Evidence map›Paper›PMID 41960573›Full record

ArticleJournal of pharmaceutical analysis2026

Covalent modification of Keap1 Cys489 by NU6300 activates Nrf2 signaling and suppresses NLRP3 inflammasome-mediated pyroptosis.

Xueqin Jiang, Hongyu Zheng, Xinlu Zhang, Minghai Tang, Jing Peng, Xiaoying Cai, Kaiyue Su, Ruijia Zhang, Neng Ye, Lei Lin and 4 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of pharmaceutical analysis, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
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

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.

3 · Its place in the literature

Who cites it

1 citing paper in PubMed.

  1. Review
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

14 authors.

Xueqin JiangDepartment of Biotherapy, Cancer Center and State Key Laboratory of Biotherapy, West China Hospital, Sichuan University, Chengdu, 610041, China.
Hongyu ZhengSchool of Pharmacy, Chengdu Medical College, Chengdu, 610500, China.
Xinlu ZhangDepartment of Biotherapy, Cancer Center and State Key Laboratory of Biotherapy, West China Hospital, Sichuan University, Chengdu, 610041, China.
Minghai TangDepartment of Biotherapy, Cancer Center and State Key Laboratory of Biotherapy, West China Hospital, Sichuan University, Chengdu, 610041, China.
Jing PengDepartment of Biotherapy, Cancer Center and State Key Laboratory of Biotherapy, West China Hospital, Sichuan University, Chengdu, 610041, China.
Xiaoying CaiDepartment of Biotherapy, Cancer Center and State Key Laboratory of Biotherapy, West China Hospital, Sichuan University, Chengdu, 610041, China.
Kaiyue SuDepartment of Biotherapy, Cancer Center and State Key Laboratory of Biotherapy, West China Hospital, Sichuan University, Chengdu, 610041, China.
Ruijia ZhangDepartment of Biotherapy, Cancer Center and State Key Laboratory of Biotherapy, West China Hospital, Sichuan University, Chengdu, 610041, China.
Neng YeScaled Manufacturing Center of Biological Products, Management Office of National Facility for Translational Medicine, West China Hospital, Sichuan University, Chengdu, 610041, China.
Lei LinDepartment of Biotherapy, Cancer Center and State Key Laboratory of Biotherapy, West China Hospital, Sichuan University, Chengdu, 610041, China.
Rupei MaDepartment of Biotherapy, Cancer Center and State Key Laboratory of Biotherapy, West China Hospital, Sichuan University, Chengdu, 610041, China.
Caiyun ShenDepartment of Biotherapy, Cancer Center and State Key Laboratory of Biotherapy, West China Hospital, Sichuan University, Chengdu, 610041, China.
Wenshuang WuDivision of Thyroid Surgery, Department of General Surgery and Laboratory of Thyroid and Parathyroid Disease, Frontiers Science Center for Disease-related Molecular Network, West China Hospital, Sichuan University, Chengdu, 610041, China.
Haoyu YeDepartment of Biotherapy, Cancer Center and State Key Laboratory of Biotherapy, West China Hospital, Sichuan University, Chengdu, 610041, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Nuclear factor erythroid 2-related factor 2 (Nrf2), a master regulator of oxidative stress and inflammasome, plays a critical role in modulating pyroptosis. In this study, we identified NU6300 as a novel small-molecule activator of Nrf2 that restores mitochondrial function, alleviates oxidative stress, and suppresses inflammasome activation and pyroptosis. Mechanistically, NU6300 covalently modified Kelch-like ECH-associated protein 1 (Keap1) at cysteine-489, disrupting the Keap1-Nrf2 interaction, thereby promoting Nrf2 nuclear translocation and transcription of antioxidant genes. Notably, NU6300 inhibits NOD-like receptor family pyrin domain containing 3 (NLRP3) inflammasome activation and gasdermin D (GSDMD)-mediated pyroptosis through redox-dependent mechanisms, representing the first evidence that covalent modification of Keap1 at cysteine-489 by NU6300 bridges Nrf2 activation and inflammasome suppression.

Indexed as

Keap1-Nrf2Liver injuryNLRP3 inflammasomeNU6300Pyroptosis

Identifiers

PMID41960573
PMCPMC13059001

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Registered trials

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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.