IGF-1 LR3: what it is, what it does, side effects and evidence

Insulin-like growth factor-1 (IGF-1) is a 70-amino-acid hormone, made mainly in the liver in response to growth hormone, that drives growth and tissue building. Most IGF-1 in the blood is bound to IGF-binding proteins (IGFBPs), which limit how much reaches tissues. IGF-1 LR3 is an engineered version with two changes: the glutamic acid at position 3 is replaced by arginine, and an extension peptide derived from the first 11 amino acids of porcine growth hormone is attached to the start of the chain ^[1]. It is much larger than most peptides discussed on this site.

The name describes the changes. “Long” refers to the 13-amino-acid extension (the first 11 amino acids of methionyl porcine growth hormone followed by valine and asparagine) added to the front of the molecule, and “R3” refers to the arginine (R in the one-letter code) at position 3 ^[1]. The full IGF-1 LR3 peptide is therefore 83 amino acids long, against 70 for native IGF-1 ^[1][9]. Vendors write the name in several ways, including IGF1 LR3, IGF-1 LR3 and Long R3 IGF-I; they all describe the same molecule.

The analogue was made by researchers in Adelaide, Australia, who also studied the truncated analogue des(1-3)IGF-I, as a tool to separate the effects of receptor binding from binding-protein interactions ^[1]. It is used as a laboratory reagent ^[6]. It is also sold by research peptide vendors and on the black market as a body-composition drug, which is a use that has never been tested in controlled human studies. It is related in purpose, though not in mechanism, to growth hormone secretagogues such as CJC-1295 and ipamorelin.

IGF-1 LR3 acts on the same type 1 IGF receptor as native IGF-1, and can also act through the insulin receptor. Its main difference is that it binds IGFBPs very weakly. In cell lines that secrete these binding proteins, it was more potent than native IGF-1 at stimulating protein and DNA synthesis and at inhibiting protein breakdown; in cells that do not secrete binding proteins, it was actually less potent than IGF-1 ^[1]. It binds the type 1 IGF receptor about three times less well than IGF-1, yet in rats it was about 2.5 times more potent, which the researchers attributed to its escape from binding proteins ^[2].

Because it is not held in reserve by binding proteins, its effects in animals are stronger and longer-lasting than native IGF-1, including its insulin-like effect of lowering blood glucose ^[3].

In short, what does IGF-1 LR3 do in the body is best answered as: it acts like IGF-1 but is far less restrained by the binding proteins that normally buffer IGF-1. In human blood more than 80% of IGF-1 is carried in a complex with IGFBP-3 and a second protein, the acid-labile subunit ^[9], and that is the reserve LR3 largely escapes.

IGF-1 DES, or des(1-3)IGF-I, is native IGF-1 with its first three amino acids removed. LR3 keeps the full chain, swaps position 3 and adds the 13-amino-acid extension. Both changes achieve the same thing, weaker binding to IGFBPs, and in the original Adelaide experiments LR3 and des(1-3)IGF-I were about equally potent in cells that secrete binding proteins, ranking LR3 ≈ des(1-3) > Long Gly3 > Long IGF-I > IGF-I ^[1]. In dexamethasone-treated rats, the two analogues were likewise about 2.5 times as potent as IGF-1 ^[2]. We found no head-to-head human data for IGF-1 DES vs LR3, and anti-doping laboratories screen for both as prohibited substances ^[7].

Native IGF-1 is available as a licensed medicine, mecasermin (Increlex), which is recombinant human IGF-1 identical to the body’s own 70-amino-acid hormone ^[9]. IGF-1 LR3 has never been approved as a medicine, and the approved drug’s data cannot be transferred to it, because LR3 behaves differently in the body.

Many sellers state an IGF-1 LR3 half-life of 20 to 30 hours. We could not find any published human measurement to support that figure, because no human pharmacokinetic study has been published. The animal evidence points the other way: in rats given a single intravenous dose, radiolabelled LR3 was removed from the circulation more rapidly than native IGF-1 ^[10]. Its longer-lasting effect on blood sugar in pigs ^[3] reflects more free, active peptide rather than a proven long half-life.

For comparison, the licensed medicine mecasermin has a mean half-life of about 5.8 hours after a subcutaneous dose in children with severe IGF-1 deficiency ^[9].

Claimed IGF-1 LR3 benefits online include muscle growth, fat loss and faster recovery. The published evidence is narrower. In catabolic rats it improved weight gain and nitrogen retention ^[2], and in mdx mice it protected muscle from contraction damage ^[5]. But in food-restricted rats it did not preserve muscle protein ^[4], and in finishing pigs a four-day infusion of 180 µg/kg per day reduced daily weight gain and food intake, and lowered blood levels of growth hormone, IGFBP-3, the pigs’ own IGF-1 and insulin ^[11].

No study we found measured muscle growth, weight loss or testosterone after IGF-1 LR3 in people, so these IGF-1 LR3 peptide benefits remain untested in humans.

In rats made catabolic with the steroid dexamethasone, infused IGF-1 LR3 and des(1-3)IGF-I were about 2.5-fold more potent than IGF-1 at improving weight gain and nitrogen retention, and all of the IGF peptides markedly increased gut weight ^[2]. In food-restricted rats, a week-long infusion helped maintain body weight and nitrogen balance but did not preserve muscle protein; in adult rats it increased muscle protein breakdown and reduced protein synthesis ^[4]. The author concluded it did not prevent loss of lean tissue during food restriction.

In pigs, IGF-1 LR3 and related analogues lowered blood glucose two to three times more potently than IGF-1 and kept it suppressed for longer, with roughly a four- to eight-fold greater cumulative hypoglycaemic effect over four hours ^[3]. In mdx mice, a model of Duchenne muscular dystrophy, four weeks of continuous IGF-1 LR3 reduced muscle damage from lengthening contractions ^[5].

These studies were designed to understand IGF biology in animals. None tested whether IGF-1 LR3 builds muscle or reduces fat in healthy people.

We found no published clinical trials of IGF-1 LR3 in humans, and no registered trial results. Evidence about human use comes from anti-doping and forensic work: one analysis of a black-market injection vial found IGF-1 LR3 carrying a “His-tag”, a purification label typically used in laboratory reagents, whose effects in humans have never been described ^[6]. A 2026 clinical review grouped IGF-1 LR3 with other unregulated growth-hormone-axis compounds and listed reported adverse effects across the class, including blood-sugar disturbances, fluid retention and joint and muscle pain ^[8].

Searches for IGF-1 LR3 before and after photos and IGF-1 LR3 results mostly lead to forum posts and vendor pages. These cannot show what a vial contained, what else the person used alongside it, or how diet and training changed. Black-market IGF-1 LR3 has contained His-tagged laboratory versions ^[6] and oxidised forms ^[7], and many users combine it with anabolic steroids or growth hormone, so any change in a photo cannot be attributed to IGF-1 LR3.

The only controlled results are from animals, and they were mixed, as set out above. We found no study that measured how long IGF-1 LR3 takes to show results in people.

All published doses are from animals. Examples include continuous infusion of about 98 nmol per kg per day in rats ^[4], bolus injections of 20 and 50 µg/kg in pigs ^[3], around 1.5 mg/kg per day by osmotic pump in mice ^[5], and a single 100 µg/kg intramuscular dose in rats for detection testing ^[7]. No human dose has been established, and animal doses cannot simply be converted to human doses.

There is no evidence-based IGF-1 LR3 dosage for people, and none for bodybuilding. The only human IGF-1 dosing information on a label is for the different drug mecasermin, given to children with severe primary IGF-1 deficiency: a starting dose of 0.04 to 0.08 mg/kg twice a day, up to a maximum of 0.12 mg/kg twice a day, given under the skin within 20 minutes of a meal or snack, and withheld if the child cannot eat ^[9]. That regimen is supervised by a specialist and does not apply to LR3.

IGF-1 LR3 is sold by weight, commonly as 1 mg vials, and is not measured in international units (IU). For the arithmetic only, 1 mg mixed with 1 mL of liquid gives 1 mg per mL, which is 10 µg in each 0.01 mL, one unit on a U-100 insulin syringe. Our peptide calculator handles other volumes and our guide to bacteriostatic water covers diluents, but neither can confirm what a vial actually contains. We found no studies of IGF-1 LR3 as a nasal spray, tablet or pen.

The best-documented effect in animals is low blood sugar (hypoglycaemia), which was more potent and more prolonged than with native IGF-1 ^[3]. IGF-1 signalling also promotes cell growth, and a recent review described mitogenic (growth-promoting) concerns about IGF-1 analogues as biologically plausible but unproven ^[8]. There are no controlled human safety data. Black-market products have been found to contain unexpected variants and oxidised or degraded forms, so the content of any vial cannot be assumed ^[6][7].

The clearest guide to IGF-1 LR3 side effects in humans is the label for native IGF-1. With mecasermin, hypoglycaemia was reported by 42% of children in clinical trials, five had severe episodes needing help, and four had seizures or loss of consciousness; it was most common early in treatment ^[9]. The label tells patients to avoid high-risk activities such as driving or exercise for 2 to 3 hours after a dose ^[9]. Other effects listed include enlarged tonsils in 15% of children, raised pressure inside the skull and, with long-term overdose, signs of acromegaly ^[9]. LR3 lowered blood sugar more potently and for longer than native IGF-1 in animals ^[3], so these risks cannot be assumed to be smaller.

On IGF-1 LR3 cancer risk, there is no direct evidence either way. The concern comes from IGF biology: a Lancet meta-analysis found that people with higher circulating IGF-1 had a modestly higher risk of prostate cancer and of breast cancer before the menopause ^[12]. Mecasermin is contraindicated in anyone with active or suspected cancer, and its label reports post-marketing cases of malignant tumours in children, while noting it is unknown whether the drug caused them ^[9]. On current evidence, the question of whether IGF-1 LR3 is safe cannot be answered, because it has never been tested in people.

Growth hormone (HGH, somatropin) acts partly by making the liver release IGF-1, and the approved GH-releasing drug tesamorelin works by stimulating the body’s own growth hormone, with some of its effects mediated by IGF-1 ^[15]. IGF-1 LR3 skips those steps and acts directly on IGF receptors. In the one animal study that combined them, adding growth hormone to LR3 in pigs did not reverse its suppression of growth hormone, insulin and IGF-1 levels ^[11].

The evidence gap is large. Somatropin is a licensed medicine with human trial data, and tesamorelin is approved in the US for excess abdominal fat in people with HIV ^[15], whereas IGF-1 LR3 has no human trials. Tesamorelin vs IGF-1 LR3 and IGF-1 LR3 vs HGH are therefore comparisons between tested medicines and an untested reagent. See our guides to tesamorelin and sermorelin for the GH-releasing approach.

IGF-1 LR3 is not approved as a medicine anywhere. It is different from mecasermin, the licensed recombinant form of native human IGF-1 used for severe primary IGF-1 deficiency in children. For sport, exogenous IGF-1 is prohibited at all times under the World Anti-Doping Agency (WADA) Prohibited List, and anti-doping laboratories describe IGF-1 analogues including LongR3-IGF-I as prohibited substances ^[7]. See our legal status overview for country-level rules.

The 2026 WADA Prohibited List names “insulin-like growth factor 1 (IGF-1, mecasermin) and its analogues” under S2.3 growth factors, prohibited at all times ^[13]. IGF-1 LR3 is a protein hormone analogue, not a steroid, so it is not an anabolic steroid under anti-doping rules or in law. In the UK, Class C of the Misuse of Drugs Act names somatropin and chorionic gonadotrophin but not IGF-1 or its analogues ^[14]; selling an unlicensed medicine for human use is still an offence under the Human Medicines Regulations. Our UK legal status page has more detail.

IGF-1 LR3 is usually supplied as a freeze-dried powder. Anti-doping laboratories found abundant oxidised forms in black-market samples, a sign that product quality and degradation are real concerns ^[7]. General guidance is in our peptide storage guide.

Identity testing matters more than usual for IGF-1 LR3 because it is a larger molecule with known variants, such as His-tagged forms, turning up in black-market products. You can compare prices, learn how to read a COA, and see our list of third-party tested suppliers.

UK buyers can see IGF-1 LR3 prices in the UK. Because a mass spectrometry test is the only way to tell LR3 from His-tagged and oxidised versions ^[6][7], read our guides to third-party peptide testing and how to spot a fake peptide supplier before relying on a label.