HNG Reconstitution Calculator

No. HNG (S14G-humanin) has no FDA approval, no human clinical trials, and no published human dosing. The evidence ceiling is preclinical: rodent disease models, in-vitro human cell lines, and one porcine cardiac study (animal). Two early Alzheimer's-related HNG papers were retracted and should be excluded from evidence weighting. Any human use is experimental, off-label, and outside any regulatory framework (community protocol).

HNG is a synthetic analogue of the endogenous mitochondrial-derived peptide humanin; the Ser14→Gly substitution confers ~1,000-fold greater potency than native humanin in cell assays (in-vitro). Core actions across models: restoring glutathione/SOD and lowering MDA; suppressing NF-κB/TLR4-driven inflammation; inhibiting apoptosis through Bax/Bcl-2 and caspases; preserving mitochondrial ATP and complex I (animal). Protection is documented in kidney, heart, brain, lung, ovary, and male germ cells. No lifespan or aging-biomarker study exists; the longevity designation is inference from this cytoprotective profile.

No oral data exist; a 24-amino-acid peptide would predictably fail GI absorption, and the published literature is not exclusively parenteral: i.v., i.p., i.c.v., and intranasal delivery systems have all been studied for brain exposure (animal). Systemic i.p. dosing did protect brain in ICH and TBI models. For human use, subcutaneous injection is the standard route for this injectable peptide (community protocol); no SC pharmacokinetic data exist.

No established human dose, all figures are animal disease models: 2 mg/kg i.v. single bolus in rat renal I/R and porcine myocardial I/R; 2.5–5 mg/kg i.p. (asthma); 3–6 mg/kg i.p. (acute lung injury); 5 mg/kg/day i.p. ×21 days (intrauterine adhesions); 10 mg/kg i.p. (ovarian insufficiency). Community longevity-type protocols use far lower, microgram-range daily SC doses (community protocol), orders of magnitude below demonstrated animal effect sizes. Any human number is extrapolation.

No human safety data; rodent exposures run from hours to ~3 months (animal). In diabetic pregnant mice, HNG reduced maternal glucose, raised insulin, and improved fetal survival and growth. In cyclophosphamide-treated male mice, HNG spared germ cells and leukocytes, enhanced the drug's anti-metastatic effect, and suppressed IGF-1. Children with IBD show low endogenous humanin, a biomarker finding, not a treatment basis. Pregnancy, lactation, pediatrics: no data, avoid (community consensus).

Unknown in humans. Tested in animals: single bolus in ischemia-reperfusion; 16 days (asthma); 21 days (intrauterine adhesions); ~3 months daily i.p. improved cognition and reduced amyloid in middle-aged AD-model mice without reported toxicity. Beyond ~3 months, nothing is published. Community use is typically cyclical, week-scale courses (community protocol).

The only direct comparison (human myotubes, in-vitro): against dexamethasone-induced atrophy, MOTS-c fully preserved myotube area and fusion index, raised Akt phosphorylation, and blunted MURF1; HNG preserved area and blunted STAT3 but did not rescue fusion index or E3-ligase expression. HNG's edge is breadth: large-animal cardiac data, ovarian and anti-fibrotic effects, and ~1,000-fold potency over native humanin. No human comparative data exists.

HNG remains disordered and stable in aqueous buffer at 37°C, resisting the irreversible β-sheet transition seen in native humanin (in-vitro). Practical handling: store lyophilized powder frozen (−20°C); reconstitute with bacteriostatic water; refrigerate and use within ~30 days (community protocol). No official reconstituted-product stability data exist. Travel: HNG is not a controlled substance in most jurisdictions but is unapproved for human use; syringes carry separate rules, check local law (practical guidance).