Neurohypophyseal diabetes insipidus

Summary

Neurohypophyseal diabetes insipidus (MONDO:0007450) is a disease caused by AVP (GenCC Strong), with 1 cohort gene and 10 clinical trials. Top therapeutic interventions include estradiol valerate, urea, and vasopressin.

At a glance

• Prevalence: Unknown (Worldwide)
• Causal gene: AVP (GenCC Strong)
• Cohort genes: 1
• ClinVar variants: 66
• Phenotypes (HPO): 9
• Clinical trials: 10

Clinical features

Signs & symptoms

Clinical features (HPO)

9 HPO clinical features (Orphanet curated; top 9 by frequency):

HPO ID	Term	Frequency
HP:0000873	Diabetes insipidus	Very frequent (80-99%)
HP:0001959	Polydipsia	Very frequent (80-99%)
HP:0000737	Irritability	Frequent (30-79%)
HP:0001254	Lethargy	Frequent (30-79%)
HP:0001510	Growth delay	Frequent (30-79%)
HP:0001824	Weight loss	Frequent (30-79%)
HP:0001945	Fever	Frequent (30-79%)
HP:0002013	Vomiting	Frequent (30-79%)
HP:0002014	Diarrhea	Frequent (30-79%)

Identifiers

Disease identifiers

Field	Value
Canonical name	neurohypophyseal diabetes insipidus
Mondo ID	MONDO:0007450
OMIM	125700
Orphanet	30925
DOID	DOID:12388
ICD-11	97299603
NCIT	C84933
SNOMED CT	45369008
UMLS	C0342394
MedGen	574999
GARD	0016629
Anatomy (UBERON)	UBERON:0000007
Is cancer (heuristic)	no

Also known as: ADH deficiency · antidiuretic hormone deficiency · Arginine vasopressin deficiency · AVP deficiency · diabetes insipidus of pituitary gland · hereditary CDI · hereditary neurogenic diabetes insipidus · pituitary gland diabetes insipidus · vasopressin deficiency

Data availability: 66 ClinVar variants · 3 GenCC gene-disease records.

Disease family

Classification path: disease › human disease › disease by etiologic mechanism › disease of genetic or genomic mechanism › hereditary disease › autosomal genetic disease › autosomal dominant disease › neurohypophyseal diabetes insipidus

Related subtypes (191): autosomal dominant polycystic liver disease, cerebral arteriopathy, autosomal dominant, with subcortical infarcts and leukoencephalopathy, type 1, tuberous sclerosis, Treacher-Collins syndrome, hereditary breast ovarian cancer syndrome, autosomal dominant polycystic kidney disease, Lynch syndrome, branchio-oto-renal syndrome, autosomal dominant Aarskog syndrome, acroosteolysis dominant type, ADULT syndrome, autosomal dominant Alport syndrome, amelogenesis imperfecta type 1B, Townes-Brocks syndrome, nevoid basal cell carcinoma syndrome, blepharophimosis, ptosis, and epicanthus inversus syndrome, autosomal dominant brachyolmia, branchiooculofacial syndrome, pheochromocytoma/paraganglioma syndrome 4, cataract-aberrant oral frenula-growth delay syndrome, cherubism, autosomal dominant chondrodysplasia punctata, autosomal dominant popliteal pterygium syndrome, blepharocheilodontic syndrome, cochleosaccular degeneration-cataract syndrome, renal coloboma syndrome, Beare-Stevenson cutis gyrata syndrome, autosomal dominant vibratory urticaria, autosomal dominant Kenny-Caffey syndrome, Rapp-Hodgkin syndrome, Ehlers-Danlos syndrome, classic type, autosomal dominant Ehlers-Danlos syndrome, vascular type, multiple endocrine neoplasia type 1, Coffin-Siris syndrome 1, isolated congenital adermatoglyphia, Flynn-Aird syndrome, Frasier syndrome, hand-foot-genital syndrome, Holt-Oram syndrome, hyperkeratosis-hyperpigmentation syndrome, autosomal dominant ichthyosis vulgaris, hyper-IgE recurrent infection syndrome 1, autosomal dominant, autosomal dominant keratitis, autosomal dominant keratitis-ichthyosis-hearing loss syndrome, LADD syndrome, trichorhinophalangeal syndrome type II, Noonan syndrome with multiple lentigines, microcephaly with or without chorioretinopathy, lymphedema, or intellectual disability, Marfan syndrome, melanoma, cutaneous malignant, susceptibility to, 2, autosomal dominant primary microcephaly, autosomal dominant progressive external ophthalmoplegia, monilethrix, Muir-Torre syndrome, autosomal dominant myoglobinuria, autosomal dominant centronuclear myopathy, nail-patella syndrome, multiple endocrine neoplasia type 2B, autosomal dominant omodysplasia, pheochromocytoma/paraganglioma syndrome 1, Pelger-Huet anomaly, multiple endocrine neoplasia type 2A, piebaldism, autosomal dominant medullary cystic kidney disease with or without hyperuricemia, generalized juvenile polyposis/juvenile polyposis coli, juvenile polyposis/hereditary hemorrhagic telangiectasia syndrome, Peutz-Jeghers syndrome, contractures, pterygia, and spondylocarpotarsal fusion syndrome 1A, autosomal dominant distal renal tubular acidosis, retinoschisis, autosomal dominant, autosomal dominant Robinow syndrome, scapuloperoneal spinal muscular atrophy, autosomal dominant, autosomal dominant sideroblastic anemia, spondyloepiphyseal dysplasia tarda, autosomal dominant, proximal symphalangism, calcaneonavicular coalition, thanatophoric dysplasia type 1, trichorhinophalangeal syndrome type I, Muckle-Wells syndrome, autosomal dominant hypophosphatemic rickets, von Hippel-Lindau disease, Denys-Drash syndrome, autosomal dominant severe congenital neutropenia, Costello syndrome, EEC syndrome, multiple cutaneous and mucosal venous malformations, diffuse nonepidermolytic palmoplantar keratoderma, Timothy syndrome, pheochromocytoma/paraganglioma syndrome 2, spondyloepimetaphyseal dysplasia with multiple dislocations, Brooke-Spiegler syndrome, macrocephaly-autism syndrome, pheochromocytoma/paraganglioma syndrome 3, Duane-radial ray syndrome, PCWH syndrome, heart-hand syndrome, Slovenian type, congenital stationary night blindness autosomal dominant 3, mandibulofacial dysostosis-microcephaly syndrome, multiple endocrine neoplasia type 4, juvenile cataract-microcornea-renal glucosuria syndrome, Crouzon syndrome-acanthosis nigricans syndrome, Birk-Barel syndrome, thrombophilia due to protein S deficiency, autosomal dominant, dyskeratosis congenita, autosomal dominant 2, dyskeratosis congenita, autosomal dominant 3, colorectal cancer, hereditary nonpolyposis, type 6, colorectal cancer, hereditary nonpolyposis, type 7, brain small vessel disease 2A, autosomal dominant, intellectual disability, autosomal dominant 14, intellectual disability, autosomal dominant 15, intellectual disability, autosomal dominant 16, hypopigmentation-punctate palmoplantar keratoderma syndrome, intellectual disability-facial dysmorphism syndrome due to SETD5 haploinsufficiency, postaxial polydactyly-anterior pituitary anomalies-facial dysmorphism syndrome, intellectual developmental disorder with microcephaly and with or without ocular malformations or hypogonadotropic hypogonadism, intellectual disability, autosomal dominant 29, intellectual disability, autosomal dominant 30, Houge-Janssens syndrome 2, severe achondroplasia-developmental delay-acanthosis nigricans syndrome, dyskeratosis congenita, autosomal dominant 6, epidermolysis bullosa simplex 6, generalized, with scarring and hair loss, autosomal dominant complex spastic paraplegia, early-onset autosomal dominant Alzheimer disease, muscular dystrophy, limb-girdle, autosomal dominant, Feingold syndrome, Carney complex, neuronopathy, distal hereditary motor, autosomal dominant, autosomal dominant coarctation of aorta, autosomal dominant spondylocostal dysostosis, autosomal dominant hypohidrotic ectodermal dysplasia, Cowden disease, autosomal dominant distal myopathy, autosomal dominant rhegmatogenous retinal detachment, palmoplantar keratoderma-spastic paralysis syndrome, Alagille syndrome due to a JAG1 point mutation, PTEN hamartoma tumor syndrome, gastric adenocarcinoma and proximal polyposis of the stomach, autosomal dominant proximal renal tubular acidosis, autosomal dominant spastic ataxia, Waardenburg syndrome, hereditary retinoblastoma, autosomal dominant hypocalcemia, Li-Fraumeni syndrome, Loeys-Dietz syndrome, hereditary hemorrhagic telangiectasia, hereditary inclusion body myopathy-joint contractures-ophthalmoplegia syndrome, microcephalic osteodysplastic dysplasia, Saul-Wilson type, autosomal dominant intermediate Charcot-Marie-Tooth disease, autosomal dominant cutis laxa, autosomal dominant nonsyndromic hearing loss, autosomal dominant optic atrophy, autosomal dominant Emery-Dreifuss muscular dystrophy, autosomal dominant cerebellar ataxia, autosomal dominant osteopetrosis, autosomal dominant epidermolytic ichthyosis, ventricular arrhythmias due to cardiac ryanodine receptor calcium release deficiency syndrome, distal arthrogryposis type 2B1, neurofibromatosis, autosomal dominant cataract, arthrogryposis, distal, type 2B2, arthrogryposis, distal, type 2B3, Charcot-Marie-Tooth disease, demyelinating, type 1G, Delpire-McNeill syndrome, LAMA5-related multisystemic syndrome, autosomal dominant oculocutaneous albinism, Charcot-Marie-tooth disease, axonal, type 2DD, Pilarowski-Bjornsson syndrome, intellectual disability, autosomal dominant, fatty acyl-CoA reductase 1 upregulation, GUCY2D-related dominant retinopathy, RPE65-related dominant retinopathy, autosomal dominant titinopathy, NOG-related symphalangism spectrum disorder, ALPL-related autosomal dominant hypophosphatasia, MYH10-related neurodevelopmental disorder with congenital anomalies, spastic paraplegia 30A, autosomal dominant, TMEM127-related tumor predisposition, MAX-related tumor predisposition, BMPR1A-related juvenile polyposis syndrome, RP1-related dominant retinopathy, Birt-Hogg-Dube syndrome, inclusion body myopathy and brain white matter abnormalities, KINSSHIP syndrome, autosomal dominant nebulin-related myopathy, IMPG1-related dominant retinopathy, PROM1-related dominant retinopathy, PURA-related severe neonatal hypotonia-seizures-encephalopathy syndrome, ALG8-related autosomal dominant polycystic kidney and/or liver disease, NOTCH1-related AOS spectrum disorder, FLNB-associated autosomal dominant filamin related bone disorder, familial antiphospholipid syndrome

Genetics & variants

GWAS landscape

No GWAS associations recorded — common-variant (GWAS) studies don’t cover this disease (typical for Mendelian / rare diseases). See the curated gene cohort and Mendelian overlap below.

Variant details and genetic-evidence tiers

ClinVar germline variants

66 retrieved; paginated sample, class counts are floors:

34 uncertain significance, 15 pathogenic, 8 likely pathogenic, 4 conflicting classifications of pathogenicity, 3 likely benign, 2 benign/likely benign

ClinVar	Variant (HGVS)	Gene	Classification	Review
12204	NM_000490.5(AVP):c.262G>A (p.Gly88Ser)	AVP	Pathogenic	no assertion criteria provided
12205	NM_000490.5(AVP):c.143G>T (p.Gly48Val)	AVP	Pathogenic	no assertion criteria provided
12206	NM_000490.5(AVP):c.55G>A (p.Ala19Thr)	AVP	Pathogenic	criteria provided, multiple submitters, no conflicts
12208	NM_000490.5(AVP):c.294C>A (p.Cys98Ter)	AVP	Pathogenic	no assertion criteria provided
12209	NM_000490.5(AVP):c.277G>T (p.Gly93Trp)	AVP	Pathogenic	no assertion criteria provided
12210	NM_000490.5(AVP):c.3del (p.Met1fs)	AVP	Pathogenic	no assertion criteria provided
12212	NM_000490.5(AVP):c.56C>T (p.Ala19Val)	AVP	Pathogenic	no assertion criteria provided
12214	NM_000490.5(AVP):c.160G>C (p.Gly54Arg)	AVP	Pathogenic	criteria provided, multiple submitters, no conflicts
12215	NM_000490.5(AVP):c.337G>T (p.Glu113Ter)	AVP	Pathogenic	no assertion criteria provided
12216	NM_000490.5(AVP):c.260C>T (p.Ser87Phe)	AVP	Pathogenic	criteria provided, single submitter
12218	NM_000490.5(AVP):c.200T>C (p.Val67Ala)	AVP	Pathogenic	no assertion criteria provided
12220	NM_000490.5(AVP):c.346T>G (p.Cys116Gly)	AVP	Pathogenic	no assertion criteria provided
12221	NM_000490.5(AVP):c.61T>C (p.Tyr21His)	AVP	Pathogenic	no assertion criteria provided
1699275	NM_000490.5(AVP):c.347G>A (p.Cys116Tyr)	AVP	Pathogenic	criteria provided, single submitter
3587176	NM_000490.5(AVP):c.77C>T (p.Pro26Leu)	AVP	Pathogenic	criteria provided, single submitter
12213	NM_000490.5(AVP):c.161G>T (p.Gly54Val)	AVP	Likely pathogenic	criteria provided, single submitter
12217	NM_000490.5(AVP):c.275G>A (p.Cys92Tyr)	AVP	Likely pathogenic	criteria provided, single submitter
3065457	NM_000490.5(AVP):c.290G>A (p.Arg97His)	AVP	Likely pathogenic	criteria provided, single submitter
3236029	NM_000490.5(AVP):c.328T>A (p.Cys110Ser)	AVP	Likely pathogenic	criteria provided, single submitter
3358364	NM_000490.5(AVP):c.287G>A (p.Gly96Asp)	AVP	Likely pathogenic	criteria provided, single submitter
3587173	NM_000490.5(AVP):c.120+1G>A	AVP	Likely pathogenic	criteria provided, single submitter
369949	NM_000490.5(AVP):c.131G>T (p.Cys44Phe)	AVP	Likely pathogenic	no assertion criteria provided
4081199	NM_000490.5(AVP):c.174C>A (p.Cys58Ter)	AVP	Likely pathogenic	criteria provided, single submitter
12211	NM_000490.5(AVP):c.287G>T (p.Gly96Val)	AVP	Conflicting classifications of pathogenicity	criteria provided, conflicting classifications
1700421	NM_000490.5(AVP):c.262G>T (p.Gly88Cys)	AVP	Conflicting classifications of pathogenicity	criteria provided, conflicting classifications
383370	NM_000490.5(AVP):c.329G>A (p.Cys110Tyr)	AVP	Conflicting classifications of pathogenicity	criteria provided, conflicting classifications
976038	NM_000490.5(AVP):c.229GAG[1] (p.Glu78del)	AVP	Conflicting classifications of pathogenicity	criteria provided, conflicting classifications
12222	NM_000490.5(AVP):c.64_66del (p.Phe22del)	AVP	Uncertain significance	criteria provided, single submitter
2186055	NM_000490.5(AVP):c.322+4C>A	AVP	Uncertain significance	criteria provided, multiple submitters, no conflicts
2302621	NM_000490.5(AVP):c.118C>G (p.Gln40Glu)	AVP	Uncertain significance	criteria provided, multiple submitters, no conflicts

Genes & proteins

Mendelian disease overlap and somatic drivers

GenCC: 3 · Orphanet: 1 · OMIM-shared: 0 · Dual-evidence (GWAS+Mendelian): 0

GenCC gene–disease validity (cohort genes)

the Disease column is the GenCC-asserted condition — a cohort gene’s strongest validity may be for a related predisposition syndrome.

Gene	Classification	Inheritance	Disease	Records
AVP	Strong	Autosomal dominant	neurohypophyseal diabetes insipidus	3

Orphanet rare-disease linkage (cohort genes)

Gene	Orphanet ID	Rare disease
AVP	Orphanet:30925	Hereditary arginine vasopressin deficiency

Cohort genes → proteins

1 cohort genes, 1 distinct canonical proteins.

Evidence partition

Subset	Genes
multi_evidence	1

Cohort genes (full)

Symbol	HGNC	Ensembl	UniProt	Name	Evidence
AVP	HGNC:894	ENSG00000101200	P01185	Vasopressin-neurophysin 2-copeptin	gencc,clinvar

Cohort function summary

Lead sentence per gene, UniProt-curated.

Symbol	Protein name	Function (lead sentence)
AVP	Vasopressin-neurophysin 2-copeptin	Has a direct antidiuretic action on the kidney, it also causes vasoconstriction of the peripheral vessels.

Protein-family classification

Druggable: 0 · Difficult: 0 · Unknown: 1 · Druggable fraction: 0.0

Family distribution

Cohort families vs a genome-wide background (hypergeometric, BH-FDR; fold = observed/expected). Counts kept; sorted by enrichment, so the catch-all Other/Unknown bucket no longer leads.

Family	Genes	Fold	FDR
Other/Unknown	1	1.8×	0.558

Per-gene assignment

Symbol	Family	Druggable?	EC	InterPro (top 3)
AVP	Other/Unknown	no		Neurhyp_horm, Neurohypophysial_hormone_CS, Neurhyp_horm_dom_sf

Expression context

Cohort genes with no expression data: 0.

1 cohort gene are a single-cell marker in ≥1 SCXA experiment.

Breadth distribution (Bgee present_calls)

Bucket	Genes
narrow (1-5 tissues)	0
moderate (6-20)	0
broad (>20)	1
unknown	0

Top tissues across cohort

Tissue	Cohort genes
buccal mucosa cell	1
hypothalamus	1
ileal mucosa	1

Per-gene tissue summary (top 30)

Symbol	Bgee breadth	FANTOM5 breadth	SCXA	Top tissues
AVP	125	tissue_specific	marker	hypothalamus, ileal mucosa, buccal mucosa cell

Protein interactions among cohort

Intra-cohort edges: 0.

Hub genes (top 10 by interactor count)

Symbol	Interactor count
AVP	2,070

Structural data

PDB: 1 · AlphaFold-only: 0 · No structure: 0

Cohort genes with PDB structures (top 30)

Symbol	UniProt	PDB entries
AVP	P01185	5

Function

Pathway analysis

Distinct Reactome pathways touched by cohort: 26. Enrichment computed across 1 evidence-associated genes (1 with Reactome annotation).

Pathways by enrichment

Over-representation of cohort genes vs the genome-wide background (hypergeometric test, Benjamini-Hochberg FDR; fold = observed/expected over 1 annotated cohort genes). Counts and members are kept as ground-truth; sorted by enrichment.

Pathway	Cohort genes	Fold	FDR	Sample cohort genes
Defective AVP does not bind AVPR2 and causes neurohypophyseal diabetes insipidus (NDI)	1	5710.0×	0.003	AVP
Defective AVP does not bind AVPR1A,B and causes neurohypophyseal diabetes insipidus (NDI)	1	3806.7×	0.003	AVP
Vasopressin-like receptors	1	1903.3×	0.005	AVP
Organic anion transport by SLCO transporters	1	1038.2×	0.006	AVP
BMAL1:CLOCK,NPAS2 activates circadian expression	1	423.0×	0.011	AVP
Aquaporin-mediated transport	1	368.4×	0.011	AVP
R-HSA-400253	1	346.1×	0.011	AVP
Transport of vitamins, nucleosides, and related molecules	1	271.9×	0.011	AVP
Vasopressin regulates renal water homeostasis via Aquaporins	1	265.6×	0.011	AVP
SLC transporter disorders	1	203.9×	0.013	AVP
Disorders of transmembrane transporters	1	139.3×	0.017	AVP
Cargo recognition for clathrin-mediated endocytosis	1	104.8×	0.021	AVP
Clathrin-mediated endocytosis	1	85.2×	0.022	AVP
Class A/1 (Rhodopsin-like receptors)	1	74.2×	0.022	AVP
Peptide ligand-binding receptors	1	74.2×	0.022	AVP
G alpha (s) signalling events	1	73.2×	0.022	AVP
GPCR ligand binding	1	64.2×	0.024	AVP
SLC-mediated transmembrane transport	1	59.2×	0.024	AVP
G alpha (q) signalling events	1	57.4×	0.024	AVP
GPCR downstream signalling	1	43.4×	0.030	AVP
Signaling by GPCR	1	40.1×	0.031	AVP
Membrane Trafficking	1	37.1×	0.032	AVP
Vesicle-mediated transport	1	34.8×	0.032	AVP
Transport of small molecules	1	25.1×	0.043	AVP
Disease	1	13.1×	0.080	AVP
Signal Transduction	1	10.2×	0.098	AVP

GO biological processes by enrichment

Over-representation of cohort genes vs the genome-wide background (hypergeometric test, Benjamini-Hochberg FDR; fold = observed/expected over 1 annotated cohort genes). Counts and members are kept as ground-truth; sorted by enrichment.

GO term	Cohort genes	Fold	FDR	Sample cohort genes
response to nerve growth factor	1	5617.3×	0.002	AVP
maternal aggressive behavior	1	4213.0×	0.002	AVP
obsolete positive regulation of cellular pH reduction	1	4213.0×	0.002	AVP
negative regulation of female receptivity	1	3370.4×	0.002	AVP
response to 2,3,7,8-tetrachlorodibenzodioxine	1	3370.4×	0.002	AVP
positive regulation of glutamate secretion	1	2407.4×	0.002	AVP
negative regulation of transmission of nerve impulse	1	2407.4×	0.002	AVP
renal water absorption	1	2407.4×	0.002	AVP
response to salt stress	1	1872.4×	0.002	AVP
positive regulation of prostaglandin biosynthetic process	1	1872.4×	0.002	AVP
positive regulation of systemic arterial blood pressure	1	1404.3×	0.002	AVP
multicellular organismal response to stress	1	1296.3×	0.002	AVP
grooming behavior	1	1123.5×	0.002	AVP
maternal behavior	1	1123.5×	0.002	AVP
response to peptide	1	1123.5×	0.002	AVP
water transport	1	991.3×	0.002	AVP
vasoconstriction	1	887.0×	0.002	AVP
response to electrical stimulus	1	648.1×	0.003	AVP
positive regulation of vasoconstriction	1	601.9×	0.003	AVP
response to testosterone	1	468.1×	0.004	AVP
response to nicotine	1	421.3×	0.004	AVP
symbiont entry into host cell	1	401.2×	0.004	AVP
generation of precursor metabolites and energy	1	343.9×	0.004	AVP
social behavior	1	271.8×	0.005	AVP
positive regulation of cell growth	1	183.2×	0.008	AVP
locomotory behavior	1	179.3×	0.008	AVP
response to ethanol	1	146.5×	0.009	AVP
positive regulation of cytosolic calcium ion concentration	1	117.0×	0.011	AVP
cell-cell signaling	1	69.6×	0.017	AVP
response to xenobiotic stimulus	1	69.1×	0.017	AVP

Therapeutics

Drug target analysis

Approved (phase 4): 0 · Phase ≥3: 0 · Phased (≥1): 0 · Undrugged: 1

Druggability breadth: 0 of 1 evidence-associated genes (0%) have a ChEMBL target (buckets above are over the deeply-mined display cohort).

Top cohort targets by molecule count

Symbol	Molecules	Max phase
AVP	0	0

Bioactivity and enzyme data

Enzyme cohort genes (≥1 EC): 0.

Pharmacogenomics

Cohort genes with a PharmGKB record: 1; with CPIC/DPWG dosing guidelines: 0.

No cohort gene has a CPIC/DPWG genotype-guided dosing guideline (PharmGKB).

Chemical tractability of cohort targets

0 approved/phased compounds have measured bioactivity against a cohort gene (and aren’t yet in disease-level trials). This is a research / tractability signal, NOT a therapeutic recommendation — a bioactivity row often reflects off-target or screening binding (e.g. promiscuous kinase inhibitors against a cohort kinase), implying no disease mechanism.

Druggability pyramid

Cohort genes binned by druggability tier (high → low):

Tier	Definition	Genes	Symbols
A	Approved (phase 4 drug)	0
B	Phased (≥1) drug, not yet approved	0
C	Druggable family + PDB, no drug	0
D	Druggable family + AlphaFold only, no drug	0
E	Difficult family or no structure, no drug	1	AVP

Undrugged target profiles

1 cohort genes are undrugged. Ranked by ‘starting-point quality’ (assay depth + drugged-partner adjacency).

Symbol	ChEMBL assays	Drugged partners (top 3)
AVP	0	—

Clinical trials & evidence

Clinical trials

Clinical trials: 10.

Phase distribution (across all retrieved trials)

Phase	Trials
Not specified	5
PHASE2	2
EARLY_PHASE1	2
PHASE1	1

Top trials by phase / activity

NCT	Phase	Status	Title
NCT06676774	PHASE2	RECRUITING	Effect of Intranasal Oxytocin on Emotion Recognition and Acute Psycho-Social Stress-induced Cortisol Increase in Patients With Central Diabetes Insipidus and Healthy Controls
NCT06808516	PHASE2	RECRUITING	Effects of Intranasal Oxytocin on Sexual Well-Being in Patients With Arginine Vasopressin Deficiency and Healthy Controls
NCT04789148	PHASE1	RECRUITING	Effects of Intranasal Oxytocin in Patients With Arginine-vasopressin Deficiency
NCT07568509	EARLY_PHASE1	RECRUITING	Identifying Oxytocin Deficiency in Pediatric Patients With Pituitary Disease
NCT06460948	EARLY_PHASE1	COMPLETED	Identifying Oxytocin Deficiency in Adults With Pituitary Disease
NCT06422975	Not specified	RECRUITING	Registry of Patients in Shock Treated With Vasopressin
NCT07361263	Not specified	RECRUITING	Plasma Oxytocin Response to Oral Estrogens in Healthy Controls and AVP-Deficiency
NCT07569861	Not specified	NOT_YET_RECRUITING	Copeptin Measurement After Mannitol and Hypertonic Saline for the Diagnosis of Polyuria-polydipsia Syndrome
NCT05890690	Not specified	COMPLETED	Plasma Copeptin in Response to Oral Urea in Healthy Adults and Patients With Polyuria-polydipsia Syndrome
NCT06542198	Not specified	COMPLETED	Mannitol-induced Release of Copeptin in Healthy Adults and Patients With Polyuria-Polydipsia Syndrome (MARS Study)

Drugs tested across these trials (top 30)

Molecule	Max phase	Trials referencing
ESTRADIOL VALERATE	4	1
UREA	4	1
VASOPRESSIN	4	1