IGF-1 LR3 Prices

How it works

What has been studied in humans

As of October 2026, no human administration study of IGF-1 LR3 has been published or registered ^[15][28]. A ClinicalTrials.gov search for the terms IGF-1 LR3, Long R3, Long-R3 and LR3IGF returns zero studies, and the antidoping literature describes the peptide as never approved for use in humans ^[15][28]. There is therefore no human dose, exposure, efficacy or adverse-event dataset for the molecule itself ^[15][16].

The human IGF-1 literature concerns native recombinant human IGF-1 or its binding-protein complex, which handle binding proteins and clearance differently from LR3 ^[6][17]. The human studies summarized here are indirect for that reason. Mecasermin is the recombinant native hormone, sold as Increlex, and it is the reference approved IGF-1 medicine ^[17][18].

The label's pivotal data come from five studies, four open-label and one double-blind placebo-controlled, in 71 children with severe primary IGF-1 deficiency, a condition in which the body cannot make enough IGF-1, often because growth hormone cannot signal properly ^[17]. Open-label means participants and investigators knew which treatment was given, while a double-blind trial keeps that information hidden. Among children treated for at least a year, 87% had Laron syndrome, a rare inherited form of the same problem ^[17]. Mean height velocity rose from 2.8 centimeters a year before treatment to 8.0 centimeters in year one and 4.3 centimeters in year eight ^[17]. Registry and long-term reports are uncontrolled and overlap with this program, so they add follow-up length rather than independent confirmation ^[17].

The controlled neurology experience is mixed. The European ALS trial randomized 183 patients from eight centers to placebo or rhIGF-I, and the regimen reported in the cited human trial was 0.1 milligrams per kilogram per day given subcutaneously, meaning under the skin, for nine months; it found no significant difference in change on the Appel ALS rating scale ^[20]. The Appel scale scores function across bulbar, respiratory, muscle and limb domains, with higher scores meaning more impairment. A Cochrane review found three trials with 779 participants: pooling the European and one North American trial gave a mean difference of minus 4.75 (95% confidence interval, the range likely to contain the true value, minus 8.41 to minus 1.09) in favor of treatment, a separate North American trial found no difference on a manual muscle strength endpoint, all three were at high risk of bias, and there was no evidence of longer survival ^[21]. Injection-site reactions were more frequent with rhIGF-I (risk ratio 1.26, 95% CI 1.04 to 1.54) ^[21].

In Rett syndrome, a neurodevelopmental disorder that mainly affects girls, 30 girls with the classic form were randomized to placebo or mecasermin for 20 weeks, then crossed over to the other assignment for 20 weeks, with a 28-week washout, a break in which no treatment is given, between periods ^[22]. No significant differences appeared on the primary endpoints, which covered anxiety, mood, fear, parent-nominated concerns, global impression and a severity scale ^[22]. The Kerr severity scale, a depressed mood subscale and a hyperventilation measure all worsened, EEG power measures deteriorated, and 12 serious adverse events occurred, although most adverse events were mild to moderate ^[22]. A secondary analysis that excluded subjects involved in a placebo recall confirmed most findings and showed improvements in stereotypic behavior and social communication ^[22].

In preterm infants, the question was whether replacing IGF-1 could prevent retinopathy of prematurity, a disorder in which abnormal retinal blood vessels grow in babies born too early ^[23]. A Cochrane review found two randomized trials with 140 extremely preterm infants, both testing intravenous mecasermin rinfabate, given into a vein, beginning on the day of birth, and rated the evidence very low certainty ^[23]. For Type 1 retinopathy, the stage requiring treatment, the risk ratio was 0.94 (95% CI 0.38 to 2.35); for serious adverse events it was 1.18 (95% CI 0.94 to 1.47) ^[23]. A post-hoc analysis, one chosen after the data were seen, of the larger trial suggested more serious adverse events with treatment (risk ratio 1.28, 95% CI 1.01 to 1.62; number needed to harm 5.9), and both trials carried high risk of bias and industry funding ^[23]. The number needed to harm of 5.9 means about one extra serious adverse event for every six infants treated ^[23].

Observational epidemiology adds a background signal. A systematic review of 21 studies with 26 datasets, 3,609 cancer cases and 7,137 controls, compared participants at the 75th percentile of circulating IGF-1 with those at the 25th ^[24]. Higher IGF-1 was associated with prostate cancer (odds ratio 1.49, 95% CI 1.14 to 1.95) and premenopausal breast cancer (odds ratio 1.65, 95% CI 1.26 to 2.08), and higher IGFBP-3 with premenopausal breast cancer (odds ratio 1.51, 95% CI 1.01 to 2.27) ^[24]. An odds ratio compares the odds of an outcome between two groups, and these associations were modest and varied by cancer site. The studies measured the body's own hormone at one point in time, so they describe a background risk signal rather than an effect of any injected analogue ^[24].

The gaps for LR3 are specific. There is no dose-finding study, no pharmacokinetic study, meaning a study of how the body absorbs, distributes and clears the peptide, no measurement of IGF-1 or IGFBP response, no immunogenicity assessment, meaning a check for an immune response, no controlled efficacy endpoint and no long-term safety follow-up ^[15][16]. Native-product data cannot simply be rescaled, because LR3's escape from binding proteins and faster clearance change the relationship between an injected dose and the free hormone that reaches tissue ^[6]. A 2026 review of growth-hormone-axis peptides notes that clinical experience with this class now includes self-directed use, with reports of dysglycemia, fluid retention, musculoskeletal symptoms and injection-site reactions ^[16].

Doses studied in human trials

As of October 2026, IGF-1 LR3 remains unapproved for any human use and without a registered clinical trial. Regimens below are those reported in the cited human trials.

Lab and animal studies

The animal literature is small enough to read in full, and the main findings are set out in the mechanism section: potency and binding proteins in rats, the pig growth reversal, glucose lowering ^[4][8], fetal sheep and the Alzheimer mouse model ^[7][10][12]. This section adds the design details that bear on how far each result can be pushed. No chronic toxicology, carcinogenicity (the potential to cause cancer), genotoxicity (the potential to damage DNA) or reproductive study of LR3 has been published, and no study has measured serum IGF-1 or IGFBP profiles in humans ^[15][16].

The rat studies used osmotic pumps, small implants that release a drug at a steady rate. The dexamethasone model gave animals 20 micrograms a day for seven days ^[4]. The gut study used female rats weighing 115 grams, six per group, at 0, 44, 111 or 278 micrograms a day for 14 days ^[5]. LR3 is the stronger analogue in these models, but in the delivery comparison injected LR3 was barely equipotent with IGF-1 for reversing carcass muscle loss, even though it cut 3-methylhistidine excretion threefold more ^[6].

The glucose work is the most reproducible animal finding. The maximum glucose fall was 4.8, 3.7 and 2.5 millimoles per liter in pigs, conscious marmosets and anesthetized marmosets ^[7]. Only LR3 was more potent than IGF-1 at lowering plasma amino acids in pigs, and the effect was greatest at the high dose; the authors proposed that suppressed glucagon or a direct hepatic insulin-receptor effect could explain the prolonged glucose fall ^[7].

The neonatal pig experiments used 2-kilogram animals that were artificially reared. The limit-fed study gave 8 days of IGF-1 or LR3 at 2, 4 or 8 micrograms an hour, and the free-milk study gave LR3 at 8 then 16 micrograms an hour ^[9]. In fetal sheep, an earlier study in normal fetuses at 6.6 micrograms per kilogram per hour did increase body weight while lowering insulin and insulin secretion, which contrasts with the null result in growth-restricted fetuses ^[11].

The Alzheimer model used male 5XFAD mice, 19 to 27 per group, dosed from 3 to 10 months of age and assessed at 8 to 9 months ^[12]. In culture, LR3 increased amyloid-beta uptake by BV-2 microglial cells and promoted gene pathways involved in actin remodeling and endocytosis ^[12]. In rat L6 myoblasts, muscle precursor cells, the analogues were more potent than IGF-1 at stimulating protein and DNA synthesis and inhibiting protein breakdown ^[1].

Research in detail

History and where it stands today

IGF-1 LR3 moved from a recombinant production project to a laboratory standard, while the clinical record belongs to native IGF-1.

1. 1992 to 2000An Adelaide group reported the recombinant production of Long [Arg3]-IGF-I in Escherichia coli and showed that the analogue bound IGF-binding proteins poorly and was more potent than IGF-1 in cells and rats ^[1][2][4]. An NMR structure in 2000 showed the IGF-1 core essentially unchanged, with the 13-amino-acid extension flexible in solution ^[3].
2. 1998The European ALS trial randomized 183 patients at eight centers to placebo or recombinant human IGF-1 for nine months and reported no significant difference on the Appel ALS rating scale ^[20].
3. August 2005FDA approved mecasermin, sold as Increlex, for growth failure in children aged 2 years and older with severe primary IGF-1 deficiency ^[17][18]. The European Medicines Agency authorized the same product for patients aged 2 to 18 years ^[19].
4. 2010A black market product contained a His-tagged Long-R3-IGF-I, a form that still carried a purification tag normally removed before use ^[14].
5. 2012A Cochrane review pooled three ALS trials with 779 participants, found no survival benefit and rated all three at high risk of bias ^[21].
6. 2018A double-blind crossover in 30 girls with Rett syndrome found no significant difference on the primary endpoints, worsening on several secondary measures and 12 serious adverse events ^[22].
7. December 2018Promise Pharmacy of Palm Harbor, Florida, recalled 3 milligram and 620 microgram LR3 injections for lack of sterility assurance, and FDA classified both recalls as Class II in February 2019 ^[27][29].
8. 2021Antidoping laboratories published an immunopurification and high-resolution mass spectrometry method that detects LongR3-IGF-I, des(1-3)-IGF-I and R3-IGF-I ^[15].
9. 2026A review of growth-hormone-axis peptides grouped LR3 with other unapproved research compounds that clinicians now encounter in self-directed use ^[16].
10. October 2026No study of LR3 is registered ^[28], FDA lists it in none of the 503A categories in the May 14, 2026 update and none of the 503B categories in the March 21, 2025 update ^[30][31], and FDA's Pharmacy Compounding Advisory Committee has not reviewed the peptide. WADA's 2026 Prohibited List covers IGF-1 and its analogues in section S2.3 ^[25], and the NCAA banned list covers peptide hormones and growth factors as a class ^[26].

How it compares with related peptides

Side effects and safety signals

Human safety data are absent for IGF-1 LR3, so the record below comes from animal work and from the approved native IGF-1 product.

• No human safety data exist for IGF-1 LR3, so the evidence is animal data or label and trial data for native recombinant IGF-1 ^[15][17].
• The mecasermin label reports hypoglycemia in 30 of 71 treated children, or 42%, severe hypoglycemia requiring assistance in five, and hypoglycemic seizures or loss of consciousness in four ^[17].
• Tonsillar hypertrophy, enlargement of the tonsils, occurred in 11 of 71 children, or 15%, with tonsillectomy or adenoidectomy in seven, and intracranial hypertension, raised pressure inside the skull, occurred in three children ^[17].
• Lipohypertrophy, enlargement of fat at injection sites, hypersensitivity including anaphylaxis and postmarketing malignant neoplasms are also labeled, and the malignancy warning is bounded: tumors were mostly reported in patients with rare genetic conditions that already raise cancer risk and more often at doses above the recommended level, and the label states that a causal relationship is unknown ^[17]. Malignant neoplasia or a history of malignancy is a contraindication in pediatric patients ^[17].
• Binding-protein-sparing variants, LR3 among them in pigs, produced about 4 to 8 times greater cumulative hypoglycemia than IGF-1 over four hours ^[7]. Fetal sheep infusions lowered insulin by 84% ^[10], growth-restricted fetuses lost circulating amino acids without gaining growth ^[11], and pigs given LR3 showed suppressed growth hormone, IGFBP-3, IGF-1 and insulin alongside reduced growth ^[8]. None of these studies was designed as a toxicology study, and exposures were short ^[7][8].
• IGF-1 is a mitogen, meaning it drives cells to divide, and the receptor it activates is implicated in several tumors ^[17]. The epidemiology of circulating IGF-1 shows modest associations with prostate and premenopausal breast cancer ^[24], and LR3's poor binding-protein affinity may expose tissues to more free hormone than native IGF-1, though the cited studies have not demonstrated that in humans ^[1][6].
• A 2010 case report identified a His-tagged Long-R3-IGF-I in an injection vial, with the tag being a purification handle normally removed before use, and antidoping analysis found oxidized forms of the peptide in some products ^[14][15]. In December 2018 Promise Pharmacy recalled 3 milligram and 620 microgram LR3 injections for lack of sterility assurance, and FDA classified both recalls as Class II in February 2019 ^[27][29]. Purity and identity testing on vendor certificates is tracked in the COA library.
• Research-grade LR3 has no published impurity, endotoxin or immunogenicity data, and its long-term safety is unknown ^[15][16]. A 2026 clinical review of growth-hormone-axis peptides reports dysglycemia, fluid retention syndromes, musculoskeletal symptoms and injection-site reactions across the class, and those reports set the questions that an early human study of LR3 would need to answer ^[16].

The future: what's next for IGF-1 LR3

No registered study of IGF-1 LR3 is recruiting as of October 2026. The ClinicalTrials.gov search for the terms IGF-1 LR3, Long R3, Long-R3 and LR3IGF returns zero studies, so there are no NCT numbers or trial results to follow ^[28]. Current work is laboratory based: cell-culture production ^[13], antidoping detection ^[15] and disease models such as the 5XFAD mouse study ^[12].

Regulatory timing is quiet. LR3 appears on no 503A category list in the May 14, 2026 update and on no 503B list in the March 21, 2025 update, and FDA's compounding committee has not scheduled a review ^[30][31]. Any future decision would begin with a nomination, and no dated action is pending for this peptide ^[30][31].

A future clinical program would need a dose-finding and pharmacokinetic study before efficacy work. LR3's weak binding-protein affinity and faster clearance make dose comparisons with native IGF-1 unreliable, and no study has measured free IGF-1 or IGFBP-3 after LR3 exposure in humans ^[6][15]. The species disagreement in growth response, with rats gaining and finisher pigs losing weight, makes the choice of a human indication the central design question ^[8][9].

• What human pharmacokinetics look like, including the half-life of intact LR3 and its effect on free IGF-1 and IGFBP-3, remains unmeasured ^[15][16].
• Whether chronic exposure reproduces the mecasermin label signals, including hypoglycemia, tonsillar hypertrophy, intracranial hypertension and malignancy, is unknown ^[17].
• Whether insulin-receptor cross-activation produces clinically important hypoglycemia at the exposures used in animals is unresolved ^[7][13].
• Whether any controlled human signal exists for muscle, gut or cognitive endpoints, and whether the pig growth reversal predicts the human response, is untested ^[8][12][28].
• Whether free-hormone exposure can be measured well enough to compare LR3 with native IGF-1 remains an open methods question ^[6].