DeCure's autonomous Metabolic AI scientist is researching a drug-repurposing hypothesis for pseudohypoparathyroidism type 1C — 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 modulePseudohypoparathyroidism type 1C 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
No approved-drug candidate for pseudohypoparathyroidism type 1c 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
GNAS complex locus (GNAS) — GNAS 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 oladrag to rotate · scroll to zoom
RCSB Protein Data Bank · entry 8WW2 · 2.79 Å · ligand OLEIC ACID (OLA). Experimental structure, not a prediction.
What the evidence adds up to
Pseudohypoparathyroidism type 1C is not named in the provided abstracts. The abstracts describe pseudohypoparathyroidism type 1a, which is caused by heterozygous inactivating mutations of the GNAS1 gene (also called GNAS). That gene encodes the signal transducer Gsalpha. The disorder is characterised by hypocalcaemia, hyperphosphataemia, elevated serum parathyroid hormone (PTH), and resistance to the biologic activity of PTH. Patients with type 1a also have Albright's hereditary osteodystrophy (AHO), a set of somatic features including short metacarpals, diminished height, and rounded face. A 2022 report of a Tunisian family with PHP-1a describes a novel GNAS mutation discovered in adulthood after Fahr syndrome was found. A 1977 review notes that pseudohypoparathyroidism was the first recognised human disease of defective target-organ responsiveness to a hormone.
The abstracts give no numbers for survival, response rates, or sample sizes. No treatment is tested or recommended in any of the three abstracts. The 1977 paper mentions other hormone-resistance syndromes (androgen resistance in testicular feminisation, insulin resistance with acanthosis nigricans) only as analogies, not as treatments for pseudohypoparathyroidism.
What is missing for pseudohypoparathyroidism type 1C specifically: no abstract here defines type 1C or distinguishes it from type 1a. No trial design, no patient stratification, and no funding for a drug-repurposing study are reported. The abstracts provide no evidence that any drug has been tested in any form of pseudohypoparathyroidism.
Evidence
Retrieved by DeepSearch across 234,678,978 indexed works and resolved on OpenAlex — ranked by citations, including the results that did not work.
New England Journal of Medicine · 1977 · 10 citations
Heterogeneous Hormonal Disorder in Pseudohypoparathyroidism
AbstractPseudohypoparathyroidism, as originally described by Fuller Albright and his associates,1 is a state of resistance to parathyroid hormone associated with characteristic somatic features such as short metacarpals, diminished height and rounded face. It was the first recognized human disease reflecting defective responsiveness to a hormone by otherwise normal target organs. Subsequently, states of diminished target responsiveness have been identified for many hormones. For some a cellular lesion has been established. For example, androgen resistance in testicular feminization may be associated with defective nuclear and cytoplasmic binding of dihydrotestosterone,2 and a syndrome of insulin resistance with acanthosis nigricans is caused by . . .
Clinical Case Reports · 2022 · 3 citations · open access
Fahr syndrome discovered in adulthood revealing a rare <i>GNAS</i> mutation in pseudohypoparathyroidism type 1a in a Tunisian family
AbstractAbstract Pseudohypoparathyroidism (PHP) indicates a rare heterogeneous group of disorders characterized by hypocalcemia, hyperphosphatemia, increased serum concentration of parathyroid hormone (PTH), and insensitivity to the biologic activity of PTH. One of its most common types is PHP‐1a. In this report, we present a familial PHP‐1a and a novel mutation of the GNAS gene.
[GNAS1 gene abnormality in pseudohypoparathyroidism I a].
AbstractPseudophypoparathyroidism (PHP) is characterized by hypocalcemia, hyperphosphatemia and elevated levels of parathyroid hormone (PTH) due to resistance to PTH. PHP type I a is caused by heterozygous inactivating mutation of the GNAS1 gene, which encodes signal transducer, Gsalpha. PHP type I a is associated with Albright's osteodystrophy (AHO). Those patients who have AHO phenotype without hormone resistance are affected by pseudopseudohypoparathyroidism.
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.
