Evidence map›Paper›PMID 42842344›Full record

ArticleCNS neuroscience & therapeutics2026

GFH312 Reduces Neuronal Death by Inhibiting RIPK1-Mediated Apoptosis and Necroptosis After Ischemic Stroke.

Ze Liu, Shengju Wu, Qian Suo, Chang Liu, Rubing Shi, Jing Ye, Haroon Khan, Jing-Yang Zhang, Yaohui Tang, Zhijun Zhang and 3 more

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Article in CNS neuroscience & therapeutics, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
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1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

The trial behind it

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Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

13 authors.

Ze LiuSchool of Biomedical Engineering, Shanghai Jiao Tong University, Shanghai, China.ORCID https://orcid.org/0000-0001-8874-5127
Shengju WuSchool of Biomedical Engineering, Shanghai Jiao Tong University, Shanghai, China.
Qian SuoSchool of Biomedical Engineering, Shanghai Jiao Tong University, Shanghai, China.
Chang LiuSchool of Biomedical Engineering, Shanghai Jiao Tong University, Shanghai, China.
Rubing ShiSchool of Biomedical Engineering, Shanghai Jiao Tong University, Shanghai, China.
Jing YeSchool of Biomedical Engineering, Shanghai Jiao Tong University, Shanghai, China.ORCID https://orcid.org/0009-0007-7738-6748
Haroon KhanSchool of Biomedical Engineering, Shanghai Jiao Tong University, Shanghai, China.ORCID https://orcid.org/0000-0002-4867-2901
Jing-Yang ZhangGenFleet Therapeutics Inc., Shanghai, China.
Yaohui TangSchool of Biomedical Engineering, Shanghai Jiao Tong University, Shanghai, China.ORCID https://orcid.org/0000-0002-9603-2650
Zhijun ZhangSchool of Biomedical Engineering, Shanghai Jiao Tong University, Shanghai, China.
Wanlu LiSchool of Biomedical Engineering, Shanghai Jiao Tong University, Shanghai, China.ORCID https://orcid.org/0000-0002-7637-1364
Fu-Sheng ZhouGenFleet Therapeutics Inc., Shanghai, China.
Guo-Yuan YangSchool of Biomedical Engineering, Shanghai Jiao Tong University, Shanghai, China.ORCID https://orcid.org/0000-0003-3105-9307

Funding

GenFleet Therapeutics (Shanghai) Inc GF-107
6 · The paper itself

Abstract

aimsTo investigate the role of the RIPK1 inhibitor GFH312 in ischemic stroke and identify its potential mechanisms.

methodsGFH312 was administered to adult mice in an ischemic stroke model. To ascertain the effectiveness of treatment, neurobehavioral tests and assessments of brain damage were carried out. Brain tissues were examined using immunofluorescence as well as western blot and real-time quantitative PCR at various intervals following ischemia to evaluate inflammatory gene expression and signaling pathways linked to apoptosis and necroptosis.

resultsTemporal analysis revealed that necroptosis and apoptosis were rapidly activated following ischemia, peaking at 1-3 days. GFH312 significantly improved neurological function and reduced brain injury in stroke mice. Mechanistically, GFH312 markedly inhibited apoptosis and necroptosis via suppression of the RIPK1-related signaling pathway (RIPK1-RIPK3-MLKL). In addition, GFH312 greatly decreased inflammatory gene expression in the brain.

conclusionApoptosis and necrotic apoptosis occur primarily during the acute poststroke phase. GFH312 exerts neuroprotective effects after ischemic stroke, which are associated with suppression of RIPK1-related apoptosis, necroptosis, and neuroinflammation.

Indexed as

ApoptosisIschemic StrokeNecroptosisNeuronsNeuroprotective AgentsReceptor-Interacting Protein Serine-Threonine KinasesAnimalsBrain IschemiaMaleMiceMice, Inbred C57BLNeuroprotective AgentsReceptor-Interacting Protein Serine-Threonine KinasesRipk1 protein, mouseapoptosisGFH312necroptosisRIPK1

Identifiers

PMID42842344
PMCPMC13644914

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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.