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MyDeficiencies

Desmopressin

Vasopressin V2-Receptor Agonist

Also sold as DDAVP, Stimate, Minirin, Noctiva, Nocdurna.

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Findings for this medication

Research about this medication, graded for how strongly each finding can be attributed to it. Nothing here describes your own levels.

Desmopressin is not appreciably metabolized, induces or inhibits no CYP450 enzyme, and is cleared mainly unchanged in urine, with oral bioavailability of only about 5% via passive absorption and no named transporter or chelation step. On that basis alone it has essentially none of the classical depletion machinery (no absorption interference, no enzyme induction, no renal wasting, no cofactor antagonism, no accelerated catabolism) that drives most drug-nutrient depletion findings. But desmopressin does have one very well documented, clinically important electrolyte effect, and it runs in the excess/retention direction, not the deficiency direction: as a selective renal V2-receptor agonist, its entire pharmacologic purpose is to promote free-water reabsorption, and when fluid intake is not restricted this produces dilutional hyponatremia. This is carried on the US label as a named risk with an explicit contraindication in patients with hyponatremia, and a large population-based cohort study found a roughly 13-fold higher hazard of hyponatremia with desmopressin versus a comparator drug for a related indication.

Posterior pituitary hormone analog, V2-receptor agonist · ATC H01BA02 · also sold as DDAVP and Stimate and Minirin and Noctiva and Nocdurna · reviewed 2026-09-23. This describes research about the medication. It does not say anything about your own levels or health.

How to read the evidence grades

These colours describe how strongly a finding can be attributed to the medication in the research. They are not a severity score and they say nothing about your own health.

Grades describe how strongly a finding can be attributed to Desmopressin in the research — not how common it is, how serious it would be, and not anything about you personally.

Red — Severe
severe: ≥2 independent Tier A sources, this drug in the cohort, the nutrient directly measured, consistent direction, clinically meaningful magnitude, a named mechanism, no substantial contradicting Tier A evidence.
Orange — Moderate
moderate: ≥1 Tier A source with this drug in the cohort showing a real deficit or effect, but bounded by exposure window, subgroup, frequency, or a functional rather than circulating change.
Yellow — Low
low/theoretical: mechanistic plausibility only (Tier B), or class extrapolation (Tier C) where at least one class member has real data but this drug does not; also used for context flags and reverse-direction findings.
Not graded — disclosed evidence gap
Nothing has been measured here, so this finding cannot be graded. That does not establish either safety or harm, and it is not the same as a White result.Source definition: evidence gap: no Tier B/C evidence exists to support even a yellow grade, and no circulating claim exists to rebut as white. A disclosed gap in the literature or in what could be accessed this review, never reworded as reassurance.

What the research found

Sodium

Red — Severe

See study details

Desmopressin's antidiuretic mechanism causes clinically significant, sometimes severe dilutional hyponatremia. This is a retention risk, not a nutrient deficiency, and higher sodium or fluid intake is not the remedy.

Full detail and limits

What the grade means here: severe: ≥2 independent Tier A sources, this drug in the cohort, the nutrient directly measured, consistent direction, clinically meaningful magnitude, a named mechanism, no substantial contradicting Tier A evidence. Excess / retention risk

Limits on what this shows

  • Key negative/null findings: None found contradicting the direction of effect. The Fralick cohort's comparators (oxybutynin, tamsulosin) are active drugs for a related indication, not placebo or no treatment, so the hazard ratios show relative risk against other nocturia therapies rather than absolute background risk; this active-comparator limitation is noted explicitly.
  • At-risk subgroups: Adults ≥50 (the studied cohort); pediatric enuresis patients on the intranasal route (per source [4]); concomitant SSRIs, TCAs, NSAIDs, carbamazepine, lamotrigine, opiates, or chlorpromazine (label-named); renal impairment; unrestricted free-water intake.
  • Counter-evidence on record: The label itself calls postmarketing hyponatremia reports "very rare," while the active-surveillance cohort study measured rates far higher (146 vs. 11 per 1,000 person-years). This gap between passive postmarketing reporting and active cohort ascertainment is a real discrepancy worth flagging to a reader, not a contradiction of the underlying signal.

Regulatory status

US label carries an explicit hyponatremia/water-intoxication warning, is contraindicated in patients with, or a history of, hyponatremia, and advises fluid restriction with use. [1]

Population evidence

Fralick et al. 2019, retrospective propensity-matched cohort (Optum Clinformatics commercial claims, 2006–2017), n=3,137 new desmopressin users age ≥50 vs. matched oxybutynin users: HR 13.19 (95% CI 6.69–26.01) for hyponatremia; HR 19.41 (95% CI 7.11–52.99) within 30 days of starting; HR 29.83 (95% CI 4.11–216.45) for hospitalization-level hyponatremia; incidence rate 146 vs. 11 per 1,000 person-years. A sensitivity analysis vs. tamsulosin gave HR 12.10 (95% CI 6.54–22.37). [3]

Mechanism

Named. V2-receptor-mediated aquaporin-2 upregulation drives renal free-water reabsorption independent of solute; without fluid restriction this produces dilutional (not deficiency) hyponatremia. [1]

Supporting reviews

Williford & Bernstein 1996, drug-specific review of intranasal-desmopressin-induced hyponatremia cases [4]; Achinger & Ayus 2019, review of the mechanism and risk of desmopressin-associated hyponatremia [5].

Counter-evidence held on record

This is a retention/excess-risk relationship, not a deficiency. Do not present sodium supplementation, increased salt intake, or increased fluid intake as a "fix." The standard clinical response to desmopressin-associated hyponatremia is fluid restriction and dose review with the prescriber.

The five body-system areas

Each finding is counted once, in a single area. Where a study is mentioned in a second area it is context only.

Mitochondrial Burden

Each finding below is counted once, in this area only.

Mitochondrial burden

Yellow — Low

See study details

One 2026 in vitro study found desmopressin triggers mitochondrial fragmentation and dysfunction in a human glioma cell line via a CaMKII-Drp1 signaling pathway. Relevance to desmopressin's labeled patient population (diabetes insipidus, enuresis, bleeding disorders) is unestablished.

Full detail and limits

What the grade means here: low/theoretical: mechanistic plausibility only (Tier B), or class extrapolation (Tier C) where at least one class member has real data but this drug does not; also used for context flags and reverse-direction findings. Mechanism-only · non-representative model

Limits on what this shows

  • Key negative/null findings: None found. The full abstract could not be opened (publisher returned a 403 error on fetch), so exact concentrations and magnitude of effect are not independently confirmed beyond the title-level description; this is disclosed rather than filled in.
  • At-risk subgroups: None identifiable. The study context is oncology cell-biology research; desmopressin/V2-agonism has been explored experimentally in glioma models, which is a different use case from standard diabetes-insipidus, enuresis, or hemostasis dosing.
  • Counter-evidence on record: None found.

Regulatory status

Not addressed on the label.

Population evidence

None in humans or patients. Tier B in vitro study only: Liang et al. 2026, Drug Development Research, human U87 MG glioma cell line treated with desmopressin. [7]

Mechanism

Named: CaMKII–Drp1-mediated mitochondrial fission pathway.

Counter-evidence held on record

This finding comes from a cancer cell line in an experimental context, not standard therapeutic dosing in the labeled indications. It should not be read as evidence of mitochondrial harm in patients taking desmopressin for diabetes insipidus, enuresis, or bleeding disorders.

Oxidative Stress

Each finding below is counted once, in this area only.

Oxidative stress

Yellow — Low

See study details

A 2026 mechanistic study found desmopressin generates glycolysis-dependent reactive oxygen species as part of its mechanism for reversing antiplatelet-drug-induced platelet dysfunction. This documents drug-induced ROS generation in a directed therapeutic role, not established tissue oxidative damage.

Full detail and limits

What the grade means here: low/theoretical: mechanistic plausibility only (Tier B), or class extrapolation (Tier C) where at least one class member has real data but this drug does not; also used for context flags and reverse-direction findings. Mechanism-only · therapeutic-context signal

Limits on what this shows

  • Key negative/null findings: None found. Full abstract could not be independently re-opened this review (bot-verification block on the PubMed article page, and Crossref/Europe PMC/Semantic Scholar lookups were all rate-limited on follow-up attempts), so this entry is based on the search-listing title and topic only.
  • At-risk subgroups: None established. The study context is short-term reversal of antiplatelet therapy (a deliberate clinical use), not chronic dosing.
  • Counter-evidence on record: None found. Note that the source frames this ROS signal as mediating a beneficial hemostatic effect, not a harm signal.

Regulatory status

Not addressed on the label.

Population evidence

Wang et al. 2026, Medical Gas Research: title/journal/year/PMID confirmed via PubMed search listing. [8]

Mechanism

Named: glycolysis-dependent reactive oxygen species mediating rescue of platelet function after antiplatelet therapy.

Counter-evidence held on record

Do not present this as evidence that desmopressin depletes antioxidant capacity or requires antioxidant supplementation. No antioxidant-capacity or depletion marker was measured in this source.

Copper and Iron Balance

Copper and iron are assessed separately. Nothing here is counted twice.

Iron

Yellow — Low

See study details

Iron deficiency is common in the bleeding disorders desmopressin treats, but this reflects the underlying disease, not the drug. Desmopressin's therapeutic action (raising factor VIII/von Willebrand factor to reduce bleeding) would be expected to reduce, not increase, bleeding-related iron loss.

Full detail and limits

What the grade means here: low/theoretical: mechanistic plausibility only (Tier B), or class extrapolation (Tier C) where at least one class member has real data but this drug does not; also used for context flags and reverse-direction findings. Context flag · likely protective direction

Limits on what this shows

  • Key negative/null findings: No direct desmopressin-iron mechanism found despite searching "desmopressin copper OR desmopressin iron deficiency" and related phrasings.
  • At-risk subgroups: Patients with von Willebrand disease, hemophilia A, or menorrhagia carry disease-driven iron-deficiency risk independent of desmopressin treatment.
  • Counter-evidence on record: None found suggesting a direct drug-caused iron effect. Per confounding-by-indication logic, the deficiency risk in this population predates and is caused by the bleeding disorder, not by starting desmopressin.

Regulatory status

DDAVP injection label indications include von Willebrand disease Type I and hemophilia A (factor VIII >5%), populations with well-documented bleeding-related iron-deficiency risk from the disease itself. [2]

Population evidence

No Tier A or Tier B study found measuring iron or ferritin status as a direct effect of desmopressin exposure. A multi-phrasing PubMed search found iron deficiency discussed only as a feature of the treated bleeding disorders (e.g., heavy menstrual bleeding, hereditary hemorrhagic telangiectasia), not as a drug effect.

Mechanism

None identified connecting desmopressin itself to iron absorption, transport, or storage. The only plausible relationship runs through the drug's intended hemostatic effect reducing blood (and thus iron) loss.

Counter-evidence held on record

Do not present this as a drug-caused deficiency. The causal direction in the evidence found runs the other way: an indication-linked risk that the drug's therapeutic effect would tend to reduce, not cause.

Copper

Not graded — disclosed evidence gap

See study details

No drug-specific or class-level evidence, and no circulating consumer claim, was found connecting desmopressin to copper or ceruloplasmin status.

Full detail and limits

What the grade means here: Nothing has been measured here, so this finding cannot be graded. That does not establish either safety or harm, and it is not the same as a White result. Ungraded · re-confirmed with full tool budget

Limits on what this shows

  • Why no grade: This category was re-researched on 2026-09-23 with a full WebSearch/WebFetch budget (not shared across a batch run), specifically to test whether the original ungraded result was a tooling artifact. Multiple phrasings were tried across multiple channels: PubMed search listings ("desmopressin copper," "vasopressin copper metabolism"), the Crossref API ("desmopressin copper," 10 results reviewed), and general web search ("desmopressin copper ceruloplasmin," "desmopressin copper deficiency," "vasopressin V2 receptor copper transporter ATP7A ATP7B ceruloplasmin," "desmopressin DDAVP trace mineral serum copper zinc," "SIADH hemodilution serum ceruloplasmin copper plasma volume expansion"). The only desmopressin-plus-copper result located in any channel was Mercorio et al. 2003, Human Reproduction [11], a pilot study of desmopressin for menorrhagia caused by a copper intrauterine device; this is copper as a device material, not as a nutrient or mineral status, and does not support a copper-status finding. The hemodilution-analogy search (whether plasma-volume expansion, the mechanism already graded orange for hematocrit/hemoglobin, might also dilute serum ceruloplasmin/copper) returned no study measuring ceruloplasmin or copper under desmopressin, SIADH, or comparable water-loading conditions. No mechanism from the Step 1/2 screen implicates copper (no chelation, no enzyme induction, no cofactor antagonism identified). No circulating consumer claim about desmopressin and copper was found. Both conditions for UNGRADED are met, and this is assessed as a genuine literature gap rather than a tooling limitation.

Tooling note

The Europe PMC REST API (www.ebi.ac.uk) returned HTTP 429 on the one attempt made for this category this session, so that single channel's coverage is still incomplete; however, PubMed search listings, Crossref, and general web search all returned genuine, on-topic results for this drug and consistently found no copper-status connection, so the absence of a Europe PMC result is not treated as the reason for the ungraded status.

Gut Microbiome Risk

Each finding below is counted once, in this area only.

Gut microbiome risk

Yellow — Low

See study details

No study of desmopressin itself and the gut microbiome was found. One animal study of the endogenous hormone desmopressin mimics found that genetically vasopressin-deficient rats show sex-specific shifts in gut microbiome composition, establishing that the vasopressin signaling axis is mechanistically linked to the microbiome, though in the reverse direction (hormone absence, not V2-receptor agonism) from what desmopressin does.

Full detail, limits and 1 references

What the grade means here: low/theoretical: mechanistic plausibility only (Tier B), or class extrapolation (Tier C) where at least one class member has real data but this drug does not; also used for context flags and reverse-direction findings. Class extrapolation · not desmopressin itself

Limits on what this shows

  • Key negative/null findings: None found for desmopressin directly. A related mouse study of V1a/V1b-receptor-deficient (not V2, not desmopressin) animals found gut-microbiome-derived butyric acid changes disrupting enteroendocrine L-cell hormone secretion (Kojima et al., 2024, PMID 39668067); it targets the receptor subtypes desmopressin does not meaningfully engage, so it is noted but not used as independent supporting evidence for this entry. [10]
  • At-risk subgroups: None established for desmopressin-treated patients; the source population is a genetic rat model of central diabetes insipidus, not drug-treated animals or humans.
  • Counter-evidence on record: None found specific to desmopressin. This entry's full source text could not be opened this review despite genuine multi-host attempts: PubMed and PMC article pages (bot-verification challenges), Tandfonline abstract and PDF pages (HTTP 403), Europe PMC (HTTP 429), and the Semantic Scholar API (robots-disallowed) were all tried; only Crossref returned usable bibliographic metadata (title, authors, journal, year, DOI) and a PubMed search-listing page confirmed the title, journal, and year. The entry therefore rests on the confirmed title and metadata, not on a directly read abstract, methods, or results section.

Regulatory status

Not addressed on the label.

Population evidence

None in humans or in desmopressin-treated animals. Tier C, class-level: Fields CT, Chassaing B, Paul MJ, Gewirtz AT, de Vries GJ. "Vasopressin deletion is associated with sex-specific shifts in the gut microbiome." Gut Microbes. 2017 (print 2018). Brattleboro rats, which lack endogenous arginine vasopressin (AVP) synthesis entirely, were compared to AVP-intact controls; the title itself is the reported finding (sex-specific shifts in gut microbiome composition with AVP absence). [9]

Mechanism

Named but only partially applicable: the study manipulates loss of the whole endogenous hormone, which signals through V1a, V1b, and V2 receptors together, not selective stimulation of the V2 receptor the way desmopressin does. Desmopressin has negligible V1 activity, so a finding built on total-AVP absence does not establish that V2-selective agonism (adding signal) would move the microbiome the same way, or at all, as removing all AVP signaling.

Counter-evidence held on record

This is not a finding about desmopressin. It is a class-level, mechanism-only signal from an animal model of the natural hormone's total absence, in the opposite direction from what a V2-selective agonist drug does. It should not be presented as evidence that desmopressin disrupts the gut microbiome, and no probiotic or microbiome-support recommendation follows from it.

Oxygen and ATP Output

Oxygen delivery and ATP production are assessed separately. Nothing here is counted twice.

Oxygen delivery/utilization

Orange — Moderate

See study details

In a small pharmacology study, DDAVP administration produced a statistically significant fall in hematocrit and hemoglobin through plasma-volume expansion, not a change in red-cell mass or iron status.

Full detail and limits

What the grade means here: moderate: ≥1 Tier A source with this drug in the cohort showing a real deficit or effect, but bounded by exposure window, subgroup, frequency, or a functional rather than circulating change. Bounded · single small study

Limits on what this shows

  • Key negative/null findings: None identified; only one study located despite a multi-phrasing search ("desmopressin hemodilution," "desmopressin hematocrit," "desmopressin dilutional anemia").
  • At-risk subgroups: The studied population received supraphysiologic or research-context dosing; plausible extension to patients on chronic higher-dose desmopressin for central diabetes insipidus is reasonable but not directly studied.
  • Counter-evidence on record: Single small study; not replicated in the drug's primary labeled populations (diabetes insipidus, hemophilia A, von Willebrand disease) in evidence located this review. Full study methodology (exact n, dose, timing) could not be independently re-confirmed: the PubMed article page and a Crossref metadata lookup were both blocked (bot-verification / rate-limit) on follow-up attempts, so this entry rests on the quoted finding from the search-listing text rather than the full paper.

Regulatory status

Not separately quantified on the label. The DDAVP injection label documents general fluid-retention warnings (heart failure, hypertension risk) without hematocrit/hemoglobin figures. [2]

Population evidence

Sanchis-Gomar et al. 2010, Int J Sports Med, a pharmacology study conducted in the context of anti-doping detection research: "After treatment with DDAVP we found a significant decrease in the hematocrit, hemoglobin and in the OFF Hr-Score values." [6]

Mechanism

Same V2-receptor-mediated free-water retention/plasma-volume-expansion mechanism as the sodium entry above; these are two measured consequences of one underlying process, not independent confirmations (see Overlap map).

Counter-evidence held on record

This is a dilutional effect from plasma-volume expansion, not anemia from blood loss or iron deficiency. Iron or B12 supplementation would not address it and should not be recommended from this evidence.

ATP production

Yellow — Low

See study details

No study directly measured ATP output with desmopressin. The only support is inferred from the mitochondrial-fragmentation and platelet-glycolysis papers above, so this entry overlaps their evidence rather than adding an independent finding.

Full detail and limits

What the grade means here: low/theoretical: mechanistic plausibility only (Tier B), or class extrapolation (Tier C) where at least one class member has real data but this drug does not; also used for context flags and reverse-direction findings. Mechanism-only · inferred, not directly measured

Limits on what this shows

  • Key negative/null findings: A dedicated search for "desmopressin ATP production / cellular energy metabolism" returned only these same two sources plus one non-drug-specific paper on mitochondrial electron transport and AMPK-dependent aquaporin-2 regulation (Carty et al. 2024, JCI Insight) that was not confirmed to have used desmopressin itself as the studied agent, so it was not used as supporting evidence here.
  • At-risk subgroups: None established.
  • Counter-evidence on record: None found; the entry's weakness is the absence of a direct measurement, which is stated rather than papered over.

Regulatory status

Not addressed on the label.

Population evidence

None direct. Inferred from Liang et al. 2026 (mitochondrial fragmentation in U87 glioma cells) [7] and Wang et al. 2026 (glycolysis-dependent ROS in platelets) [8].

Mechanism

Plausible but not demonstrated: mitochondrial fragmentation can impair oxidative ATP synthesis, and a glycolytic shift changes cellular ATP sourcing, but neither accessible source reports a direct ATP measurement.

Counter-evidence held on record

This is the thinnest entry in the dossier: two mechanism papers in non-representative models, neither directly measuring ATP. It should not be read as an established energy-metabolism effect of desmopressin.

Claims checked and not supported

These circulate online for this medication. They are listed here only so they can be answered, never as findings, and they are not graded.

A claim with no supporting evidence is not necessarily disproven. Where evidence actually argues against a claim, that is stated below.

  • Electrolyte/mineral wasting via increased urination (sodium, potassium, magnesium)

    Where it comes from: Generic, non-drug-stratified drug-nutrient depletion resources can group hormone or pituitary-axis drugs together, or read "hormone therapy" as diuretic-like, implying urinary electrolyte loss.

    Why it fails: Desmopressin is a selective V2-receptor agonist that produces antidiuresis (renal free-water retention), the pharmacologic opposite of a diuretic. Its own regulatory label describes a water-retention/hyponatremia risk, not electrolyte wasting, and no Tier A, B, or C source found in this review supports a urinary-wasting mechanism for this drug. [1][2]

All references used above
  1. DailyMed. DDAVP (desmopressin acetate) tablets, full prescribing information. — Ferring Pharmaceuticals Inc. Regulatory label, US FDA-approved prescribing information.
  2. DailyMed. DDAVP (desmopressin acetate) injection, full prescribing information. — Ferring Pharmaceuticals Inc. Regulatory label, US FDA-approved prescribing information.
  3. Fralick M, Kesselheim AS, Avorn J, Schneeweiss S. Desmopressin and the risk of hyponatremia: A population-based cohort study. — PLoS Medicine. 2019;16(10):e1002930. Retrospective propensity-matched cohort, n=3,137 desmopressin users vs. matched comparators. PMID 31634354.
  4. Williford SL, Bernstein SA. Intranasal desmopressin-induced hyponatremia. — Pharmacotherapy. 1996;16(1):66-74. PMID 8700794.Access note: title, journal, year, and PMID confirmed via PubMed search-listing fetch; a follow-up fetch of the individual article page returned a rate-limit block, so the full abstract was not independently re-opened this review.
  5. Achinger SG, Ayus JC. Use of Desmopressin in Hyponatremia: Foe and Friend. — Kidney Medicine. 2019;1(2):65-70. PMID 32734186.Access note: title, journal, year, and PMID confirmed via PubMed search-listing fetch; a follow-up fetch of the PMC full-text page returned a bot-verification challenge, so it was not independently re-opened this review.
  6. Sanchis-Gomar F, et al. Desmopressin and hemodilution: implications in doping. — International Journal of Sports Medicine. 2010. PMID 19885778. Quoted finding: "a significant decrease in the hematocrit, hemoglobin and in the OFF Hr-Score values" after DDAVP treatment.Access note: quoted finding taken from the PubMed search-listing abstract text; a follow-up fetch of the individual article page and a Crossref metadata lookup were both blocked (bot-verification / HTTP 429) on retry, so exact sample size and dosing were not independently re-confirmed this review.
  7. Liang S, Zhu Y, Su J, Luo C, Yang C. Desmopressin Induces Mitochondrial Fragmentation and Dysfunction in Human U87 MG Glioma Cells via CaMKII-Drp1 Signaling Pathway. — Drug Development Research. 2026. DOI 10.1002/ddr.70224. PMID 41527347. In vitro study, U87 MG human glioma cell line.Access note: title, authors, journal, year, and DOI confirmed via Crossref metadata lookup; the publisher page returned a 403 error on fetch, so the full text/abstract was not independently opened this review.
  8. Wang K, et al. Glycolysis-dependent reactive oxygen species mediate desmopressin acetate-induced rescue of platelet dysfunction caused by antiplatelet therapy. — Medical Gas Research. 2026. PMID 41888039.Access note: title, journal, year, and PMID confirmed via PubMed search-listing fetch only. Follow-up attempts via the individual PubMed page, Crossref, Europe PMC, and Semantic Scholar were all blocked (HTTP 429 or bot-verification) this session; the full abstract was not independently re-opened.
  9. Fields CT, Chassaing B, Paul MJ, Gewirtz AT, de Vries GJ. Vasopressin deletion is associated with sex-specific shifts in the gut microbiome. — Gut Microbes. 2017 (print 2018);9(1). Animal study, Brattleboro (AVP-deficient) rats vs. AVP-intact controls. DOI 10.1080/19490976.2017.1356557. PMID 28759308.Access note: title, authors, journal, and year confirmed via Crossref metadata lookup and a PubMed search-listing match (PMID 28759308); the PubMed article page, both new- and old-style PMC pages (PMC5914910), the Tandfonline abstract and PDF pages, and Europe PMC all returned bot-verification challenges, HTTP 403, or HTTP 429 on repeated attempts, and the Semantic Scholar API is robots-disallowed, so the full abstract, methods, and results were not independently opened this review; this entry is class-level (endogenous hormone deletion, not desmopressin) and is graded and framed accordingly.
  10. Kojima I, et al. Intestinal butyric acid-mediated disruption of gut hormone secretion and lipid metabolism in vasopressin receptor-deficient mice. — 2024. PMID 39668067. Mouse study, V1a/V1b-receptor-deficient (not V2-receptor, not desmopressin) strains; cited only to show it targets a different receptor subtype than desmopressin engages, not used as independent supporting evidence.
  11. Mercorio F, De Simone R, Di Carlo C, Bifulco G, Tessitore G, Di Spiezio Sardo A, Nappi C. Effectiveness and mechanism of action of desmopressin in the treatment of copper intrauterine device-related menorrhagia: a pilot study. — Human Reproduction. 2003;18(11):2319-2322. DOI 10.1093/humrep/deg449. Confirms desmopressin has no located connection to copper as a nutrient/mineral; the only desmopressin+copper hit found in any channel concerns a copper IUD as a bleeding-cause device, not copper status.
  12. WHO Collaborating Centre for Drug Statistics Methodology. ATC/DDD Index: H01BA02 (desmopressin). — Classification: H01B Posterior pituitary lobe hormones > H01BA Vasopressin and analogues.