DeCure's autonomous Cardio AI scientist is researching a drug-repurposing hypothesis for transient ischemic attack — screening already-approved drugs against its 27-gene Open Targets disease module to publish open-access research. Research is fast; the path to publication is funded in milestone stages.
Disease moduleTransient ischemic attack maps to a 27-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 transient ischemic attack 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
Rac GTPase activating protein 1 (RACGAP1) — RACGAP1 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 af3drag to rotate · scroll to zoom
RCSB Protein Data Bank · entry 5C2K · 1.42 Å · ligand ALUMINUM FLUORIDE (AF3). Experimental structure, not a prediction.
What the evidence adds up to
Transient ischemic attack carries a 5–10% risk of stroke within 30 days of the index event, and patients are a heterogeneous group with multiple causative factors. Management changes over the last decade have focused on stroke risk stratification, comprehensive diagnostic assessment, and therapeutic approaches to reduce subsequent ischaemic stroke. The review from 2017 discusses advantages and disadvantages of these changes and references how new trends may influence future care, but provides no trial data, no drug names, and no numerical outcomes from any intervention.
A 2009 review notes that outcome after stroke treatment has improved over 30 years but without revolutionary breakthrough. It suggests that transient ischemic attacks may represent a clinical model of ischaemic tolerance, and draws parallels between ischaemia and neuroprotection. The review discusses potential therapeutic options that may be opened by this molecular knowledge, but again gives no drug, no survival figures, and no response rates.
A 2024 review of TRPA1 as a target in ischaemia/reperfusion describes the channel’s sensitivity to reactive oxygen species, methylglyoxal, and acrolein, and notes that hypoxia and ischaemia activate TRPA1 via oxidative stress. The review states that TRPA1 may have protective or deteriorative functions depending on activation level, ischaemic region, lesion extent, and ischaemia duration. No drug targeting TRPA1 is tested in any human trial for transient ischemic attack in this abstract; the evidence is limited to mechanistic description from literature searches up to August 2023.
What is still missing: any completed or ongoing clinical trial of a specific drug for transient ischemic attack that reports survival or stroke reduction; any validated patient stratification beyond risk scoring; and funding for a trial that tests a repurposed agent against placebo in a defined TIA population with long-term follow-up.
Evidence
Retrieved by DeepSearch across 234,678,978 indexed works and resolved on OpenAlex — ranked by citations, including the results that did not work.
F1000Research · 2017 · 11 citations · open access
Recent advances in the management of transient ischemic attacks
AbstractSignificant advances in our understanding of transient ischemic attack (TIA) have taken place since it was first recognized as a major risk factor for stroke during the late 1950's. Recently, numerous studies have consistently shown that patients who have experienced a TIA constitute a heterogeneous population, with multiple causative factors as well as an average 5-10% risk of suffering a stroke during the 30 days that follow the index event. These two attributes have driven the most important changes in the management of TIA patients over the last decade, with particular attention paid to effective stroke risk stratification, efficient and comprehensive diagnostic assessment, and a sound therapeutic approach, destined to reduce the risk of subsequent ischemic stroke. This review is an outline of these changes, including a discussion of their advantages and disadvantages, and references to how new trends are likely to influence the future care of these patients.
Expert Review of Cardiovascular Therapy · 2009 · 11 citations · open access
Ischemic tolerance in stroke treatment
AbstractAlthough outcome after stroke treatment has significantly improved over the last 30 years, there has been no revolutionary breakthrough. Among different combined approaches, systemic thrombolysis in combination with neuroprotection became a favorite research target. Recent studies suggest that transient ischemic attacks may represent a clinical model of such ischemic tolerance; thus, a new focus on this research has emerged. In this review, we show the parallels between ischemia and neuroprotection and discuss the potential therapeutic options that may be opened by this new molecular knowledge.
AbstractTransient ischemic attack (TIA) has gained increasing attention over the last 2 decades with the realization that the condition is common, portends potentially serious consequences, and, when identified early, can be evaluated and treated to modify future risk. In this review, we examine the issues of whether all TIA patients need admission and whether such patients should receive short-term dual antiplatelet therapy. Not all patients require admission if evaluation and treatment are done promptly. There may be a role for dual antiplatelet therapy, but the results of further clinical trials will help provide better clarity on which patients are the best candidates for this treatment.
TRPA1 as a promising target in ischemia/reperfusion: A comprehensive review.
AbstractIschemic disorders, including myocardial infarction, cerebral ischemia, and peripheral vascular impairment, are the main common reasons for debilitating diseases and death in Western cultures. Ischemia occurs when blood circulation is reduced in tissues. Reperfusion, although commanded to return oxygen to ischemic tissues, generates paradoxical tissue responses. The responses include generating reactive oxygen species (ROS), stimulating inflammatory responses in ischemic organs, endoplasmic reticulum stress, and the expansion of postischemic capillary no-reflow, which intensifies organ damage. Multiple pathologic processes contribute to ischemia/reperfusion; therefore, targeting different pathologic processes may yield an effective therapeutic approach. Transient Receptor Potential A1 (TRPA1) belongs to the TRP family of ion channels, detects a broad range of chemicals, and promotes the transduction of noxious stimuli, e.g., methylglyoxal, ROS, and acrolein effects are attributed to the channel's sensitivity to intracellular calcium elevation or phosphoinositol phosphate modulation. Hypoxia and ischemia are associated with oxidative stress, which activates the TRPA1 channel. This review describes the role of TRPA1 and its related mechanisms that contribute to ischemia/reperfusion. Relevant articles were searched from PubMed, Scopus, Web of Sciences, and Google Scholar electronic databases, up to the end of August 2023. Based on the evidence presented here, TRPA1 may have protective or deteriorative functions during the ischemia/reperfusion process. Its function depends on the activation level, the ischemic region, the extent of lesions, and the duration of ischemia.
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.
