DeCure's autonomous Rare AI scientist is researching a drug-repurposing hypothesis for gastritis — screening already-approved drugs against its 36-gene Open Targets disease module to publish open-access research. Research is fast; the path to publication is funded in milestone stages.
Disease moduleGastritis maps to a 36-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 gastritis 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
KRas proto-oncogene, GTPase (KRAS) — KRAS 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 gnpdrag to rotate · scroll to zoom
RCSB Protein Data Bank · entry 7VVB · 1.7 Å · ligand PHOSPHOAMINOPHOSPHONIC ACID-GUANYLATE ESTER (GNP). 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.
Jundishapur Journal of Microbiology · 2015 · 23 citations · open access
Correlation Between Mucosal IL-6 mRNA Expression Level and Virulence Factors of Helicobacter pylori in Iranian Adult Patients With Chronic Gastritis
AbstractBACKGROUND: Helicobacter pylori infection is associated with gastritis and marked infiltration of the gastric mucosa by several cytokines secreting inflammatory cells that contribute to sustained local inflammation. In this study, we sought to examine IL-6 expression in H. pylori-infected and uninfected gastric mucosa and elucidate the implication in the pathogenesis of H. pylori-associated gastritis in human. OBJECTIVES: The current study aimed to determine mucosal IL-6 mRNA expression level and their correlation with virulence factors and the grade of chronic gastritis among H. pylori infected patients with chronic gastritis from Shahrekord, Iran. PATIENTS AND METHODS: Mucosal IL-6 mRNA levels was measured by real-time PCR using endoscopic biopsies taken from the gastric antrum of 58 subjects infected with H. pylori and 44 uninfected subjects. Presence of vacA and cagA virulence factors was evaluated using PCR. RESULTS: The IL-6 mRNA expression levels were significantly more elevated in H. pylori-positive patients than uninfected individuals and expression of this cytokine was independent from the virulence factors. There was a correlation between IL-6 expression level and the grade of chronic gastritis. CONCLUSIONS: Enhanced induction of IL-6 may be involved in the pathogenesis of H. pylori-associated gastritis.
AbstractBACKGROUND: Helicobacter pylori is widely accepted as a major pathogen in gastritis. The histologic features of H. pylori gastritis are the numerous infiltrating mononuclear cells (MNCs) and neutrophils. It is not clear what role the infiltrating MNCs and neutrophils play in H. pylori gastritis. METHODS: In this study, we have established enzyme-linked immunospot (ELISPOT) assay for the measurement of H. pylori antibody-producing cells in gastric mucosa. RESULTS: Using ELISPOT assay, we found that H. pylori-specific IgA-producing cells as well as IgG-producing cells were distributed in gastric mucosa. These H. pylori-specific antibodies in gastric mucosa and neutrophils are responsible for the induction of cytotoxic effect to cultured Vero cells. CONCLUSIONS: These observations suggest that a mucosal immune response specific to H. pylori is closely associated with the pathogenesis of gastritis.
Gastritis Associated with Initially Pediatric Crohn's Disease and Ulcerative Colitis
AbstractThe aim of this study is to determine the involvement of the upper gastrointestinal system (GIS) in patients diagnosed with Crohn's disease (CD), ulcerative colitis (UC), and non-inflammatory bowel disease (IBD) and to compare their differences. Methods: This study included patients aged between 2 and 18 years who underwent colonoscopy and esophagogastroduodenoscopy (EGD) for the first time due to the prediagnosis of IBD. In EGD, samples were taken from duodenum, antrum, corpus, and esophagus; and gastritis, duodenitis, and esophagitis were identified through histopathologic examination. The data gathered the ends of the research were compared between IBD with non-IBD groups and between CD-UC with non-IBD groups, and the presence of significant differences between groups were determined. Results: In our study, 16 patients were diagnosed with CD, 13 with UC, 3 with undeterminate colitis, and 13 with non-IBD. In the histopathological examination of the groups, GIS involvement was found in 94.1% of patients diagnosed with IBD and in 38.5% of non-IBD patients. Moreover, the difference was found to be statistically significant (p=0.032). No significant difference was found between the CD and UC groups. Gastritis was mostly observed in 93.8% of CD-diagnosed patients, 76.8% of UC-diagnosed patients, 81.2% of IBD-diagnosed patients, and 38.5% of non-IBD-diagnosed patients. On the other hand, significant differences were found between CD and non-IBD groups (p=0.03), UC and non-IBD groups (p=0.047), and IBD and non-IBD groups (p=0.03).
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.
