DeCure for Glucosephosphate dehydrogenase deficiency
DeCure's autonomous Rare AI scientist is researching a drug-repurposing hypothesis for glucosephosphate dehydrogenase deficiency — 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 moduleGlucosephosphate dehydrogenase deficiency 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 glucosephosphate dehydrogenase deficiency 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
glucose-6-phosphate dehydrogenase (G6PD) — G6PD 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 napdrag to rotate · scroll to zoom
RCSB Protein Data Bank · entry 6E08 · 1.9 Å · ligand NADP NICOTINAMIDE-ADENINE-DINUCLEOTIDE PHOSPHATE (NAP). Experimental structure, not a prediction.
What the evidence adds up to
Glucose-6-phosphate dehydrogenase (G6PD) deficiency is a hereditary condition caused by mutations on chromosome X with sex-linked inheritance, but a 2022 narrative review describes an "acquired" form phenotypically indistinguishable from the primary deficiency. This acquired impairment results from biochemical mechanisms that inhibit the enzyme in the absence of a structural gene-level defect, and the review identifies hyperaldosteronism and diabetes as the most common culprits, with additional endocrine and metabolic conditions causing deficiency in both hospitalised and outpatients. Unlike the inherited defect, acquired G6PD deficiency is potentially curable by removing the factor responsible for enzyme inhibition. The review does not provide any patient numbers, response rates, or survival data.
A 2010 study from Iraq reviewed records of 156 under-5-year-olds with G6PD deficiency admitted to three hospitals in Baghdad over six years. A preponderance of males was noted in both Baghdad and Mosul (ratios of 1.6:1 and 3.4:1 respectively). Family history of G6PD deficiency was positive in 19.2% of patients in Baghdad and 13.6% in Mosul. The majority of patients in Baghdad (69.2%) and Mosul (76.1%) showed haemolysis within one to three days of exposure to noxious agents. A 2007 study from Saudi Arabia aimed to investigate mutations and clinical significance of the G6PD gene but its abstract provides no results, patient numbers, or outcome data. A 2008 case report and review on kernicterus by G6PD deficiency is cited but its abstract contains no usable data.
What is still missing is any controlled trial of a treatment for either inherited or acquired G6PD deficiency, any data on whether removing the causative factor in acquired cases actually reverses the deficiency in a measurable way, and any patient stratification by specific G6PD variant or precipitating agent. No drug is mentioned in any of these abstracts.
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 Medicine · 2022 · 14 citations · open access
AbstractGlucose-6-phosphate dehydrogenase (G6PD) deficiency is a hereditary condition caused by mutations on chromosome X and is transmitted by a sex-linked inheritance. However, impairment of G6PD activity may result from biochemical mechanisms that are able to inhibit the enzyme in specific clinical conditions in the absence of a structural gene-level defect. In this narrative review, a number of clinical settings associated with an "acquired" G6PD deficiency, phenotypically undistinguishable from the primary deficiency, as well as the mechanisms involved, were examined. Hyperaldosteronism and diabetes are the most common culprits of acquired G6PD deficiency. Additional endocrine and metabolic conditions may cause G6PD deficiency in both hospitalized and outpatients. Contrary to the inherited defect, acquired G6PD deficiency is a condition that is potentially curable by removing the factor responsible for enzyme inhibition. Awareness regarding acquired G6PD deficiency by physicians might result in improved recognition and treatment.
Eastern Mediterranean Health Journal · 2010 · 6 citations · open access
Epidemiological, clinical and laboratory profile of glucose-6-phosphate dehydrogenase deficiency in the middle and north of Iraq: a comparative study
AbstractThis study determined the epidemiological, clinical and laboratory profile of glucose-6-phosphate dehydrogenase (G6PD) deficiency in Baghdad (central Iraq) and compared it with previous data from Mosul (northern Iraq). We reviewed the records of 156 under-5-year-olds with G6PD deficiency admitted to 3 hospitals in Baghdad over a 6-year period. A preponderance of males was noted in both Baghdad and Mosul (1.6:1 and 3.4:1 respectively). Family history of G6PD deficiency was positive in 19.2% of patients in Baghdad and 13.6% in Mosul. A majority of patients in Baghdad (69.2%) and Mosul (76.1%) showed haemolysis within 1-3 days of exposure to noxious agents. Similarities in the profiles from Baghdad and Mosul suggest that there are similar G6PD variants and similar exposure to precipitating agents.
Journal of King Abdulaziz University-Medical Sciences · 2007 · 1 citations · open access
Glucose-6-Phosphate Dehydrogenase Deficiency Correlation between Genotype and Phenotype
AbstractIn Saudi Arabia, Glucose-6-phosphate dehydrogenase deficiency exists at variable frequency in different regions in the Kingdom. The aim of this study was to investigate the mutations and clinical significance of the Glucose-6-phosphate dehydrogenase gene among the population in this area.
Kernicterus by glucose-6-phosphate dehydrogenase deficiency: a case report and review of the literature-0
Abstract<b>Copyright information:</b>Taken from "Kernicterus by glucose-6-phosphate dehydrogenase deficiency: a case report and review of the literature"http://www.jmedicalcasereports.com/content/2/1/146Journal of Medical Case Reports 2008;2():146-146.Published online 6 May 2008PMCID:PMC2391151.
Kernicterus by glucose-6-phosphate dehydrogenase deficiency: a case report and review of the literature-0
Abstract<b>Copyright information:</b>Taken from "Kernicterus by glucose-6-phosphate dehydrogenase deficiency: a case report and review of the literature"http://www.jmedicalcasereports.com/content/2/1/146Journal of Medical Case Reports 2008;2():146-146.Published online 6 May 2008PMCID:PMC2391151.
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.
