DeCure for Intestinal disaccharide deficiency and disaccharide malabsorption
DeCure's autonomous Rare AI scientist is researching a drug-repurposing hypothesis for intestinal disaccharide deficiency and disaccharide malabsorption — screening already-approved drugs against its 7-gene Open Targets disease module to publish open-access research. Research is fast; the path to publication is funded in milestone stages.
Disease moduleIntestinal disaccharide deficiency and disaccharide malabsorption maps to a 7-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 intestinal disaccharide deficiency and disaccharide 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
glucokinase (GCK) — GCK 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 2rdrag to rotate · scroll to zoom
RCSB Protein Data Bank · entry 4DCH · 1.79 Å · ligand (2R)-3-cyclopentyl-2-[4-(methylsulfonyl)phenyl]-N-(1,3-thiazol-2-yl)propanamide (4DC). Experimental structure, not a prediction.
What the evidence adds up to
A 1967 case report describes a young child with gastroenteritis who developed a temporary secondary disaccharidase deficiency linked to intestinal mucosal damage. The report stresses that without complete diagnostic studies, confusion can arise in distinguishing this reversible deficiency from a primary, congenital enzyme absence. The child was given oral carbohydrate tolerance tests using 2 grams of sugar per kilogram of body weight, with blood sugar measured in duplicate by the Nelson-Somogyi method, but the abstract gives no survival or response rate numbers.
A 2024 Norwegian study of 40 patients referred for gastroscopy due to gastrointestinal complaints measured disaccharidase activity in duodenal pinch biopsies using the Dahlqvist method. Lactase deficiency was found in 22 patients (55%), maltase deficiency in 11 (28%), sucrase deficiency in 9 (23%), isomaltase deficiency in 13 (33%), and glucoamylase deficiency in 12 (30%). All five enzymes were reduced in 8 patients (20%). Twenty-one patients met Rome IV criteria for irritable bowel syndrome. Moderate to severe gastrointestinal symptoms were reported by 16 of 24 patients (67%) with disaccharidase deficiency and by 14 of 16 patients (88%) with normal enzyme activity. The study found no association between the degree of disaccharidase deficiency and either the severity of gastrointestinal symptoms or the diagnosis of IBS. Enzyme levels were not associated with symptom scores.
A 2002 review article mentions disaccharidase deficiencies only as one topic among several malabsorptive diseases, including coeliac disease, short bowel syndrome, and Crohn disease. It offers no new data on prevalence, treatment, or outcomes for disaccharidase deficiency.
What is still missing is a prospective trial that stratifies patients by specific enzyme deficiency and measures symptom response to dietary intervention or enzyme replacement, rather than relying on cross-sectional associations. The 2024 study’s negative finding suggests that biochemical deficiency alone does not predict symptoms, so any future trial would need to account for mucosal healing, concurrent disease, and patient-reported outcomes. Funding for such a stratified, placebo-controlled dietary trial has not been reported.
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 · 1964 · 18 citations
CHRONIC DIARRHEA AND FAILURE TO THRIVE DUE TO INTESTINAL DISACCHARIDASE INSUFFICIENCY
AbstractAn infant with chronic diarrhea due to suspected generalized disaccharidase insufficiency is described. The clinical condition of the infant improved following the removal of lactose and sucrose from the diet. The fermentative and acidic stool with free lactose and lactic acid also improved. However, the infant was too ill to undergo direct assay of intestinal mucosal tissue for disaccharidase activity or for challenge with offending sugars. Postmortem tissue assay revealed less than 10% of normal activity for lactase, sucrase, maltase, and isomaltase in the intestinal mucosa.
Current Opinion in Gastroenterology · 2002 · 8 citations
Malnutrition and gastrointestinal disease
AbstractThe recognition of several disease processes that cause or are associated with gastrointestinal malabsorption has led to extensive investigation into their pathogenesis, diagnosis, and treatment. This review of selected articles covers a range of subjects related to some of the more common malabsorptive disease. Selected topics including celiac disease, disaccharidase deficiencies, short bowel syndrome, and Crohn disease are discussed.
Archives of Pediatrics and Adolescent Medicine · 1967 · 5 citations
Reversible Secondary Disaccharidase Deficiency
AbstractDIETARY disaccharides are hydrolyzed by specific enzymes in the brush border membrane of the small intestinal surface epithelial cells.<sup>1</sup>Disaccharide malabsorption may be primary and result from the congenital or acquired absence of a specific functional element of the digestive-absorptive surface or may be secondary and caused by a reduction in the total available digestive-absorptive surface, as a consequence of other disease.<sup>2</sup>Young children whose initial symptoms are consistent with gastroenteritis may develop a temporary secondary disaccharidase deficiency associated with intestinal mucosal damage.<sup>3</sup>This report will present such a patient and discuss the confusion that may arise in diagnosis, if complete studies are not performed. <h3>Methods</h3> Oral carbohydrate-tolerance tests were performed in a uniform fashion using 2 gm of sugar per kilogram of body weight. The blood sugar was determined in duplicate by the Nelson-Somogyi method<sup>4</sup>on samples obtained from the fasting patient and at one-half
Scandinavian Journal of Gastroenterology · 2024 · 1 citations · open access
Disaccharidase deficiencies and gastrointestinal symptoms in patients referred to gastroscopic examination: a single center study from Norway
AbstractOBJECTIVE: Gastrointestinal illnesses have been reported in relation to low disaccharidase activity, yet both the prevalence of disaccharidase deficiency and its association with gastrointestinal symptoms and irritable bowel syndrome (IBS) are largely unknown. We aimed to determine the association between low activity of disaccharidase enzymes on gastrointestinal symptoms and presence of IBS. METHODS: Patients referred for gastroscopic examination due to gastrointestinal complaints were consecutively included. A pinch biopsy was taken from the distal part of duodenum, and disaccharidase activity was measured using the Dahlqvist method. Gastrointestinal symptom severity was measured using IBS-Symptom Severity Score (IBS-SSS). RESULTS: = 21) had IBS according to Rome IV criteria. A majority (75%) of all patients reported moderate to severe gastrointestinal symptoms. Moderate to severe gastrointestinal symptoms were reported by 16 patients (67%) with disaccharidase deficiency and in 14 patients (88%) with normal disaccharidase activity. Lactase deficiency was detected in 22 patients (55%), maltase deficiency in 11 patients (28%), sucrase deficiency in 9 patients (23%), isomaltase deficiency in 13 patients (33%) and glucoamylase deficiency in 12 patients (30%). The activity of all enzymes was reduced in 8 patients (20%). Degree of disaccharidase deficiency was not associated with either the severity of gastrointestinal symptoms or the diagnosis of IBS. Enzymes levels were not associated with gastrointestinal symptom scores. CONCLUSION: Our findings did not reveal any association between biochemically measured disaccharidase deficiency and gastrointestinal symptoms or the presence of IBS.
Экспериментальная и клиническая гастроэнтерология · 2025 · 1 citations · open access
Multicomponent biocomplex consisting of Bifidobacterium lactis HN019TM, Lactobacillus acidophilus NCFM® 109 and 1010, alphaand beta-galactosidase, extracts of lemon balm, chamomile, passionflower, and ginger for the treatment of lactase deficiency and irritable bowel syndrome
AbstractOne of the diseases that occurs under the “mask” of irritable bowel syndrome (IBS) is disaccharidase deficiency, which develops due to the deficiency of disaccharide hydrolysis enzymes. The probability of disaccharidase deficiency in a patient with IBS-like symptoms is quite high and reaches 22-26%. Disaccharide intolerance develops against the background of congenital or acquired galactosidase deficiency. Beta-galactosidase is an enzyme, often called lactase, that catalyzes the reaction of hydrolytic cleavage of non-reducing residues of beta-D-galactose in milk sugar, the disaccharide lactose. Impaired or decreased synthesis of beta-galactosidase is the cause of intolerance to milk and dairy products. Lactose intolerance is diagnosed based on a thorough collection of complaints, anamnesis, physical examination and medical tests. A connection between symptoms and the intake of dairy products is traced. In this regard, a patient who has come to the doctor for the first time with IBS symptoms is recommended to keep a food diary. Poor milk tolerance appears within 1-1.5 hours after consuming dairy products. Rumbling, abdominal pain, loose stools and bloating appear. The severity of clinical manifestations of lactase deficiency often does not correlate with the degree of decrease in enzyme activity. Lactose intolerance is associated not only with the level and activity of the enzyme, but also with the number of lactose-fermenting bacteria. Lactase deficiency is combined with manifestations of excessive bacterial growth in the small intestine, which affects the clinical symptoms and their duration. Diagnosis is made by performing a hydrogen breath test to confirm excessive colonization of the small intestine. Treatment of lactose intolerance involves dietary changes, taking lactase-containing enzymes, and treating the underlying disease in patients with secondary lactase deficiency.
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.
