IGF-1 LR3Growth Factor Analog PeptideSafety Rating 4/10

TypeSynthetic IGF-1 analog
CAS143045-27-6
MW9,117.60 g/mol
AAs83
Primary research areaMuscle / IGF research

Research-literature reference data, NOT patient instructions. Not for human use. Consult a licensed clinician for any human application.

Research dose rangeLimited human clinical data; research protocols 20–50 mcg/day SCsource ↗
AdministrationSubcutaneous injection
Half-life~20–30 hours
Safety4/10 · Not FDA-approved
NCAA D1Banned

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Overview

About IGF-1 LR3

Mechanism of action

Analogue of IGF-1 with arginine substitution at position 3 and N-terminal extension; binds IGF-1 receptors; promotes muscle cell hyperplasia and hypertrophy; inhibits apoptosis; enhances nutrient uptake.

Safety profile

Hypoglycemia (most significant risk), jaw/organ growth with high doses, insulin resistance, acromegaly risk, water retention, potential cancer promotion. · Potent growth factor; proven hypoglycemia risk; potential tumor promotion concern backed by mechanistic data

Storage

Stability & handling

❄️Lyophilized (powder)−20°Cstable long-term
💉Reconstituted2–8°Cwithin 30 days
📈

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Safety & Interactions

Contraindications & Drug Interactions

Research use only — not medical advice. Consult a licensed physician before using any peptide. Sources are cited where available.

⚠ CriticalContraindication

Active malignancy — IGF-1 is a potent growth factor with documented tumor-promoting activity in preclinical models.

⚠ CriticalContraindication

Severe hypoglycemia history or type 1 diabetes — IGF-1 causes significant hypoglycemia.

⚠ CriticalContraindication

Hypersensitivity to IGF-1 or benzyl alcohol.

Sources: FDA

Related pages

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Research

Studies & key findings

  • Long R3 modification (Arg substitution at position 3 + 13-aa N-terminal extension) reduces IGF-binding protein (IGFBP) affinity by >95%, extending half-life from ~10 min to 20–30 hours.
  • Demonstrated superior anabolic potency vs native IGF-1 in dexamethasone-treated catabolic rat models, supporting use in muscle-wasting and recovery contexts.

5 peer-reviewed sources cited — clinical, preclinical, and regulatory.

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