Mecasermin
Mecasermin (Increlex), recombinant human IGF-1
Written by Aaron CuhaReviewed Sep 2026
Also known as: Increlex, rhIGF-1, Recombinant human insulin-like growth factor 1, IGF-1
An approved medicine, and only for a rare paediatric deficiency. In 76 children with severe IGF-1 deficiency, height velocity rose from 2.8 cm per year at baseline to 8.0 cm per year in the first year, and 49 percent had hypoglycaemia. Among registry patients followed to the end of puberty, mean height moved from about 3.7 to about 2.6 standard deviations below the mean in boys: better, still short.
Overview
Mecasermin is recombinant human IGF-1, the mature 70 amino acid hormone, given by subcutaneous injection twice daily with food. It is the only entry in this batch that is an approved medicine, and it is approved for one narrow thing: growth failure in children and adolescents with severe primary IGF-1 deficiency, and in children with growth hormone gene deletion who have developed neutralising antibodies to growth hormone.
Those children make growth hormone but cannot respond to it, so giving more growth hormone does nothing. Giving the downstream hormone directly works, and that is the whole clinical case. In the pivotal long-term experience, 76 children with severe IGF-1 deficiency due to growth hormone insensitivity were treated for up to 12 years under a predominantly open-label design at doses of 60 to 120 micrograms per kilogram twice daily. Height velocity rose from a mean of 2.8 cm per year at baseline to 8.0 cm per year in the first year (p less than 0.0001), was dose dependent, and fell in subsequent years while staying above baseline for up to 8 years.
The honest limit sits in the registry data. Among European registry patients who reached the end of puberty, 25 boys and 11 girls, mean height standard deviation score improved from minus 3.7 at registry baseline to minus 2.6 at Tanner stage 5 in boys, and from minus 3.1 to minus 2.3 in girls. Treatment moves these children meaningfully up the curve. It does not make them average height.
Safety is not incidental here. Hypoglycaemia was reported by 49 percent of treated subjects in the long-term study, injection site lipohypertrophy by 32 percent and tonsillar or adenoidal hypertrophy by 22 percent. In the European registry, 80 of 306 enrolled patients had at least one hypoglycaemia adverse event, at a rate of 0.11 events per patient per treatment year with serious events at 0.01, and prior hypoglycaemia and a Laron syndrome diagnosis predicted it.
What mecasermin is not approved for, and has not been shown to do, is anything an adult buyer is usually looking for: muscle, recovery, ageing, sarcopenia or performance. IGF-1 signalling also runs the wrong way in cancer epidemiology, and that belongs on the page rather than in a footnote.
Mechanism of action
Mecasermin binds the IGF-1 receptor, a receptor tyrosine kinase, activating PI3K/Akt and MAPK signalling to drive cell growth, protein synthesis and, at the growth plate, linear bone growth. It also has meaningful affinity for the insulin receptor, which is the direct reason hypoglycaemia is the principal adverse effect and why the product is dosed with a meal. Endogenous IGF-1 circulates almost entirely bound to IGFBP-3 and the acid-labile subunit, a complex whose formation depends on growth hormone signalling. In severe primary IGF-1 deficiency that signalling is broken, so the binding proteins are low, free IGF-1 exposure after a dose is higher and clearance faster than the endogenous hormone would suggest. That is the pharmacological difference between replacing IGF-1 and having made it yourself.
Human evidence
Substantial human evidence in one rare condition, almost all of it open-label and registry-based rather than randomised, and none of it in adults or for any non-growth purpose.
- 76 children with growth hormone insensitivity, up to 12 years of treatment: height velocity 2.8 cm per year at baseline to 8.0 cm per year in year one (p less than 0.0001), staying above baseline for up to 8 years.
- Same study, adverse events: hypoglycaemia in 49 percent, injection site lipohypertrophy in 32 percent, tonsillar or adenoidal hypertrophy in 22 percent.
- European registry, 306 patients: 80 had at least one hypoglycaemia event, 0.11 events per patient-year overall and 0.01 serious. Laron syndrome and prior hypoglycaemia predicted events.
- European registry, 242 patients: 56 percent of treatment-naive prepubertal non-Laron patients met the first-year responder threshold; treatment-emergent adverse events in 65.3 percent.
- Registry patients reaching Tanner stage 5: mean height moved from minus 3.7 to minus 2.6 standard deviations in boys and minus 3.1 to minus 2.3 in girls. Puberty started about 1.5 years late.
- No randomised placebo-controlled trial of mecasermin in adults for muscle, recovery, sarcopenia or ageing was located.
What this does not tell you: The pivotal experience is predominantly open-label and the follow-up evidence is observational registry data, so growth is compared against each child's own baseline rather than against a randomised control. That design is defensible in a condition this rare and it is still not a randomised trial. Nothing here tells you what mecasermin does in a person with normal IGF-1: the entire evidence base is replacement in deficiency, where the starting point is pathologically low. Hypoglycaemia is common rather than rare. And the IGF-1 axis is associated with higher cancer incidence in general-population epidemiology, which is a reason for caution about raising IGF-1 in someone who is not deficient, not a finding about treated children.
Reading the research record
Mecasermin is on this site because IGF-1 is one of the most sought-after molecules in the grey market and almost nobody selling it is describing the approved drug.
The site already covers IGF-1 LR3, IGF-1 DES and the mechano growth factor variants, all of them analogues designed to evade binding proteins and none of them approved. This page is the reference point: the real hormone, manufactured to pharmaceutical standard, tested in the population that cannot make it, approved by four regulators, and indicated for children who are severely short.
Two things follow from that. The first is that IGF-1 demonstrably does something powerful in humans, which is more than most compounds here can say. The second is that everything it has been shown to do is correct a deficiency in a growing child. There is no randomised trial of IGF-1 for muscle mass in healthy adults, none for sarcopenia, none for recovery, and none for ageing.
The direction of the ageing evidence is, if anything, the opposite of the one buyers assume. Reduced IGF-1 signalling extends lifespan in several model organisms, and in human epidemiology higher circulating IGF-1 is associated with higher prostate cancer incidence and mortality, with Mendelian randomisation supporting causality. Those are associations in people with naturally varying IGF-1 and they say nothing about a child receiving replacement. They say a great deal about an adult choosing to raise their own.
Hypoglycaemia is the practical fact. It affected roughly half the children in the long-term study, it is why the drug is taken with food, and it is the reason self-administration without monitoring is dangerous rather than merely unapproved.
The evidence, charted
Fig. 1 · evidence composition
5of 5 citations (100%) are in people
Every citation cited here is Human work; no other study type is cited on this page. This count is of our own citation list and understates any literature larger than the sources we cite.
Fig. 2 · evidence over time
Evidence spans 4 distinct years, 2007 to 2023, counted from the citation list on this page.
Fig. 3 · legal status at a glance
US
Approved
UK
Approved
AU
Approved
CA
Approved
Approved in all four jurisdictions shown. A jurisdiction's classification is a regulatory fact, not a verdict on the science; see Legal status below for the full text and any notes.
Fig. 4 · dose response
No human dose response curve exists
We draw this figure where the data supports it. For this compound in humans it does not, so the panel stays empty rather than borrowing an animal curve and implying it transfers.
Key studies & citations
- Human2007
Long-term treatment with recombinant insulin-like growth factor (IGF)-I in children with severe IGF-I deficiency due to growth hormone insensitivity
The long-term efficacy and safety experience behind the approval. 76 children with IGF-1 deficiency due to growth hormone insensitivity treated with recombinant human IGF-1 for up to 12 years under a predominantly open-label design, at 60 to 120 micrograms per kilogram subcutaneously twice daily. Height velocity rose from a mean of 2.8 cm per year at baseline to 8.0 cm per year in the first year (p less than 0.0001) and was dose dependent; velocities were lower in subsequent years but stayed above baseline for up to 8 years. The most common adverse event was hypoglycaemia, reported by 49 percent of treated subjects and observed both before and during therapy, followed by injection site lipohypertrophy (32 percent) and tonsillar or adenoidal hypertrophy (22 percent). Note the design: predominantly open label, not randomised against placebo.
Journal of Clinical Endocrinology and Metabolism - Human2023
Frequency and Predictive Factors of Hypoglycemia in Patients Treated With rhIGF-1: Data From the Eu-IGFD Registry
Surveillance registry data from December 2008 to May 2021, 306 patients enrolled, 84.6 percent with severe primary IGF-1 deficiency. 80 patients had at least one hypoglycaemia adverse event against 224 with none. Total hypoglycaemia events were 0.11 per patient per treatment year and serious events 0.01 per patient per treatment year. Prior history of hypoglycaemia and a Laron syndrome diagnosis both predicted future events. The affected group started treatment younger (mean 8.7 against 9.8 years).
Journal of Clinical Endocrinology and Metabolism - Human2021
Effectiveness and safety of rhIGF1 therapy in patients with or without Laron syndrome
Ongoing open-label observational registry (NCT00903110), 242 children and adolescents from ten European countries enrolled between 2008 and 2017. In the treatment-naive prepubertal cohort of 138, height standard deviation score gain after one year was greater in the 21 patients with Laron syndrome than in the 117 without (p less than 0.05), and 56 percent of the non-Laron group met the responder threshold of a first-year height SDS gain of at least 0.3. Younger age at baseline predicted response (p less than 0.001). Treatment-emergent adverse events occurred in 65.3 percent of patients, hypoglycaemia most commonly. Observational, not randomised.
European Journal of Endocrinology - Human2022
Pubertal Timing and Growth Dynamics in Children With Severe Primary IGF-1 Deficiency: Results From the European Increlex Growth Forum Database Registry
The number that sets expectations honestly. 213 registry patients, 132 boys and 81 girls. Among those reaching the end of puberty, 25 boys and 11 girls, mean height standard deviation score rose from minus 3.7 at registry baseline to minus 2.6 at Tanner stage 5 in boys, and from minus 3.1 to minus 2.3 in girls. Median pubertal peak height velocity was 8.0 cm per year in boys and 6.8 in girls. Puberty started about 1.5 years late and peak height velocity was delayed and slightly lower, but the height gain made before puberty was maintained through it. Treatment improves final height substantially without normalising it.
Frontiers in Endocrinology - Human2021
Circulating insulin-like growth factor-I, total and free testosterone concentrations and prostate cancer risk in 200 000 men in UK Biobank
The epidemiology that any page about giving people more IGF-1 has to state. 199,698 men in UK Biobank followed a mean of 6.9 years, 5,402 diagnosed with and 295 dying from prostate cancer. Higher circulating IGF-1 was associated with prostate cancer diagnosis (hazard ratio 1.09 per 5 nmol/L increment, 95 percent CI 1.05 to 1.12) and with prostate cancer mortality (1.15, 1.02 to 1.29), with hazard ratios corrected for regression dilution using repeat measurements. A two-sample Mendelian randomisation analysis using genetic instruments and outcome data from 79,148 cases and 61,106 controls supported a causal role (cis-MR odds ratio 1.34 per 5 nmol/L, 1.07 to 1.68). This is an association study in men with naturally varying IGF-1, not a study of mecasermin, and it does not establish that treating a deficient child raises cancer risk.
International Journal of Cancer
Frequently asked questions
What is mecasermin approved for?
Growth failure in children and adolescents with severe primary IGF-1 deficiency, and in children with growth hormone gene deletion who have developed neutralising antibodies to growth hormone. It is approved in the United States, the United Kingdom, Australia and Canada for that paediatric indication and nothing else.
Does it work?
In the population it is approved for, yes, measurably. Height velocity rose from a mean of 2.8 cm per year to 8.0 cm per year in the first year across 76 children, and stayed above baseline for up to 8 years. The honest qualifier is what the endpoint is: registry patients followed to the end of puberty reached a mean height around 2.6 standard deviations below average in boys, up from 3.7. That is a large improvement and it is not a normal height.
Can adults take it for muscle or recovery?
There is no trial evidence for that at all. Mecasermin has never been approved for adults and no randomised trial of it for muscle mass, recovery, sarcopenia or performance was located. The entire evidence base is replacement in children whose IGF-1 is pathologically low.
What is the main risk?
Hypoglycaemia, because IGF-1 has meaningful affinity for the insulin receptor. It was reported by 49 percent of children in the long-term study and is the reason the drug is given twice daily with food. In the European registry, prior hypoglycaemia and Laron syndrome both predicted further events.
Does raising IGF-1 increase cancer risk?
In general-population epidemiology, higher circulating IGF-1 is associated with more prostate cancer. In 199,698 UK Biobank men the hazard ratio was 1.09 per 5 nmol/L for diagnosis and 1.15 for mortality, and a Mendelian randomisation analysis supported a causal role. That is an association in men with naturally varying IGF-1, not a study of treated patients, but it is the correct thing to weigh before deliberately raising your own.
How is this different from IGF-1 LR3 sold online?
Mecasermin is the native 70 amino acid hormone made to pharmaceutical standard and approved by regulators. IGF-1 LR3 and IGF-1 DES are modified analogues designed to escape the binding proteins that normally control IGF-1 exposure, they are not approved anywhere, and they have no controlled human trials. They are not the same molecule and not the same evidence base.