Evidence map›Paper›PMID 36089608›Full record

ReviewJournal of experimental & clinical cancer research : CR2022

Elesclomol: a copper ionophore targeting mitochondrial metabolism for cancer therapy.

Peijie Zheng, Chuntao Zhou, Liuyi Lu, Bin Liu, Yuemin Ding

Open access · goldAbstract readReview
In one paragraph

Review in Journal of experimental & clinical cancer research : CR, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 220 papers.

0numbers the graph read from it
0cells of the map it votes in
220citing papers in PubMed
26.3field-weighted citation impact, top 1% of its field
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

220 citing papers in PubMed, 328 citations in OpenAlex.

  1. Review
  2. Cuproptosis and the bioinorganic basis of copper-induced cell death.Journal of biological inorganic chemistry : JBIC : a publication of the Society of Biological Inorganic Chemistry · 2026
    Review
  3. Review
  4. Article
  5. Effects of copper overload on mitochondrial parameters in GBM-1, U-87 MG, and C6 glioma cell lines.Biometals : an international journal on the role of metal ions in biology, biochemistry, and medicine · 2026
    Article
  6. Review
  7. Article
  8. Review
  9. Review
  10. Review
  11. Review
  12. Article
  13. Article
  14. Article
  15. Review
  16. Review
  17. Review
  18. Article
  19. Role of Ferredoxin 1Cancer pathogenesis and therapy · 2026
    Review
  20. Review

160 more citing papers are in PubMed but not listed here.

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

5 authors at 1 institution in 1 country.

Peijie ZhengDepartment of Clinical Medicine, School of Medicine, Zhejiang University City College, Hangzhou, 310015, China.
Chuntao ZhouDepartment of Clinical Medicine, School of Medicine, Zhejiang University City College, Hangzhou, 310015, China.
Liuyi LuDepartment of Clinical Medicine, School of Medicine, Zhejiang University City College, Hangzhou, 310015, China.
Bin LiuDepartment of Clinical Medicine, School of Medicine, Zhejiang University City College, Hangzhou, 310015, China.
Yuemin DingDepartment of Clinical Medicine, School of Medicine, Zhejiang University City College, Hangzhou, 310015, China. dingyuemin@zucc.edu.cn.ORCID http://orcid.org/0000-0003-0547-5358
Zhejiang University · CN

Funding

Zhejiang Provincial Public Welfare Technology Research Program/Experimental Animal Project LGD19H090008
6 · The paper itself

Abstract

Elesclomol is an anticancer drug that targets mitochondrial metabolism. In the past, elesclomol was recognized as an inducer of oxidative stress, but now it has also been found to suppress cancer by inducing cuproptosis. Elesclomol's anticancer activity is determined by the dependence of cancer on mitochondrial metabolism. The mitochondrial metabolism of cancer stem cells, cancer cells resistant to platinum drugs, proteasome inhibitors, molecularly targeted drugs, and cancer cells with inhibited glycolysis was significantly enhanced. Elesclomol exhibited tremendous toxicity to all three kinds of cells. Elesclomol's toxicity to cells is highly dependent on its transport of extracellular copper ions, a process involved in cuproptosis. The discovery of cuproptosis has perfected the specific cancer suppressor mechanism of elesclomol. For some time, elesclomol failed to yield favorable results in oncology clinical trials, but its safety in clinical application was confirmed. Research progress on the relationship between elesclomol, mitochondrial metabolism and cuproptosis provides a possibility to explore the reapplication of elesclomol in the clinic. New clinical trials should selectively target cancer types with high mitochondrial metabolism and attempt to combine elesclomol with platinum, proteasome inhibitors, molecularly targeted drugs, or glycolysis inhibitors. Herein, the particular anticancer mechanism of elesclomol and its relationship with mitochondrial metabolism and cuproptosis will be presented, which may shed light on the better application of elesclomol in clinical tumor treatment.

Indexed as

CopperNeoplasmsHumansHydrazinesIonophoresPlatinumProteasome InhibitorsCopperelesclomolHydrazinesIonophoresPlatinumProteasome InhibitorsAnticancer drugsCancerCancer stem cellsClinical trialsCuproptosisDrug safetyElesclomolMitochondrial metabolism

Identifiers

PMID36089608
PMCPMC9465867
OpenAlexW4295517279

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.