Evidence map›Paper›PMID 29769258›Full record

ArticleEMBO molecular medicine2018

Anti-tumor efficacy of a novel CLK inhibitor via targeting RNA splicing and MYC-dependent vulnerability.

Kenichi Iwai, Masahiro Yaguchi, Kazuho Nishimura, Yukiko Yamamoto, Toshiya Tamura, Daisuke Nakata, Ryo Dairiki, Yoichi Kawakita, Ryo Mizojiri, Yoshiteru Ito and 16 more

Open access · goldAbstract read
In one paragraph

Article in EMBO molecular medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 68 papers.

0numbers the graph read from it
0cells of the map it votes in
68citing papers in PubMed
5.4field-weighted citation impact, top 4% 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

68 citing papers in PubMed, 89 citations in OpenAlex.

  1. Review
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  5. Phase I Study of Rogocekib in Patients with Advanced, Relapsed, or Refractory Malignant Solid Tumors.Clinical cancer research : an official journal of the American Association for Cancer Research · 2026
    Article
  6. Review
  7. Review
  8. Article
  9. Article
  10. Review
  11. RNA Splicing as a Therapeutic Target in Cancer.Annual review of pharmacology and toxicology · 2026
    Review
  12. Article
  13. A Chemically Induced CRISPR/dCas13Journal of medicinal chemistry · 2025
    Article
  14. Article
  15. Review
  16. Article
  17. Article
  18. Article
  19. Targeting RNA splicing modulation: new perspectives for anticancer strategy?Journal of experimental & clinical cancer research : CR · 2025
    Review
  20. Research towards selective inhibition of the CLK3 kinase.Beilstein journal of organic chemistry · 2025
    Article

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

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

26 authors at 2 institutions in 2 countries.

Kenichi IwaiOncology Drug Discovery Unit, Takeda Pharmaceutical Company, Limited, Fujisawa, Japan.
Masahiro YaguchiOncology Drug Discovery Unit, Takeda Pharmaceutical Company, Limited, Fujisawa, Japan.
Kazuho NishimuraOncology Drug Discovery Unit, Takeda Pharmaceutical Company, Limited, Fujisawa, Japan.
Yukiko YamamotoOncology Drug Discovery Unit, Takeda Pharmaceutical Company, Limited, Fujisawa, Japan.
Toshiya TamuraOncology Drug Discovery Unit, Takeda Pharmaceutical Company, Limited, Fujisawa, Japan.
Daisuke NakataOncology Drug Discovery Unit, Takeda Pharmaceutical Company, Limited, Fujisawa, Japan.
Ryo DairikiOncology Drug Discovery Unit, Takeda Pharmaceutical Company, Limited, Fujisawa, Japan.
Yoichi KawakitaOncology Drug Discovery Unit, Takeda Pharmaceutical Company, Limited, Fujisawa, Japan.
Ryo MizojiriOncology Drug Discovery Unit, Takeda Pharmaceutical Company, Limited, Fujisawa, Japan.
Yoshiteru ItoOncology Drug Discovery Unit, Takeda Pharmaceutical Company, Limited, Fujisawa, Japan.
Moriteru AsanoOncology Drug Discovery Unit, Takeda Pharmaceutical Company, Limited, Fujisawa, Japan.
Hironobu MaezakiOncology Drug Discovery Unit, Takeda Pharmaceutical Company, Limited, Fujisawa, Japan.
Yusuke NakayamaIntegrated Technology Research Laboratories, Takeda Pharmaceutical Company, Limited, Fujisawa, Japan.
Misato KaishimaIntegrated Technology Research Laboratories, Takeda Pharmaceutical Company, Limited, Fujisawa, Japan.
Kozo HayashiIntegrated Technology Research Laboratories, Takeda Pharmaceutical Company, Limited, Fujisawa, Japan.
Mika TerataniIntegrated Technology Research Laboratories, Takeda Pharmaceutical Company, Limited, Fujisawa, Japan.
Shuichi MiyakawaBiomolecular Research Laboratories, Takeda Pharmaceutical Company, Limited, Fujisawa, Japan.
Misa IwataniBiomolecular Research Laboratories, Takeda Pharmaceutical Company, Limited, Fujisawa, Japan.
Maki MiyamotoDrug Metabolism & Pharmacokinetics Research Laboratories, Takeda Pharmaceutical Company, Limited, Fujisawa, Japan.
Michael G KleinDepartment of Structural Biology, Takeda California Inc., San Diego, CA, USA.
Wes LaneDepartment of Structural Biology, Takeda California Inc., San Diego, CA, USA.
Gyorgy SnellDepartment of Structural Biology, Takeda California Inc., San Diego, CA, USA.
Richard TjhenDepartment of Structural Biology, Takeda California Inc., San Diego, CA, USA.
Xingyue HeOncology Drug Discovery Unit, Takeda Pharmaceuticals International Co., Cambridge, MA, USA.
Sai PulukuriOncology Drug Discovery Unit, Takeda Pharmaceuticals International Co., Cambridge, MA, USA.
Toshiyuki NomuraOncology Drug Discovery Unit, Takeda Pharmaceutical Company, Limited, Fujisawa, Japan toshiyuki.nomura@takeda.com.ORCID 0000-0003-4122-0301
Takeda (Japan) · JPTakeda (United States) · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The modulation of pre-mRNA splicing is proposed as an attractive anti-neoplastic strategy, especially for the cancers that exhibit aberrant pre-mRNA splicing. Here, we discovered that T-025 functions as an orally available and potent inhibitor of Cdc2-like kinases (CLKs), evolutionally conserved kinases that facilitate exon recognition in the splicing machinery. Treatment with T-025 reduced CLK-dependent phosphorylation, resulting in the induction of skipped exons, cell death, and growth suppression

Indexed as

AnimalsCell Line, TumorDiaminesGenes, mycHumansMiceMice, TransgenicPhosphorylationProtein Kinase InhibitorsProtein Serine-Threonine KinasesProtein-Tyrosine KinasesProto-Oncogene Proteins c-mycPyrimidinesQuinolinesRNA SplicingClk dual-specificity kinasesCLK inhibitor T-025DiaminesProtein Kinase InhibitorsProtein Serine-Threonine KinasesProtein-Tyrosine KinasesProto-Oncogene Proteins c-mycPyrimidinesQuinolinesalternative splicingCdc2‐like kinase inhibitorCLK2MYC

Identifiers

PMID29769258
PMCPMC5991599
OpenAlexW2803686670

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.