Evidence map›Paper›PMID 41490840›Full record

ArticleJournal of advanced research2026

Structural optimization and functional evaluation of cytisine for redox homeostasis regulation in lung cancer cells.

Zhicui Qin, Zilu Xin, Xueli Zhang, Xin Liu, Yang Yang, Feng Feng, Zongwei Xia, Xiuling Yu

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Article in Journal of advanced research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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5 · Who and what money

Authors and funding

8 authors.

Zhicui QinCollege of Medicine, Linyi University, Linyi 276000, China.
Zilu XinCollege of Medicine, Linyi University, Linyi 276000, China.
Xueli ZhangCollege of Medicine, Linyi University, Linyi 276000, China.
Xin LiuCollege of Medicine, Linyi University, Linyi 276000, China.
Yang YangCollege of Medicine, Linyi University, Linyi 276000, China.
Feng FengCollege of Medicine, Linyi University, Linyi 276000, China.
Zongwei XiaCollege of Resources and Environment, Linyi University, Linyi 276000, China. Electronic address: xiazongwei@lyu.edu.cn.
Xiuling YuCollege of Medicine, Linyi University, Linyi 276000, China. Electronic address: yuxiuling@lyu.edu.cn.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionTargeting redox homeostasis represents a promising strategy to selectively eliminate cancer cells through oxidative stress-mediated apoptosis. However, developing specific molecular entities capable of effectively disrupting this balance remains a key challenge.

objectivesThis study aimed to construct a novel library of cytisine derivatives through rational drug design to discover lead compounds with potent redox-disrupting activity and validate their potential as precision therapy candidates for lung cancer.

methodsA focused library of 77 derivatives was designed and synthesized via rational modification of key pharmacophores in cytisine. The antitumor activity and mechanism of action of candidate compounds were evaluated using in vitro cellular models and in vivo animal models.

resultsAmong these, YU-C-ThioU-9 emerged as a lead compound with potent antitumor activity. Mechanistic investigations revealed that YU-C-ThioU-9 disrupts intracellular redox balance, leading to a marked accumulation of reactive oxygen species (ROS) and consequent oxidative damage. This redox perturbation, marked by oxidative stress accumulation, ultimately induces apoptotic cell death in lung cancer cells. Importantly, YU-C-ThioU-9 exhibited robust anticancer efficacy in both in vitro and in vivo models.

conclusionThese findings establish redox disruption as a clinically actionable avenue for precision oncology and position YU-C-ThioU-9 as a lead cytisine-derived candidate for lung cancer therapy.

Indexed as

AlkaloidsAntineoplastic AgentsAzocinesHomeostasisLung NeoplasmsQuinolizinesAnimalsApoptosisCell Line, TumorCell ProliferationHumansMiceOxidation-ReductionOxidative StressQuinolizidine AlkaloidsReactive Oxygen SpeciesAlkaloidsAntineoplastic AgentsAzocinescytisineQuinolizidine AlkaloidsQuinolizinesReactive Oxygen SpeciesAnti-lung cancer activityCytisineReactive oxygen speciesRedox homeostasisStructural optimization

Identifiers

PMID41490840
PMCPMC13539262

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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.