Evidence map›Paper›PMID 39520729›Full record

ArticleEuropean journal of medicinal chemistry2025

Discovery of the first selective and potent PROTAC degrader for the pseudokinase TRIB2.

Chaowei Wen, Prathibha R Gajjala, Yihan Liu, Bingzhong Chen, Mehtab S Bal, Payal Sutaria, Qiao Yuanyuan, Yang Zheng, Yang Zhou, Jinwei Zhang and 6 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in European journal of medicinal chemistry, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing 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

3 citing papers in PubMed.

  1. Article
  2. Article
  3. 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

16 authors.

Chaowei WenInternational Cooperative Laboratory of Traditional Chinese Medicine Modernization and Innovative Drug Development, Ministry of Education (MoE) of People's Republic of China, College of Pharmacy, Jinan University, 601 Huangpu Avenue West, Guangzhou, 510632, China.
Prathibha R GajjalaMichigan Center for Translational Pathology, University of Michigan, Ann Arbor, MI, 48109, United States; Department of Pathology, University of Michigan, Ann Arbor, MI, 48109, United States.
Yihan LiuMichigan Center for Translational Pathology, University of Michigan, Ann Arbor, MI, 48109, United States; Cancer Biology Program, University of Michigan, Ann Arbor, MI, 48109, United States.
Bingzhong ChenInternational Cooperative Laboratory of Traditional Chinese Medicine Modernization and Innovative Drug Development, Ministry of Education (MoE) of People's Republic of China, College of Pharmacy, Jinan University, 601 Huangpu Avenue West, Guangzhou, 510632, China.
Mehtab S BalMichigan Center for Translational Pathology, University of Michigan, Ann Arbor, MI, 48109, United States.
Payal SutariaMichigan Center for Translational Pathology, University of Michigan, Ann Arbor, MI, 48109, United States.
Qiao YuanyuanMichigan Center for Translational Pathology, University of Michigan, Ann Arbor, MI, 48109, United States; Department of Pathology, University of Michigan, Ann Arbor, MI, 48109, United States.
Yang ZhengMichigan Center for Translational Pathology, University of Michigan, Ann Arbor, MI, 48109, United States; Department of Pathology, University of Michigan, Ann Arbor, MI, 48109, United States.
Yang ZhouInternational Cooperative Laboratory of Traditional Chinese Medicine Modernization and Innovative Drug Development, Ministry of Education (MoE) of People's Republic of China, College of Pharmacy, Jinan University, 601 Huangpu Avenue West, Guangzhou, 510632, China.
Jinwei ZhangState Key Laboratory of Chemical Biology, Shanghai Institute of Organic Chemistry, University of Chinese Academy of Sciences, Chinese Academy of Sciences, 345 Lingling Road, Shanghai, 200032, China.
Weixue HuangState Key Laboratory of Chemical Biology, Shanghai Institute of Organic Chemistry, University of Chinese Academy of Sciences, Chinese Academy of Sciences, 345 Lingling Road, Shanghai, 200032, China.
Xiaomei RenState Key Laboratory of Chemical Biology, Shanghai Institute of Organic Chemistry, University of Chinese Academy of Sciences, Chinese Academy of Sciences, 345 Lingling Road, Shanghai, 200032, China.
Zhen WangState Key Laboratory of Chemical Biology, Shanghai Institute of Organic Chemistry, University of Chinese Academy of Sciences, Chinese Academy of Sciences, 345 Lingling Road, Shanghai, 200032, China.
Ke DingInternational Cooperative Laboratory of Traditional Chinese Medicine Modernization and Innovative Drug Development, Ministry of Education (MoE) of People's Republic of China, College of Pharmacy, Jinan University, 601 Huangpu Avenue West, Guangzhou, 510632, China; State Key Laboratory of Chemical Biology, Shanghai Institute of Organic Chemistry, University of Chinese Academy of Sciences, Chinese Academy of Sciences, 345 Lingling Road, Shanghai, 200032, China. Electronic address: dingk@sioc.ac.cn.
Arul M ChinnaiyanMichigan Center for Translational Pathology, University of Michigan, Ann Arbor, MI, 48109, United States; Department of Pathology, University of Michigan, Ann Arbor, MI, 48109, United States; Rogel Cancer Center, University of Michigan, Ann Arbor, MI, 48109, United States; Department of Urology, University of Michigan, Ann Arbor, MI, 48109, United States; Howard Hughes Medical Institute, University of Michigan, Ann Arbor, MI, 48109, United States. Electronic address: arul@med.umich.edu.
Fengtao ZhouInternational Cooperative Laboratory of Traditional Chinese Medicine Modernization and Innovative Drug Development, Ministry of Education (MoE) of People's Republic of China, College of Pharmacy, Jinan University, 601 Huangpu Avenue West, Guangzhou, 510632, China. Electronic address: fengtaozhou@jnu.edu.cn.

Funding

Howard Hughes Medical Institute
6 · The paper itself

Abstract

Pseudokinase TRIB2, a member of the CAMK Ser/Thr protein kinase family, regulates various cellular processes through phosphorylation-independent mechanisms. Dysregulation of TRIB2 has been implicated in promoting tumor growth, metastasis, and therapy resistance, making it a promising target for cancer treatment. In this study, we designed and synthesized a series of TRIB2 PROTAC degraders by conjugating a TRIB2 binder 1 with VHL or CRBN ligands via linkers of varying lengths and compositions. Among these compounds, 5k demonstrated potent TRIB2 degradation with a DC

Indexed as

Antineoplastic AgentsApoptosisCell ProliferationCalcium-Calmodulin-Dependent Protein KinasesCell Line, TumorDose-Response Relationship, DrugDrug DiscoveryDrug Screening Assays, AntitumorHumansMolecular StructureProteolysisStructure-Activity RelationshipAntineoplastic AgentsCalcium-Calmodulin-Dependent Protein KinasesTRIB2 protein, humanApoptosisProliferationPROTACsProtein degradationPseudokinaseTRIB2

Identifiers

PMID39520729
PMCPMC12135709

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LicenceCC BY
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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.