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Comparison

IGF-1 DES vs MGF

Both are IGF & growth factors, so the meaningful differences are in kinetics, evidence and regulatory status.

IGF-1 DES MGF
Class IGF & growth factors IGF & growth factors
Evidence Animal models only Animal models only
Human trials None published ~1
Half-life ~20-30 minutes ~5-7 minutes
Reported range 50-150 mcg 100-200 mcg
Frequency Once daily, peri-workout Post-training, localised
Routes Subcutaneous, Intramuscular Subcutaneous, Intramuscular
FDA approved No No
Research use only Yes Yes
Banned in sport Yes Yes
Studied for Localised hypertrophy research, Satellite cell studies Satellite cell activation research, Muscle repair studies
Reported side effects Hypoglycaemia, Injection-site reactions, Headache Injection-site reactions, Transient fatigue

IGF-1 DES

IGF-1 DES lacks the N-terminal tripeptide glycine-proline-glutamate, a deletion that greatly reduces binding-protein affinity while increasing intrinsic receptor potency. The result is a compound reported as around tenfold more potent than native IGF-1 but cleared within roughly half an hour. That kinetic profile is the basis for its use in localised post-training protocols rather than systemic ones.

MGF

Mechano growth factor is the IGF-1Ec splice variant, produced locally in skeletal muscle after mechanical overload or injury. Its distinct C-terminal E-domain peptide acts independently of the IGF-1 receptor to activate satellite cells and promote myoblast proliferation, positioning it upstream of the differentiation signalling that mature IGF-1 drives. Its extremely short half-life in circulation is the central practical problem and the reason the pegylated form was developed.

IGF-1 DES vs MGF: common questions

What is the difference between IGF-1 DES and MGF?

Both are IGF & growth factors. IGF-1 DES: A truncated IGF-1 variant missing the first three residues, roughly ten times more potent than native IGF-1 but very short-acting. MGF: A splice variant of IGF-1 expressed by muscle in response to mechanical loading and damage.

Which has stronger evidence, IGF-1 DES or MGF?

They sit at the same evidence level: animal models only. IGF-1 DES has about 0 human studies and MGF about 1.

Are IGF-1 DES and MGF FDA approved?

Neither is FDA approved for any indication.

References

Regulatory and primary sources

  1. WADA Prohibited List ↗ · current year
  2. FDA: Unapproved drugs and "research use only" products ↗ · regulatory status of non-approved products

Published literature

  1. Espinosa G, Esposito R, Kazzazi A, et al.. Vitamin D and benign prostatic hyperplasia -- a review.Can J Urol 2013.PubMed 23930605
  2. Werther GA, Russo V, Baker N, et al.. The role of the insulin-like growth factor system in the developing brain.Horm Res 1998.PubMed 9554468 · doi:10.1159/000053066
  3. Ricort JM, Binoux M. Insulin-like growth factor (IGF) binding protein-3 inhibits type 1 IGF receptor activation independently of its IGF binding affinity.Endocrinology 2001.PubMed 11145572 · doi:10.1210/endo.142.1.7915
  4. Forbes B, Szabo L, Baxter RC, et al.. Classification of the insulin-like growth factor binding proteins into three distinct categories according to their binding specificities.Biochem Biophys Res Commun 1988.PubMed 2973786 · doi:10.1016/s0006-291x(88)80032-9
  5. Li YM, Schacher DH, Liu Q, et al.. Regulation of myeloid growth and differentiation by the insulin-like growth factor I receptor.Endocrinology 1997.PubMed 8977425 · doi:10.1210/endo.138.1.4847
  6. Pamuklar ZN, Chen J, Muehlbauer M, et al.. Necdin-E2F4 interaction provides insulin-sensitizing effect after weight loss induced by gastric bypass surgery.Surg Obes Relat Dis 2013.PubMed 22138333 · doi:10.1016/j.soard.2011.10.014
  7. Viñals F, Ventura F. Myogenin protein stability is decreased by BMP-2 through a mechanism implicating Id1.J Biol Chem 2004.PubMed 15322112 · doi:10.1074/jbc.M408059200
  8. Kaplan-Lefko PJ, Sutherland BW, Evangelou AI, et al.. Enforced epithelial expression of IGF-1 causes hyperplastic prostate growth while negative selection is requisite for spontaneous metastogenesis.Oncogene 2008.PubMed 18026134 · doi:10.1038/sj.onc.1210943
  9. Goldspink G, Harridge SD. Growth factors and muscle ageing.Exp Gerontol 2004.PubMed 15501012 · doi:10.1016/j.exger.2004.08.010
  10. Goldspink G, Wessner B, Bachl N. Growth factors, muscle function and doping.Curr Opin Pharmacol 2008.PubMed 18353722 · doi:10.1016/j.coph.2008.02.002
  11. Harridge SD. Ageing and local growth factors in muscle.Scand J Med Sci Sports 2003.PubMed 12535315 · doi:10.1034/j.1600-0838.2003.20235.x
  12. Dai Z, Wu F, Yeung EW, et al.. IGF-IEc expression, regulation and biological function in different tissues.Growth Horm IGF Res 2010.PubMed 20494600 · doi:10.1016/j.ghir.2010.03.005
  13. Janssen JA. Impact of Physical Exercise on Endocrine Aging.Front Horm Res 2016.PubMed 27348867 · doi:10.1159/000445158
  14. Goldspink G. Gene expression in skeletal muscle.Biochem Soc Trans 2002.PubMed 12023866
  15. Goldspink G. Age-related loss of skeletal muscle function; impairment of gene expression.J Musculoskelet Neuronal Interact 2004.PubMed 15615114
  16. Heilig CW, Deb DK, Abdul A, et al.. GLUT1 regulation of the pro-sclerotic mediators of diabetic nephropathy.Am J Nephrol 2013.PubMed 23817135 · doi:10.1159/000351989

Literature retrieved from PubMed on October 16, 2026, favouring human studies and reviews. Numbered markers in the text show which paper supports which statement; uncited entries are background reading.

Read this first This page compares published reference data. It is not medical advice and not a recommendation to use either compound. Several compounds documented on this site are not approved for human use.