Humanin

Humanin (HN) is a 24-amino-acid mitochondrial-derived peptide (MDP) — the founding member of that class, encoded from the 16S ribosomal RNA region of mitochondrial DNA and first identified in 2001 in surviving neurons from an Alzheimer's-disease patient's brain — the first mitochondrial-derived peptide (MDP) to be described. It acts as a cytoprotective, anti-apoptotic signaling peptide. It is not approved for any use and is supplied strictly for research use only.

Source: A rescue factor abolishing neuronal cell death by a wide spectrum of familial Alzheimer's disease genes and Aβ, Hashimoto Y., Niikura T., Tajima H., et al. (optional, non-blocking: complete list), Proc Natl Acad Sci U S A, 2001

What is Humanin and why does the mitochondrial-derived-peptide mechanism matter?

Humanin was the discovery that showed mitochondrial DNA encodes small bioactive peptides that act outside the mitochondrion — a retrograde signal from mitochondria to the rest of the cell. It protects cells against stress-induced apoptosis by two routes: intracellularly, it binds and antagonizes pro-apoptotic proteins (Bax, BID, IGFBP-3); extracellularly, it signals through a CNTFR/WSX-1/gp130 receptor complex (STAT3) and FPRL1 (ERK1/2). It sits in the same family as MOTS-C — both are mtDNA-encoded MDPs studied for metabolic and longevity effects, though they act on different pathways.

What does the research on Humanin show?

A large preclinical literature (well over 100 studies) reports neuroprotective, cytoprotective, insulin-sensitizing, and anti-inflammatory effects in cell and animal models — but there are no controlled human efficacy trials. As of August 2026 no interventional human clinical trial of administered humanin (or its potent analog HNG) has been published — the "well over 100 studies" are cell and animal experiments plus observational human work measuring naturally occurring (endogenous) humanin, such as reports that circulating humanin declines with age. The cytoprotective, neuroprotective, and metabolic findings all come from those preclinical models. Reported findings include protection against amyloid-β toxicity, reduced apoptosis and reactive oxygen species, and improved metabolic markers, with circulating humanin levels declining with age.

Evidence level: preclinical (in vitro / animal) only

What are the known side effects and safety concerns?

Because Humanin has not been administered to humans in controlled trials, there is no established human side-effect profile or safe dose. As an endogenous cytoprotective peptide its preclinical safety signals are mild, but the absence of human data is the primary consideration. Evidence level: No human data. See the legal status guide.

Why does vendor verification matter, and how does Peptigrity verify?

As a longer (24-residue) synthetic peptide, Humanin is prone to synthesis impurities and truncation, so HPLC purity and mass-spec identity confirmation are the objective checks. Peptigrity collects independent third-party Certificates of Analysis for humanin from shops' official channels and verifies each for authenticity before publishing. Because shops choose which COAs to publish, results reflect the batches shops have made public rather than every production batch — a selection bias we state openly. A community-funded Testing Grant to purchase and test vials anonymously is in development. Tests in the database come from independent labs such as Janoshik Analytical, Freedom Diagnostics, and Chromate; the trust score weights independent lab purity and community reviews equally (50/50). See the independent humanin lab tests on file. See how to read lab results.

Educational information only; not medical advice. Humanin is not approved by the FDA or any regulator for human use. Consult a qualified healthcare provider before using any research compound. Peptigrity does not sell, endorse, or recommend products or vendors.

Frequently asked questions