Copeptin
The stable peptide released alongside vasopressin, and what measuring it in blood can and cannot tell
Vasopressin, the body's water-conserving hormone, is hard to measure: it is unstable and sticks to platelets. Copeptin is cut from the same precursor and released with it in equal amounts, but it survives in a blood sample, so laboratories measure copeptin instead. A copeptin test after a salt infusion now diagnoses disorders of vasopressin more accurately than the old water-deprivation test, and copeptin levels mark risk in stroke, heart and kidney disease. Copeptin is never given as a drug.
No established human dose Details ↓
Recommended Dosing
No established human dose
Copeptin is a diagnostic marker, not a treatment: in every study here it is measured in blood, never given. The tests that stimulate it raise copeptin by other means, an infusion of concentrated salt, an arginine or glucagon injection, and then measure the copeptin the body releases.
What is it?
Copeptin is the tail end of the protein the body makes to produce vasopressin. One precursor, pre-pro-vasopressin, is cut into vasopressin, a carrier protein, and copeptin, so copeptin comes out in the same amount as the hormone. Unlike vasopressin, which is unstable and binds to platelets, copeptin is stable in a tube of blood and easy to measure, which is why it is used as a stand-in for vasopressin.
Copeptin rises with the same signals as vasopressin: a rise in blood saltiness, a fall in blood volume, and stress. In one study copeptin tracked the stress of illness and surgery more finely than cortisol did. It barely changes with food, though even a little water to drink can lower it. A 2025 review puts its initial half-life at roughly twice vasopressin's, without giving an exact figure.
Its clearest use is in the polyuria-polydipsia syndrome, where a person passes and drinks large volumes and the question is whether the cause is a lack of vasopressin, resistance to it, or simply drinking too much. The old water-deprivation test is uncomfortable and often wrong. Measuring copeptin after an infusion of hypertonic (concentrated) salt raised the diagnostic accuracy from about 77% to 97% in a trial of 141 patients. A single baseline copeptin above a high cutoff identifies vasopressin resistance outright.
Simpler versions of the test have been compared. Arginine-stimulated copeptin is gentler but less accurate than the salt test in a head-to-head trial; glucagon-stimulated copeptin showed promise in a small study. After pituitary surgery, a low copeptin on the first day flagged patients who would develop diabetes insipidus, while a high level almost ruled it out.
Beyond vasopressin disorders, copeptin is studied as a risk marker. Higher levels carry a worse outlook after stroke, in heart failure, in coronary artery disease and in polycystic kidney disease, and predict new diabetes. Added to a troponin test it helps rule out heart attack quickly in the emergency department. In most of these settings copeptin reflects general stress rather than a specific disease, and whether measuring it changes treatment is still largely untested.
Mechanism of Action
Copeptin is the stable C-terminal piece of the protein that yields vasopressin; made and released with the hormone, it rises with the same stimuli and is measured in its place.
Released with vasopressin
Cut from the same precursor, copeptin comes out in equal amounts with vasopressin in response to raised blood saltiness, low blood volume and stress.
Stable and measurable
Where vasopressin degrades and binds platelets, copeptin lasts in a blood sample, so it is what the assay actually measures.
No action of its own
Copeptin is not known to do anything in the body; its value is entirely as a readout of vasopressin release.
Published Research
These are studies of copeptin read from their PubMed abstracts: the diagnostic trials in vasopressin disorders, studies after pituitary surgery and in hyponatraemia, the stress study, prognostic cohorts and meta-analyses in heart, stroke and kidney disease, and three reviews. Copeptin is measured throughout, not given.
Salt-stimulated copeptin beats the water-deprivation test
In 141 patients with hypotonic polyuria across 11 centres, measuring plasma copeptin after a hypertonic saline infusion (cutoff above 4.9 pmol/L) gave the correct diagnosis in 96.5% of cases, against 76.6% for the indirect water-deprivation test. One serious adverse event, desmopressin-induced low sodium, occurred during the water-deprivation test.
Salt beats arginine as the stimulus
In 158 patients tested on two days, hypertonic saline-stimulated copeptin reached 95.6% diagnostic accuracy against 74.4% for arginine-stimulated copeptin, a difference of about 21 percentage points. Adverse events were generally mild, but 72% of patients preferred the arginine test.
Arginine-stimulated copeptin as a gentler test
Across development and validation cohorts, copeptin 60 minutes after an arginine infusion separated diabetes insipidus from primary polydipsia with 93% accuracy at a 3.8 pmol/L cutoff. Levels rose in healthy people and in primary polydipsia but barely in diabetes insipidus, and the test was well tolerated.
Glucagon as a stimulus, tested small
In 22 healthy participants, 10 with central diabetes insipidus and 10 with primary polydipsia, subcutaneous glucagon raised copeptin in healthy people and in primary polydipsia but not in diabetes insipidus; a 4.6 pmol/L cutoff separated the two patient groups with 100% sensitivity and 90% specificity in this small study.
Predicting diabetes insipidus after pituitary surgery
In 205 patients, 50 of whom developed diabetes insipidus after surgery, a low day-one copeptin (below 2.5 pmol/L) predicted it with 81% positive predictive value, while a level above 30 pmol/L virtually excluded it (95% negative predictive value). Low copeptin despite surgical stress reflected damage to the posterior pituitary.
Useful mainly for primary polydipsia in hyponatraemia
In 106 patients with low blood sodium and 32 controls, copeptin below 3 pmol/L with dilute urine identified primary polydipsia in every suspected case, but copeptin alone separated the other causes poorly; the copeptin-to-urine-sodium ratio told volume-depleted from normal-volume hyponatraemia with 85% sensitivity and 87% specificity.
A stable marker of stress
Copeptin rose with stress across three groups: 4.3 pmol/L in unstressed healthy controls, 17.5 in hospitalised medical patients and 67.5 in surgical patients just after extubation. It tracked the stress gradient more finely than cortisol did and correlated with cortisol.
Copeptin kinetics in healthy ageing
In a crossover trial of 16 older and 16 younger healthy adults, the within-person copeptin range was similar in both groups and the response to a salt infusion was comparable, but older adults suppressed copeptin less after drinking water, which may bear on their higher rate of low blood sodium.
Predicts new-onset diabetes
In 4,742 people followed 12.6 years, higher copeptin at baseline was linked to insulin resistance and to developing diabetes, with the odds roughly doubling across quartiles even after adjusting for fasting glucose and insulin; the link held in people with normal baseline glucose.
Tracks progression in polycystic kidney disease
In 241 patients with autosomal dominant polycystic kidney disease followed about 8.5 years (the CRISP cohort), higher baseline copeptin was independently associated with faster kidney growth, and borderline with a steeper fall in measured filtration rate; copeptin did not track plasma osmolality, suggesting a disease-promoting role for vasopressin.
Added to troponin to rule out heart attack
In 317 emergency patients with recent chest pain, copeptin was higher in the 45 with heart attack (23.2 vs 9.9 pmol/L). Copeptin at or above 10.7 pmol/L with troponin detected heart attack with 98% sensitivity against 71% for troponin alone, raising the negative predictive value to 99%.
Single copeptin-plus-troponin test for early discharge
In a randomised trial of 902 low-to-intermediate-risk patients with suspected acute coronary syndrome, discharging those with a negative troponin and copeptin at admission gave a 30-day adverse-event rate no higher than standard care; discharged copeptin-negative patients had a 0.6% event rate.
Meta-analysis: prognosis after stroke
Pooling six studies of 1,976 acute ischaemic stroke patients, a high admission copeptin carried about four times the risk of death and over twice the risk of poor functional outcome, and added to standard scores for predicting recurrence after transient ischaemic attack.
Meta-analysis: prognosis in heart failure
Across ten cohorts with 4,473 heart-failure patients, a raised copeptin was associated with about 2.6 times the risk of death from any cause, with a predictive value comparable to NT-proBNP.
Meta-analysis: prognosis in coronary disease
In 22 studies of 19,821 patients with coronary artery disease, a high baseline copeptin carried about 1.76 times the mortality risk and 1.49 times the risk of major cardiovascular events, consistently across age, sex and disease subtype.
Copeptin as a vasopressin surrogate: a 2025 review
This review sets out copeptin's biology and assays: it is a 39-amino-acid glycosylated peptide released with vasopressin, with an initial half-life about twice as long, measured now by an automated immunofluorescent assay. It summarises the diagnostic use in polyuria-polydipsia (a baseline above 21.4 pmol/L identifies vasopressin resistance) and the prognostic signals in cardiovascular, kidney and metabolic disease.
Copeptin in endocrine disorders
The review describes copeptin's stability and ease of measurement as the reason it replaces vasopressin, its established use in telling vasopressin resistance and deficiency from primary polydipsia and in flagging deficiency after pituitary surgery, and the gaps still to fill in the syndrome of inappropriate antidiuresis and in children.
Copeptin and stroke prognosis
Reviewing 25 studies, the authors report that copeptin predicts functional outcome and death after stroke about as well as established clinical variables, with signals also in transient ischaemic attack, intracerebral haemorrhage and subarachnoid haemorrhage.
No Established Human Dose
Copeptin is a diagnostic marker, not a treatment: in every study here it is measured in blood, never given. The tests that stimulate it raise copeptin by other means, an infusion of concentrated salt, an arginine or glucagon injection, and then measure the copeptin the body releases. There is no copeptin preparation to give and no dose to state.
What this rests on: PMID 30067922, PMID 37966286, PMID 35521789.
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 Copeptin 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 Copeptin 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 Copeptin, 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 Copeptin stays intact once mixed.
How it is taken
Unknown: with no established human dose, there is no established way of taking Copeptin. 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 Copeptin 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: The hypertonic saline test raises blood sodium and needs close monitoring; adverse events in the diagnostic trials were generally mild (PMID 37966286); A serious event in the diagnostic trial, low sodium needing hospital care, occurred during the old water-deprivation test, not with copeptin (PMID 30067922). Full list and cautions ↓
When to stop or get help: unknown; no label or trial on file sets rules for stopping Copeptin. Treat a severe or unexpected reaction as a reason to stop and see a doctor.
Source: the Side Effects section below (“Copeptin is measured, not given, so it has no side effects of its own”).
Interactions
Unknown: a PubMed search for human interaction studies of Copeptin (reviewed 2026-10-28) 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 Copeptin 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. Trust & Verification explains what independent testing can and cannot show.
Legal status
US: Research Chemical (Not a medicine: copeptin is measured with laboratory assays, including an automated immunofluorescent assay (PMID 39086073)). 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
Copeptin is measured, not given, so it has no side effects of its own. These notes concern the tests that stimulate it.
Contraindications & Cautions
Copeptin is a blood test, not a medicine.
Legal Status
Copeptin is a laboratory biomarker measured in blood, not a medicine; it has no drug approval status.
Frequently Asked Questions
?What is copeptin?
A 39-amino-acid peptide cut from the same precursor as vasopressin and released with it in equal amounts. It is measured in blood as a stable stand-in for vasopressin, which is hard to measure directly.
?Is copeptin a medicine?
No. It is a laboratory marker. In every study it is measured, never given, and there is no copeptin product to take.
?What is copeptin used to diagnose?
Mainly the polyuria-polydipsia syndrome: a copeptin test after a hypertonic saline infusion tells vasopressin deficiency and resistance from drinking too much more accurately than the old water-deprivation test.
?Why measure copeptin instead of vasopressin?
Vasopressin is unstable and binds to platelets, so it is hard to measure. Copeptin comes from the same precursor in the same amount but survives in a blood sample.
?Does a high copeptin predict disease?
Higher copeptin carries a worse outlook after stroke and in heart failure, coronary disease and polycystic kidney disease, and predicts new diabetes. It mostly reflects general stress, and whether measuring it changes treatment is largely untested.
?How long does copeptin last in the blood?
No exact figure was found in the sources read; a 2025 review estimates its initial half-life at roughly twice that of vasopressin.
References
- [clinical-trial] Fenske W, et al. "A Copeptin-Based Approach in the Diagnosis of Diabetes Insipidus." N Engl J Med, 2018;379(5):428-439. PMID: 30067922.
- [clinical-trial] Refardt J, et al. "Arginine or Hypertonic Saline-Stimulated Copeptin to Diagnose AVP Deficiency." N Engl J Med, 2023;389(20):1877-1887. PMID: 37966286.
- [clinical-trial] Winzeler B, et al. "Arginine-stimulated copeptin measurements in the differential diagnosis of diabetes insipidus: a prospective diagnostic study." Lancet, 2019;394(10198):587-595. PMID: 31303316.
- [clinical-trial] Atila C, et al. "Glucagon-stimulated copeptin measurements in the differential diagnosis of diabetes insipidus: a double-blind, randomized, placebo-controlled study." Eur J Endocrinol, 2022;187(1):65-74. PMID: 35521789.
- [pubmed] Winzeler B, et al. "Postoperative Copeptin Concentration Predicts Diabetes Insipidus After Pituitary Surgery." J Clin Endocrinol Metab, 2015;100(6):2275-82. PMID: 25923040.
- [pubmed] Fenske W, et al. "Copeptin in the differential diagnosis of hyponatremia." J Clin Endocrinol Metab, 2009;94(1):123-9. PMID: 18984663.
- [pubmed] Katan M, et al. "Copeptin, a stable peptide derived from the vasopressin precursor, correlates with the individual stress level." Neuro Endocrinol Lett, 2008;29(3):341-6. PMID: 18580851.
- [clinical-trial] Lustenberger S, et al. "Copeptin kinetics in healthy aging." J Clin Endocrinol Metab, 2026;111(9):2436-2444. PMID: 41964423.
- [pubmed] Enhörning S, et al. "Plasma copeptin and the risk of diabetes mellitus." Circulation, 2010;121(19):2102-8. PMID: 20439785.
- [pubmed] Boertien WE, et al. "Relationship of copeptin, a surrogate marker for arginine vasopressin, with change in total kidney volume and GFR decline in autosomal dominant polycystic kidney disease: results from the CRISP cohort." Am J Kidney Dis, 2013;61(3):420-9. PMID: 23089511.
- [pubmed] Chenevier-Gobeaux C, et al. "Copeptin for rapid rule out of acute myocardial infarction in emergency department." Int J Cardiol, 2013;166(1):198-204. PMID: 22104994.
- [clinical-trial] Möckel M, et al. "Early discharge using single cardiac troponin and copeptin testing in patients with suspected acute coronary syndrome (ACS): a randomized, controlled clinical process study." Eur Heart J, 2015;36(6):369-76. PMID: 24786301.
- [review] Xu Q, et al. "Copeptin as a biomarker for prediction of prognosis of acute ischemic stroke and transient ischemic attack: a meta-analysis." Hypertens Res, 2017;40(5):465-471. PMID: 27904159.
- [review] Zhong Y, et al. "Copeptin in heart failure: Review and meta-analysis." Clin Chim Acta, 2017;475:36-43. PMID: 28982590.
- [review] Shi Z, et al. "Copeptin and the prognosis of patients with coronary artery disease: a meta-analysis." Ir J Med Sci, 2023;192(5):2129-2141. PMID: 36719516.
- [review] Choy KW, et al. "Copeptin as a surrogate marker for arginine vasopressin: analytical insights, current utility, and emerging applications." Crit Rev Clin Lab Sci, 2025;62(1):24-44. PMID: 39086073.
- [review] Moodley N. "Copeptin analysis in endocrine disorders." Front Endocrinol (Lausanne), 2023;14:1230045. PMID: 37859988.
- [review] Karatzetzou S, et al. "Copeptin Implementation on Stroke Prognosis." Neurol Int, 2023;15(1):83-99. PMID: 36648972.
- [other] UniProt P01185 (NEU2_HUMAN), peptide residues 126-164, copeptin; read October 28, 2026. https://www.uniprot.org/uniprotkb/P01185/entry
Sources & Citations
Every study on this page was read from its PubMed record on October 28, 2026. Status comes from Drugs@FDA (openFDA) and the EMA medicines list, 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.