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Insulin-like growth factor 1 (IGF-1), also called somatomedin C, is a peptide hormone that is structurally close to insulin and serves as the principal mediator of growth hormone action. Produced chiefly by the liver but also locally in tissues, it signals through the IGF-1 receptor to drive cell proliferation, differentiation, and protein synthesis, and it feeds back on the hypothalamus and pituitary to help regulate the growth hormone axis. A notable feature is the alternative splicing of the IGF-1 gene in skeletal muscle to yield mechano growth factor, a variant rapidly induced by mechanical loading or injury that is associated with satellite (stem) cell activation and repair, though its distinct peptide activity remains debated. A recombinant form, mecasermin, is an approved therapy for children with severe primary IGF-1 deficiency, and the hormone remains a central focus in research on aging, longevity, neuroprotection, and cancer risk.
- Drives muscle protein synthesis
- Tissue growth and repair
- Central to normal growth
- Medical use in growth disorders
- Growth hormone's main tissue-building messenger
- Low blood sugar (hypoglycemia), especially when taken without food
- Overgrowth of tonsils and other lymphoid tissue
- Fat accumulation and coarsening of facial features
- Theoretical cancer risk from its growth-promoting, anti-apoptotic action
Overview
Insulin-like growth factor 1 is a single-chain protein of about seventy amino acids, structurally similar to proinsulin, which is how it got its name. It is produced chiefly in the liver, and its synthesis is stimulated by pituitary growth hormone, making IGF-1 the main messenger through which growth hormone exerts many of its effects on the body [3]. Local tissues also make their own IGF-1 that acts nearby. In the bloodstream almost all IGF-1 travels bound to a family of IGF-binding proteins, especially IGFBP-3, which regulate how much free, active hormone is available. Blood levels are low in infancy, peak during puberty, and gradually decline with age [3].
IGF-1 promotes the growth of muscle, cartilage, bone and internal organs, and it influences the metabolism of protein, carbohydrate and fat; it is essential for normal childhood growth and for fetal development of the brain and other organs [3]. Because it reflects growth hormone activity, measuring IGF-1 in blood is used to help screen for growth hormone deficiency, acromegaly and gigantism. A recombinant human version, mecasermin, is approved for the long-term treatment of growth failure in children with severe primary IGF-1 deficiency or growth hormone insensitivity such as Laron syndrome, where it stimulates the linear growth that growth hormone cannot [1][2]. IGF-1 also acts as an insulin-sensitizing agent and has been explored in a long list of conditions, from severe insulin resistance and diabetes to muscle wasting, though most of these uses remain experimental and its clinical role stays largely confined to rare growth disorders [2].
Because IGF-1 builds tissue and, like insulin, can influence muscle and metabolism, it and related growth factors have been misused in sport as performance-enhancing agents and are banned by anti-doping authorities. The hormone has a complex relationship with disease: higher IGF-1 is associated with lower cardiovascular risk but also with increased risk of certain cancers, since its ability to drive cell proliferation and block apoptosis can favor tumor growth, and both very high and very low levels are linked to higher mortality [3]. Prescription IGF-1 (mecasermin) is given by injection and its most common adverse effect is low blood sugar; other effects include lymphoid tissue overgrowth and fat accumulation, and its growth-promoting, anti-apoptotic nature raises theoretical cancer concerns with long-term use [2].
Mechanism
acts mainly by binding to the IGF-1 receptor (IGF1R) on the surface of cells, a receptor tyrosine kinase closely related to the receptor. When IGF-1 attaches, the receptor's two halves phosphorylate each other and recruit adaptor proteins, switching on two major intracellular cascades: the - pathway, which drives cell growth, protein synthesis and survival while suppressing programmed cell death, and the Ras-MAPK pathway, which promotes cell proliferation [3]. Through these pathways stimulates the division and enlargement of muscle, bone and cartilage cells and mediates much of the anabolic action attributed to growth hormone.
Because is structurally similar to , it can also weakly activate the insulin receptor and lower blood glucose, which explains both its insulin-sensitizing effect and the risk of hypoglycemia when it is given as a drug [2]. The amount of that reaches its receptor is tightly controlled by IGF-binding proteins, which hold the hormone in the circulation and release it to tissues as needed [3]. The same proliferative, anti-apoptotic signaling that supports healthy growth is what links elevated activity to cancer risk.
receptor fingerprint
receptoragonist
/ pathwayactivates
receptorweak agonist
Satellite cellsactivates
Dosingtypical ranges, not medical advice
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Safetyrisks and cautions, not medical advice
This is a high-risk hormone. Acute danger includes hypoglycemia, sometimes severe, because of its insulin-like activity. Longer-term concerns include organ and tissue overgrowth, joint pain, and a theoretical increase in cancer risk from sustained IGF-1 signaling. It's not approved for athletic use, purity of black-market product is unreliable, and it should only ever be used under genuine medical supervision for approved conditions.
Resources
This entry is here for reference.
Research
- 2001first citedIntranasal administration of insulin-like growth factor-I bypasses the blood-brain barrier and…
- 2021most active year3 papers
- 2024most recentClinical characteristics and treatment efficacy in patients with primary severe IGF-1 deficienc…
- 1.Mecasermin (recombinant human IGF-I): drug profile
- 2.Mecasermin (recombinant human insulin-like growth factor I)
- 3.Insulin-like Growth Factors in a clinical setting: Review of IGF-I
- 4.The Role of Insulin-like Growth Factor-1 (IGF-1) in the Control of Neuroendocrine Regulation of Growth.
- 5.Intranasal IGF-1 Reduced Rat Pup Germinal Matrix Hemorrhage.
- 6.Molecular and cellular pathways contributing to brain aging.
- 7.Clinical characteristics and treatment efficacy in patients with primary severe IGF-1 deficiency treated with recombinant IGF-1.
- 8.Alterations in Stem Cell Populations in IGF-1 Deficient Pediatric Patients Subjected to Mecasermin (Increlex) Treatment.
- 9.Treatment of severe primary IGF-1 deficiency using rhIGF-1 preparation - first three years of Polish experience.
- 10.Mecasermin: new drug. Insufficient improvement in statural growth.
- 11.Increased longevity due to sexual activity in mole-rats is associated with transcriptional changes in the HPA stress axis.
- 12.Expression and splicing of the insulin-like growth factor gene in rodent muscle is associated with muscle satellite (stem) cell activation following local tissue damage.
19 listed here; entry last updated August 2026
Reviews
My notesprivate to this device
FAQ
Does deer antler velvet give you IGF-1?
Any IGF-1 in it is negligible and destroyed by digestion, so oral products don't meaningfully raise IGF-1.
Is IGF-1 safe for building muscle?
No. It's a potent hormone with hypoglycemia and cancer-risk concerns, not a supplement to experiment with.
What is IGF-1 LR3?
An engineered analog with a much longer active half-life; it's used illicitly and is not medically approved for athletes.
How is it used medically?
Recombinant IGF-1 (mecasermin) treats specific severe growth failure disorders under close medical supervision.
Adverse effects
- Low blood sugar (hypoglycemia), especially when taken without food
- Overgrowth of tonsils and other lymphoid tissue
- Fat accumulation and coarsening of facial features
- Theoretical cancer risk from its growth-promoting, anti-apoptotic action
Notes and cautions
- Banned in sport as a performance-enhancing agent
- Intranasal delivery of IGF-1 is well documented in animals. Radiolabelled IGF-1 given into the nasal passages of rats reached the olfactory bulbs, brainstem and spinal cord within thirty minutes and activated IGF-1 signalling there, at tissue concentrations the intravenous route did not match [16]. Nasal IGF-1 cut infarct volume by roughly sixty percent and improved neurologic scores in rats after middle cerebral artery occlusion [17][18], and the same route has since been used in rodent models of neonatal brain injury [19]. No human trial of intranasal IGF-1 has been published and no nasal IGF-1 product exists.