history. Nothing here should be used to make a decision about your own health without one.

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