DeCure's autonomous Rare AI scientist is researching a drug-repurposing hypothesis for glucose-galactose malabsorption — 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 moduleGlucose-galactose malabsorption 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 glucose-galactose malabsorption 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 5 member 1 (SLC5A1) — SLC5A1 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 y01drag to rotate · scroll to zoom
RCSB Protein Data Bank · entry 7SLA · 3.15 Å · ligand CHOLESTEROL HEMISUCCINATE (Y01). Experimental structure, not a prediction.
What the evidence adds up to
Glucose-galactose malabsorption is a genetic disorder caused by a defect in the Na+-glucose cotransporter SGLT1, which normally transports glucose and galactose across the intestinal brush border. Mutations causing the transport defect have been identified in patients from 33 kindreds, and functional studies have established how these mutations cause the disease. Domestic research about the congenital form is rare, and no cases had been discovered in that setting as of a 2017 review.
Eight children from eight different Arab families, six Saudi and two from other Arab nationalities, presented with chronic watery diarrhoea present since birth and failure to thrive. The mean age at presentation was 10.6 months. Diagnosis was confirmed by small-bowel biopsy, histology, and small-bowel enzyme assay. One child had a renal stone at the first visit, and another was discovered to have one on follow-up. All eight children responded clinically to a fructose-based formula and were thriving at follow-up.
No drug treatment is described in any of these abstracts. The only intervention reported is dietary: replacing glucose and galactose with fructose. No data on survival, response rates beyond clinical improvement, or sample sizes larger than eight patients are provided. The 2017 review notes that the condition can involve hypertonic dehydration and hypernatraemia, but gives no new trial results.
What is still missing is any controlled trial of a pharmacological intervention, any attempt to correct the SGLT1 defect at the molecular level, and any systematic patient registry that would allow stratification by mutation type or severity. No funding for drug development is mentioned.
Evidence
Retrieved by DeepSearch across 234,678,978 indexed works and resolved on OpenAlex — ranked by citations, including the results that did not work.
American Journal of Physiology-Gastrointestinal and Liver Physiology · 1998 · 85 citations
I. Glucose Galactose Malabsorption
AbstractGlucose Galactose Malabsorption is a genetic disorder caused by a defect in glucose and galactose transport across the intestinal brush border. Normally, lactose in milk is broken down into glucose and galactose by lactase, an ectoenzyme on the brush border, and the hexoses are transported into the cell by the Na+-glucose cotransporter SGLT1. The mutations causing the defect in sugar transport have been identified in patients from 33 kindreds, and functional studies have established how these mutations cause the disease.
Journal of Pediatric Gastroenterology and Nutrition · 1996 · 23 citations
Congenital Glucose-Galactose Malabsorption in Arab Children
AbstractEight children with chronic diarrhea from glucose-galactose malabsorption from eight different families are presented. Six children are Saudi Arabs and two are of the other Arab nationalities. The mean age of the children at the time of presentation was 10.6 months. They were first seen for chronic watery diarrhea, present since birth, and failure to thrive. Laboratory investigations, including small-bowel biopsy, histology, and small-bowel enzyme assay, confirmed the diagnosis of glucose-galactose malabsorption. One child had a renal stone at the first visit, and another was discovered to have one on follow-up. All the children responded clinically to fructose-based formula, and they are thriving at follow-up.
International journal of pediatrics · 2017 · 0 citations
Progress of the congenital glucose-galactose malabsorption
AbstractCongenital glucose-galactose malabsorption(CGGM), also known as congenital glucose-galactose intolerance syndrome, is a rare autosomal recessive hereditary disease.Domestic research about CGGM is rare and there was no discovery of the cases for this disease.This review summarizes the mechanism, clinical characteristics, diagnosis and treatment of CGGM.
Key words:
Congenital glucose-galactose malabsorption; Hypertonic dehydration; Hypernatremia
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.
