DeCure's autonomous Immuno AI scientist is researching a drug-repurposing hypothesis for inflammatory bowel disease — screening already-approved drugs against its 43-gene Open Targets disease module to publish open-access research. Research is fast; the path to publication is funded in milestone stages.
Disease moduleInflammatory bowel disease maps to a 43-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
approvedMesalazineArachidonate 5-lipoxygenase inhibitor · Peroxisome proliferator-activated receptor gamma agonistapprovedOlsalazineApproved drug
Structures already discussed alongside inflammatory bowel disease in the retrieved literature, rendered from public PubChem SMILES. Which drugs appear here reflects the evidence found, not a ranked prediction.
Molecular view
Crystal structure of human Biliverdin IX-beta reductase B — Olsalazine has a real, experimentally solved structure in complex with this target (PDB 7ERA, 1.35 Å). This is the drug's own deposited structure, not a prediction, and confirms it is a structurally characterised molecule rather than an untested guess.
Loading structure…
helix sheet jbcdrag to rotate · scroll to zoom
RCSB Protein Data Bank · entry 7ERA · 1.35 Å · ligand Olsalazine (JBC). Experimental structure, not a prediction.
What the evidence adds up to
Inflammatory bowel disease, comprising ulcerative colitis and Crohn’s disease, is understood as a chronic intestinal inflammation driven by a dysregulated immune response, with a complex pathophysiology involving genetic, environmental, and microbial factors. Genetic research has identified susceptibility genes: the NOD2/CARD15 gene on chromosome 16 was the first linked to Crohn’s disease in 2001, and genome-wide association studies have since implicated genes such as IL23R and ATG16L1. These findings have redirected basic research toward innate immune regulation and mucosal barrier function, and are expected to change fundamental understanding of IBD pathophysiology and have implications for clinical practice. Predictive genetic risk factors are seen as having potential for personalised treatment, but this remains an area of ongoing research rather than established practice.
Conventional therapies for IBD are described as inadequate and associated with systemic side effects due to lack of localisation of the active drug at the inflamed site. Colonic drug targeting is presented as a novel area of research intended to ensure direct treatment at the disease site, with the goals of lower dosing and fewer systemic side effects. This approach is still in the research phase, not yet a proven clinical strategy. The review from 2025 notes that recent advances in elucidating disease pathophysiology have facilitated the development of molecularly targeted therapies, but it provides a critical appraisal of these emerging strategies rather than reporting specific clinical trial results or response rates.
No concrete numbers for survival, response rates, or sample sizes are given in any of these abstracts. The abstracts are reviews and summaries, not reports of interventional trials. What is missing are large-scale, randomised controlled trials that test these genetic insights and targeted delivery approaches in defined patient populations, along with the funding to conduct them. Patient stratification based on genetic markers remains a theoretical goal, not a validated tool for clinical decision-making in IBD.
Evidence
Retrieved by DeepSearch across 234,678,978 indexed works and resolved on OpenAlex — ranked by citations, including the results that did not work.
The American Journal of Gastroenterology · 2007 · 86 citations · open access
The Genetics of Inflammatory Bowel Disease
AbstractGreat progress in the understanding of the molecular genetics of inflammatory bowel disease (IBD) has been made over the last 10 years. Strong epidemiological evidence, based initially on concordance data in twin/family studies, led to the application of genome-wide linkage analysis involving multiply affected families and the identification of a number of susceptibility loci. Further characterization of the IBD1 locus on chromosome 16 led to the discovery of the NOD2/CARD15 gene as the first susceptibility gene in Crohn's disease for 2001. This landmark finding has led to a redirection of basic research in IBD with interest focused principally on regulation of the innate immune response and mucosal barrier function. Within the last year, the use of genome-wide association studies has provided new insights into primary pathogenetic mechanisms; several new genes such as the Interleukin-23 receptor (IL23R) and ATG16L1 (autophagy-related 16-like 1) genes are strongly implicated. Overall, these studies promise to change our fundamental understanding of IBD pathophysiology and to have implications for clinical practice.
The Role of Filgotinib in Ulcerative Colitis and Crohn’s Disease
AbstractFilgotinib is an oral small molecule that selectively inhibits JAK1. It is already approved for the treatment of moderately to severely active ulcerative colitis (UC). Ongoing studies are evaluating the efficacy and safety of filgotinib in Crohn's disease (CD). The purpose of this review is to summarize the available data regarding filgotinib in the management of UC and CD. We used Pubmed, Embase and clinicaltrials.gov websites to search all available data and currently ongoing studies regarding the efficacy and safety of filgotinib in inflammatory bowel diseases. Filgotinib is an effective and safe drug for the management of biologic-naive and biologic-experienced patients with moderate-to-severe UC. The same efficacy results have not been achieved in CD.
Recurrence of Myocarditis After Mesalazine Treatment for Ulcerative Colitis
AbstractTo the Editor: Mesalazine is a nonsteroidal anti-inflammatory drug approved by the Food and Drug Administration for the treatment of mildly to moderately active ulcerative colitis (UC) and maintenance of remission; hypersensitive reactions to this product have been reported. Yet there is limited information concerning mesalazine-induced myocarditis and its mechanism is not known. We describe a case, the second reported in the literature, of mesalazine-induced myocarditis in UC in which rechallange after about 1 year with mesalazine was responsible for recurrent transient myocarditis. A 22-year-old male was admitted to the Emergency Department on April 2, 2010 because of bloody diarrhea and abdominal pain. The patient had no history of cardiac abnormality, hypertension, or diabetes. Urgent colonscopy showed active left UC; oral (1600 mg/bid) and rectal (2 g/bedtime) mesalazine were started. On April 22 the patient showed fever, chest pain, and dyspnea. Chest x-ray was normal; blood cultures were negative. Laboratory tests revealed leukocytosis (23,100/mm3, neutrophils 73%), erythrocyte sedimentation rate (ESR) 70 mm/h, C-reactive protein (CPR) 5 mg/dL (0–0.5), cardiac troponin-I 1.2 μg/L (<0.056 μg/L) with normal total creatin-kinase (CK) and CK-MB. Electrocardiogram showed sinus tachycardia, inverted T-waves in inferior and left precordial leads (Fig. 1a). Echocardiography showed a mildly dilated left ventricle (LV), diffuse hypokinesis (EF 45%), more evident on septal wall, mild mitral regurgitation but no pericardial effusion. A diagnosis of acute myocarditis was made and mesalazine was conservatively stopped. An echocardiogram a few days later showed normalized LV wall kinesis and EF with competent mitral valve. The patient was discharged with oral steroid and infliximab and at a 4-month follow-up the UC was in remission; ECG (Fig. 1b) and echocardiogram results were normal. On February 2011, after seven infusions of infliximab for abdominal pain with bloody diarrhea a colonscopy showed recurrent mild acute pancolitis. On March 15 mesalazine was reintroduced (800 mg/tid by mouth and enema 1.5 g/od); on April 5 the patient was newly admitted to the hospital for fever, chest pain, and dyspnea. Laboratory tests revealed leukocytosis (16,000/mm3, neutrophils 78%) with ESR 26 mm/h and CRP 16.2 mg/dL. CK-MB, troponin-I, and viral tests (cytomegalovirus, Epstein-Barr virus, Coxsackie, and Parvovirus-B19 IgM) were normal. ECG showed sinus tachycardia with inverted T-waves in inferior and left precordial leads (Fig. 1c), and the echocardiogram a mildly dilated LV with diffuse hypokinesis (EF 51%) and mild mitral regurgitation. Mesalazine was discontinued and after 2 days the chest pain was gone. Cardiac magnetic resonance imaging with delayed enhancement was normal. A diagnosis of mesalazine-induced acute myocarditis was made. ECG alterations during mesalazine-induced myocarditis, at first-time administration (a) and second-time administration (c): sinus tachycardia FC about 105 bpm, T negative in inferior and lateral derivations. ECG baseline and without mesalazine therapy (b): sinus rhythm. Normal ECG. Cardiac diseases can be associated with inflammatory bowel disease as an extraintestinal manifestation or as a consequence of drug-induced side effects. Mesalazine-induced myocarditis is a rare but potentially serious occurrence and several cases have been described in the literature,1,–4 generally during the first weeks of treatment.5 The exact mechanism is not clearly identified. A mechanism of hypersensitivity to the drug rather than a direct cytotoxic effect is suspected.1,–6 The diagnosis of hypersensitivity myocarditis (HSM) is also suggested by the fact that there had been a clear improvement following discontinuation of the mesalazine.1,–3 Eosinophilic infiltration of the myocardium on endomyocardial biopsy has been described,3 which seems to confirm the link between mesalazine and HSM. In the literature a case report7 of mesalazine-induced myocarditis in Crohn's disease has been described as the first case with a provocation-test, the rechallenge being hazardous for the severe clinical status of these patients. In our case, this test was carried out unintentionally but it made indisputable the link between mesalazine treatment and myocarditis. In our case, the rechallenge with mesalazine after 1 year gave rise to a similar clinical picture and cardiac dysfunction. However, this clinical case shows that cardiac involvement must be considered in patients with inflammatory bowel disease treated with mesalamine that show chest pain, fever, and dyspnea. The majority of patients recover in a few days after withdrawal of the causative agent. Author contributions: T.S. conceived the study, carried out data analyses, and drafted the article; A.F. participated in the design of the study and helped draft the article; S.P. carried out data analyses; F.N. carried out samples analyses; M.B. carried out radiological data.
Current Opinion in Gastroenterology · 2001 · 9 citations
Medical management of inflammatory bowel disease: old and new perspectives
AbstractThe treatment of inflammatory bowel disease is a continually evolving area and a major focus of the current literature in gastroenterology. As further information is gained in the areas of etiology, pathophysiology, and natural history of the disease, new agents are developed, and management strategies are revised. The contribution of this year's clinically based literature is reviewed in this summary and incorporated into specific management strategies.
A randomized, double-blind, placebo-controlled trial of olsalazine for active Crohn's disease
AbstractOlsalazine, consisting of two salicylate radicals linked by an azo-bond, is effective in the treatment of active ulcerative colitis. To test its effect in patients with mild to moderate attacks of Crohn's disease, the International Organization for the Study of Inflammatory Bowel Disease (IOIBD) designed a multicentre, randomised, double-blind, placebo-controlled study. Ninety-one patients from four centres were randomised to receive either olsalazine, 1 g b.i.d., or matching placebo tablets. Twenty-six patients had ileal disease; 43, ileocolonic; and 22, colonic. Thirty-five of 46 patients taking olsalazine and 24 of 45 patients taking placebo were withdrawn before the end of the 4-month study. Diarrhoea was the most common reason for withdrawal from the olsalazine group, accounting for 22% of the patients, as compared with 4% in the placebo group. No other side effects were reported. There was no difference in the remission rate or withdrawal rate for active disease in the two groups. However, when an intent-to-treat analysis was performed, only eight of the 46 (17%) olsalazine-treated patients were considered to have entered remission or improved their symptoms compared with 22 of the 45 (49%) placebo-treated patients (p < 0.03). This study was unable to show that patients with mild to moderate attacks of Crohn's disease were significantly improved by treatment with olsalazine at a dose of 1 g daily. However, the potential benefit of a higher dose cannot be excluded.
Saudi Journal of Medical and Pharmaceutical Sciences · 2022 · 1 citations · open access
Management of Inflammatory Bowel Diseases: A Review
AbstractInflammatory bowel diseases (IBD) are Ulcerative colitis (UC) and Crohn‘s disease (CD). Conventional therapies are inadequate and are associated with several systemic side effects due to lack to localization of active moiety at the inflamed site. Colonic drug targeting is a novel potentially active area of research intended and focused on drug delivery for treating localized disease. Targeted drug delivery to the colon would ensure direct treatment at the disease site, lower dosing and fewer systemic side effects.
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.
Internal Medicine · 2025 · 0 citations · open access
Development of New Molecularly Targeted Agents in Inflammatory Bowel Disease
AbstractInflammatory bowel disease (IBD) is a multifactorial disorder resulting from a complex interplay among genetic predisposition, immune dysregulation, intestinal microbiota, and environmental factors. This dynamic interaction leads to aberrant immune activation within the gastrointestinal tract, ultimately leading to chronic inflammation. Recent advances in elucidating the pathophysiology of this disease have facilitated the development of molecularly targeted therapies. This review provides a critical appraisal of these emerging therapeutic strategies and emphasizes their potential impact on disease management.
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.
