Dr. Pep

Peptides · Mitochondrial-derived peptide

Humanin: what the studies show

Every line below comes from a study, label or regulator record, checked by two models, with the source linked. Information, not medical advice. For adults 18+.

What it is

  • Humanin is a short peptide the body makes from a gene in its own mitochondria, the cell's energy units. It is endogenous, which means people already have it in their blood and tissues. The lab version used in most animal work is humanin-G (S14G-humanin, HNG), a more potent analogue.[1][2]
  • Humanin is a different molecule from MOTS-c, another mitochondrial peptide. Several papers study both together, but results for one are not results for the other.[3]

Bottom line

  • Almost everything known about humanin comes from rodents and cells, plus human studies that only measure the body's own humanin levels. Those levels change with age, diabetes, exercise and illness, but that does not show that taking humanin treats anything. The corpus has no human trial in which people were given humanin.[4][5][6]

What the human studies found

  • Human studies in the corpus measure humanin that the body already makes. In 225 adults, blood humanin was lower in type 2 diabetes and fell with age and HbA1c. This is a cross-sectional study and shows association only.[4]
  • In a small randomised study (10 per group), 45 minutes of cycling raised plasma humanin, but resistance exercise did not. This shows exercise changes the body's own level. It does not show that giving humanin has any effect.[5]
  • In an 8-week trial in 90 women with type 2 diabetes, combined training raised humanin levels, with astaxanthin (8 mg/day, an antioxidant, not humanin) adding to the effect on other markers. The trial gave no humanin. The authors suggest humanin may mediate the benefit, which the trial design cannot show.[7]
  • In a hospital study, serum humanin was higher in 20 patients with a serious Klebsiella bloodstream infection than in 20 healthy controls. In atrial fibrillation, humanin and MOTS-c were lower in human atrial tissue, and plasma MOTS-c was lower in 39 patients than in 39 controls. Both findings are about natural levels.[6][3]
  • COPD (observational, 165 patients with stable COPD and 49 smokers without it): higher blood humanin was linked to more flare-ups and to malnutrition over 12 months of follow-up. This is an association with the body's own levels.[8]
  • Chronic hemodialysis (83 patients followed for 24 months): both low and high blood humanin were linked to more cardiovascular events (33 patients had one), a curved pattern. Observational only.[9]

Known risks and side effects

  • No human safety data for given humanin exist in the corpus. The animal studies above are short and mostly report benefits, so they say little about harm.[6][10]
  • Some high-profile humanin papers have been retracted, so the early literature should be read with care.[11][12]

Legal status

  • The corpus holds no regulatory document about humanin. FDA's July 2026 briefing document in the corpus covers MOTS-c, not humanin, and names humanin only in a reference list.[13]

Sources

  1. [1] Humanin and Its Pathophysiological Roles in Aging: A Systematic Review.
  2. [2] S14G-humanin attenuates renal ischaemia-reperfusion injury, potentially through activation of STAT3 and ERK1/2 signalling pathways in rats.
  3. [3] Humanin and MOTS-c Attenuate Atrial Fibrillation by Suppressing Fibrosis and Mitochondrial Dysfunction.
  4. [4] Mitochondrial-Derived Peptides Are Down Regulated in Diabetes Subjects.
  5. [5] Acute endurance exercise stimulates circulating levels of mitochondrial-derived peptides in humans.
  6. [6] Humanin Attenuates Inflammatory Liver Injury and NF-κB Activation During Systemic Hypervirulent Klebsiella pneumoniae Infection.
  7. [7] Redox-sensitive miRNAs and Humanin could mediate effects of exercise and astaxanthin on oxidative stress and inflammation in type 2 diabetes.
  8. [8] Associations between serum mitokine levels and outcomes in stable COPD: an observational prospective study.
  9. [9] Circulating Humanin Improves the Prognostic Accuracy of Cardiovascular Risk Models in Chronic Hemodialysis Patients.
  10. [10] Repeated Humanin Treatment Attenuates Oxidative Stress, Inflammation, and Apoptosis in Diabetic Cardiac Tissue.
  11. [11] S14G-humanin inhibits Aβ1-42 fibril formation, disaggregates preformed fibrils, and protects against Aβ-induced cytotoxicity in vitro.
  12. [12] Protective Effects of Colivelin Against Alzheimer's Disease in a PDAPP Mouse Model.
  13. [13] July 23-24, 2026, Meeting of the Pharmacy Compounding Advisory Committee – FDA Briefing Document for MOTS-c-Related Bulk Drug Substances (MOTS-c (free base) and MOTS-c acetate)