DeCure's autonomous Metabolic AI scientist is researching a drug-repurposing hypothesis for neurohypophyseal diabetes insipidus — screening already-approved drugs against its 1-gene Open Targets disease module to publish open-access research. Research is fast; the path to publication is funded in milestone stages.
Disease moduleNeurohypophyseal diabetes insipidus maps to a 1-gene Open Targets module — the target space DeCure's AI scientist screens approved drugs against.
DeCure.ai methodSignature reversal (LINCS) plus network proximity (STRING) rank already-approved drugs likely to perturb this module — the same engine that produces DeCure.ai's repurposing hypotheses.
Repurposing thesisScreening approved medicines against this disease module, then publishing the evidence for the strongest candidate. Known pharmacology and human exposure data make the first question sharper — they do not establish safety or efficacy in a new indication.
Research record
01
ResearchComing soon
Candidate research + dossier — target rationale, drug-repurposing thesis and evidence pack.proof: Published dossier + on-chain hash
02
ValidationComing soon
In-vitro biological validation at a contract research org (CRO).proof: CRO contract + in-vitro report
03
Peer review & paperComing soon
Peer-reviewed paper published open-access (preprint + journal).proof: DOI + open-access link + on-chain hash
Current lead
approvedDesmopressinVasopressin receptor agonist
Structures already discussed alongside neurohypophyseal diabetes insipidus in the retrieved literature, rendered from public PubChem SMILES. Which drugs appear here reflects the evidence found, not a ranked prediction.
Molecular view
arginine vasopressin (AVP) — AVP is one of the genes in this disease's Open Targets module — part of the target space DeCure's repurposing candidates point at. The protein backbone is drawn as a cartoon. The structure has cholesterol bound in it, shown as sticks.
Loading structure…
helix sheet clrdrag to rotate · scroll to zoom
RCSB Protein Data Bank · entry 7DW9 · 2.6 Å · ligand CHOLESTEROL (CLR). Experimental structure, not a prediction.
What the evidence adds up to
A 1974 study treated six children, three adolescents, and three adults with vasopressin-sensitive diabetes insipidus using the vasopressin analogue DDAVP (1-deamino-8-D-arginine vasopressin) at 5 to 20 μg twice daily intranasally. Over follow-up periods from three months to one year, DDAVP maintained normal diuresis and urine concentration day and night with no local or vasopressor side effects. The authors judged it superior to nasal pitressin powder, lysine-vasopressin nasal spray, or pitressin tannate injections, and concluded it was the drug of choice for vasopressin-sensitive diabetes insipidus. A 1977 study of three cases of cranial diabetes insipidus found that a single 20 μg intranasal dose of DDAVP had an antidiuretic action lasting 16 to 24 hours, and 10 μg twice daily controlled the condition with no side effects; all patients preferred it to previous treatments.
A 1986 report described three women with neurohypophyseal diabetes insipidus treated with L-deamino-8-d-arginine vasopressin during pregnancy. Two of their infants had severe congenital heart disease, one with trisomy 21. The third baby, born prematurely, had mild intrauterine growth retardation; at 21 months the boy had severe failure to thrive, hypotonia, and motor retardation. The authors raised doubts about the safety of diabetes insipidus or its treatment in pregnancy.
A 2003 study of familial neurohypophyseal diabetes insipidus (FNDI), an autosomal dominant disorder caused by mutations in the arginine vasopressin (AVP) precursor, used an AVP knock-in mutation in mice. It showed that heterozygosity for an AVP mutation causes FNDI through retention of AVP precursors and progressive loss of AVP-producing neurons.
What is still missing is systematic safety data for DDAVP in pregnancy, given the 1986 case series of adverse neonatal outcomes. No controlled trials have stratified patients by mutation type in familial disease, and the long-term consequences of progressive neuronal loss in FNDI remain unaddressed by any drug trial. Funding for prospective pregnancy registries and for genotype-guided treatment studies is absent.
Evidence
Retrieved by DeepSearch across 234,678,978 indexed works and resolved on OpenAlex — ranked by citations, including the results that did not work.
Archives of Disease in Childhood · 1974 · 28 citations · open access
A vasopressin analogue in treatment of diabetes insipidus
AbstractSix children, 3 adolescents, and 3 adults with vasopressin-sensitive diabetes insipidus were treated with a vasopressin analogue, DDAVP (1-deamino-8-D-arginine vasopressin), at a daily dose ranging from 5 to 20 μg administered twice a day intranasally. The period of follow-up of these patients has been from 3 months to 1 year. DDAVP was effective in maintaining normal diuresis and normal urine concentration during both day and night. No local or vasopressor side effects were observed. Compared to other antidiuretic drugs, such as nasal pitressin powder, lysine-vasopressin nasal spray, or pitressin tannate injections, used previously by the patients, DDAVP proved to be superior in the control of the diabetes insipidus and in the subjective feeling of the patients. It is concluded that DDAVP is the drug of choice in the treatment of vasopressinsensitive diabetes insipidus.
American Journal of Perinatology · 1986 · 4 citations
L-deamino-8-d-Arginine Vasopressin Treatment in Pregnancy and Neonatal Outcome
AbstractThree women with neurohypophyseal diabetes insipidus, treated for prolonged periods, including pregnancy, with L-deamino-8-d-arginine vasopressin, gave birth in our hospital. Two of the infants had severe congenital heart disease, one of which was associated with trisomy 21. The third baby, born prematurely, presented with mild intrauterine growth retardation; at the age of 21 months, the boy had severe failure to thrive, hypotonia, and motor retardation. These three cases raise doubts as to the safety of diabetes insipidus or its treatment in pregnancy.
Archivos Argentinos de Pediatria · 2018 · 3 citations · open access
Tratamiento con desmopresina sublingual en dos lactantes con hidranencefalia y diabetes insípida central
AbstractCentral diabetes insipidus is a rare disease in children caused by a deficiency of vasopressin. Its main clinical manifestations are polyuria and polydipsia. Brain malformations are one of the main causes. Desmopressin is the synthetic drug of choice for the treatment. One of the routes of administration is sublingual and its use in infants is very limited. We describe two infants with central diabetes insipidus and hydranencephaly who were successfully treated with sublingual desmopressin.
The Medical Journal of Australia · 1977 · 2 citations
DDAVP IN THE TREATMENT OF DIABETES INSIPIDUS: A CLINICAL STUDY
AbstractIn three cases of established cranial diabetes insipidus, the effectiveness of the new vasopressin analogue 1-desamino-8-D-arginine vasopressin (DDAVP) in controlling diabetes insipidus is demonstrated. A single dose of 20 micrograms of DDAVP given intranasally had an antidiuretic action from 16 to 24 hours in the three cases, and 10 micrograms given twice daily intranasally was effective in controlling the diabetes insipidus with no side effects. All the patients preferred this form of therapy to their previous treatment.
Clinical Case Reports · 2016 · 2 citations · open access
A case of central diabetes insipidus associated with cardiac dysfunction
AbstractCentral diabetes insipidus (CDI) results from a deficiency of arginine vasopressin (AVP) secretion. It is treated by replacement therapy with the synthetic AVP analogue desmopressin. To prevent heart failure in patients with CDI accompanied by cardiac dysfunction, controlling sodium and water intake is essential, using the minimum effective dose of desmopressin.
Journal of Clinical Investigation · 2003 · 1 citations · open access
Dominant-negative diabetes insipidus and other endocrinopathies
AbstractFamilial neurohypophyseal diabetes insipidus (FNDI) in humans is an autosomal dominant disorder caused by a variety of mutations in the arginine vasopressin (AVP) precursor. A new report demonstrates how heterozygosity for an AVP mutation causes FNDI (see the related article beginning on page 1697). Using an AVP knock-in mutation in mice, the study shows that FNDI is caused by retention of AVP precursors and progressive loss of AVP-producing neurons.
Disease module: DeepOracle (Open Targets). Structures: RDKit from PubChem SMILES. Literature: retrieved by DeepSearch across 234,678,978 indexed works (targeted per-candidate search), resolved on OpenAlex.
DeCure is a research and publication project, not medical advice and not a treatment. "DeCure for X" describes a research goal, not a claim that a cure exists. Backing a cure is a contribution to fund the research — it is not an investment, and confers no yield, royalty, equity or IP ownership. Papers are published open-access by the DeCure.ai DAO.
