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approvedGrowth & Recovery

Mecasermin

Also known as: Increlex, Recombinant Human IGF-1, rhIGF-1, Mecasermin (rDNA origin)

Mecasermin (brand name Increlex) is recombinant human insulin-like growth factor-1 (rhIGF-1), a 70-amino-acid peptide identical to endogenous IGF-1. FDA-approved in 2005, it is the only approved therapy for severe primary IGF-1 deficiency (also called Laron syndrome or GH insensitivity), a rare condition where the body cannot produce adequate IGF-1 despite normal or elevated growth hormone levels. Mecasermin directly replaces the missing IGF-1, bypassing the defective GH signaling pathway to promote linear growth in children with this condition.

3 cited references·5 researched benefits

Quick Answer

Mecasermin (Increlex) is recombinant human IGF-1, a 70-amino-acid peptide FDA-approved in 2005 for severe primary IGF-1 deficiency (Laron syndrome). It directly replaces missing IGF-1 in patients whose bodies cannot produce it despite having normal or elevated growth hormone. By bypassing the defective GH-IGF-1 axis, mecasermin promotes linear bone growth, improves body composition, and normalizes metabolic parameters in affected children. It is the only approved treatment for this rare condition.

Key Facts

Mechanism
Mecasermin is identical to endogenous IGF-1 and binds to the IGF-1 receptor (IGF-1R), a receptor tyrosine kinase expressed on virtually all cell types. Activation of IGF-1R triggers the PI3K/Akt pathway (promoting cell survival and glucose uptake) and the MAPK/ERK pathway (promoting cell proliferation and differentiation). At the growth plate, IGF-1R activation stimulates chondrocyte proliferation and hypertrophy, driving longitudinal bone growth. In muscle, it promotes protein synthesis and satellite cell differentiation. In metabolically active tissues, it enhances glucose uptake through a mechanism partially overlapping with insulin signaling. Unlike exogenous GH, which works by stimulating hepatic IGF-1 production, mecasermin provides IGF-1 directly, making it effective in patients with GH receptor defects.
Research Status
approved
Half-Life
~5.8 hours
Molecular Formula
C₃₃₁H₅₁₂N₉₄O₁₀₁S₇
Primary Use
Growth & Recovery
Table of Contents

Benefits

  • Promotes linear bone growth in children with severe primary IGF-1 deficiency — increases growth velocity from ~2–3 cm/year to ~8 cm/yearstrong
  • Normalizes body composition — reduces excess body fat and increases lean mass in IGF-1 deficient patientsstrong
  • Improves metabolic parameters including insulin sensitivity and lipid profilesmoderate
  • Supports organ growth and development in IGF-1 deficient children (brain, kidney, heart)moderate
  • Potential therapeutic application in neurodegenerative conditions due to IGF-1 neuroprotective effectspreliminary

Dosage Protocols

RouteDosage RangeFrequencyNotes
Subcutaneous injection0.04–0.12 mg/kgTwice daily (before meals)FDA-approved dosing. Start at 0.04 mg/kg twice daily, increase by 0.04 mg/kg increments. Maximum dose 0.12 mg/kg twice daily. Must eat within 20 minutes of injection to prevent hypoglycemia.
Subcutaneous injection0.04–0.08 mg/kgTwice dailyConservative dosing used in younger children or those with higher hypoglycemia risk. Slower titration schedule with close glucose monitoring.

Medical disclaimer

Dosage information is provided for educational reference only. Always follow your prescriber's instructions and consult a qualified healthcare provider before starting any peptide protocol.

Side Effects

  • Hypoglycemia — the most common serious side effect (up to 49% of patients); must eat within 20 minutes of injectionserious
  • Injection site lipohypertrophy — fatty tissue buildup at frequently used injection sitescommon
  • Tonsillar and adenoidal hypertrophy — lymphoid tissue growth, sometimes requiring surgical interventioncommon
  • Intracranial hypertension (pseudotumor cerebri) — presents as headache, visual changes, papilledemaserious
  • Coarsening of facial features with long-term use at high dosesrare

Frequently Asked Questions

What is Laron syndrome and why is mecasermin needed?
Laron syndrome (growth hormone insensitivity) is a rare genetic disorder caused by mutations in the GH receptor gene. Patients produce normal or elevated levels of growth hormone, but their cells cannot respond to it because the GH receptor is defective. Since GH normally stimulates the liver to produce IGF-1 (the hormone that actually drives growth), Laron patients have very low IGF-1 levels and severe short stature. Growth hormone therapy is useless in these patients because their receptors cannot respond to it. Mecasermin bypasses this defect by providing IGF-1 directly.
How does mecasermin differ from IGF-1 LR3?
Mecasermin is identical to natural human IGF-1 — a 70-amino-acid peptide that binds normally to IGF-binding proteins and the IGF-1 receptor. IGF-1 LR3 is a modified analog with an arginine-to-glutamic acid substitution at position 3 and a 13-amino-acid N-terminal extension, which dramatically reduces binding to IGF-binding proteins. This gives LR3 a much longer effective half-life and greater bioavailability, but it is not FDA-approved and remains a research compound. Mecasermin is the only approved rhIGF-1 product.
Why does mecasermin cause hypoglycemia?
IGF-1 has structural similarity to insulin and can activate the insulin receptor at high concentrations. Even through the IGF-1 receptor, it promotes glucose uptake in muscle and adipose tissue. When administered exogenously, especially before meals when blood glucose is lower, mecasermin can drive blood glucose to dangerously low levels. This is why the FDA label requires that patients eat a meal within 20 minutes of each injection and that the dose is skipped if the patient cannot eat. Hypoglycemia occurs in up to 49% of patients.

References

  1. 1
    Mecasermin (recombinant human IGF-1) therapy for growth failure in primary IGF-1 deficiency: long-term efficacy and safety(2006)PubMed ↗
  2. 2
    Recombinant human IGF-1 (mecasermin) for treating growth failure in children with severe primary IGF-1 deficiency(2009)PubMed ↗
  3. 3
    IGF-1 deficiency, IGF-1 receptor signaling, and growth hormone insensitivity: clinical and molecular insights(2011)PubMed ↗

Latest Research

Last updated: 2026-02-19