ArticleNeuropharmacology2023
Preclinical development of an EP2 antagonist for post-seizure cognitive deficits.
Article in Neuropharmacology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 16 citations in OpenAlex.
- Development of highly potent EP2 antagonists as novel anti-inflammatory neuroprotectants.Bioorganic & medicinal chemistry · 2026Article
- Novel EP2 Antagonist Attenuates Microgliosis and Memory Deficits in Pilocarpine-Induced Status Epilepticus Mice.Journal of medicinal chemistry · 2026Article
- Antagonism of the EP2 Receptor Reveals Sex-Specific Protection in a Two-Hit Mouse Model of Alzheimer's Disease.ACS chemical neuroscience · 2026Article
- Neuroinflammation and Disease: Pathways and Opportunities.Annual review of pharmacology and toxicology · 2026Review
- Brain-invading monocytes promote seizure-associated cognitive deficits and neurodegeneration.Neuropharmacology · 2025Article
- Modulating inflammatory prostaglandin E2 signaling to mitigate neurobehavioral comorbidities associated with seizure disorders.Acta pharmaceutica Sinica. B · 2025Review
- Disease modification upon 2 weeks of tofacitinib treatment in a mouse model of chronic epilepsy.Science translational medicine · 2025Article
- Suppressing the Inflammatory Prostaglandin Signaling after Thrombotic Stroke Ameliorates Ischemic Brain Injury and Facilitates Poststroke Recovery.ACS pharmacology & translational science · 2024Article
- Targeting EP2 Receptor for Drug Discovery: Strengths, Weaknesses, Opportunities, and Threats (SWOT) Analysis.Journal of medicinal chemistry · 2023Review
- Pharmacological inhibition of the inflammatory receptor CCR2 relieves the early deleterious consequences of status epilepticus.Scientific reports · 2023Article
- Neuroinflammatory mediators in acquired epilepsy: an update.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2023Review
Corrections and comments
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Authors and funding
12 authors at 1 institution in 1 country.
Funding
Abstract
Cognitive comorbidities can substantially reduce quality of life in people with epilepsy. Inflammation is a component of all chronic diseases including epilepsy, as well as acute events like status epilepticus (SE). Neuroinflammation is the consequence of several broad signaling cascades including cyclooxygenase-2 (COX-2)-associated pathways. Activation of the EP2 receptor for prostaglandin E2 appears responsible for blood-brain barrier leakage and much of the inflammatory reaction, neuronal injury and cognitive deficit that follows seizure-provoked COX-2 induction in brain. Here we show that brief exposure of mice to TG11-77, a potent, selective, orally available and brain permeant EP2 antagonist, eliminates the profound cognitive deficit in Y-maze performance after SE and reduces delayed mortality and microgliosis, with a minimum effective i.p. dose (as free base) of 8.8 mg/kg. All in vitro studies required to submit an investigational new drug (IND) application for TG11-77 have been completed, and non-GLP dose range-finding toxicology in the rat identified no overt, organ or histopathology signs of toxicity after 7 days of oral administration at 1000 mg/kg/day. Plasma exposure in the rat was dose-linear between 15 and 1000 mg/kg dosing. TG11-77 thus appears poised to continue development towards the initial clinical test of the hypothesis that EP2 receptor modulation after SE can provide the first preventive treatment for one of the chief comorbidities of epilepsy.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.