DeCure's autonomous Rare AI scientist is researching a drug-repurposing hypothesis for iminoglycinuria — 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 moduleIminoglycinuria 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 iminoglycinuria 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
solute carrier family 6 member 20 (SLC6A20) — SLC6A20 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 3phdrag to rotate · scroll to zoom
RCSB Protein Data Bank · entry 7Y75 · 3.1 Å · ligand 1,2-DIACYL-GLYCEROL-3-SN-PHOSPHATE (3PH). Experimental structure, not a prediction.
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 · 1968 · 51 citations
Familial Iminoglycinuria
AbstractClinical, biochemical and genetic studies in a family with inherited, renal iminoglycinuria showed that the proband had a prominent renal tubular defect for reabsorption of glycine, proline and hydroxyproline. His parents and several relatives had hyperglycinuria only. No defect in intestinal absorption or transport of glycine or the imino acids was found in the proband. Familial iminoglycinuria is concluded to represent another specific inborn error of transport due to an autosomal mutation. Homozygotes for this mutation are believed to excrete abnormal quantities of the imino acids and glycine whereas heterozygotes excrete excessive glycine only. Glycine is reabsorbed by more than one renal transport system, and the biochemical mechanisms that control intestinal transport of glycine and the imino acids are not identical. The abnormal phenotype noted in iminoglycinuria is very probably due to more than a single abnormal genotype.
New England Journal of Medicine · 1968 · 31 citations
Cystathioninuria and Renal Iminoglycinuria in a Pedigree
AbstractCystathioninuria and hyperglycinuria both occurred in a male Ashkenazi-Jewish Infant. Both traits were dominantly inherited as the heterozygous forms of two independent mutant alleles. The patient was thus a double heterozygote. Renal iminoglycinuria appeared as an autosomal recessive trait in the mother of the proband and In four of her sibs. This condition is the homozygous form of the trait that presents as hyperglycinuria in the heterozygote; it is a benign inborn error of amino acid transport. Cystathioninuria is probably also a benign trait. Knowledge of the precise phenotypes and their significance were of practical value in counseling the family.
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.
