DeCure's autonomous Cardio AI scientist is researching a drug-repurposing hypothesis for brain ischemia — 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 moduleBrain ischemia 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 brain ischemia 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
erythropoietin receptor (EPOR) — EPOR 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 nh4drag to rotate · scroll to zoom
RCSB Protein Data Bank · entry 8VUI · 2.1 Å · ligand AMMONIUM ION (NH4). Experimental structure, not a prediction.
What the evidence adds up to
Acute ischemic stroke still has no effective therapy to improve outcome. A 2008 review notes that thrombolytic agents, both clot-specific and non-specific, are being evaluated in clinical trials, and that neuroprotective therapies designed to correct the metabolic abnormalities caused by focal brain ischaemia are also in trials. The key feature of all these trials is rapid initiation of therapy. The same review anticipates future combined therapy trials with both neuroprotective and thrombolytic drugs, an approach it says is likely to be more beneficial than either alone.
A 2021 review states that effective and rapid reperfusion significantly improves patient survival and functional outcomes, but that other approaches to brain infarction treatment have not proved their effectiveness in large clinical trials. Dozens of neuroprotective drugs are being studied to compensate isolated pathological pathways and increase cellular survival, but they were ineffective in large clinical trials. The reason for this ineffectiveness may be a lack of understanding of the drug targets’ real importance. Many drugs that showed promising results in preclinical studies have not been studied in large clinical trials until now.
Earlier work from 1997 on global brain ischaemia notes that a cascade of injurious events begins within minutes of ischaemia and that both ischaemic and post-ischaemic events cause significant neuronal damage. It describes a therapeutic window of opportunity during which interventions might improve neurologic outcome, but does not report any drug that has achieved this in practice. A 1997 volume on cellular and molecular mechanisms of ischaemic brain damage is a review of pathophysiological events and a forum for discussion of new ideas, not a report of effective treatments.
What is still missing is large-scale clinical trial evidence for the dozens of neuroprotective drugs that have failed so far, a clearer understanding of which molecular targets actually matter in human stroke, and trial designs that test combined thrombolytic and neuroprotective regimens rather than single agents. Money and patient stratification for the heterogeneous mechanisms of brain ischaemia also remain absent.
Evidence
Retrieved by DeepSearch across 234,678,978 indexed works and resolved on OpenAlex — ranked by citations, including the results that did not work.
European Neurology · 2008 · 36 citations
Potentially Effective Therapies for Acute Ischemic Stroke
AbstractAcute ischemic stroke remains without an effective therapy to improve outcome. As knowledge about the basic pathophysiology has expanded, rational approaches to therapy have evolved. The frequent presence of arterial occlusion suggested that thrombolytic therapy might be a viable approach. Both clot-specific and nonspecific thrombolytic agents are currently being evaluated in clinical trials. Focal brain ischemia induces a variety of cellular consequences. Neuroprotective therapies designed to ameliorate these metabolic abnormalities are also being evaluated in clinical trials. A key feature of all these clinical trials is the rapid initiation of therapy. In the future, we can anticipate combined therapy trials with both neuroprotective and thrombolytic drugs, an approach which is likely to be more beneficial than either one in isolation.
Cellular and Molecular Mechanisms of Ischemic Brain Damage
AbstractEnthusiasm for clinical and basic science research in cerebrovascular disease is increasing because of recent findings of new effective treatments for stroke. This volume of the "Advances in Neurology" series is well timed to coincide with this recrudescence of interest in brain ischemia. This volume includes background papers, articles, and discussions from the Eric K. Fernström symposium "Cellular and Molecular Mechanisms of Ischemic Brain Damage," in Lund, Sweden, June 13 through 16, 1994, as well as invited chapters from other investigators. The goal of this symposium was to use current knowledge about the mechanisms of ischemia to stimulate discussion about novel strategies for identifying and treating the causes of ischemic brain damage. This book, then, is both a review of current knowledge about the pathophysiological events in ischemic brain injury and a forum for discussion of new ideas. Chapters are grouped into the following sections based on the cellular pro
AACN Clinical Issues Advanced Practice in Acute & Critical Care · 1997 · 24 citations
Cerebral Resuscitation After Global Brain Ischemia: Linking Research to Practice
AbstractDespite significant advances in resuscitation medicine, neurologic recovery continues to be the major limiting factor in achieving successful resuscitation outcomes. Clinicians must recognize that successful resuscitation outcomes are not limited to the restoration of normal cardiac rhythm and hemodynamics, but rather the restoration of human mentation. It is well recognized that a cascade of injurious events begins within minutes of ischemia and that ischemic and postischemic events cause significant neuronal damage. An increased understanding of the pathophysiology of global brain ischemia provides evidence of a therapeutic window of opportunity during which interventions hold the potential to improve neurologic outcome. The research basis for understanding global brain ischemia, its clinical prognosis, and potential intervention strategies are examined.
Regional blood circulation and microcirculation · 2021 · 4 citations · open access
Brain acute ischemia mechanisms: implications to experimental and clinical treatment
AbstractWe have reviewed current understanding of ischemic brain damage and the main therapeutic approaches. Pathological factors affecting the survival of neurons and glial cells in the focus of ischemia are outlined: depolarization, cytotoxic and vasogenic edema, calcium overload, excitotoxicity, inflammation, free radical damage. Effective and rapid reperfusion significantly improves patient’s survival and functional outcomes, but other approaches to brain infarction treatment did not approve their effectiveness in large clinical trials. Dozens of drugs (neuroprotectors) are being studied in order to compensate isolated pathological brain ischemia pathways and to increase cellular survival, but they were ineffective in large clinical trials.The reason for the ineffectiveness of neuroprotective drugs may be a lack of understanding of the drug targets real importance. Many drugs that have shown promising results in preclinical studies have not been studied in large clinical trials until now. Additional pathogenetic mechanisms revealed in the last decade expand our knowledge about the brain infarction and may become promising directions for the development of new therapeutic approaches.
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.
