IGF-1 LR3

Origin and structure

IGF-1 LR3 is a laboratory-made variant of insulin-like growth factor 1 (IGF-1), the growth factor that the liver and other tissues release in response to growth hormone and that relays many of its effects. Natural IGF-1 is a single chain of 70 amino acids. LR3 changes it in two places: the glutamic acid at position 3 is replaced by arginine (the "R3"), and a 13-amino-acid extension is added at the front, made of an 11-residue stretch from the start of pig growth hormone and a two-residue linker. The result is 83 amino acids long. The "Long" in the name refers to that extension, not to how long the molecule lasts.

It was made by Francis, Ballard and colleagues at the Cooperative Research Centre for Tissue Growth and Repair and the CSIRO Division of Human Nutrition in Adelaide, Australia, and described in 1992 as one of several variants built to test a question: is IGF-1's activity held back by the binding proteins that carry it in the blood? Their experiments showed that it is. A sibling variant from the same work, des(1-3)IGF-1, takes the opposite route and lacks the first three amino acids; in cell culture the two were about equally potent. LR3 was never developed into a medicine. It is sold as a laboratory reagent, for cell culture and animal research, and outside the lab it circulates as an unlicensed performance drug.

How it is thought to work

LR3 acts on the same target as IGF-1: the type 1 IGF receptor, found on muscle, bone, gut and most other cells, which drives cell growth and division and, like insulin, moves glucose into tissues. What differs is access. Most of the body's own IGF-1 circulates in a complex with the binding protein IGFBP-3 and a third protein, which keeps it in the blood and releases it slowly. LR3 binds the binding proteins about 1,000 times less well than IGF-1, so far more of it is free to reach the receptor. How much more depends on the species: in a 1994 test-tube comparison by the same Adelaide group, the variants bound very weakly in rat plasma but clearly in human plasma.

That, not a stronger grip on the receptor, explains its potency. LR3 binds the receptor itself about three times less well than IGF-1, and in chick cells that make no binding proteins it was weaker than IGF-1. Where binding proteins are present the picture flips: it was 5 to 10 times as potent in rat muscle cells, about 2.5 times as potent in rats made catabolic with a steroid, 6 times as potent for growth in normal rats, and 2 to 3 times as potent at lowering blood sugar in pigs.

Despite the name, it is not cleared slowly. In rats it left the blood much faster than IGF-1, because nothing holds it there, although in pigs its blood-sugar lowering lasted longer than that of IGF-1. Nobody has measured how long it stays in human blood, so the half-lives of 20 to 30 hours quoted online have no published source. Like IGF-1, it also feeds back on the pituitary: in pigs, four days of LR3 cut the area under the growth-hormone peaks by 60% and lowered the animals' own IGF-1.

Is IGF-1 LR3 approved?

No. No medicines regulator has authorised IGF-1 LR3 for use in people, and it is not an ingredient of any licensed medicine. In the Netherlands it is not a registered medicine, so it may not be sold or promoted for use in people. Selling it as research material is a different status.

The approved form of IGF-1 is mecasermin, sold as Increlex: recombinant IGF-1 with exactly the natural 70-amino-acid sequence. Its approvals cover that molecule only, not LR3.

• EU: Increlex was authorised on 3 August 2007, under exceptional circumstances because the disease is too rare for complete data to be collected, for the long-term treatment of growth failure in children and adolescents aged 2 to 18 with severe primary IGF-1 deficiency. It is a medicine on restricted prescription, in the Netherlands as elsewhere in the EU; the marketing authorisation is held by Esteve Pharmaceuticals.
• US: Increlex has been approved since 2005; the label covers children from 2 years with severe primary IGF-1 deficiency or with a growth-hormone gene deletion and neutralising antibodies to growth hormone. IGF-1 LR3 has no FDA approval.
• Sport: the WADA Prohibited List names "insulin-like growth factor 1 (IGF-1, mecasermin) and its analogues" in class S2.3, growth factors, prohibited in and out of competition. The Netherlands publishes the list in the Tractatenblad as an appendix to the Council of Europe anti-doping convention; the 2026 list appeared as Tractatenblad 2026, no. 25.

What the research shows

There are no human data on IGF-1 LR3. No clinical trial has been published, none is registered on ClinicalTrials.gov, and no study has measured how the body handles it in people. Everything below comes from cells and animals, much of the early work from the Adelaide group that made it, and the results depend heavily on the species and the model. None of it tests muscle growth in healthy, well-fed adults.

• Catabolic rats (Tomas et al., 1992): in rats losing weight on the steroid dexamethasone, IGF-1 partly reversed the losses, and LR3 did so at about 2.5 times lower doses, raising muscle protein synthesis and slowing muscle protein breakdown.
• Normal rats (Ballard et al., 1993): over 14 days LR3 raised body weight, nitrogen retention and feed efficiency at a sixth of the IGF-1 dose, and kept the gut, spleen and thymus at the relatively larger size typical of younger animals.
• Pigs (Dunaiski et al., 1997): the opposite result. A four-day infusion of 180 µg/kg per day reduced daily weight gain and food intake, cut the area under the growth-hormone peaks by 60% and lowered the animals' own IGF-1, IGFBP-3 and insulin.
• Pigs (Tomas et al., 1997): single injections of 20 or 50 µg/kg lowered blood sugar 2 to 3 times more potently than IGF-1, and the variants kept it down for longer.
• Mice with cancer (Levolger et al., Erasmus MC Rotterdam, 2019): in mice carrying C26 colon tumours, a model of cancer-related muscle wasting, LR3 limited the loss of muscle mass, but the tumours grew faster.

IGF-1 LR3 versus mecasermin: what carries over

Mecasermin is the natural IGF-1 sequence and has two decades of clinical use behind it; LR3 is a different molecule with none. Because both act on the same receptor, some of what is known about mecasermin applies to LR3. Much of it does not.

What carries over are the effects of the receptor itself. Across 413 trial patients, the EU product information for Increlex reports headache in 44%, low blood sugar in 28%, vomiting in 26%, thickening at injection sites in 17% and ear infections in 17%, with raised pressure inside the skull in about 1%. The US label counts low blood sugar in 42% of 71 children, including seizures, and both labels warn about enlarged tonsils and adenoids. Both rule it out in people with cancer, and the EU text warns of an increased risk of benign and malignant tumours, possibly higher with unapproved use or doses above the label. The animal data on LR3 point the same way: stronger blood-sugar lowering than IGF-1 in pigs and faster tumour growth in mice.

What does not carry over is the dose, the safety record and the benefit. Increlex is dosed per kilogram in children with a hormone defect; LR3 was 2 to 6 times as potent as IGF-1 in animals and behaves differently in blood, so mecasermin doses say nothing about LR3. The benefit of Increlex is height in children who cannot make IGF-1: in the five studies summarised in the EU product information, growth rose from 2.6 to 8.0 cm a year in the first year, and 21 children followed to near-adult height ended about 13 cm taller than expected after an average of 11 years of treatment. In adults, IGF-1 has not shown the muscle effect LR3 is sold for. In a year-long randomised trial in 16 healthy women over 60, IGF-1 raised blood levels into the young range but did not change lean mass, fat mass or strength compared with placebo; in a two-year placebo-controlled trial in 330 people with ALS it did not slow the loss of muscle strength; and in seven obese people with type 2 diabetes, 120 to 160 µg/kg twice daily gave all of them side effects, among them swelling of the face and hands, jaw pain, joint and muscle pain and a racing heart, and the treatment was stopped early.

Frequently asked questions

Is IGF-1 LR3 the same as mecasermin (Increlex)?

No. Mecasermin is IGF-1 with the natural 70-amino-acid sequence, a licensed medicine for children with severe primary IGF-1 deficiency, made and tested under pharmaceutical rules. IGF-1 LR3 has 83 amino acids, a different amino acid at position 3 and an extension at the front, and has never been tested in people. Research-grade IGF-1 LR3 is a lyophilised peptide sold for laboratory use; its identity and purity are what a certificate of analysis says, nothing more, and it may not be used in people.

Is IGF-1 LR3 legal in the Netherlands?

It is not a registered medicine in the Netherlands or anywhere else in the EU, so it may not be sold or advertised for use in people; it is sold only as research material. The IGF-1 medicine authorised in the EU, Increlex, is on restricted prescription and licensed only for children with a rare growth disorder. In sport it is prohibited at all times.

Is IGF-1 LR3 banned in sport?

Yes, in and out of competition. The WADA Prohibited List names IGF-1, including mecasermin, and its analogues in class S2.3, growth factors, and IGF-1 LR3 is such an analogue. In the Netherlands the list is published in the Tractatenblad; the 2026 version is Tractatenblad 2026, no. 25.

How long does IGF-1 LR3 stay in the body?

In people, nobody knows: it has never been measured. In rats it was cleared from the blood much faster than IGF-1, because it does not shelter in the binding-protein complex, while in pigs its blood-sugar lowering lasted longer than that of IGF-1. The half-lives of 20 to 30 hours often quoted online have no published source. For comparison, the half-life of mecasermin in children with IGF-1 deficiency is about 5.8 hours.

Does IGF-1 LR3 build muscle?

That has never been tested in people. In rats it countered muscle loss and boosted growth; in pigs it reduced growth; in mice with cancer it limited muscle loss but sped up the tumours. In a placebo-controlled trial, natural IGF-1 given to healthy older women for a year did not change their lean mass or strength.

Storage and handling

Store according to product-label instructions and batch handling notes. Lyophilized research peptides are commonly kept dry, protected from light, and handled with clean laboratory technique.

References

Checked against these sources on 28 October 2026.

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