Overview
Mecasermin is recombinant human insulin-like growth factor-1 (rhIGF-1), a 70-amino-acid polypeptide with three disulfide bonds that is identical in sequence to the endogenous hormone. It is produced in Escherichia coli using recombinant DNA technology. IGF-1 is the principal mediator of many of growth hormone's effects, produced mainly in the liver in response to GH, and it was originally described in the 1950s as a sulfation factor before being sequenced in the 1970s.
Mecasermin was approved by the FDA in 2005 and by the EMA in 2007, marketed as Increlex, for severe primary IGF-1 deficiency. This condition, which includes Laron syndrome caused by GH receptor mutations, involves very low IGF-1 despite normal or elevated GH, so GH itself is ineffective. Research with mecasermin focuses on linear growth in GH insensitivity, IGF-1 receptor signalling and the metabolic consequences of IGF-1 replacement. Because IGF-1 shares signalling features with insulin, hypoglycaemia is the most closely monitored adverse effect in clinical studies. WADA lists IGF-1 and its analogues as prohibited.
Mechanism studied
- Mecasermin
- IGF-1 receptor
- Growth-plate signalling
- Linear growth
Mecasermin binds the IGF-1 receptor, a receptor tyrosine kinase structurally related to the insulin receptor. Ligand binding triggers autophosphorylation and recruitment of insulin receptor substrate proteins, activating the PI3K-Akt and Ras-MAPK pathways. These pathways promote cell proliferation, differentiation and survival. At the growth plate, IGF-1 stimulates chondrocyte proliferation and hypertrophy, driving longitudinal bone growth. In GH insensitivity, where hepatic IGF-1 production fails, exogenous rhIGF-1 bypasses the defective GH receptor step. At higher concentrations IGF-1 can also activate insulin receptors and hybrid receptors, which explains its glucose-lowering effects.
Research highlights
- 01IGF-1 was first described as a GH-dependent sulfation factor in the 1950s, then sequenced in the 1970s.
- 02Recombinant production in E. coli enabled study of IGF-1 replacement in GH insensitivity.
- 03Laron syndrome research established the distinction between GH deficiency and GH insensitivity.
- 04Approved in the US in 2005 and the EU in 2007 for severe primary IGF-1 deficiency.
- 05Open questions include long-term metabolic and neoplastic considerations of sustained IGF-1 receptor activation.
Latest published research
256 papers on PubMed →Real world data on rhIGF-1 therapy in children with severe primary IGF-I deficiency - The European experience
Saavedra J et al. · Growth hormone & IGF research : official journal of the Growth Hormone Research Society and the International IGF Research Society · 2026 Jun 21 · PMID 42341624
Clinical spectrum of extreme insulin resistance syndromes treated with rhIGF-1: A single-center experience
Improda N et al. · The Journal of clinical endocrinology and metabolism · 2026 Jun 17 · PMID 41606799
Recombinant human IGF-1 alleviates dyslipidemia induced by lactational maternal dietary restriction
Liu X et al. · Frontiers in pediatrics · 2026 · PMID 42327899
Placental hormones, IGF-1, and early-life growth: endocrine links between birth size and infant metabolic programming-a systematic review
Soliman AT et al. · European journal of pediatrics · 2026 Apr 28 · PMID 42050034
Insulin-like growth factor-1 for the prevention or treatment of retinopathy of prematurity
Trzaski JM et al. · The Cochrane database of systematic reviews · 2026 Apr 15 · PMID 41983451
Recombinant human insulin-like growth factor 1 complex preserves lung development in mechanically ventilated preterm lambs
Albertine KH et al. · American journal of respiratory and critical care medicine · 2026 Apr 1 · PMID 41738171
Therapeutic approaches for endocrine dysregulation in anorexia nervosa in adolescents
Hoskens L et al. · Frontiers in pediatrics · 2026 · PMID 41937902
Randomised Phase 2b trial of rhIGF-1/rhIGFBP-3 (OHB-607) for bronchopulmonary dysplasia prevention in preterm neonates: study protocol
Baraldi E et al. · BMJ paediatrics open · 2026 Mar 5 · PMID 41786363
Live feed from PubMed (NCBI) for “Mecasermin”, updated 2026-10-30. Listing a paper is not an endorsement of its findings.
Registered studies
37 on ClinicalTrials.gov →- Not yet recruiting
Personalized Care for Prenatal Stress Reduction & Prevention of Preterm Birth (PTB) Disparities
NCT06915428 · University of North Carolina, Chapel Hill · 2026-10-01
- Active not recruitingPhase 2
A Clinical Efficacy and Safety Study of OHB-607 in Preventing Bronchopulmonary Dysplasia in Extremely Premature Infants
NCT03253263 · OHB Neonatology Ltd. · 2019-05-09
- Recruiting
Biomarkers of Response to SEEG Thermocoagulation
NCT07399327 · Assistance Publique Hopitaux De Marseille · 2026-06-19
- Withdrawn
Increlex Treatment of Children With Chronic Liver Disease and Short Stature
NCT01314508 · University of California, Los Angeles · 2011-06
- Completed
User Testing of an End of Life Medication Support Intervention for Lay Carers (Palliate).
NCT06526637 · Imperial College London · 2024-09-26
- Recruiting
Global Patient Registry to Monitor Long-term Safety and Effectiveness of Increlex® in Children and Adolescents With Severe Primary Insulin-like Growth Factor-1 Deficiency (SPIGFD).
NCT00903110 · Esteve Pharmaceuticals, S.A. · 2008-12-09
- Recruiting
Cellular Markers in Treated or Untreated Non-tuberculous Mycobacterial Respiratory Infection in Patients With Cystic Fibrosis
NCT06602869 · University Hospital, Montpellier · 2024-09-17
- CompletedPhase 1Phase 2
IGF-1 Treatment for Individuals With Short Stature Due to PAPP-A2 Deficiency
NCT02636270 · Children's Hospital Medical Center, Cincinnati · 2015-12-21
From the public ClinicalTrials.gov registry for “Mecasermin”, updated 2026-10-30. Shown for research context only; Purity Peptides products are not for human use.
Key references
- [1]Manufacturer's prescribing information — FDA / EMA / ANVISA
- [2]Chernausek et al., 2007 — J Clin Endocrinol Metab
- [3]WADA — Prohibited List of Substances and Methods
FAQ
In severe primary IGF-1 deficiency, such as Laron syndrome, the GH receptor or its signalling is defective. Supplying growth hormone cannot raise IGF-1, so recombinant IGF-1 is used to bypass the blocked step.
IGF-1 is structurally similar to insulin and can activate insulin and hybrid receptors at higher concentrations. This promotes glucose uptake, so hypoglycaemia is the most carefully tracked adverse effect in clinical studies.
Mecasermin is approved by the FDA and EMA as a prescription medicine for severe primary IGF-1 deficiency. WADA lists IGF-1 as prohibited. Research material is supplied for laboratory investigation only.
FOR RESEARCH USE ONLY.Not for human or veterinary use. Not intended to diagnose, treat, cure, or prevent any disease.



