Humanin
Mitochondrial-derived peptide
Humanin (Mitochondrial-derived peptide) is a longevity & bioregulators research compound. Mitochondrial-encoded cytoprotective peptide — anti-apoptotic and metabolic-protective signaling, sibling to MOTS-c.
Humanin quick facts
| Reported research dose | 0.5mg-2mg |
| Route | Subq |
| Frequency | 1x Daily · Varies |
| Half-life | ~1.5 hrs |
| Forms | Injectable |
| Evidence level | Animal + early |
Longevity/cytoprotection interest, still early-stage. In the MOTS-c family.
How Humanin works
Mitochondrial-encoded cytoprotective peptide — anti-apoptotic and metabolic-protective signaling, sibling to MOTS-c.
Proposed benefits
Researched for mitochondrial and cellular-energy support, tissue-specific bioregulation and healthy-aging pathways.
Where to get Humanin
Buy Humanin at Disguised Alpha →Bacteriostatic water is the diluent — sterile water with 0.9% benzyl alcohol, which is what lets a vial be drawn from more than once. It does not come with the vial, and unlike the compound it is bought again every time.
Need bacteriostatic water? Get it at AminoWell USA (my company) → Code CAMERON.
The evidence for Humanin
Graded by what exists behind each claim.
✅ Clinically validated
- No randomized trials of administered humanin. The human evidence is observational and about endogenous levels: circulating humanin declines with age, and higher levels have been reported in the offspring of centenarians and in long-lived individuals.
- That is association, not causation, and the direction is not established — higher humanin may be a marker of better mitochondrial health rather than a cause of it.
📊 Correlative data
- Limited community use, generally as part of a mitochondrial or longevity stack. The analog HNG is more potent in the animal work than native humanin and is what most research material claims to be.
- Beyond that the record is self-reported: community dosing logs are real information about tolerability and almost none about efficacy.
🧪 Theoretical / extrapolated
- A mitochondrial-derived peptide — encoded in mitochondrial DNA rather than nuclear DNA, which is itself notable; it was the first of its kind identified. It is cytoprotective, anti-apoptotic, and improves insulin sensitivity in rodent models.
- It signals through cell-surface receptors including the formyl peptide receptor, so it acts as a retrograde signal from mitochondria to the rest of the body — a genuinely novel category of biology.
- Anti-apoptotic is the double edge. Preventing cell death is protective in neurons and cardiomyocytes and is precisely what you do not want in a cell that has accumulated damage. No one has characterized where that line sits.
What community dosing logs are worth →
How to read these tiers: they say how much human evidence exists, not how well something works — and ✗ flags harm, never a disappointing trial. How the evidence tiers work →
What Humanin actually does
Humanin is a 24-amino-acid peptide Matsuoka 2010 Gong 2014 encoded not by the nuclear genome but by a short open reading frame inside the mitochondrial 16S ribosomal RNA gene. It was not designed and not predicted — it was found in a functional screen for cDNAs that stopped neurons dying from familial Alzheimer's mutations, it turned out to be secreted into the culture medium, and its rescue activity depended on its primary structure Hashimoto 2001.
The sequence is MAPRGFSCLLLLTSEIDLPVKRRA, and the chemistry that follows from it is not on any vendor's page. Computed from the sequence: molecular weight 2,687.28 Da, isoelectric point 9.82, net charge about +2 at blood pH — a cationic peptide, not an anionic one. It carries one free cysteine (C8) and one methionine (M1). A single unpaired thiol is a dimerization site: two humanin molecules in one vial can form a disulfide, and copper catalyzes exactly that reaction, which is a real constraint on mixing this peptide with a copper complex.
There is no such thing as "the humanin receptor." Two distinct systems are documented. Neuroprotection runs through a trimeric IL-6-family receptor made of CNTFRα, WSX-1 and gp130 Matsuoka 2010. Separately, the analog [Gly14]-humanin restores cathepsin D activity in human endothelial cells through the formyl peptide receptor FPRL1 — an effect abolished by FPRL1 siRNA and by the FPRL1 inhibitor Boc-MLF Ding 2020. Different receptor families, different cell types, both real.
And here is the fact that reframes everything below. The peptide sold as humanin is native humanin. Almost none of the animal work used it. Yen 2020 treated mice with the HNG analog; Ding 2020 used [Gly14]-humanin; Muzumdar 2009 reproduced the peripheral effect with HN derivatives and lowered glucose in diabetic rats with potent HN analogs. A single-residue substitution at position 14 is what most of the in-vivo literature is actually about, and it is not what is in the vial.
Cell, rodent, human — and where it stops
Step one, in cells. Functional cDNA screening identified humanin as a factor that abolished neuronal death caused by a wide spectrum of familial Alzheimer's genes and by amyloid-β; the peptide was secreted, and activity tracked its primary structure Hashimoto 2001.
Step two, in a worm and in transgenic mice. Overexpression in C. elegans extended lifespan in a daf-16/FOXO-dependent manner; humanin-transgenic mice showed overlapping phenotypes with increased protection from toxic insult Yen 2020. Genetic gain of function, not a drug.
Step three, rodents given the peptide, and the route matters enormously. Muzumdar 2009 improved insulin sensitivity with continuous intraventricular infusion — directly into the cerebral ventricles — acting through hypothalamic STAT-3. Peripherally delivered HN derivatives reproduced the effect, and the authors are explicit that it remained centrally mediated. Yen 2020 gave the HNG analog biweekly and reported improved metabolic healthspan and reduced inflammatory markers.
Step four, humans, and this is where it stops being a drug story. There is no interventional human study of humanin. What exists is observational, and it contradicts itself. On one side: humanin declines with age in rodents, mice and humans Muzumdar 2009, stays flat in the exceptionally long-lived naked mole-rat, is lower in Alzheimer's disease and MELAS, and is higher in the children of centenarians Yen 2020. On the other side, a dedicated human mitokine study found humanin increased in old age, highest in centenarians, associated with worsened health parameters, and inversely correlated with survival in the oldest subjects — which the authors read as a stress response, a marker of biological age rather than a cause of longevity Conte 2019.
The obstacle, in one sentence. The literature cannot yet agree on whether a high humanin level in a person is a sign of resilience or a sign of damage, and nobody has run the trial that would settle it — so injecting the peptide is an intervention whose desired direction is genuinely uncertain, on top of the separate problem that the molecule with the animal data behind it is an analog rather than this one.
Humanin pharmacokinetics — how much of it actually gets in
Route: subcutaneous, and no human pharmacokinetic study of humanin exists by that route or any other. The half-life on this site's card, about 1.5 hours, cannot be traced to a published measurement in the papers this page is built on. Treat it as unsourced.
What degrades it. A 24-residue peptide with a free N-terminal amine and a free C-terminal carboxyl is an ordinary substrate for plasma aminopeptidases and endopeptidases; there are no D-amino acids, no cyclization and no terminal protecting groups in the native sequence to slow that down. The strongest indirect evidence for this is that the field itself moved to analogs: HNG and [Gly14]-humanin carry a substitution at position 14 and are what the in-vivo work uses Yen 2020 Ding 2020.
The oral barrier is absolute. At 2,687 Da and about +2 net charge, humanin is far outside the size range for passive intestinal absorption, and gastric and brush-border proteolysis would act on it before size ever became the limiting factor. There is no oral humanin study, and there is no plausible route by which an oral dose reaches a mitochondrion.
The injection reaches the blood; the mechanism is in the brain. The insulin-sensitizing result that people take this for was produced by intracerebroventricular infusion and was explicitly centrally mediated Muzumdar 2009. A subcutaneous injection of 0.5–2 mg has to clear the blood-brain barrier to reproduce that, and no measurement of humanin in human cerebrospinal fluid after a peripheral dose has ever been published. The vial chemistry adds one practical constraint: the free cysteine means reconstituted peptide should be used promptly and should not share a syringe with a copper-containing peptide.
What would have to be true, and how you would know it was not
Four predictions. The fourth runs directly against the reason people buy it.
1. If the insulin mechanism transfers, insulin falls before anything else. The rodent result is improved insulin sensitivity Muzumdar 2009. Draw fasting insulin and HbA1c at baseline and at 12 weeks, holding training and diet constant. This is the cleanest available test of whether a peripheral injection is doing anything a central infusion did.
2. Inflammatory markers should fall, modestly. Yen 2020 reported reduced inflammatory markers with the HNG analog. Add hs-CRP to the same two draws. A person starting at 0.4 mg/L has no room to show this; someone starting at 2–3 mg/L does, which is worth knowing before you spend the money.
3. IGF-1 should not rise. The association described in the review literature runs between humanin and the growth hormone/IGF-1 axis Gong 2014, with the highest humanin levels in long-lived, growth-signaling-deficient models. Measure IGF-1 alongside. A rise would point away from the mechanism this compound is sold on and toward something else in the stack.
4. The prediction that cuts against it: if more humanin were simply better, the people with the most of it should be doing best — and in the oldest human cohort measured, they were doing worst. Conte 2019 found circulating humanin highest in centenarians, associated with worse health parameters, and inversely correlated with survival. The falsifiable form of that is a population claim, not a personal one: if humanin supplementation were beneficial, then baseline humanin should predict outcome positively in a prospective cohort. It did the opposite. Anyone injecting it is betting that the cross-sectional correlation is confounded by underlying illness — a reasonable bet, and an untested one.
What nobody has tested yet
Nobody has drawn a humanin level before and after injecting humanin into a person. The assay plainly exists — Conte 2019 measured circulating humanin across an entire aging cohort including centenarians. Pairing that assay with a single 1 mg subcutaneous dose in ten volunteers would produce the first human pharmacokinetic curve for this peptide, and it would immediately settle whether an injection moves the number at all.
Nobody has run native humanin against HNG head to head, at the same dose, in the same experiment. This is the experiment that matters most commercially, because the product is the native peptide and the animal data are largely about the analog Yen 2020 Ding 2020. A two-arm mouse study with a metabolic read-out would tell buyers whether they are holding the molecule the literature is about.
Nobody has followed humanin longitudinally in the same people. The declines-with-age and rises-with-age findings are both cross-sectional. Annual draws in one cohort over a decade would distinguish "humanin falls as you age" from "humanin rises as you get sick," and those two sentences imply opposite therapeutic strategies.
Nobody has checked whether the vial contains monomer. One free cysteine per molecule makes disulfide-linked dimer the obvious degradation product in solution, and a mass-spectrometry check on reconstituted vendor peptide at day 0 and day 14 is a cheap, publishable answer to a question nobody has asked.
Humanin — its own safety story, not its class's
The risk here is not toxicity, it is what the mechanism is for. Humanin's defining action is the suppression of apoptosis. That is what was screened for Hashimoto 2001, and a molecule selected for keeping stressed cells alive does not distinguish a neuron you want to keep from a cell you do not.
That is not a hypothetical, and the paper is recent. Cheng 2024 reports that nanomolar concentrations of humanin promote temozolomide resistance in glioblastoma by activating the DNA damage response through GP130 signaling, that models recapitulating intratumoral humanin release showed accelerated blood-tumor barrier formation, and that blocking GP130 restored chemotherapy efficacy. GP130 is one of the three components of the receptor complex humanin's neuroprotection runs through Matsuoka 2010. The protective mechanism and the chemoresistance mechanism are the same mechanism.
The second thing that is specific to this peptide: the human correlation points the wrong way in the oldest people. Humanin was highest in centenarians, associated with worse health parameters and inversely correlated with survival Conte 2019. Whatever the explanation, "raise it further" is not obviously the conclusion.
Three practical items nothing else on this site will tell you. (1) The product is native humanin; the in-vivo literature is largely HNG. (2) One free cysteine means the reconstituted peptide can dimerize, and copper accelerates it — do not co-reconstitute with a copper peptide. (3) There is no human dose-finding study of any kind, so the 0.5–2 mg on this site's card is not a dose derived from a trial; it is a convention. Anyone on active cancer treatment should read the paragraph above about GP130 as a reason to stay away entirely rather than as a caution.
Sources read for this page
- Hashimoto Y, Niikura T, Tajima H, Yasukawa T, Sudo H, Ito Y, Kita Y, Kawasumi M, Kouyama K, Doyu M, Sobue G, Koide T, Tsuji S, Lang J, Kurokawa K, Nishimoto I. A rescue factor abolishing neuronal cell death by a wide spectrum of familial Alzheimer's disease genes and Abeta.. Proc Natl Acad Sci U S A 2001 · PMID 11371646
- Matsuoka M. Humanin and the receptors for humanin.. Mol Neurobiol 2010 · PMID 19997871
- Muzumdar RH, Huffman DM, Atzmon G, Buettner C, Cobb LJ, Fishman S, Budagov T, Cui L, Einstein FH, Poduval A, Hwang D, Barzilai N, Cohen P. Humanin: a novel central regulator of peripheral insulin action.. PLoS One 2009 · PMID 19623253
- Yen K, Mehta HH, Kim SJ, Lue Y, Hoang J, Guerrero N, Port J, Bi Q, Navarrete G, Brandhorst S, Lewis KN, Wan J, Swerdloff R, Mattison JA, Buffenstein R, Breton CV, Wang C, Longo V, Atzmon G, Wallace D, Barzilai N, Cohen P. The mitochondrial derived peptide humanin is a regulator of lifespan and healthspan.. Aging (Albany NY) 2020 · PMID 32575074
- Conte M, Ostan R, Fabbri C, Santoro A, Guidarelli G, Vitale G, Mari D, Sevini F, Capri M, Sandri M, Monti D, Franceschi C, Salvioli S. Human Aging and Longevity Are Characterized by High Levels of Mitokines.. J Gerontol A Biol Sci Med Sci 2019 · PMID 29955888
- Gong Z, Tas E, Muzumdar R. Humanin and age-related diseases: a new link?. Front Endocrinol (Lausanne) 2014 · PMID 25538685
- Ding Y. [Gly14]-humanin restores cathepsin D function via FPRL1 and promotes autophagic degradation of Ox-LDL in HUVECs.. Nutr Metab Cardiovasc Dis 2020 · PMID 32917500
- Cheng J. Myeloid cells coordinately induce glioma cell-intrinsic and cell-extrinsic pathways for chemoresistance via GP130 signaling. Cell Rep Med 2024 · PMID 39053460
Humanin — safety, predicted from mechanism
Predicted from mechanism, not from a human safety trial. How that reasoning works →
What the mechanism predicts
Derived from the molecule, not a trial.
- These act on mitochondrial function, NAD+ availability, sirtuin signaling or cellular clearance. The honest prediction is that acute harm is unlikely and the interesting risks are theoretical and long-range — which is a different shape of risk, not an absence of one.
- Growth and clearance signals cut both ways. Anything that improves the efficiency of cell survival is also improving it for cells you would rather not keep. Anything that pushes clearance hard is doing so indiscriminately.
- The near-term, practical ones: NAD+ precursors and infusions commonly cause flushing and a strong sensation if pushed fast, and several compounds in this class are stimulating enough to disrupt sleep.
What has actually been reported
- Generally well tolerated at studied doses. NAD+ infusion discomfort is rate-dependent and resolves by slowing down.
- The human evidence is mostly short trials with surrogate endpoints — a marker moved, not a life changed. That is worth knowing before you build a decade-long habit on it.
How to reduce the risk
Same mechanism as the prediction.
- Slow the infusion rate. Almost all NAD+ discomfort is rate, not dose. There is no prize for finishing quickly.
- Dose earlier in the day. Several of these are subtly stimulating, and sleep is where most of the repair you are paying for happens.
- Pick an endpoint you can actually measure, and take the baseline before you start. This is the class most prone to spending years on something with no way of knowing whether it did anything.
- Fix the basics first. Sleep, training and bloodwork move the same markers further than anything on this list, and they are free. A longevity compound stacked on four hours of sleep is a rounding error.
What it does to your bloodwork
A fact about the assay.
- There is no NAD+ assay worth ordering clinically. Judge this class on downstream markers — inflammatory markers, lipids, fasting glucose, and whatever your baseline panel showed as out of range.
Don't run this if
- Active malignancy, for the survival-signaling reasoning above.
- Pregnancy — uncharacterized.
The honest unknown
- Whether any of it extends healthspan in humans. Every honest person in this field is running on mechanism and animal data, and this catalog should say so rather than imply otherwise.
Not medical advice. If you take prescription medication or have a diagnosed condition, check this with a pharmacist or doctor.
Humanin — interference & stacking
Predicted from mechanism, not from an interaction study. How mechanism-predicted claims are made →
What Humanin moves on your bloodwork
Expected direction, not a measured one.
- hs-CRP (High-Sensitivity C-Reactive Protein) — ↓ expected to fall
If a repair peptide is doing anything systemic, inflammation is where it would plausibly show.
What to do: Worth a baseline if you are running one for a chronic issue rather than an acute injury. - Comprehensive Metabolic Panel (CMP) — ◆ worth watching
Standard baseline. Nothing in this class predicts a specific abnormality — which is itself worth saying rather than inventing one.
What to do: Annual is fine unless something changes.
The honest position on this class is that the proliferation question is unresolved — anything that accelerates tissue repair is acting on pathways cancer also uses. Nobody has studied it properly either way.
- How to work up to it, and when not to
- When to take it, and why that window
- Cycle length
- Time off between cycles
- Fasted or fed, and when in the day
- Needle gauge and injection site
- Coach Cam's personal notes
- Which compounds push the same lever, and why the dose adds up faster than people count
- What blunts it — the stacks that waste your money
- What compounds the risk, so a side effect arrives sooner than any one of them suggests
- Coach Cam's read on running it alongside the rest of your protocol
Everything above is free and stays free. Skool is where it becomes a plan — Humanin in an order, with the rest of what you're running.
Unlock in Skool — $10/mo →Bloodwork to run alongside Humanin
Baseline first, then again at 8–12 weeks.
| Marker | What it’s watching for |
|---|---|
| hs-CRP (High-Sensitivity C-Reactive Protein) | Chronic low-grade inflammation is the process most of these target |
| ApoB (Apolipoprotein B) | Counts the particles that actually cause plaque, unlike LDL-C |
| HbA1c (Hemoglobin A1c) | Glycation, which is the other half of the ageing story |
| Comprehensive Metabolic Panel (CMP) | Liver and kidney — the two organs that clear everything you take |
| Complete Blood Count (CBC) with Differential | The cheapest broad screen there is |
The Longevity Baseline panel covers these in one order — 13 markers, $219.10 with the discount applied.
Check results you already have → · All 103 markers A–Z
Humanin — frequently asked questions
What is Humanin?
Humanin (Mitochondrial-derived peptide) is a longevity & bioregulators research compound. Mitochondrial-encoded cytoprotective peptide — anti-apoptotic and metabolic-protective signaling, sibling to MOTS-c.
Is the full Humanin protocol on this page?
The reported research dose is on this page, along with how Humanin works and the evidence behind it. The protocol — how to work up to it, frequency, cycle length, time off, what not to stack it with and Coach Cam's notes — is inside Skool.
What is the half-life of Humanin?
Humanin has an approximate half-life of ~1.5 hrs, which is part of what determines how often it's dosed.
What's the evidence behind Humanin?
Current evidence level: Animal + early. Humanin is offered for research purposes only and is not an approved medicine.
Humanin inside a finished plan
One arm of 1 Protocol Blueprint, free to read in full.
What Humanin is used for
Humanin appears under 3 goals in the goal router.
Related Longevity & Bioregulators compounds
Where this goes next
Humanin is the mitochondrial arm of this plan. The page above is the free breakdown of one compound; the plan it belongs to — the dosing, the order to correct things in, the week-by-week schedule and what to retest — is a lesson inside Skool.