Peptide Evidence Index

IGF-1 LR3

Evidence last reviewed: September 2026

Quick answers

What is it?: IGF-1 LR3 is a laboratory-re-engineered version of insulin-like growth factor 1 (IGF-1), a growth factor the body already makes. One amino acid is swapped and 13 more are added so the body's normal binding proteins can't latch onto it, making it longer-acting and more potent than natural IGF-1.
Why are people interested in it?: It's marketed for muscle growth and fat loss, and its potency makes it attractive to people wanting stronger effects than natural IGF-1 — but no human being has ever been studied taking it, in any published record.
What has actually been studied?: Exclusively mice, rats, sheep, cattle, and cell- or yeast-based lab systems, for purposes ranging from Alzheimer's pathology and cancer cachexia to lactation and manufacturing efficiency — never a human trial of any kind.
How strong is the evidence?: None. This is a complete absence of human evidence, not just thin evidence — no dose, safety profile, or outcome has ever been documented in a person.
What don't we know yet?: Whether IGF-1 LR3 has ever been given to a human being in any documented setting, and whether its longer-acting, harder-to-bind design makes it more dangerous than natural IGF-1, given IGF-1's role in cell growth and division.
Where can I read the original research?: Sources at the bottom of this page: Engel et al., Journal of Alzheimer's Disease 2024; Levolger et al., Scientific Reports 2019.

Plain-English overview

IGF-1 LR3 is not a natural hormone — it is insulin-like growth factor 1 (IGF-1), a growth factor the body already produces under the control of growth hormone, deliberately re-engineered in a laboratory. One amino acid is swapped and thirteen more are added to the front of the molecule, changes designed to stop the body's IGF-binding proteins from grabbing hold of it, making it act longer and more potently than natural IGF-1. It has never been approved as a medicine anywhere, and it is prohibited at all times in competitive sport by the World Anti-Doping Agency. Every study located for this review — in mice, rats, sheep, cattle, or laboratory cell and yeast-expression systems — was designed around a specific animal-research question, not around testing IGF-1 LR3 as a product for people. No clinical trial of IGF-1 LR3 is registered on ClinicalTrials.gov, and no published human study of any kind was found. That absence of any human data at all is the single most important thing to know about this compound.

What researchers are studying it for

muscle preservation in cancer cachexia (animal)
cognitive/Alzheimer's pathology (animal)
lactation (animal)
cardiac and reproductive cell signaling (animal, in vitro)

Current evidence level

Animal only

Regulatory status: Not an approved medicine. Evidence strength and approval are scored separately; approval is a regulatory decision about a specific use, not a measure of how much research exists.

Human research

None. No trial of IGF-1 LR3 is registered on ClinicalTrials.gov, and no published study — a case report, a Phase 1 safety trial, or anything else — describing IGF-1 LR3 given to a human being could be located. This is a more complete absence than 'early' or 'thin' evidence; it is the total absence of any human research record for this compound. No human dose, safety profile, or effect of any kind has ever been documented.

Animal and preclinical research

In a mouse model of Alzheimer's disease (5XFAD mice), 7 months of intranasal IGF-1 LR3 treatment improved body composition and reduced some measures of amyloid plaque burden in the brain, but failed to preserve cognitive or memory function, the study's main goal. In a separate mouse model of cancer-related muscle wasting (cachexia), IGF-1 LR3 limited muscle loss — but at the cost of accelerating tumor growth in the same animals, a trade-off the study's authors reported directly. In lactating mice, IGF-1 LR3 modestly increased milk production and altered mammary-gland gene expression. In cultured bovine ovarian follicles, IGF-1 LR3 increased follicle growth and estrogen production, but at higher concentrations was also linked to more oocyte degeneration than physiological levels of natural IGF-1. In fetal sheep heart cells studied outside the body, IGF-1 LR3 stimulated cell division through the same growth-signaling pathways (ERK and PI3K) that natural IGF-1 uses. Separately, IGF-1 LR3 has been produced in yeast (Pichia pastoris) as a manufacturing exercise to make production more efficient — a lab-production study, not a biological or human study.

Major findings

In an Alzheimer's mouse model, 7 months of IGF-1 LR3 improved body composition and reduced some measures of brain amyloid plaque, but did not preserve cognitive function, the study's primary goal.
In a mouse cancer-cachexia model, IGF-1 LR3 limited muscle loss but accelerated tumor growth in the same animals — a direct, reported trade-off.
In lactating mice, IGF-1 LR3 modestly increased milk production.
In cultured bovine ovarian follicles, IGF-1 LR3 increased follicle growth and estrogen production, but was linked to more oocyte degeneration at higher concentrations.
In fetal sheep heart cells outside the body, IGF-1 LR3 stimulated cell division through the same signaling pathways used by natural IGF-1.
IGF-1 LR3 has been manufactured in a yeast expression system (Pichia pastoris) with bioactivity comparable to standard IGF-1, a production study rather than a biological one.
No clinical trial or published human study of IGF-1 LR3, of any kind, could be located.

What has not been established

Whether IGF-1 LR3 has ever been given to a human being in any documented, published setting.
Whether its longer-acting, harder-to-bind design makes it more dangerous than natural IGF-1, given IGF-1's established role in promoting cell growth and division.
Whether the cachexia-model trade-off — less muscle loss, faster tumor growth — has any relevance to a healthy person using it for muscle gain.
What an effective or safe human dose would even look like, since none has been tested.
What purity or content an unregulated vial sold online actually contains.

Important limitations

There is no human research of any kind to evaluate — every finding here comes from a different species or an isolated cell system.
The studies that do exist were each designed around a narrow animal-research question (cachexia, memory, lactation, fertility, manufacturing) rather than around testing the compound broadly.
The cachexia-model finding of accelerated tumor growth alongside preserved muscle is a specific and concerning trade-off that has not been explored further.
Every human dosing figure in circulation is an animal-to-human weight conversion that has never itself been tested.

Regulatory status

IGF-1 LR3 is not approved as a medicine anywhere. It has never been tested in a registered human trial and is sold only as an unregulated laboratory research chemical. It is prohibited at all times by the World Anti-Doping Agency as an IGF-1 and analogue (category S2).

Primary research sources

Engel MG, Narayan S, Cui MH, et al., "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": Journal of Alzheimer's Disease 2024; PMID 39610283, DOI 10.1177/13872877241299056
Levolger S, Wiemer EAC, van Vugt JLA, et al., "Inhibition of activin-like kinase 4/5 attenuates cancer cachexia associated muscle wasting": Scientific Reports 2019; PMID 31285507, DOI 10.1038/s41598-019-46178-9
Hadsell DL, Parlow AF, Torres D, George J, Olea W, "Enhancement of maternal lactation performance during prolonged lactation in the mouse by mouse GH and long-R3-IGF-I": Journal of Endocrinology 2008; PMID 18577570, DOI 10.1677/JOE-07-0556
Thomas FH, Campbell BK, Armstrong DG, Telfer EE, "Effects of IGF-I bioavailability on bovine preantral follicular development in vitro": Reproduction 2007; PMID 17636166, DOI 10.1530/REP-06-0382
Sundgren NC, Giraud GD, Schultz JM, Lasarev MR, Stork PJS, Thornburg KL, "Extracellular signal-regulated kinase and phosphoinositol-3 kinase mediate IGF-1 induced proliferation of fetal sheep cardiomyocytes": American Journal of Physiology - Regulatory, Integrative and Comparative Physiology 2003; PMID 12947030, DOI 10.1152/ajpregu.00232.2003
Lu Z, Liu N, Huang H, et al., "Recombinant expression of IGF-1 and LR3 IGF-1 fused with xylanase in Pichia pastoris": Applied Microbiology and Biotechnology 2023; PMID 37261455, DOI 10.1007/s00253-023-12606-0
Dominikowski A, Rękoś Z, Olejarz M, et al., "The emerging landscape of performance-enhancing peptides modulating the GH-IGF1 axis" (review including IGF-1 LR3 among unregulated self-administered peptides): Frontiers in Endocrinology 2026; PMID 42395176, DOI 10.3389/fendo.2026.1822475

Full evidence entry (complete data, registry records, dosing evidence)

Animal only

Studied in animals; human evidence absent or minimal

At a glance

Also known as: Long R3 IGF-1, LR3-IGF-1, Long R3 Insulin-like Growth Factor 1
Class: Laboratory-modified analogue of insulin-like growth factor 1 (IGF-1)
Derived from: Human IGF-1 with a substituted arginine at position 3 and a 13-amino-acid extension added to the front of the molecule, engineered so that IGF-binding proteins in the blood cannot latch onto it — intended to keep more of it active for longer than natural IGF-1
Registered human trials: 0
…with published results: 0
Largest human trial: None identified. Every study of LR3-IGF-1 located in this review was conducted in mice, rats, sheep, or cattle, or in laboratory cell and yeast-expression systems — not in people.
Studied for: muscle preservation in cancer cachexia (animal), cognitive/Alzheimer's pathology (animal), lactation (animal), cardiac and reproductive cell signaling (animal, in vitro)
Dosing evidence: No human dose establishedNo human study of IGF-1 LR3, at any dose, could be located. Every dosing figure that exists in the scientific literature comes from mice, rats, sheep, or cattle.
Regulatory status: Not approved as a medicine anywhere. IGF-1 LR3 has never been tested in a registered human trial and is sold only as an unregulated laboratory research chemical.
Anti-doping status: Prohibited at all times by the World Anti-Doping Agency, as an IGF-1 and analogue (S2)

What it is

IGF-1 LR3 is not a natural hormone. It's a version of insulin-like growth factor 1 (IGF-1) — a growth factor the body already produces, largely under the control of growth hormone — that has been deliberately re-engineered in a laboratory. One amino acid is swapped and thirteen more are added to the front of the molecule, changes designed to stop the body's natural IGF-binding proteins from grabbing hold of it. The idea is a longer-acting, more potent version of IGF-1.

It is not approved as a medicine anywhere, and it is prohibited in competitive sport at all times.

What the studies actually found

The published research on IGF-1 LR3 is exclusively preclinical — and spans an unusually wide range of species and purposes for a single compound. In mice, it improved body composition but failed to protect against memory and thinking decline in an Alzheimer's disease model. In a separate mouse model of cancer-related muscle wasting (cachexia), it limited muscle loss — but at the cost of accelerating tumor growth, a real and concerning trade-off reported in the same study. In lactating mice, it modestly increased milk production. In cattle ovarian tissue and fetal sheep heart cells studied outside the body, it activated cell growth and division pathways, as expected for an IGF-1-like molecule.

Across all of it, one pattern holds: every study was designed around a specific animal-research question — cachexia, memory, lactation, cell signaling — not around testing IGF-1 LR3 as a product for people.

What exists in humans

None. No clinical trial of IGF-1 LR3 is registered on ClinicalTrials.gov, and this review could not locate a single published study — of any size, design, or purpose — that gave IGF-1 LR3 to a human being. The compound has also been produced in yeast (Pichia pastoris) as a manufacturing exercise, to make production more efficient — a lab-production study, not a human study.

Every fact known about IGF-1 LR3 comes from mice, rats, sheep, cattle, or cells in a dish. That is the single most important thing to know about this compound before considering it.

What doses have been studied in humans

No human dose of any kind, for any purpose, has been studied or published. This section exists in every profile on this site because it's usually possible to say something about what dosing evidence does or doesn't exist — for IGF-1 LR3, the honest answer is that there is no human dosing evidence to describe at all.

Every number that circulates online for IGF-1 LR3 — for injury recovery, muscle growth, or fat loss — traces back to an animal study: a dose given to a mouse, rat, sheep, or cow, scaled to a human's body weight using a standard conversion formula. That conversion estimates a comparable exposure between a person and an animal. It says nothing about whether the resulting amount does anything in a person, or whether it's safe — because no one has published a study that gave any dose of this compound to a human being and reported what happened.

What remains unknown

Whether IGF-1 LR3 has ever been given to a human being in any documented, published setting
Whether its longer-acting, harder-to-bind design makes it more dangerous than natural IGF-1, given IGF-1's established role in promoting cell growth and division
Whether the cachexia-model trade-off — less muscle loss, faster tumor growth — has any relevance to a healthy person using it for muscle gain
What an effective or safe dose would even look like, since none has been tested
What purity or content an unregulated vial sold online actually contains

Registry and study records

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: PubMed · DOI: 10.1177/13872877241299056 — mice only, 7-month treatment, failed its cognitive endpoint
Inhibition of activin-like kinase 4/5 attenuates cancer cachexia associated muscle wasting: PubMed · DOI: 10.1038/s41598-019-46178-9 — mice; LR3 IGF-1 limited muscle loss but accelerated tumor growth in a cachexia model
Enhancement of maternal lactation performance during prolonged lactation in the mouse by mouse GH and long-R3-IGF-I...: PubMed · DOI: 10.1677/JOE-07-0556 — mice only
Effects of IGF-I bioavailability on bovine preantral follicular development in vitro: PubMed · DOI: 10.1530/REP-06-0382 — cattle ovarian tissue, in vitro
Extracellular signal-regulated kinase and phosphoinositol-3 kinase mediate IGF-1 induced proliferation of fetal sheep cardiomyocytes: PubMed · DOI: 10.1152/ajpregu.00232.2003 — sheep, fetal heart cells

See the full Evidence Index →

Evidence last reviewed: September 2026. Peptide Proof reports what studies found. We do not give medical advice, dosing guidance, or treatment recommendations.