MGF Reconstitution Calculator

No. MGF (Mechano Growth Factor, IGF-1Ec) has no regulatory approval for any therapeutic or performance indication in any jurisdiction,. It circulates as an unregulated "research compound" and on the black market, where seized products often differ chemically from endogenous MGF, e.g., C-terminal amidated analogues. The World Anti-Doping Agency (WADA) classifies MGF as a banned substance. All efficacy data are animal or in-vitro; no human trial of exogenous MGF administration exists.

MGF is one of three IGF-1 splice variants, defined by its unique Ec E-domain tail. Two distinct products circulate. Full-length MGF directly activates the IGF-1 receptor, reaching the same maximal activation as recombinant IGF-1 at high equimolar doses but with ~9-fold lower potency (EC50 7.83 vs 0.86 nmol/L); it also stimulates insulin receptors. The synthetic 24-amino-acid E-domain fragment (MGF-Ct24E) increases cell proliferation, stem-cell homing, and neuroprotection through IGF-1R-independent receptors,. PEGylated MGF (PEG-MGF) is a third form marketed for longer half-life. Note the E-peptide is a laboratory synthetic; endogenous MGF is produced only as the full prohormone.

No human dose-finding data exist. Mouse cardiac studies used E-domain peptides at 2.25–9 mg/kg/day, with paradoxically opposing dose-dependent effects; in-vitro tissue repair responses occur at 10–100 ng/mL. Community protocols (community protocol): full-length MGF 100–400 mcg injected intramuscularly, split bilaterally into the trained or injured muscle, immediately post-training or post-injury, 1–3×/week in 4–8 week cycles; PEG-MGF 200–500 mcg subcutaneous 2–3×/week. MGF is injectable only: no effective oral form. Reconstitute with bacteriostatic water, refrigerate at 2–8°C, and use within ~30 days of reconstitution (practitioner consensus).

(animal) The E-domain increases myoblast proliferation while delaying terminal differentiation. Aged rodents lose the ability to express MGF after mechanical overload, correlating with failed hypertrophy and satellite-cell activation,. A dual IGF-1Ea/Ec plasmid increased muscle mass in rodent injury and age-atrophy models. Human data cover only endogenous expression: IGF-1Ec mRNA rises acutely after eccentric exercise, and blunted exercise-induced IGF-1Ec under hypogonadism tracks reduced hypertrophy (RCT). One in-vitro study found MGF E-peptide had no effect on myoblasts or primary muscle stem cells. No human efficacy data exist for exogenous MGF; anabolic claims rest on animal work and anecdote.

IGF-1 LR3 and mature IGF-1 signal primarily through the IGF-1 receptor; full-length MGF binds the same receptor with ~9-fold lower affinity yet equal maximal activation. MGF's distinct claim is E-domain bioactivity, anti-apoptotic, pro-migratory, and stem-cell-homing effects that do not require IGF-1R,. IGF-1 LR3 is engineered for extended half-life, while PEG-MGF extends the E-peptide's exposure. No head-to-head comparative studies exist. Practical convention (community protocol): MGF is used for site-specific muscle, tendon, and joint healing claims; LR3 and GH secretagogues for systemic growth.

(observational/in-vitro) The E-domain is mitogenic through IGF-1R-independent signaling. MGF/IGF-1Ec is overexpressed in prostate cancer, colorectal adenomas and carcinomas (expression rises with dysplasia grade), and osteosarcoma, where exogenous MGF-E promoted proliferation, migration, and invasion. Conversely, an anti-Ec antibody reduced tumor growth in mice. No human carcinogenicity data exist; these findings argue against use with any cancer history or elevated risk. Cardiomyocyte and mouse data show dose-dependent, partly paradoxical depression of systolic/diastolic function. Full-length MGF's insulin-receptor activation also implies hypoglycemia risk at high doses (mechanistic). Human long-term safety is unknown.

Yes. WADA prohibits MGF and all IGF-1-related peptides, with validated urine screening detecting this peptide class at limits of 5–50 pg/mL. Seized black-market MGF is frequently a C-terminal amidated analogue distinguishable from endogenous MGF by a diagnostic transition at m/z 717.8→431.1, confirming routine detection is feasible. Unregulated supply chains mean product identity, dose, and stacking are uncontrolled. For drug-tested athletes, use carries zero-tolerance exposure risk; no reliable detection window or clearance data have been published (community protocol).