DeCure's autonomous Immuno AI scientist is researching a drug-repurposing hypothesis for inflammatory bowel disease 30 — 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 moduleInflammatory bowel disease 30 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
Structures already discussed alongside inflammatory bowel disease 30 in the retrieved literature, rendered from public PubChem SMILES. Which drugs appear here reflects the evidence found, not a ranked prediction.
Molecular view
TetR(D) — Minocycline has a real, experimentally solved structure in complex with this target (PDB 2XPV, 1.49 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 miydrag to rotate · scroll to zoom
RCSB Protein Data Bank · entry 2XPV · 1.49 Å · ligand Minocycline (MIY). Experimental structure, not a prediction.
What the evidence adds up to
Over the past two decades, genetic studies have identified several susceptibility genes for inflammatory bowel disease. The NOD2/CARD15 gene on chromosome 16 was the first susceptibility gene found in Crohn's disease, reported in 2001. More recent genome-wide association studies have implicated the Interleukin-23 receptor (IL23R) and ATG16L1 (autophagy-related 16-like 1) genes. These findings have redirected basic research toward regulation of the innate immune response and mucosal barrier function.
Biological agents have been used to treat IBD for about two decades with what the 2019 review calls impressive results. However, these drugs are costly and carry significant side-effects, including risk of malignancy. Patients often request to discontinue biological therapy because of cost and fear of adverse effects. The review discusses strategies to de-escalate therapy, the risk of relapse when agents are discontinued, and the success of retreatment with the same or a similar biological agent. No concrete numbers for relapse rates or retreatment success are given in the abstract.
A 2022 review states that conventional therapies for ulcerative colitis and Crohn's disease are inadequate and cause systemic side-effects because the active drug does not localise at the inflamed site. Colonic drug targeting is described as a novel research area intended to deliver treatment directly to the disease site, which would allow lower dosing and fewer systemic side-effects. No clinical trial results or patient outcome data are reported in this abstract.
What is still missing are large-scale, randomised controlled trials that test colonic drug delivery systems in patients, with clear endpoints for relapse rates and side-effect profiles. The genetic findings have not yet translated into new treatments that change clinical practice. Cost-effectiveness data for de-escalation strategies are absent, and no patient stratification method based on genetic markers has been validated in prospective studies.
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.
South African Medical Journal · 2019 · 6 citations · open access
De-escalation of biological therapy in inflammatory bowel disease: Benefits and risks
AbstractThe treatment of inflammatory bowel disease (IBD) is often challenging. It has a vexing and waning course with frequent relapses, despite adequate maintenance therapy. Biological agents have been available for the treatment of IBD for the last two decades, with impressive results. However, these drugs are costly and often have significant side-effects. Therefore, the benefit of aggressive treatment must be carefully balanced against the risk of serious adverse events. Despite good clinical outcomes, patients often request to discontinue the drugs because of cost and detrimental effects, especially the risk of malignancy. This review focuses on the benefits of biological treatment, strategies to de-escalate therapy, risk of relapse when these agents are discontinued and success with retreatment with the same or a similar biological agent.
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.
Naunyn-Schmiedeberg s Archives of Pharmacology · 2025 · 1 citations · open access
Repurposing minocycline as an added-on treatment for ulcerative colitis patients on mesalamine: a randomized clinical pilot study
AbstractOne of the most prevalent forms of chronic inflammatory bowel disease is ulcerative colitis (UC). The key characteristics observed in UC patients involve fecal urgency, abdominal discomfort, and bloody diarrhea, all of which significantly lower their quality of life. Preclinical studies investigated the protective effect of minocycline in animal models of colitis. This study aimed to assess minocycline's potential efficacy and safety in mesalamine-treated UC patients. This randomized, controlled pilot clinical research included 46 individuals with mild to moderate UC who met the inclusion criteria. The mesalamine group (n = 23) received 1 g of mesalamine three times a day for 6 months. The minocycline group (n = 23) received minocycline 100 mg twice daily and mesalamine 1 g three times a day. Patients were evaluated by a gastroenterologist using the Short Inflammatory Bowel Disease Questionnaire (SIBDQ), Truelove and Witts Severity Index, Brief Pain Inventory (BPI), and the non-invasive Partial Mayo Score (PMS). Before and after 6 months of treatment, each patient's levels of nitric oxide (NO), matrix metalloproteinase-12 (MMP-12), and intracellular adhesion molecule 1 (ICAM-1) were measured. Serum levels of MMP-12, ICAM-1, and NO were statistically lower in the minocycline group than in the mesalamine group. In the minocycline group, the Truelove and Witts Severity Index, PMS, and BPI pain intensity all significantly dropped, whereas SIBDQ was substantially elevated compared to the mesalamine group. Minocycline could serve as a potential adjunctive remedy for enhancing clinical outcomes, improving quality of life, and modulating inflammation in patients with mild to moderate UC.Trial registration: ClinicalTrials.gov ID: NCT06201793. Trial registration date 22-1-2024.
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.
