DeCure's autonomous Rare AI scientist is researching a drug-repurposing hypothesis for pseudohypoaldosteronism — screening already-approved drugs against its 2-gene Open Targets disease module to publish open-access research. Research is fast; the path to publication is funded in milestone stages.
Disease modulePseudohypoaldosteronism maps to a 2-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
No approved-drug candidate for pseudohypoaldosteronism is corroborated in the literature DeepSearch retrieved. Some conditions are managed with non-pharmacological care — a device, surgery or physical therapy — rather than a medicine; that may be the case here, or the literature we found may simply be too sparse yet to support a drug-repurposing angle.
Molecular view
nuclear receptor subfamily 3 group C member 2 (NR3C2) — NR3C2 is one of the genes genetically linked to this disease in Open Targets — shown as context, not as a drug target we're pursuing: no approved-drug candidate for this disease is yet corroborated in the literature we found.
Loading structure…
helix sheet 2,2-difluoro-3-hydroxypropyldrag to rotate · scroll to zoom
RCSB Protein Data Bank · entry 4PF3 · 1.1 Å · ligand 6-[1-(2,2-difluoro-3-hydroxypropyl)-5-(4-fluorophenyl)-3-methyl-1H-pyrazol-4-yl]-2H-1,4-benzoxazin-3(4H)-one (HFN). Experimental structure, not a prediction.
What the evidence adds up to
Two unrelated male infants with pseudohypoaldosteronism presented with failure to thrive. Renal and adrenal function were normal. Sodium balance studies showed abnormal urinary salt loss despite very high aldosterone secretion rates. Daily oral salt supplement resulted in complete therapeutic success in these two cases.
A 6-month-old boy with pseudohypoaldosteronism did not respond adequately to considerable quantities of supplemental sodium. Indomethacin, a prostaglandin inhibitor, greatly reduced his sodium requirement. Treatment was maintained for nine months, at which point re-evaluation showed he was dependent on indomethacin for satisfactory control.
A 1994 review article titled "The enigma of pseudohypoaldosteronism" was published in The Journal of Clinical Endocrinology & Metabolism. A 2024 article describes a 15-year-old female patient diagnosed with type IIE pseudohypoaldosteronism, a rare monogenic cause of secondary arterial hypertension that can remain undiagnosed or be misclassified as primary hypertension. The article emphasises the role of differential diagnosis and molecular genetic testing in paediatric and adolescent hypertension.
What is still missing is evidence from larger, controlled studies comparing salt supplementation, indomethacin, and no treatment across the different genetic subtypes of pseudohypoaldosteronism. The long-term outcomes of indomethacin therapy beyond nine months are not reported, and no trial has stratified patients by the specific molecular defect to predict which will respond to prostaglandin inhibition versus salt alone.
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 Pediatrics and Adolescent Medicine · 1973 · 21 citations
Pseudohypoaldosteronism
AbstractTwo unrelated male infants with pseudohypoaldosteronism are reported. Their main clinical symptom was failure to thrive. Renal and adrenal function were normal. Sodium balance studies showed an abnormal urinary salt loss in the presence of very high aldosterone secretion rates. A daily oral administration of salt supplement resulted in a complete therapeutic success. A brief review of the literature on this rare condition is given and the pathophysiology is discussed.
Archives of Disease in Childhood · 1982 · 14 citations · open access
Pseudohypoaldosteronism: Response to long-term treatment with indomethacin
AbstractA 6-month-old boy presented with features of pseudohypoaldosteronism. Considerable quantities of supplemental sodium failed to compensate his natriuresis but indomethacin, a prostaglandin inhibitor, greatly reduced his sodium requirement. Treatment was maintained for 9 months when re-evaluation showed him to be dependent on indomethacin for satisfactory control.
The Journal of Clinical Endocrinology & Metabolism · 1994 · 9 citations
The enigma of pseudohypoaldosteronism.
AbstractJournal Article The enigma of pseudohypoaldosteronism. Get access D Corvol, D Corvol Search for other works by this author on: Oxford Academic Google Scholar J Funder J Funder Search for other works by this author on: Oxford Academic Google Scholar The Journal of Clinical Endocrinology & Metabolism, Volume 79, Issue 1, 1 July 1994, Pages 25–26, https://doi.org/10.1210/jcem.79.1.8027237 Published: 01 July 1994
Russian Journal for Personalized Medicine · 2024 · 0 citations · open access
Rare monogenic cause of arterial hypertension
AbstractSecondary arterial hypertension is characterized by a diverse range of etiological factors, making the clarification of its underlying causes a fundamental aspect of both diagnosis and treatment. Accurate identification of the etiology of hypertension directly influences therapeutic strategies and has significant implications for patient prognosis. In certain instances, molecular genetic testing may be necessary to pinpoint the specific etiological factor with greater precision. Among the rare but noteworthy causes of secondary arterial hypertension is pseudohypoaldosteronism, which can often remain undiagnosed for prolonged periods or be misclassified as primary hypertension. This article presents the clinical case of a 15-year-old female patient diagnosed with type IIE pseudohypoaldosteronism, emphasizing the critical role of differential diagnosis in managing arterial hypertension in pediatric and adolescent populations. We will explore the principal clinical manifestations of the condition, as well as the laboratory, instrumental, and molecular genetic findings that facilitated the accurate diagnosis and optimization of treatment for this patient.
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.
