IGF-1 LR3
Also known as: Long R3 IGF-1 · Long-Arg3 IGF-1 · insulin-like growth factor 1 LR3
A synthetic long-acting analogue of insulin-like growth factor 1 with reduced IGF-binding-protein affinity, providing sustained systemic IGF-1 signalling with direct hippocampal-neurogenesis implications.
IGF-1 LR3 is a long-acting IGF-1 analogue with reduced IGFBP binding, providing direct systemic IGF-1 signalling with hippocampal-neurogenesis implications.
Evidence tier: C — preclinical / mechanistic evidence only
- Category
- Neurogenesis
- Half-life
- Approximately 20-30 hours plasma (vs ~10 minutes for native IGF-1)
Section 1
Overview
IGF-1 LR3 (Long R3 IGF-1) is a synthetic modified analogue of insulin-like growth factor 1 (IGF-1) — the primary anabolic mediator of GH-axis signalling — engineered with two structural modifications: an arginine substitution at position 3 (R3) that reduces binding to IGF-binding proteins (IGFBPs), and a 13-amino-acid N-terminal extension (Long) that further extends plasma half-life. The combined modifications produce a molecule with substantially greater bioavailable IGF-1 signalling than native IGF-1 at the same nominal dose.
The compound's research relevance to cognitive-endpoint applications rests on the well-established role of IGF-1 signalling in adult hippocampal neurogenesis and cognitive-plasticity mechanisms. Central IGF-1 receptor engagement drives adult neurogenesis in the dentate gyrus and supports BDNF-mediated synaptic plasticity — the same cognitive-plasticity mechanisms targeted by BDNF-inducing peptides through a different upstream pathway.
IGF-1 LR3 is used in research-peptide practice both as a standalone compound and as a downstream component of GH-axis research protocols (where GH-axis peptides raise endogenous IGF-1 via hepatic IGF-1 production). Direct cognitive-endpoint clinical trials of IGF-1 LR3 have not been completed, but the mechanistic framework and preclinical evidence support continued cognitive-relevance research interest.
Section 2
Discovery & History
- Developed as a modified IGF-1 analogue with structural changes designed to reduce IGFBP binding and extend plasma half-life relative to native IGF-1.
- Widely adopted in the sports-medicine and research-peptide communities despite absence of licensed clinical development.
- Preclinical cognitive-endpoint research has emerged from academic groups exploring the IGF-1 signalling contribution to adult hippocampal neurogenesis and cognitive-plasticity mechanisms.
- No entry for IGF-1 LR3 was found in the electronic medicines compendium (emc) on 17 October 2026.
- Insulin-like growth factor 1 and its analogues are listed in section S2.3 of the WADA 2026 Prohibited List (prohibited at all times).
Section 3
Mechanism of Action
- 1Direct IGF-1 receptor (IGF-1R) agonism providing the full spectrum of IGF-1 signalling effects — anabolic, metabolic, and neurotrophic — with substantially greater bioavailable signalling than native IGF-1 owing to the reduced IGFBP binding.
- 2Central IGF-1 receptor engagement in the hippocampus and other cognitively-relevant brain regions, driving adult hippocampal neurogenesis in the dentate gyrus — the primary cognitive-relevance mechanism-of-action angle.
- 3Support of BDNF-mediated synaptic plasticity — IGF-1 signalling supports BDNF expression and downstream cognitive-plasticity mechanisms, providing mechanistic convergence with the BDNF-inducing peptide family.
- 4Systemic anabolic effects on muscle, tendon, ligament, and bone tissue via the well-characterised IGF-1 systemic mechanism.
- 5Metabolic effects including improved glucose regulation and lipid profile modulation via the systemic IGF-1 mechanism.
- 6Reported effects on synaptic protein expression (PSD-95, synaptophysin), dendritic spine density, and long-term potentiation in preclinical models, providing cellular-level substrates for the cognitive-plasticity mechanism.
- 7Neuroprotective effects in preclinical models of cerebral ischaemia, oxidative stress, and neurodegenerative disease models, supporting a broader neuroprotection research angle.
Section 4
Researched Benefits
Findings reported in the published preclinical and clinical literature. Effects in research contexts do not constitute claims of therapeutic benefit in humans.
- 1Direct central IGF-1 signalling providing adult hippocampal neurogenesis induction — a distinctive cognitive-plasticity mechanism-of-action angle.
- 2Substantially greater bioavailable IGF-1 signalling than native IGF-1 owing to the reduced IGFBP binding — the pharmacological advantage over native IGF-1.
- 3Mechanistic convergence with the BDNF-inducing peptide family via IGF-1's support of BDNF signalling.
- 4Systemic anabolic effects on tissue-repair and body-composition endpoints providing broader research application contexts.
- 5Well-characterised IGF-1 signalling pharmacology from the extensive endogenous-IGF-1 research literature.
- 6Downstream mechanism of the GH-axis peptides — provides a direct-action alternative to raising endogenous IGF-1 via GH-axis stimulation.
- 7Neuroprotective effects in preclinical models providing broader neuroprotection research applications.
Section 5
Theoretical Dosing & Protocols
| Route | Dosage | Frequency | Duration | Source |
|---|---|---|---|---|
| Subcutaneous injection (research) | No sourced dose | Not stated | Not stated | None cited |
Note: No dose figure is shown because none could be confirmed from a cited human trial abstract or a regulatory label.
Section 6
Administration Routes
- Subcutaneous injection — the primary research route.
- Intramuscular administration in some research contexts, particularly for localised anabolic-effect research applications.
- Oral administration is not viable — the peptide is degraded by gastrointestinal proteases.
- Intravenous administration in some acute-mechanistic research contexts.
Section 7
Safety Profile
Commonly reported
- · Injection-site reactions with subcutaneous administration.
- · Transient effects on blood glucose (typically mild hypoglycaemia via the IGF-1 hypoglycaemic mechanism) — requires monitoring in susceptible research subjects.
- · Occasional headache during initial dosing.
- · Fluid retention and mild peripheral oedema.
- · Occasional mild fatigue reported at higher doses.
Rare / theoretical
- · Severe hypoglycaemia in susceptible research subjects — the most clinically-significant acute concern.
- · Theoretical tumour-growth promotion in active malignancy — a substantial theoretical concern given IGF-1's role in cell proliferation.
- · Long-term chronic-use safety concerns extrapolated from the broader IGF-1 biology literature — chronic elevated IGF-1 is associated with increased cancer risk epidemiologically.
- · Acromegaly-like effects with chronic supraphysiological IGF-1 exposure.
- · Rare hypersensitivity reactions.
Contraindications
- · No entry for IGF-1 LR3 was found in the electronic medicines compendium (emc) on 17 October 2026.
- · Active or historic malignancy — substantial theoretical contraindication via the IGF-1 proliferative mechanism.
- · Diabetes and severe glucose-metabolism disorders.
- · Pregnancy and lactation.
- · Concurrent use with insulin or oral hypoglycaemic agents without careful monitoring.
Section 8
UK & EU Regulatory Context
United Kingdom
No entry for IGF-1 LR3 was found in the electronic medicines compendium (emc) on 17 October 2026. The emc is not a complete record of UK authorisations, so check the MHRA Products database.
European Union
Not approved by the EMA.
Section 9
Clinical Studies Summary
IGF-1 signalling in adult hippocampal neurogenesis
Foundational neuroscience characterisation of IGF-1 signalling's role in adult hippocampal neurogenesis in the dentate gyrus, establishing the mechanism-of-action framework for IGF-1's cognitive-relevance research applications and providing the neuroscience scaffold for the IGF-1 LR3 cognitive-endpoint research angle.
IGF-1 LR3 pharmacokinetic characterisation
Clinical pharmacology characterisation of IGF-1 LR3's pharmacokinetic profile relative to native IGF-1, demonstrating substantially extended plasma half-life and reduced IGFBP binding — the pharmacological advantages that motivated the analogue design.
IGF-1 in cognitive-plasticity research
Extensive research characterising IGF-1's contributions to synaptic plasticity, learning, and memory across preclinical models. Reports effects on synaptic protein expression, dendritic spine density, long-term potentiation, and BDNF expression that provide the cellular-substrate scaffold for the cognitive-endpoint research.
IGF-1 in Alzheimer's disease and cognitive-decline research
Research characterising IGF-1's role in Alzheimer's disease pathophysiology and its potential as a cognitive-therapeutic research target. Reports effects on amyloid-beta processing, tau pathology, and cognitive-endpoint outcomes in AD-model preparations, extending the cognitive-relevance research angle into disease-relevant contexts.
Section 10
Frequently Asked Questions
Section 10a
Practical Research Guidance
Cycle guidance
Reconstitution & storage
UK sourcing notes
Section 11
Sourcing for Laboratory Research
Sourcing IGF-1 LR3 for laboratory research
Researchers in the United Kingdom and elsewhere typically obtain IGF-1 LR3 from specialist research-chemical suppliers. Purity, third-party testing, and supplier transparency are the principal differentiators worth evaluating before placing an order. The two suppliers below are commonly referenced in UK research contexts.
Reminder: this page is educational. Regulation 46(1) of the Human Medicines Regulations 2012 prohibits selling or supplying an unauthorised medicinal product, and some compounds on this site, such as semaglutide, are authorised prescription-only medicines in the UK.