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MUSCLE & GROWTHPEPTIDE PROFILE

IGF-1 LR3

Also known as Long R3 IGF-1, Insulin-like Growth Factor-1 LR3, IGF1-LR3, LR3-IGF-1

IGF-1 LR3 (Long R3 Insulin-like Growth Factor-1) is a 83-amino acid recombinant analog of native IGF-1, engineered with a 13-amino acid N-terminal extension and an arginine substitution at position 3. These modifications greatly reduce binding to IGF-binding proteins (IGFBPs) and extend its circulating half-life well beyond that of native IGF-1, which is cleared within minutes when unbound. The specific half-life and potency multiples quoted in community sources are not supported by any published human pharmacokinetic study.

Last updated June 25, 2026

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IGF-1 LR3: quick citable summary

IGF-1 LR3 is listed by PeptaHub as a muscle & growth peptide with a research only legal-status classification. The page summarizes mechanism, research context, common routes, safety notes, and references for writers and AI answer engines.

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PeptaHub. “IGF-1 LR3: Mechanism, Research Context, Safety.” peptahub.com, 2026. https://peptahub.com/peptides/igf-1-lr3. Licensed CC BY 4.0.

License: Creative Commons Attribution 4.0 International. Link back to https://peptahub.com/peptides/igf-1-lr3.

SAMEAS / EXTERNAL IDS
IGF-1 LR3 CAS: 946870-92-4
QUICK ANSWER

What is IGF-1 LR3?

IGF-1 LR3 is an 83-amino acid recombinant analog of IGF-1 engineered to escape IGF-binding-protein sequestration, which extends its circulating half-life well beyond native IGF-1. It is a laboratory research reagent: no controlled human trial of IGF-1 LR3 has been published.

§ 01

Overview

IGF-1 LR3 (Long R3 Insulin-like Growth Factor-1) is a 83-amino acid recombinant analog of native IGF-1, engineered with a 13-amino acid N-terminal extension and an arginine substitution at position 3. These modifications greatly reduce binding to IGF-binding proteins (IGFBPs) and extend its circulating half-life well beyond that of native IGF-1, which is cleared within minutes when unbound. The specific half-life and potency multiples quoted in community sources are not supported by any published human pharmacokinetic study.

§ 02

Mechanism of action

IGF-1 LR3 binds to the IGF-1 receptor (IGF-1R), a receptor tyrosine kinase, with high affinity. Receptor activation triggers autophosphorylation and downstream signaling through two primary pathways: the PI3K/Akt/mTOR axis, which drives protein synthesis, suppresses protein degradation, and promotes cell survival; and the MAPK/ERK pathway, which stimulates cell proliferation and differentiation. The near-complete bypass of IGFBPs — which normally sequester native IGF-1 in circulation — means systemically administered IGF-1 LR3 is substantially more bioavailable at tissue IGF-1R. Satellite cell activation in skeletal muscle is a key mechanism for hypertrophic adaptation. IGF-1 LR3 also exhibits insulin-like metabolic activity at high concentrations, activating insulin receptors and driving glucose uptake into muscle tissue.

§ 03

Reported study ranges

PurposeRouteReported rangeFrequency
Muscle anabolism / body recomposition researchsubcutaneous2050 mcgonce daily, post-workout
Recovery from injuryintramuscular2040 mcgonce daily

Reported ranges are for research context only. Consult a qualified healthcare professional before using any peptide.

Convert IGF-1 LR3 research-range units

Need to convert mg to mcg, dose volume, or U-100 syringe units? The IGF-1 LR3 dose calculator is preloaded with these ranges, or use the general dose unit converter.

§ 04

Research summary

IGF-1 LR3 is an established research reagent in cell biology and metabolic research. The animal data are narrower than commonly assumed: infusion in guinea pigs stimulated organ growth while suppressing endogenous IGF-I, IGF-II and IGFBPs (Conlon, J Endocrinol 1995), and in food-restricted rats LR3-IGF-I limited body weight loss but did not preserve skeletal muscle (Tomas, Growth Horm IGF Res 2001). The muscle hypertrophy rationale rests on general IGF-1/PI3K/Akt/mTOR signalling rather than on LR3-specific in vivo hypertrophy trials. No controlled human trial of IGF-1 LR3 has been published as of 2026. Hypoglycemia is a documented class risk of IGF-1 therapy.[1][2][3][4]

📄This section cites 4 peer-reviewed sources. View all references →
§ 04b

Evidence grading

Each claimed benefit is graded by the strength of available evidence. Grades reflect study quality, not effect size.

preliminary
Skeletal muscle hypertrophy and anabolismConlon J Endocrinol 1995: LR3-IGF-I infusion in guinea pigs stimulated organ growth while lowering plasma IGF-I, IGF-II and IGFBPs. Tomas Growth Horm IGF Res 2001 found LR3-IGF-I limited body weight loss during food restriction but did not preserve skeletal muscle, so the animal evidence for muscle-specific anabolism is not consistent. No human LR3 trials
moderate
Extended half-life via reduced IGFBP bindingThe 13-amino-acid N-terminal extension plus R3 substitution sharply lowers IGFBP affinity, and animal infusion data are consistent with prolonged free exposure (Conlon J Endocrinol 1995). No human pharmacokinetic study of IGF-1 LR3 has been published, so specific half-life figures are not established
preliminary
Satellite cell activation in muscleYoshida & Delafontaine Cells 2020 review of IGF-1/PI3K/Akt/mTOR muscle signaling; mechanism established, LR3-specific evidence is in vitro
moderate
Hypoglycemia risk from insulin-receptor cross-activityEstablished IGF-1 therapeutic class effect; documented in mecasermin clinical use and animal LR3 studies
insufficient
Human body composition efficacyNo controlled human trials of IGF-1 LR3 published; WADA-banned; community use only extrapolated from animal anabolism studies

Strong = multiple RCTs · Moderate = limited trials or observational · Preliminary = animal or in vitro only · Insufficient = anecdotal or no published data

§ 05

Side effects

Hypoglycemia (dose-dependent, serious)
Fatigue
Jaw pain
Headache
Water retention / edema
Acromegaly-like symptoms with long-term use (jaw, organ growth)
Injection site pain
Nausea

Side effects vary by individual. This is not an exhaustive list. Report unusual symptoms to a healthcare professional.

§ 06

Common stacks

Peptides commonly paired with IGF-1 LR3 for synergistic effects.

§ 08

Sourcing & access

Research compound

IGF-1 LR3 is classified as a research compound. Regulatory status varies by jurisdiction. Always verify current legal status and source from vendors providing third-party certificates of analysis (COA).

§ 09

Frequently asked questions

IGF-1 LR3 (Long R3 IGF-1) is a modified version of native IGF-1 with a 13-amino acid N-terminal extension and an arginine substitution at position 3. These changes sharply reduce binding to IGF-binding proteins, increasing free bioavailability and substantially extending the circulating half-life relative to native IGF-1. No published human pharmacokinetic study of IGF-1 LR3 pins down the exact figure.

IGF-1 LR3 binds the IGF-1 receptor, activating PI3K/Akt/mTOR (driving protein synthesis and cell survival) and MAPK/ERK (stimulating proliferation) pathways. It activates satellite cells in skeletal muscle for hypertrophy and exhibits insulin-like metabolic activity at high concentrations.

Side effects include dose-dependent hypoglycemia (serious), fatigue, jaw pain, headache, water retention, and acromegaly-like symptoms with long-term use. It is not FDA-approved, is banned by WADA, and no controlled human trials specific to IGF-1 LR3 have been published.

Hypoglycemia is a serious dose-dependent risk because IGF-1 LR3 activates insulin receptors at high concentrations, driving glucose uptake into muscle tissue. Users should have fast-acting carbohydrates available and not exceed recommended dosing. Cycles should be limited to 4 weeks.

§ 10

Research references

  1. Long R3 insulin-like growth factor-I infusion stimulates organ growth but reduces plasma IGF-I, IGF-II and IGF binding protein concentrations in the guinea pigConlon MA, Tomas FM, Owens PC, Wallace JC, et al.J Endocrinol, 1995PubMed
  2. Insulin-like growth factor-I (IGF-I) analogue, LR(3)IGF-I, ameliorates the loss of body weight but not of skeletal muscle during food restrictionTomas FMGrowth Horm IGF Res, 2001PubMed
  3. Mechanisms of IGF-1-Mediated Regulation of Skeletal Muscle Hypertrophy and AtrophyYoshida T, Delafontaine PCells, 2020Review
  4. Detection of LongR3-IGF-I, Des(1-3)-IGF-I, and R3-IGF-I using immunopurification and high resolution mass spectrometry for antidoping purposesMongongu C, Coudoré F, Domergue V, Ericsson M, et al.Drug Test Anal, 2021PubMed
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