Hepcidin
The liver hormone that decides how much iron reaches the blood, and what measuring it has and has not achieved
Hepcidin is a small peptide hormone from the liver that acts as the body's iron brake. It binds ferroportin, the protein cells use to push iron out, and makes them destroy it, so less iron reaches the blood. Inflammation and iron loading raise hepcidin; a drive to make red cells lowers it. Too little causes iron overload, too much causes the anaemia of inflammation. It is measured in blood and studied to time iron supplements; hepcidin itself is not given as a treatment.
No established human dose Details ↓
Recommended Dosing
No established human dose
Hepcidin has not been given to people in any of the studies on this page. In the human work it is measured in blood or urine: to set a normal range, to follow its rise after an iron supplement or exercise, and to decide in one trial when children should receive iron.
What is it?
Hepcidin was first pulled out of human urine in 2001 as a small peptide rich in cysteine. Because its gene was active mainly in the liver and the purified peptide slowed the growth of some bacteria and fungi, it was named hepcidin and filed as an antimicrobial peptide. Within months, mice that happened to lack it were found to overload with iron, and the field changed direction: hepcidin turned out to be the hormone that controls iron.
Its job is to set how much iron enters the blood. Iron arrives in plasma from three places: the gut, which absorbs it from food; macrophages, which recycle it from old red cells; and the liver, which stores it. All three release iron through one exporter, ferroportin. Hepcidin binds ferroportin and makes the cell pull it in and break it down, so a high hepcidin level shuts the exits and a low level opens them.
The liver raises hepcidin when iron stores are full and when the body is inflamed, with interleukin-6 as the main inflammatory signal. That second effect is deliberate: lowering blood iron starves invading microbes, and newborns show a sharp, hepcidin-linked drop in blood iron in the first day of life. The cost is the anaemia of inflammation, in which iron is locked away from the marrow even though stores are adequate. When the body needs more red cells, as when growth hormone or testosterone was given to volunteers, hepcidin falls.
Faults in this system explain several diseases. Mutations in HAMP, the hepcidin gene, cause a severe juvenile form of hemochromatosis, and the common adult form involves hepcidin that is too low for the body's iron. At the other end, conditions with high hepcidin, such as chronic kidney disease and some inflammatory illnesses, restrict iron supply.
Since 2008 hepcidin can be measured in serum, and studies of it have changed advice on oral iron: a supplement raises hepcidin for about a day, which blunts absorption of the next day's dose, so alternate-day schedules absorb a larger share. A trial that used hepcidin to decide when Gambian children got iron cut the iron given but raised haemoglobin less than giving iron to every child. Hepcidin itself has not been given to people as a treatment; drugs designed to copy it, such as rusfertide, are separate molecules with their own entries.
Mechanism of Action
Hepcidin works on a single target: it binds the iron exporter ferroportin and causes its removal, so iron stays inside gut cells, macrophages and liver cells instead of entering the blood.
Shuts the iron exit
Binding ferroportin makes the cell internalise and degrade it, so less iron is absorbed from food and less is released from recycled red cells and liver stores.
Inflammation raises it
Interleukin-6 drives hepcidin up during infection and inflammation, which lowers blood iron and over time causes the anaemia of inflammation.
Red-cell demand lowers it
When the marrow needs iron, hepcidin falls; growth hormone and testosterone given to volunteers lowered it, and fasting raised it.
Too little means overload
Without working hepcidin, ferroportin stays open and iron builds up in organs, as in HAMP-related juvenile hemochromatosis.
Published Research
These are studies of hepcidin itself, read from their PubMed abstracts: its discovery, the mouse and human genetics that showed it controls iron, the cell study of how it acts, the serum assay, physiology studies in volunteers, trials that used it to time or target iron, and three reviews and meta-analyses. Hepcidin is measured in every human study here; none gave it as a drug.
Found in urine, made in the liver
Researchers purified a small cysteine-rich peptide from human urine in three forms of different length, the main two being 20 and 25 amino acids long with all eight cysteines paired in disulfide bonds. Its messenger RNA was found mainly in the liver, so they named it hepcidin. In the lab it killed or slowed several fungi and bacteria, which is why it was first described as an antimicrobial peptide.
Mice that cannot make hepcidin overload with iron
Mice lacking the transcription factor USF2 turned out to make no hepcidin, and they slowly loaded iron into the pancreas, heart and liver while their spleens held less iron than normal. The authors concluded that missing hepcidin was what caused the overload, the first sign that the peptide controls iron rather than only fighting microbes.
HAMP mutations cause juvenile hemochromatosis
Two families with a severe, early form of hereditary iron overload carried mutations in HAMP, the hepcidin gene on chromosome 19. This tied a hepcidin defect directly to human iron overload and defined a new type of juvenile hemochromatosis.
Interleukin-6 switches hepcidin on in inflammation
In human liver cell cultures, in mice and in human volunteers, interleukin-6 was the cytokine needed and sufficient to raise hepcidin during inflammation. The authors linked this interleukin-6 to hepcidin axis to the low blood iron that follows infection and inflammatory disease.
Hepcidin removes ferroportin from the cell surface
In cultured cells, hepcidin bound the iron exporter ferroportin, after which ferroportin was pulled inside the cell and broken down, and the cells released less iron. This closed the loop: iron levels set hepcidin output, and hepcidin sets how much ferroportin is left to export iron.
The first serum assay and its normal range
The first serum ELISA for hepcidin gave a 5th to 95th percentile range of about 29 to 254 ng/mL in 65 healthy men and 17 to 286 ng/mL in 49 healthy women, with a lower median in women. Levels tracked ferritin and urine hepcidin, rose from morning to evening and after iron was eaten, were very low in iron deficiency and in hemochromatosis, and were high in inflammation, myeloma and chronic kidney disease.
Daily rhythm, fasting and growth hormone
With a specific hepcidin-25 immunoassay in healthy volunteers, levels were lowest early in the morning and climbed through the day regardless of meals. Three days of fasting roughly tripled hepcidin-25, refeeding reversed it, and growth hormone given to volunteers lowered it by about 65%, presumably by driving red-cell production.
Hepcidin-20 in a general population
In the Val Borbera population study, the shorter hepcidin-20 form was detectable in 854 of 1,577 people at about 14% of the hepcidin-25 level. The ratio between the two forms rose with ferritin, which the authors said argues against hepcidin-20 being only a breakdown product, and they warned that assays which cannot tell the forms apart may misread hepcidin-25.
An iron dose raises hepcidin and blunts the next dose
In 54 iron-depleted, non-anaemic young women given isotope-labelled ferrous sulfate, iron doses of 60 mg or more raised serum hepcidin 24 hours later and cut absorption of the next day's dose by 35 to 45%. A sixfold larger dose gave only about three times more absorbed iron, and splitting iron into twice-daily doses did not add much. The authors said the day-long hepcidin rise supports giving iron on alternate days.
Newborns drop their blood iron within hours
In 120 healthy Gambian newborns, transferrin saturation fell from about 48% in cord blood to about 24% by 24 hours of age, alongside high hepcidin and interleukin-6. Serum with lower transferrin saturation supported less growth of four bacteria that cause newborn sepsis, which the authors read as a hepcidin-driven defence.
Testosterone lowers hepcidin during a calorie deficit
In a randomised, placebo-controlled trial in 50 healthy young men on a 28-day energy deficit, weekly testosterone injections lowered hepcidin by 41% compared with placebo, raised erythropoietin and preserved red-cell production. Erythroferrone did not differ between groups, so the fall in hepcidin did not seem to run through that signal.
Alternate-day iron in infants
In stable-isotope studies in Kenyan infants, two thirds of them anaemic, an iron dose raised plasma hepcidin 24 hours later and slightly reduced absorption of a dose given the next day, but not of a dose given two or three days later. Morning and afternoon doses were absorbed equally well.
Hepcidin-guided iron fell short of giving iron to all
In a randomised, double-blind trial in 407 anaemic Gambian children aged 6 to 23 months, giving iron only in weeks when plasma hepcidin was low did cut total iron given by half or more, but it raised haemoglobin less than WHO's universal daily iron and failed the non-inferiority margin. Adverse events and infections did not differ between the groups.
Exercise raises hepcidin 1.5 to 2.5 times
An individual participant data meta-analysis found that exercise raises hepcidin about 1.5 to 2.5-fold, peaking three to six hours afterwards. Pre-exercise hepcidin explained about 44% of the variation in the three-hour value, and exercise duration explained most of the size of the rise; women tended to show a smaller rise than men.
Liver disease moves hepcidin both ways
A meta-analysis of studies using ELISA found serum hepcidin lower than controls in hepatitis C, alcohol-related liver disease and cirrhosis of any cause, higher in non-alcoholic fatty liver disease, and no different in hepatitis B.
Hepcidin in health and disease
This review describes hepcidin as the hormone that sets plasma iron and total body iron by controlling ferroportin. Levels go up with iron loading and inflammation and down with stimulated red-cell production and in pregnancy; too little hepcidin causes hemochromatosis and iron loading anaemias, and too much causes iron-restricted anaemias such as the anaemia of inflammation.
No Established Human Dose
Hepcidin has not been given to people in any of the studies on this page. In the human work it is measured in blood or urine: to set a normal range, to follow its rise after an iron supplement or exercise, and to decide in one trial when children should receive iron. The drugs that act like hepcidin in people are separate molecules with their own entries, so there is no hepcidin dose to state.
What this rests on: PMID 18689548, PMID 26289639, PMID 36521942.
Educational information, not medical advice. The doses on this page come from approved labels, published studies and, where no study exists, amounts reported by users. None is a recommendation for you. An unapproved compound has no established safe or effective human dose, and products sold for “research use only” are not made or tested for people. Talk to a doctor before acting on anything on this site, including before you start, stop or change any medicine or dose. Full medical disclaimer.
What a Buyer Needs to Know
What is sold, how it is mixed, stored and taken, and what is known about its safety, quality and legal status. Each part names its source. Where we have none, it says unknown.
What is sold
Unknown: we hold no label and no published test that says what forms or vial sizes Hepcidin is sold in. A vial's own label is a seller's claim, not a source.
Mixing a vial: a worked example
Unknown: no human dose of Hepcidin has been established (see No Established Human Dose below), so there is no amount to work out. The reconstitution calculator does the arithmetic for any vial, water and dose.
Storage before and after mixing
Unknown: no label or published stability study on file says how to store Hepcidin, before or after mixing. The mixing guide sets out the general rules, with their sources: keep a mixed vial in the fridge, and use it promptly, as the bacteriostatic water label says of any drug dissolved in it. The 28 days often quoted is the limit for an opened multiple-dose vial from a manufacturer, an outer limit set for sterility, not a time a mixed solution has been shown to keep. Nobody has published how long Hepcidin stays intact once mixed.
How it is taken
Unknown: with no established human dose, there is no established way of taking Hepcidin. What the human studies gave and how is set out under No Established Human Dose.
What to expect, and when
Unknown: no cited half-life and no label or trial duration on this page says how long Hepcidin lasts or how long it was given. Results reported in the studies are under Published Research.
Side effects, and when to stop or get help
From the Side Effects section: In the hepcidin-guided iron trial, adverse events and infections did not differ between children given iron by hepcidin level and children given iron daily; none was judged related to the interventions (PMID 36521942); Using hepcidin to withhold iron lowered the haemoglobin gain compared with giving iron to all children (PMID 36521942); A single high serum hepcidin value can reflect time of day, a recent iron dose, exercise or inflammation rather than iron stores alone (PMIDs 18689548, 22679180, 37347443). Full list and cautions ↓
When to stop or get help: unknown; no label or trial on file sets rules for stopping Hepcidin. Treat a severe or unexpected reaction as a reason to stop and see a doctor.
Source: the Side Effects section below (“Hepcidin is measured, not given, so it has no side effects of its own”).
Interactions
Unknown: a PubMed search for human interaction studies of Hepcidin (reviewed 2026-10-30) found none. Unknown is not the same as safe to combine.
Every peptide's record, with its source: the interaction matrix.
Checking what you bought
Unknown: no published independent test of Hepcidin products is in our lab-results database yet, so how products sold under this name measure up is not known.
To read a certificate of analysis, paste it into the COA decoder; it checks the measured mass against Hepcidin's expected mass, 2,789.3 Da, from this entry's molecular data. Trust & Verification explains what independent testing can and cannot show.
Legal status
US: Research Chemical (Not a medicine: hepcidin is measured in blood with immunoassays and mass spectrometry and has not been approved or given as a drug). Sport: Not on the 2026 List.
Country by country ↓ · Regulatory tracker
Source: this entry's approval status and the WADA Prohibited List, as in Legal Status below.
Side Effects & Contraindications
Reported Side Effects
Hepcidin is measured, not given, so it has no side effects of its own. These notes come from the studies that used it as a guide.
Contraindications & Cautions
There is no hepcidin product to take. These cautions concern reading the test.
Legal Status
Hepcidin is a hormone measured in blood; it is not approved as a medicine anywhere in the sources read.
Frequently Asked Questions
?What is hepcidin?
A 25-amino-acid peptide hormone made mainly by the liver. It controls how much iron enters the blood by shutting down ferroportin, the protein cells use to export iron.
?What does a high hepcidin level mean?
Less iron is reaching the blood. Hepcidin is raised by inflammation, by iron loading, by a recent iron supplement and by exercise, and it rises through the day. Persistently high levels restrict iron for red cells, as in the anaemia of inflammation and chronic kidney disease.
?What does a low hepcidin level mean?
The body is letting iron in. Levels are very low in iron deficiency anaemia and when red-cell production is being driven hard, and inappropriately low in hereditary hemochromatosis, where iron then builds up in organs.
?Why do some doctors suggest taking iron every other day?
Because an iron supplement raises hepcidin for about a day, which reduces absorption of a dose taken the next day. In women and in infants, doses spaced two days apart did not meet that block, so a larger share was absorbed.
?Can a hepcidin test decide who needs iron?
It has been tried. In a Gambian trial, giving iron only when hepcidin was low cut the iron given but raised haemoglobin less than giving iron to every child, so the approach did not prove as good as standard care.
?Is hepcidin sold as a drug or supplement?
No hepcidin medicine exists, and no study here gave it to people. Drugs that imitate it, such as rusfertide, are different molecules with their own entries.
?What is hepcidin-20?
A shorter form missing five residues at the start. In a large population study it was found in about half of people at roughly a seventh of the hepcidin-25 level, and some assays detect both forms.
References
- [other] UniProt P81172 (HEPC_HUMAN), hepcidin-25 = residues 60-84, hepcidin-20 = residues 65-84, four disulfide bonds; read October 30, 2026. Formula and mass computed from the sequence with four disulfides. https://www.uniprot.org/uniprotkb/P81172/entry
- [pubmed] Park CH, et al. "Hepcidin, a urinary antimicrobial peptide synthesized in the liver." J Biol Chem, 2001;276(11):7806-10. PMID: 11113131.
- [pubmed] Nicolas G, et al. "Lack of hepcidin gene expression and severe tissue iron overload in upstream stimulatory factor 2 (USF2) knockout mice." Proc Natl Acad Sci U S A, 2001;98(15):8780-5. PMID: 11447267.
- [pubmed] Roetto A, et al. "Mutant antimicrobial peptide hepcidin is associated with severe juvenile hemochromatosis." Nat Genet, 2003;33(1):21-2. PMID: 12469120.
- [pubmed] Nemeth E, et al. "IL-6 mediates hypoferremia of inflammation by inducing the synthesis of the iron regulatory hormone hepcidin." J Clin Invest, 2004;113(9):1271-6. PMID: 15124018.
- [pubmed] Nemeth E, et al. "Hepcidin regulates cellular iron efflux by binding to ferroportin and inducing its internalization." Science, 2004;306(5704):2090-3. PMID: 15514116.
- [pubmed] Ganz T, et al. "Immunoassay for human serum hepcidin." Blood, 2008;112(10):4292-7. PMID: 18689548.
- [pubmed] Troutt JS, et al. "Circulating human hepcidin-25 concentrations display a diurnal rhythm, increase with prolonged fasting, and are reduced by growth hormone administration." Clin Chem, 2012;58(8):1225-32. PMID: 22679180.
- [pubmed] Campostrini N, et al. "Serum levels of the hepcidin-20 isoform in a large general population: the Val Borbera study." J Proteomics, 2012;76 Spec No.(5):28-35. PMID: 22951294.
- [clinical-trial] Moretti D, et al. "Oral iron supplements increase hepcidin and decrease iron absorption from daily or twice-daily doses in iron-depleted young women." Blood, 2015;126(17):1981-9. PMID: 26289639.
- [pubmed] Prentice S, et al. "Hepcidin mediates hypoferremia and reduces the growth potential of bacteria in the immediate post-natal period in human neonates." Sci Rep, 2019;9(1):16596. PMID: 31719592.
- [clinical-trial] Hennigar SR, et al. "Testosterone Administration During Energy Deficit Suppresses Hepcidin and Increases Iron Availability for Erythropoiesis." J Clin Endocrinol Metab, 2020;105(4). PMID: 31894236.
- [clinical-trial] Uyoga MA, et al. "The effect of iron dosing schedules on plasma hepcidin and iron absorption in Kenyan infants." Am J Clin Nutr, 2020;112(4):1132-1141. PMID: 32678434.
- [clinical-trial] Wegmüller R, et al. "Hepcidin-guided screen-and-treat interventions for young children with iron-deficiency anaemia in The Gambia: an individually randomised, three-arm, double-blind, controlled, proof-of-concept, non-inferiority trial." Lancet Glob Health, 2023;11(1):e105-e116. PMID: 36521942.
- [review] Fensham NC, et al. "Factors Influencing the Hepcidin Response to Exercise: An Individual Participant Data Meta-analysis." Sports Med, 2023;53(10):1931-1949. PMID: 37347443.
- [review] Sharma R, et al. "Serum hepcidin levels in chronic liver disease: a systematic review and meta-analysis." Clin Chem Lab Med, 2024;62(3):373-384. PMID: 37540837.
- [review] Nemeth E, et al. "Hepcidin and Iron in Health and Disease." Annu Rev Med, 2023;74:261-277. PMID: 35905974.
Sources & Citations
Every study on this page was read from its PubMed record on October 30, 2026. Status comes from Drugs@FDA (openFDA), read the same day. Grey Peptides sells nothing and links to no vendor.
Medical Disclaimer: This content is for educational and informational purposes only. It is not medical advice, and nothing here is an instruction to obtain or use any compound. Talk to a licensed clinician about your own situation.