What Is IGF-1?
Published Oct 15, 2026 · 15 minute read
IGF-1, short for insulin-like growth factor 1, is a protein hormone that the liver releases when growth hormone tells it to. A recombinant copy called mecasermin, sold as Increlex, is FDA-approved for one rare use: growth failure in children whose bodies make too little IGF-1 despite normal or high growth hormone. In adults, controlled trials of injected IGF-1 have not increased lean mass, and its strongest acute effect is lowering blood sugar.
Key Takeaways
- IGF-1 is a hormone made mostly by the liver in response to growth hormone. Mecasermin (Increlex) is a recombinant copy of it.
- Increlex is FDA-approved only for growth failure in children with severe primary IGF-1 deficiency or a growth hormone gene deletion with neutralizing antibodies. It has no adult, muscle-building or anti-aging approval.
- Low blood sugar is the leading risk: 42% of children in the label's trials had at least one episode, and some had seizures.
- In controlled adult trials, a year of IGF-1 in older women and 28 days of an IGF-1 complex in athletes did not change lean mass.
- The label links tumors to above-recommended doses or IGF-1 levels pushed over the normal range, and WADA bans IGF-1 at all times.
IGF-1 sits one step downstream of growth hormone, which is why it shows up in conversations about muscle, recovery and aging. For people on GLP-1 medicines, the obvious question is whether it could protect muscle during weight loss. The human trials below answer a narrower question: what happens to lean mass, blood sugar and safety when IGF-1 is actually given.
This page covers the native hormone and mecasermin. The synthetic analogues IGF-1 LR3 and IGF-1 DES have their own guides.
| IGF-1 at a glance | What to know |
|---|---|
| Other names | Insulin-like growth factor 1, IGF-I; mecasermin (Increlex) as a drug |
| Class | Peptide hormone; recombinant human IGF-1 (rhIGF-1) |
| Size | 70 amino acids with three internal disulfide bridges; about 7.6 kDa |
| US status | Increlex approved August 2005, pediatric indication only |
| EU status | Authorized August 2007 under exceptional circumstances |
| WADA status | Prohibited at all times (S2.3, growth factors) |
| Route | Subcutaneous injection; the label says never intravenous |
| Half-life | Free IGF-1 about 10–12 minutes (tracer study); mecasermin terminal half-life 5.8 hours in 3 young patients |
| Main evidence gap | No controlled adult trial showing lean-mass gain |
1. What does IGF-1 do in the body?
Growth hormone binds receptors in the liver and other tissues, and those tissues respond by producing IGF-1. IGF-1 then binds the type 1 IGF receptor, a close relative of the insulin receptor, according to the Increlex prescribing information. The label describes three main jobs:
- Lengthening bones. Working with growth hormone, IGF-1 stimulates the cartilage cells of growth plates until the plates fuse after puberty.
- Growing cells and organs. Most cell types carry IGF-1 receptors, and IGF-1 promotes cell division.
- Handling glucose. It reduces sugar output from the liver, raises sugar uptake into tissues and dampens insulin release.
The resemblance to insulin is structural as well as functional. When Rinderknecht and Humbel worked out its structure in 1978, they found it closely matched proinsulin, the molecule the body trims to make insulin. That kinship explains why IGF-1 can cause low blood sugar.
Mecasermin carries the same amino-acid sequence as human IGF-1 and is produced in E. coli bacteria engineered with the human gene. A tracer study in two healthy adults estimated the body’s own production at roughly 10 mg per day.
How IGF-1 differs from related products
| Product | What it is | Status |
|---|---|---|
| Mecasermin (Increlex) | Recombinant IGF-1, identical to the human hormone | FDA-approved 2005; EU-authorized 2007 |
| Mecasermin rinfabate (iPlex) | Recombinant IGF-1 bound to its main carrier protein, IGFBP-3 | FDA-approved December 2005; listed as discontinued |
| IGF-1 LR3 | Synthetic analogue with an added N-terminal segment and one substituted amino acid | Not approved; research chemical |
| IGF-1 DES | Synthetic, truncated IGF-1 analogue | Not approved; research chemical |
| MGF and PEG-MGF | Peptides derived from a splice variant of the IGF-1 gene | Not approved; research chemicals |
Drugs@FDA lists the Increlex approval and the iPlex record. A 2009 review by Kemp noted that iPlex had been withdrawn from short-stature use in the US and Europe because of a legal requirement. Anti-doping chemists classify LR3 and DES as synthetic IGF-1 analogues in their 2017 detection paper.
2. What is the half-life of IGF-1?
There is no single answer, because IGF-1 rarely travels alone. The label states that over 80% of circulating IGF-1 sits in a three-part complex with IGFBP-3 (IGF binding protein 3) and a second protein called the acid-labile subunit. The tighter the binding, the longer it lasts.
Guler’s 1989 tracer study, done in only two healthy adults, measured each form separately:
| Form in the blood | Apparent half-life |
|---|---|
| Unbound (free) IGF-1 | 10–12 minutes |
| Bound in the smaller complex, about 50 kDa | 20–30 minutes |
| Bound in the large complex with IGFBP-3, about 200 kDa | 12–15 hours |
For the drug itself, the Increlex label reports these values after a subcutaneous dose of 0.12 mg/kg:
| Parameter | Value | Basis |
|---|---|---|
| Bioavailability | Close to 100% | Healthy subjects; not determined in IGF-1 deficiency |
| Time to peak | 2 hours | 3 patients aged 12–22 with severe primary IGF-1 deficiency |
| Peak concentration | 234 ng/mL | Same 3 patients |
| Terminal half-life | 5.8 hours | Same 3 patients |
| Elimination | Liver and kidney | Label |
Clearance also depends on how much IGFBP-3 a person has. The label estimates clearance at 0.04 L/h/kg when IGFBP-3 is 0.5 µg/mL, falling to 0.01 L/h/kg at 3 µg/mL, the median in people with normal IGF-1. Children with severe primary deficiency have very little IGFBP-3, so they clear injected IGF-1 faster. A half-life model built from one of these numbers therefore applies only to the population and form it came from.
3. Is IGF-1 FDA-approved, and for what?
United States
FDA approved Increlex in August 2005 under biologics license 021839, per Drugs@FDA. The label limits it to growth failure in children aged 2 and older who have one of two conditions:
- Severe primary IGF-1 deficiency. Height standard deviation score (SDS, a measure of how far a value sits from the population average) of –3.0 or lower, basal IGF-1 SDS of –3.0 or lower, and normal or high growth hormone. Laron syndrome, in which the body cannot respond to growth hormone, is the classic example.
- Growth hormone gene deletion with neutralizing antibodies that block treatment with growth hormone.
The label is explicit about what Increlex is not. It does not replace growth hormone where growth hormone is approved, and it is not for secondary IGF-1 deficiency caused by growth hormone deficiency, malnutrition, an underactive thyroid or long-term corticosteroids. The current DailyMed label names Eton Pharmaceuticals as manufacturer; Ipsen issued an earlier version.
European Union
In August 2007 the European Commission cleared Increlex for children and adolescents with severe primary IGF-1 deficiency, according to EMA. The authorization was granted under “exceptional circumstances,” a route used when a disease is too rare to collect complete data. Increlex held orphan-medicine status from 2006 to 2017.
No regulator has approved IGF-1 for adults, muscle building, fat loss or aging.
4. What does the research show?
Children with severe primary IGF-1 deficiency
The label pools five studies (one placebo-controlled, four open-label) involving 71 children. At the start they averaged 6.7 years old, with a height SDS of –6.7 and an IGF-1 level of 21.6 ng/mL. Laron syndrome accounted for 87% of the 61 children treated for a year or more, and most received 0.06–0.12 mg/kg twice daily.
| Point in treatment | Children measured | Height velocity, cm/year | Height SDS |
|---|---|---|---|
| Pretreatment | 58 | 2.8 | –6.7 |
| Year 1 | 58 | 8.0 | –5.9 |
| Year 2 | 48 | 5.8 | –5.6 |
| Year 3 | 38 | 5.5 | –5.4 |
| Year 4 | 23 | 4.7 | –5.5 |
| Year 6 | 20 | 4.8 | –5.4 |
| Year 8 | 13 | 4.3 | –5.2 |
The jump was largest in the first year and tapered afterward. By years 7 and 8, growth was no longer significantly faster than before treatment. Skeletal age advanced a little faster than calendar age, 5.3 years versus 4.9 years over the same span (n = 49).
In a US cohort of 76 children treated with 60–120 µg/kg twice daily and tracked for as long as 12 years, Chernausek’s team found the first-year response was dose-dependent. Among 21 who reached adult or near-adult height after an average of 10 years, Backeljauw and colleagues reported a mean 13.4 cm above expected untreated height and a total height SDS gain of about +2. Most still finished below the normal adult range.
Blood sugar in healthy adults and type 2 diabetes
The first human study, Guler’s 1987 NEJM paper, gave eight healthy adults a single 100 µg/kg intravenous dose and compared it with insulin. Glucose bottomed out 30 minutes later at 1.98 mmol/L (about 36 mg/dL) with IGF-1, against 1.78 mmol/L (about 32 mg/dL) with insulin. Molecule for molecule, IGF-1 was about 6% as potent as insulin, and roughly 80% of the IGF-1 in blood was unbound right after the dose.
That glucose effect led to trials in type 2 diabetes. In Moses and colleagues’ study, 12 obese patients took 100 µg/kg twice daily for 6 weeks:
| Measure | Baseline | After treatment |
|---|---|---|
| HbA1c (roughly 3-month average glucose) | 10.4% | 8.1% |
| Mean 24-hour glucose | 14.7 mmol/L | 9.1 mmol/L |
| Insulin sensitivity | Reference | 3.4 times higher |
| Serum IGF-1 | 206 µg/L | 849 µg/L |
Only 6 of the 12 completed the full 6 weeks because of side effects. In Jabri’s 1994 study, all 7 patients given 120–160 µg/kg twice daily stopped early, and the authors judged high-dose rhIGF-1 unacceptable for them. IGF-1 was never approved for diabetes.
Other conditions tested
- ALS. A two-year phase 3 trial randomized 330 patients to 0.05 mg/kg twice daily or placebo and found no difference in strength, tracheostomy-free survival or functional decline (Sorenson et al., 2008).
- Preterm infants. Intravenous mecasermin rinfabate has been tested to prevent retinopathy of prematurity, an eye disease of very premature babies. A 2026 Cochrane review found two trials with 140 infants, a risk ratio of 0.94 (95% CI 0.38–2.35) for severe retinopathy and very low certainty throughout, so no conclusion was possible.
5. Does IGF-1 build muscle or protect it during GLP-1 weight loss?
The case for an effect comes mainly from infusion physiology. Fryburg’s 1994 study delivered rhIGF-1 straight into the forearm artery for 6 hours in 19 adults, and the infused forearm shifted toward net protein gain at every dose. The opposite arm, exposed only through general circulation, did not change.
Longer controlled trials of injected IGF-1 tell a different story:
| Trial | Who | What they received | Body composition result |
|---|---|---|---|
| Friedlander et al., 2001 | 16 healthy postmenopausal women, mean age 71 | rhIGF-1 15 µg/kg twice daily or placebo for 1 year | No change in lean mass, fat mass, strength or bone density |
| Guha et al., 2015 | 56 recreational athletes, 30 men and 26 women | rhIGF-1/IGFBP-3 at 30 or 60 mg/day, or placebo, for 28 days | No change in lean or fat mass |
In the 2001 trial, IGF-1 rose from about 66 to about 330 ng/mL, yet no outcome moved, and the study stopped after 16 participants. The athletes’ maximal oxygen uptake (VO₂ max, a measure of aerobic capacity) rose about 7% across the treated groups, which is not the same as muscle growth.
None of these trials enrolled people losing weight on semaglutide or tirzepatide. The evidence therefore gives no basis for expecting IGF-1 to preserve lean mass during GLP-1 treatment. The GLP-1 and muscle loss guide covers what is known about that problem.
6. What are the side effects and risks of IGF-1?
Low blood sugar
Hypoglycemia is the first warning on the Increlex label. Among 71 children treated for a mean of 3.9 years, 30 (42%) had at least one episode, although 14 of them had hypoglycemia before starting. Five needed help from another person, and four had seizures or lost consciousness. Episodes were concentrated in younger children and in the first month of treatment.
For the first 2–3 hours after a dose, especially early in treatment, the label recommends steering clear of risky activities like driving or exercise. In the long-term US cohort, 49% of children reported hypoglycemia.
Other labeled risks
| Risk | Label detail |
|---|---|
| Enlarged tonsils and adenoids | Seen in 15% during the first 1–2 years; surgery in 7, including 3 with obstructive sleep apnea |
| Intracranial hypertension | Reported in 3 children; signs include headache, vision change, nausea or vomiting from increased fluid pressure in the skull |
| Slipped capital femoral epiphysis | The upper end of the thigh bone slips at its growth plate during fast growth; may cause osteonecrosis (bone death) |
| Scoliosis | Existing spinal curvature may worsen during rapid growth |
| Allergic reactions | Anaphylaxis after marketing estimated at 0.3%; hospital care was needed in some cases |
| Injection-site changes | Fatty lumps (lipohypertrophy) and bruising; lipohypertrophy in 32% of the long-term cohort |
| Benzyl alcohol preservative | The preservative has been tied to deadly “gasping syndrome” in newborns, so infant use is not recommended |
The label also mentions kidney and spleen enlargement on ultrasound, thickening of facial soft tissue, and heart findings of uncertain relation to the drug. Prolonged overdose may produce features of acromegaly, the condition caused by excess growth hormone.
High doses in adults
Every patient in Jabri’s high-dose diabetes study developed side effects that ended treatment. They included facial and hand swelling, jaw tenderness, joint and muscle pain, fast heart rate, flushing, low blood pressure when standing up, tiredness and, at times, breathlessness.
Cancer
Increlex is contraindicated in anyone with active or past cancer. The label describes postmarketing reports of various cancers in treated children, with no established causal link, but tumors appeared more often in children with cancer-predisposing genetic conditions and in those whose doses exceeded the recommendation or lifted IGF-1 beyond its normal range. In a two-year rat study, adrenal tumors increased at exposures below human levels.
Population data point the same way without proving cause. Renehan’s 2004 meta-analysis of 21 studies found that IGF-1 at the 75th versus 25th percentile carried modestly higher odds of prostate cancer (OR 1.49) and premenopausal breast cancer (OR 1.65). At the opposite extreme, Ecuadorians with growth hormone receptor deficiency and very low IGF-1 had one nonlethal cancer over 22 years, compared with 17% among relatives (Guevara-Aguirre et al., 2011).
Who should not use it
The label lists allergy to mecasermin or its ingredients, closed growth plates, and active or prior cancer. Safety has not been established under age 2 or at 65 and over.
7. How is mecasermin dosed?
The only labeled regimen is for the pediatric indication. It is shown here to explain the label, not as guidance for anyone else.
| Label step | Dose |
|---|---|
| Start | 0.04–0.08 mg/kg twice daily |
| Increase, if tolerated for at least 1 week | +0.04 mg/kg per dose |
| Maximum | 0.12 mg/kg twice daily |
Every dose goes with food, within 20 minutes before or after a meal or snack. A child who cannot eat skips that dose, and missed doses are not made up. The label calls for pre-meal glucose checks at the start until a well-tolerated dose is established.
The adult studies above used their own research doses, from 15 µg/kg twice daily in older women to 120–160 µg/kg twice daily in the stopped diabetes study. None established an adult dose for any purpose.
8. Interactions and what you can measure
Diabetes medicines, including GLP-1s
The Increlex label tells patients to report diabetes and any insulin or other diabetes medicine, because those doses may need adjusting. No study reviewed here tested IGF-1 together with a GLP-1 medicine. Given IGF-1’s own glucose-lowering effect, any combination with glucose-lowering therapy is a question for the prescriber rather than for self-experiment.
Blood tests that matter
- Glucose. The label calls for this check early in treatment, because hypoglycemia is the dominant acute risk.
- Serum IGF-1. The label ties tumor reports partly to doses that pushed IGF-1 above the normal range, so the level relative to that range is clinically meaningful. Note that a raised level in the adult trials did not translate into more lean mass.
- Body composition. The adult trials measured lean mass directly. A scale weight or a mirror cannot separate muscle from fluid, and swelling was a common side effect at high doses.
For tracking, log the product, date, time, meal timing and any glucose readings together. A record like that helps a clinician see patterns around hypoglycemia, but it cannot show that IGF-1 caused a change in muscle or recovery.
9. Is IGF-1 legal, and what about online products?
US law treats mecasermin as a prescription biologic, and its only approved use is pediatric. The WADA 2026 Prohibited List bans “insulin-like growth factor 1 (IGF-1, mecasermin) and its analogues” at all times under S2.3, alongside mechano growth factors.
IGF-1 products and analogues turn up in online advertising and black-market sales, according to anti-doping scientists. As of 2013, Guha and colleagues noted that IGF-1 was harder to detect than growth hormone and that no misuse test was yet in place. Detection has improved since then, with mass-spectrometry assays published for LR3, DES and related synthetic analogues.
Nothing guarantees the identity, strength or sterility of IGF-1 bought outside a pharmacy, and every clinical result above came from pharmaceutical mecasermin. For the hormone upstream of IGF-1, see the growth hormone guide.
10. IGF-1 FAQ
What is IGF-1?
IGF-1, or insulin-like growth factor 1, is a protein hormone produced mainly in the liver when growth hormone signals it. It drives much of growth hormone's effect on growth and also lowers blood sugar in a way that resembles insulin.
Is IGF-1 legal?
In the US, mecasermin (Increlex) is a prescription biologic approved only for a rare pediatric growth disorder. Products sold online outside pharmacies are not regulated for identity, dose or sterility. WADA prohibits IGF-1 and its analogues at all times in sport.
Does IGF-1 build muscle?
Short forearm infusions shifted local muscle protein balance toward gain. However, a one-year placebo-controlled trial in older women and a 28-day trial in recreational athletes found no change in lean mass from injected IGF-1.
What are the side effects of IGF-1?
The Increlex label lists hypoglycemia first, followed by tonsil and adenoid enlargement, raised pressure around the brain, hip growth-plate slippage, worsening scoliosis, allergic reactions and fatty lumps at injection sites. Adults with type 2 diabetes given high doses developed swelling, joint and jaw pain, fast heart rate and fatigue.
How long does IGF-1 stay in your system?
It depends on binding. Free IGF-1 has an apparent half-life of about 10–12 minutes, while IGF-1 held in its large binding-protein complex lasts 12–15 hours. Injected mecasermin had a terminal half-life of 5.8 hours in a small group of patients with severe primary IGF-1 deficiency.
Can IGF-1 be used with semaglutide or tirzepatide?
No study reviewed here tested that combination. IGF-1 lowers blood sugar on its own, and the Increlex label asks patients to report diabetes and any insulin or other diabetes medicine because doses may need adjusting. Any combination belongs in a conversation with a prescriber.
Does high IGF-1 cause cancer?
That has not been proven. Observational data link higher natural IGF-1 to modestly higher risk of some cancers, and the Increlex label reports tumors more often with above-recommended doses. Increlex must not be used by people with active or past cancer.
What is the difference between IGF-1, IGF-1 LR3 and IGF-1 DES?
IGF-1 is the natural hormone, and mecasermin is an identical recombinant version with an FDA approval. IGF-1 LR3 and IGF-1 DES are synthetic analogues with altered structures that are sold as research chemicals and have no approval.
11. Sources
References used for this article
- Increlex (mecasermin) prescribing information, DailyMed
- Drugs@FDA: Increlex, BLA 021839
- Drugs@FDA: iPlex (mecasermin rinfabate), BLA 021884
- European Medicines Agency: Increlex EPAR
- World Anti-Doping Agency: 2026 Prohibited List
- Rinderknecht and Humbel (1978): IGF-1 structure and homology with proinsulin
- Guler et al. (1989): IGF half-lives and production rates in healthy adults
- Guler et al. (1987): Short-term metabolic effects of rhIGF-1 in healthy adults
- Kemp (2009): Treatment options for IGF-1 deficiency, including mecasermin rinfabate availability
- Chernausek et al. (2007): Long-term rhIGF-1 treatment in growth hormone insensitivity
- Backeljauw et al. (2013): Adult and near-adult height after long-term rhIGF-1
- Moses et al. (1996): rhIGF-1 and glycemic control in type 2 diabetes
- Jabri et al. (1994): Adverse effects of high-dose rhIGF-1 in type 2 diabetes
- Fryburg (1994): IGF-1 infusion and forearm muscle protein metabolism
- Friedlander et al. (2001): One year of IGF-1 in postmenopausal women
- Guha et al. (2015): rhIGF-1/IGFBP-3 in recreational athletes
- Sorenson et al. (2008): Two-year phase 3 trial of IGF-1 in ALS
- Trzaski et al. (2026): Cochrane review of IGF-1 for retinopathy of prematurity
- Renehan et al. (2004): IGF-1, IGFBP-3 and cancer risk meta-analysis
- Guevara-Aguirre et al. (2011): Growth hormone receptor deficiency, cancer and diabetes
- Guha et al. (2013): IGF-1 misuse in athletes and detection methods
- Thomas et al. (2017): LC-MS detection of LR3, R3 and DES IGF-1 analogues