Pep IQ
← Pep IQ
IGF-1 (insulin-like growth factor 1) is one of the most-studied growth factors in biology. Decades of animal work established the role in tissue growth, protein synthesis, glucose metabolism, and the GH/IGF-1 axis. The mecasermin formulation (recombinant human IGF-1) replicates endogenous IGF-1 for therapeutic use. Animal carcinogenicity studies (rats, 4–10 mg/kg/day) showed increased mammary carcinoma at supratherapeutic exposures — this is a known concern with chronic high IGF-1 levels.
Off-label community use carries real hypoglycaemia risk and is the most acute safety concern of any peptide on this platform. Always have fast carbohydrates available; never inject without food. Community doses vary widely. The IGF-1 LR3 modification (extended half-life, see separate entry) has different pharmacokinetics and risk profile to standard mecasermin — they are not interchangeable. Pep IQ does not endorse off-label IGF-1 use without medical supervision because the hypoglycaemia risk is severe and immediate, not theoretical.
Substantial in approved indications. FDA approval based on uncontrolled study in 76 children with severe primary IGF-1 deficiency (Laron syndrome and similar) — height velocity increased from 2.8 to 8.0 cm/year in the first treatment year, sustained above baseline for up to 8 years. Multiple Phase 2/3 trials in growth disorders (NCT00571727 long-term GHIS study, others). Off-label trials in Rett syndrome (Khwaja et al. 2014 Phase 1 — 40–120 mcg/kg twice daily, 12 subjects, completed without serious adverse events). Also explored in chronic liver disease, cystic fibrosis, AIDS muscle wasting, anorexia nervosa, ALS, and others — variable results, none yet leading to additional approvals.
FDA-approved as Increlex (mecasermin) for primary IGF-1 deficiency in children. FDA-approved as Iplex (mecasermin rinfabate) formerly approved, now withdrawn. Adult use is not FDA-approved. Prescription-only. WADA-banned for tested athletes. Side effects per FDA labelling: hypoglycaemia (most frequent, controlled by dosing with meals), tonsillar hypertrophy (may require tonsillectomy in children), fat redistribution, coarsening of facial features. Theoretical malignancy concern based on rat carcinogenicity at supratherapeutic doses.
Standard IGF-1 (mecasermin/Increlex) is FDA-approved with well-defined clinical dosing for paediatric IGF-1 deficiency. The off-label adult performance use is a different application — unstudied at supraphysiological doses, real hypoglycaemia risk, theoretical chronic IGF-1-elevation concerns. Standard IGF-1 is run continuously when used clinically (not cycled like LR3). Pep IQ flags this honestly: legitimate clinical use is well-evidenced; off-label adult use is uncharted and carries acute hypoglycaemia risk that has caused emergencies — hospitalisations from hypoglycaemia after IGF-1 self-administration are documented in case reports.
IGF-1 (insulin-like growth factor 1) is not a synthetic peptide developed in a lab — it is a hormone your body produces naturally, primarily in the liver, in response to growth hormone (GH) stimulation from the pituitary gland. Named for its structural similarity to insulin, IGF-1 is the key downstream mediator of growth hormone's anabolic effects on virtually every tissue in the body.
IGF-1 levels peak during puberty and adolescence — the period of most rapid growth — and then decline gradually throughout adulthood. By age 60, typical IGF-1 levels are roughly 40% of what they were at age 20. This age-related decline runs parallel to the loss of muscle mass, bone density, and tissue repair capacity associated with ageing, making IGF-1 one of the most studied targets in longevity research.
The performance and biohacking community's interest is in exogenous IGF-1 — specifically engineered analogues that are more stable or potent than native IGF-1 for injection. The two most common are IGF-1 LR3 (long-acting, 20-30 hour half-life, systemic effects) and IGF-1 DES (short-acting, ~20 minutes, site-specific effects). Both are research chemicals, not approved drugs, and both are banned by WADA.
IGF-1 works by binding to the IGF-1 receptor (IGF1R) — a tyrosine kinase receptor expressed in skeletal muscle, bone, connective tissue, and virtually every organ. Receptor activation triggers a cascade that is essentially the master switch for anabolic processes.
The Cancer Question — The Most Important Thing to Understand About IGF-1: IGF-1 promotes cell growth, division, and survival — in all cells, including cancer cells. Chronically elevated IGF-1 levels have been epidemiologically associated with increased risk of prostate, breast, colorectal, and lung cancers. This is not a theoretical concern: it is a documented signal across multiple large population studies. The IGF-1 signalling pathway (PI3K/Akt/mTOR) is one of the most frequently dysregulated pathways in cancer. Anyone with a personal or family history of cancer should consider IGF-1 use extremely carefully. The same mTOR activation that builds muscle is the activation that cancer cells exploit.