ArticleMolecular diversity2016
Novel RIPK3 inhibitors discovered through a structure-based approach exert post-ischemic neuroprotection.
Article in Molecular diversity, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
11 citing papers in PubMed, 16 citations in OpenAlex.
- Neuronal Injury after Ischemic Stroke: Mechanisms of Crosstalk Involving Necroptosis.Journal of molecular neuroscience : MN · 2025Review
- Microglia programmed cell death in neurodegenerative diseases and CNS injury.Apoptosis : an international journal on programmed cell death · 2025Review
- The molecular mechanisms, roles, and potential applications of PANoptosis in cancer treatment.Frontiers in immunology · 2025Review
- A two-center prospective cohort study of serum RIP-3 as a potential biomarker in relation to severity and prognosis after severe traumatic brain injury.Neurosurgical review · 2024Article
- Trauma diagnostic-related target proteins and their detection techniques.Expert reviews in molecular medicine · 2024Review
- Therapeutic potential of PANoptosis: innate sensors, inflammasomes, and RIPKs in PANoptosomes.Trends in molecular medicine · 2024Review
- Methodology of drug screening and target identification for new necroptosis inhibitors.Journal of pharmaceutical analysis · 2019Review
- Dabrafenib, an inhibitor of RIP3 kinase-dependent necroptosis, reduces ischemic brain injury.Neural regeneration research · 2018Article
- Is Receptor-Interacting Protein Kinase 3 a Viable Therapeutic Target forFrontiers in immunology · 2018Article
- Amikacin Inhibits miR-497 Maturation and Exerts Post-ischemic Neuroprotection.Molecular neurobiology · 2017Article
- Ischemia/Reperfusion.Comprehensive Physiology · 2016Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Necroptosis or programmed necrosis is evident in various neurological disorders such as ischemic stroke. Receptor interacting serine/threonine protein kinase 3 (RIPK3) is one of the crucial targets of necroptosis and inhibition of this protein exerts neuroprotection. However, knowledge regarding the three-dimensional structure and binding site information of this protein is lacking. In the present study, structure-based in silico methods were implemented to identify the key amino acids in the RIPK3 binding site that might be responsible for ligand interactions. Further, novel RIPK3 inhibitors were identified through a dual ensemble screening strategy. Three inhibitors exhibited binding to RIPK3 in micromolar concentrations and exerted post-ischemic neuroprotection in vitro.
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What OpenQuestion holds
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.