DeCure for Glutathione synthetase deficiency without 5-oxoprolinuria
DeCure's autonomous Rare AI scientist is researching a drug-repurposing hypothesis for glutathione synthetase deficiency without 5-oxoprolinuria — 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 moduleGlutathione synthetase deficiency without 5-oxoprolinuria 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
approvedGlutathioneApproved drug
Structures already discussed alongside glutathione synthetase deficiency without 5-oxoprolinuria in the retrieved literature, rendered from public PubChem SMILES. Which drugs appear here reflects the evidence found, not a ranked prediction.
Molecular view
GLUTATHIONE S-TRANSFERASE — Glutathione has a real, experimentally solved structure in complex with this target (PDB 13GS, 1.9 Å). This is the drug's own deposited structure, not a prediction, and confirms it is a structurally characterised molecule rather than an untested guess.
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helix sheet gshdrag to rotate · scroll to zoom
RCSB Protein Data Bank · entry 13GS · 1.9 Å · ligand Glutathione (GSH). 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.
Journal of Clinical Investigation · 1978 · 51 citations · open access
Biochemical heterogeneity in glutathione synthetase deficiency.
AbstractTwo different clinical syndromes are associated with glutathione synthetase deficiency, one presenting with hemolytic anemia and 5-oxoprolinuria, the other with isolated hemolysis. We have differentiated these disorders on an enzymatic basis. In 5-oxoprolinuria, all cell types examined have grossly deficient enzyme activity and glutathione content. In contrast, in the nonoxoprolinuric variant, erythrocytes have decreased enzyme activity and glutathione content, whereas nucleated cells maintain substantial levels of both. The enzyme in this disorder is unstable in vitro and has shortened survival in intact erythrocytes. Nucleated cells appear able to maintain sufficient enzyme activity and concentrations of glutathione to suppress overproduction of 5-oxoproline.
AbstractGlutathione synthetase (GSS) deficiency is an extremely rare autosomal recessive inborn error of metabolism. This metabolic disorder is caused by mutations in the GSS gene, which encodes GSS—an enzyme that catalyses the ATP-dependent conversion of γ-glutamyl-cysteine and glycine to glutathione. Low glutathione impairs the cellular antioxidant defence mechanism, leaving cells susceptible to oxidative stress and damage.
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.
