Comparison
Glepaglutide vs. Humanin
Two peptides side-by-side — identity, evidence base, legal status and known adverse events.
Identity
Category
Research other
Research other
CAS no.
no data
330936-69-1
Molecular weight
no data
2687.27 g/mol
Half-life
no data
no data
Sequence
no data
Met-Ala-Pro-Arg-Gly-Phe-Ser-Cys-Leu-Leu-Leu-Leu-Thr-Ser-Glu-Ile-Asp-Leu-Pro-Val-Lys-Arg-Arg-AlaMechanism of action
Glepaglutide
As a GLP-2 receptor agonist, glepaglutide has a trophic effect on the intestinal mucosa, enlarging the absorptive surface and thereby improving intestinal uptake of nutrients and fluid.
Humanin
Humanin arises from a short open reading frame within the 16S rRNA region of the mitochondrial genome (MT-RNR2) — it is therefore not encoded by nuclear DNA. Mechanistically, preclinical work describes a cytoprotective, anti-apoptotic effect via multiple pathways: an extracellular interaction with a trimeric receptor complex of gp130, CNTFR and WSX-1 with downstream activation of JAK2/STAT3 signalling, as well as intracellular interactions including inhibition of the pro-apoptotic protein BAX (and of tBID), binding to IGFBP-3 with modulation of the IGF-1 axis, and interaction with FPRL1/FPRL2 receptors. These models derive predominantly from cell culture and rodents; the extent to which they reflect human physiology after administration of exogenous synthetic humanin is not established by controlled human trials.
Evidence base
Highest evidence
Human RCT
Human trial
Studies
1
4
of which in humans
1
1
Effects recorded
2
4
Open conflicts
0
1
Documented adverse events
1
0
Legal status
Full entries
Frequently asked questions
- What is the difference between Glepaglutide and Humanin?
- Glepaglutide is classified as "Research other", while Humanin is classified as "Research other". Glepaglutide: Glepaglutide is a long-acting GLP-2 analogue (Zealand Pharma) intended to reduce the need for parenteral support in short bowel syndrome. Humanin: Humanin is a 24-amino-acid mitochondrial-encoded peptide (mitochondrial-derived peptide, MDP) whose open reading frame lies within the 16S rRNA region (gene MT-RNR2) of mitochondrial DNA. It is considered the founding member of the MDP family and was discovered in 2001 by the Hashimoto/Nishimoto group while searching for neuroprotective factors in the brain of an Alzheimer's patient. In basic research (including the laboratory of Pinchas Cohen) humanin is described as a cytoprotective, anti-apoptotic peptide and is studied in the contexts of Alzheimer's/neuroprotection, metabolism/insulin action and aging. The evidence comes almost entirely from cell and animal models and from observations of endogenous levels in humans; controlled human trials of exogenous humanin as a therapeutic are lacking. It is not approved as a medicine anywhere and is traded on the grey market as a research chemical. This page contrasts both neutrally and source-based — with no usage or dosing recommendation.
- Which peptide is better supported by science, Glepaglutide or Humanin?
- The highest available evidence level is "Human RCT" for Glepaglutide and "Human trial" for Humanin. A higher evidence level means more robust data, but says nothing about suitability for an individual. The full body of evidence is on each peptide's own page.
- What is the legal status of Glepaglutide and Humanin in Germany and the United States?
- Germany: Glepaglutide — Unapproved, Humanin — Unapproved. United States: Glepaglutide — Unapproved, Humanin — Research only. These are factual summaries with source and review date on the individual pages.