Evidence map›Paper›PMID 39759112›Full record

ArticleGenes & diseases2025

Novel oral compound Z526 mitigates cancer-associated cachexia via intervening NF-κB signaling and oxidative stress.

Xiaofan Gu, Shanshan Lu, Shuang Xu, Yiwei Li, Meng Fan, Guangyu Lin, Yiyuan Liu, Yun Zhao, Weili Zhao, Xuan Liu and 2 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Genes & diseases, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Article
  2. Article
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

12 authors.

Xiaofan GuShanghai Engineering Research Center of Molecular Therapeutics and New Drug Development, School of Chemistry and Molecular Engineering, East China Normal University, Shanghai 200062, China.
Shanshan LuShanghai Engineering Research Center of Molecular Therapeutics and New Drug Development, School of Chemistry and Molecular Engineering, East China Normal University, Shanghai 200062, China.
Shuang XuDepartment of Medicinal Chemistry, School of Pharmacy, Fudan University, Shanghai 201210, China.
Yiwei LiShanghai Engineering Research Center of Molecular Therapeutics and New Drug Development, School of Chemistry and Molecular Engineering, East China Normal University, Shanghai 200062, China.
Meng FanShanghai Engineering Research Center of Molecular Therapeutics and New Drug Development, School of Chemistry and Molecular Engineering, East China Normal University, Shanghai 200062, China.
Guangyu LinDepartment of Medicinal Chemistry, School of Pharmacy, Fudan University, Shanghai 201210, China.
Yiyuan LiuShanghai Engineering Research Center of Molecular Therapeutics and New Drug Development, School of Chemistry and Molecular Engineering, East China Normal University, Shanghai 200062, China.
Yun ZhaoShanghai Engineering Research Center of Molecular Therapeutics and New Drug Development, School of Chemistry and Molecular Engineering, East China Normal University, Shanghai 200062, China.
Weili ZhaoDepartment of Medicinal Chemistry, School of Pharmacy, Fudan University, Shanghai 201210, China.
Xuan LiuInstitute of Interdisciplinary Integrative Medicine Research, Shanghai University of Traditional Chinese Medicine, Shanghai 201203, China.
Xiaochun DongDepartment of Medicinal Chemistry, School of Pharmacy, Fudan University, Shanghai 201210, China.
Xiongwen ZhangShanghai Engineering Research Center of Molecular Therapeutics and New Drug Development, School of Chemistry and Molecular Engineering, East China Normal University, Shanghai 200062, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cancer-associated cachexia (CAC) is a severe metabolic disorder syndrome mainly characterized by muscle and fat loss, which accounts for one-third of cancer-related deaths. No effective therapeutic approach that could fully reverse CAC is available. NF-κB signaling and oxidative stress play vital roles in both muscle atrophy and fat loss in CAC. Here, we showed that our developed oral compound Z526 exhibited potent anti-CAC efficacy by inhibiting NF-κB signaling and ameliorating oxidative stress.

Indexed as

Cancer-associated cachexiaFat lipolysisMuscle atrophyNF-κB signalingOxidative stressZ526

Identifiers

PMID39759112
PMCPMC11697116

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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.