Immuno Lab · DeCure for X

DeCure for Inflammatory bowel disease 1

DeCure's autonomous Immuno AI scientist is researching a drug-repurposing hypothesis for inflammatory bowel disease 1 — screening already-approved drugs against its 5-gene Open Targets disease module to publish open-access research. Research is fast; the path to publication is funded in milestone stages.

Disease module5 genesLead labImmuno
All cures
ImmunoDOID:0110892$DeCureImmuno

The disease map

Disease moduleInflammatory bowel disease 1 maps to a 5-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 inflammatory bowel disease 1 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

heat shock protein family A (Hsp70) member 1 like (HSPA1L)HSPA1L 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 adpdrag to rotate · scroll to zoom

RCSB Protein Data Bank · entry 3GDQ · 1.8 Å · ligand ADENOSINE-5'-DIPHOSPHATE (ADP). Experimental structure, not a prediction.

What the evidence adds up to

A 2013 mouse study tested oral interleukin-10 plus anti-IL-1 antibody in dextran sodium sulphate-induced colitis. The combination restored intestinal barrier function, reduced proinflammatory cytokines, increased plasma interleukin-10, and restored tight junction architecture. The study involved BALB/c mice; no human data were reported.

A 2018 Danish population-based inception cohort followed 213 Crohn’s disease and 300 ulcerative colitis patients for 10 years. Treatment was grouped into four levels: 5-aminosalicylates ± topical steroids; oral steroids ± 5-ASA or topical steroids; immunosuppressants (azathioprine or 6-mercaptopurine ± steroids and/or 5-ASA); biologics (infliximab or adalimumab in combination with any of the above). In Crohn’s disease, only younger age at diagnosis was associated with escalation to immunosuppressants or biologics (odds ratio for age 17–40: 0.7, 95% CI 0.5–0.98; age >40: 0.5, 95% CI 0.4–0.8, reference age <17). In ulcerative colitis, former smoking (OR 1.3, 95% CI 1.0–1.6) and disease extent at diagnosis (E2 OR 1.4, 95% CI 1.2–1.8; E3 OR 1.4, 95% CI 1.1–1.7, reference E1) predicted escalation. After the first few years, treatment levels stabilised for both diseases. Crohn’s disease patients required escalation to immunomodulators and biologics more often than ulcerative colitis patients, even after the initial years.

A 2023 narrative review summarised that inflammatory bowel disease involves dysregulated immune response, complex pathophysiology, and both environmental and genetic determinants. The review stated that genetic drivers and signalling pathways may present therapeutic potential for further research, and that predictive genetic risk factors could have implications for personalised treatment. No new experimental data were presented.

A 2011 article described inflammatory bowel diseases as multifactorial, covering genetic susceptibility, innate and adaptive immune responses, and mucosal barrier function. It noted that animal models have been developed to study disease mechanisms. No clinical results were 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.

Gastroenterology Research · 2013 · 34 citations · open access

Oral Administration of Interleukin-10 and Anti-IL-1 Antibody Ameliorates Experimental Intestinal Inflammation

AbstractBACKGROUND: To elucidate the effects of a solution containing interleukin-10 and anti-IL-1 antibody in modulating experimental intestinal inflammation. METHODS: Colitis was induced in BALB/c mice by oral administration of dextran sodium sulphate; mice were then treated with interleukin-10 plus anti-IL-1 antibody at low dosage. Transepithelial electrical resistance of isolated mouse colon and colon lengths were evaluated. Cytokines concentrations in organocultures supernatants and plasma samples were evaluated by Enzyme-Linked Immuno Sorbent Assay. Tight junction proteins were evaluated by immunofluorescence, respectively. RESULTS: Oral administration of tested products restores intestinal barrier function during experimental intestinal inflammation in association with reduced levels of proinflammatory cytokines, increased interleukin-10 plasma concentrations and a tight junction architecture restoration. CONCLUSION: Obtained results may contribute to modelling an interesting strategy for the treatment of patients with inflammatory bowel diseases.

https://doi.org/10.4021/gr556w
Journal of Crohn s and Colitis · 2018 · 0 citations · open access

P786 The use and escalation of treatments in patients with inflammatory bowel disease; a 10 years follow-up of a Danish population-based inception cohort

AbstractThe long-term treatment strategies and change between medications in Inflammatory bowel disease (IBD) in the age of biologics has not been well described. We aimed to characterise the treatment strategies in IBD in a well-defined population-based inception cohort of Crohn's disease (CD) and ulcerative colitis (UC) patients after 10 years of follow-up. All patients (n = 513) diagnosed with CD, UC or IBD unclassified between January 1, 2003 and December 31, 2004 in a well-defined area were included. Clinical data regarding treatment and outcome were recorded and patient records linked with four national registries to ensure complete data capture and follow-up. Treatments were grouped into four treatment levels (TL): (1) 5-aminosalicylates (5-ASA) ± topical steroids, (2) oral steroids ± 5-ASA or topical steroids, (3) immunosuppressant (azathioprine or 6-mercaptopurine ± steroids and/or 5-ASA), (4) biologics (infliximab or adalimumab in combination with any of the above). Disease classification was made according to the Montreal classification. In a linear regression model, gender, age class, diagnostic delay, smoking behaviour, disease behaviour, location, and extent at diagnosis was used as independent variables. A total of 213 CD and 300 UC patients were followed. TL over time is shown in Figure 1 and 2. Characteristics of patients’ TL are shown in Table 1. In CD, only younger age at diagnosis was associated with the risk of escalating to TL 3 or 4 (OR (CI 95); A2: 0.7 (0.5, 0.98); A3: 0.5 (0.4,0.8) [ref: A1]). In UC patients, former smoking (OR (CI95); 1.3 (1.0–1.6) [ref: never smoker]), and extent at diagnosis was significantly associated with the risk of escalating to TL 3 or 4 (OR (CI95); E2: 1.4 (1.2,1.8), p < 0.001; E3: 1.4 (1.1,1.7) [ref: E1]). After the first initial years after diagnosis, stability occurs regarding treatment levels of both CD and UC patients. Escalation to immunomodulators and biologics was more frequently necessary in CD, even after the initial years, compared with UC patients. Crohn’s disease patients’ treatment level throughout 10 years of follow-up ulcerative colitis patients’ treatment level throughout 10 years of follow-up Characteristics of Crohn’s disease and Ulcerative colitis patients’ treatment level after 10 years of follow-up

https://doi.org/10.1093/ecco-jcc/jjx180.913
Journal of the Pakistan Medical Association · 2023 · 0 citations · open access

An insight into genetic landscape of inflammatory bowel disease

AbstractInflammatory bowel disease has been regarded to be chronic intestinal inflammation characterised by a dsyregulatory immune response. The disease pathophysiology is known to be complex. Growing pieces of evidences underpin the involvement of various environmental and genetic determinants in the disease onset. The current narrative review was planned to manifest the contribution of genetic drivers for disease onset and to target signalling pathways that might present a therapeutic potential for further research. The factors of the disease that provide the genetic nature and understanding of the pathways involved have been researched in recent times. Also, numerous diseasedeveloping factors have been studied and assessed. Among them genetic determinants of disease onset have further improved the understanding of disease development. Genetic contributors to the onset of disease as well as important therapeutic targets need to be understood as predictive genetic risk factors have a potential implication for personalised treatment.

https://doi.org/10.47391/jpma.9050
Física y sociedad · 2011 · 0 citations

El papel de la ingeniería independiente en el control del consumo y la contaminación lumínica

AbstractIBDs (inflammatory bowel diseases) are a group of diseases affecting the gastrointestinal tract. The diseases are multifactorial and cover genetic aspects: susceptibility genes, innate and adaptive responses to inflammation, and structure and efficacy of the mucosal protective barrier. Animal models of IBD have been developed to gain further knowledge of the disease mechanisms. These topics form an overlapping background to enable an improved understanding of the molecular features of these diseases. A series of articles is presented based on the topics covered at the Biochemical Society Focused Meeting The Molecular Biology of Inflammatory Bowel Diseases.

https://doi.org/10.1042/bst0391057

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.