DeCure's autonomous Rare AI scientist is researching a drug-repurposing hypothesis for hyperprolinemia type 1 — 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 moduleHyperprolinemia type 1 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 hyperprolinemia type 1 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.
What the evidence adds up to
The 1971 study of a Sicilian family found type I hyperprolinemia in several members who had no kidney disease or other hereditary anomalies. Serum proline levels ranged from about 5 to about 25 mg/100 ml. The authors concluded that hyperprolinemia is probably an inborn error of amino acid metabolism without clinical implications, inherited as "pure familial hyperprolinemia" by an autosomal and probably recessive gene, and suggested that even heterozygotes may show some degree of hyperprolinemia.
A 1974 report described three siblings with type II hyperprolinemia, a disorder typically associated with mental retardation, seizures, and EEG anomalies. These three siblings had high serum proline and urinary pyrroline-5-carboxylic acid but no signs of any associated anomalies. The authors noted that type II hyperprolinemia is a rare metabolic disorder.
A 1978 paper described a non-chromatographic screening test for hyperprolinemia using protein precipitation, color development with isatin, extraction with methylene chloride, and measurement of absorbance at 600 nm. The authors reported that the specificity and analytical recovery made the method suitable for this use.
No treatment trials, no drug interventions, and no outcome data beyond the biochemical and clinical descriptions are reported in these abstracts. What is missing is any evidence that lowering proline levels changes clinical outcomes, any randomised trial of any intervention, and any patient stratification that might identify who, if anyone, would benefit from treatment.
Evidence
Retrieved by DeepSearch across 234,678,978 indexed works and resolved on OpenAlex — ranked by citations, including the results that did not work.
PEDIATRICS · 1971 · 17 citations
PURE FAMILIAL HYPERPROLINEMIA: ISOLATED INBORN ERROR OF AMINOACID METABOLISM WITHOUT OTHER ANOMALIES IN A SICILIAN FAMILY
AbstractType I hyperprolinemia was detected in several members of a Sicilian family, in which no clinical or biological signs of nephropathy and of other hereditary anomalies were present. A family with similar findings has been reported in 1970 by Fontaine, et al. These two families indicate that hyperprolinemia is probably an inborn error of aminoacid metabolism without clinical implications, which can be inherited as "pure familial hyperprolinemia," independently of other hereditary disorders, by an autosomal and probably recessive gene. A wide range of serum proline levels (from about 5 to about 25 mg/100 ml) was found in the affected members. It is suggested that even the 0heterozygotes may show some degree of hyperprolinemia.
Clinical Chemistry · 1978 · 2 citations · open access
Non-chromatographic screening test for hyperprolinemia.
AbstractThis procedure for determining serum proline in patients with hyperprolinemia involves protein precipitation (Folin-Wu method), color development with isatin, extraction of the color with methylene chloride and measurement of its absorbance at 600 nm. The specificity and analytical recovery show the method to be suitable for this use.
Acta geneticae medicae et gemellologiae · 1974 · 0 citations · open access
Asymptomatic Type II Hyperprolinemia Associated with Hyperglycinemia in Three Siblings
AbstractType II hyperprolinemia is a rare metabolic disorder associated with mental retardation, seizures, and EEG anomalies. The authors describe a Sicilian family, detected screening for aminoacidopathies by the method of Scriver, in which three siblings have high levels of serum proline and urinary pyrroline-5-carboxylic acid, without any signs of associated anomalies.
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.
