Evidence map›Paper›PMID 35048559›Full record

ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2022

A Selective Small-Molecule c-Myc Degrader Potently Regresses Lethal c-Myc Overexpressing Tumors.

Ying Xu, Qingfeng Yu, Ping Wang, Zhaoxing Wu, Lei Zhang, Shuigao Wu, Mengyuan Li, Bowen Wu, Hongzhi Li, Haifeng Zhuang and 4 more

Open access · goldAbstract read
In one paragraph

Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
2.9field-weighted citation impact, top 8% 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

29 citing papers in PubMed, 34 citations in OpenAlex.

  1. Article
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  7. MYC as a key target for melanoma therapy.Frontiers in cell and developmental biology · 2026
    Review
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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

14 authors at 4 institutions in 2 countries.

Ying XuDepartment of Hematology and Cancer Institute (Key Laboratory of Cancer Prevention and Intervention, China National Ministry of Education, Key Laboratory of Molecular Biology in Medical Sciences, The Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, 310009, China.ORCID 0000-0003-4211-4156
Qingfeng YuDepartment of Hematology and Cancer Institute (Key Laboratory of Cancer Prevention and Intervention, China National Ministry of Education, Key Laboratory of Molecular Biology in Medical Sciences, The Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, 310009, China.
Ping WangDepartment of Hematology and Cancer Institute (Key Laboratory of Cancer Prevention and Intervention, China National Ministry of Education, Key Laboratory of Molecular Biology in Medical Sciences, The Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, 310009, China.
Zhaoxing WuDepartment of Hematology and Cancer Institute (Key Laboratory of Cancer Prevention and Intervention, China National Ministry of Education, Key Laboratory of Molecular Biology in Medical Sciences, The Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, 310009, China.
Lei ZhangDepartment of Hematology and Cancer Institute (Key Laboratory of Cancer Prevention and Intervention, China National Ministry of Education, Key Laboratory of Molecular Biology in Medical Sciences, The Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, 310009, China.
Shuigao WuWeben Pharmaceuticals, Hangzhou, 310051, China.
Mengyuan LiDepartment of Hematology and Cancer Institute (Key Laboratory of Cancer Prevention and Intervention, China National Ministry of Education, Key Laboratory of Molecular Biology in Medical Sciences, The Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, 310009, China.
Bowen WuDepartment of Hematology and Cancer Institute (Key Laboratory of Cancer Prevention and Intervention, China National Ministry of Education, Key Laboratory of Molecular Biology in Medical Sciences, The Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, 310009, China.
Hongzhi LiDepartment of Molecular Medicine, Beckman Research Institute, City of Hope National Medical Center, Duarte, CA, 91010, USA.
Haifeng ZhuangDepartment of Hematology, the First Affiliated Hospital of Zhejiang Chinese Medical University, Hangzhou, 310009, China.
Xuzhao ZhangDepartment of Hematology and Cancer Institute (Key Laboratory of Cancer Prevention and Intervention, China National Ministry of Education, Key Laboratory of Molecular Biology in Medical Sciences, The Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, 310009, China.
Yu HuangAcademy of Chinese Medical Sciences, Zhejiang Chinese Medical University, Hangzhou, 310053, China.
Xiaoxian GanWeben Pharmaceuticals, Hangzhou, 310051, China.
Rongzhen XuDepartment of Hematology and Cancer Institute (Key Laboratory of Cancer Prevention and Intervention, China National Ministry of Education, Key Laboratory of Molecular Biology in Medical Sciences, The Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, 310009, China.ORCID 0000-0002-5865-0589
Zhejiang Cancer Hospital · CNBetta Pharmaceuticals (China) · CNZhejiang Chinese Medical University · CNCity Of Hope National Medical Center · US

Funding

National Natural Science Foundation of China 81470306National Natural Science Foundation of China 81670138National Natural Science Foundation of China 81870111National Natural Science Foundation of China 82070146Natural Science Foundation of Zhejiang Province LZ21H160005Weben fund 491020-15170C
6 · The paper itself

Abstract

MYC oncogene is involved in the majority of human cancers and is often associated with poor outcomes, rendering it an extraordinarily desirable target, but therapeutic targeting of c-Myc protein has been a challenge for >30 years. Here, WBC100, a novel oral active molecule glue that selectively degrades c-Myc protein over other proteins and potently kills c-Myc overexpressing cancer cells is reported. WBC100 targets the nuclear localization signal 1 (NLS1)-Basic-nuclear localization signal 2 (NLS2) region of c-Myc and induces c-Myc protein degradation through ubiquitin E3 ligase CHIP mediated 26S proteasome pathway, leading to apoptosis of cancer cells. In vivo, WBC100 potently regresses multiple lethal c-Myc overexpressing tumors such as acute myeloid leukemia, pancreatic, and gastric cancers with good tolerability in multiple xenograft mouse models. Identification of the NLS1-Basic-NLS2 region as a druggable pocket for targeting the "undruggable" c-Myc protein and that single-agent WBC100 potently regresses c-Myc overexpressing tumors through selective c-Myc proteolysis opens new perspectives for pharmacologically intervening c-Myc in human cancers.

Indexed as

Proto-Oncogene Proteins c-mycUbiquitin-Protein LigasesAnimalsCell Line, TumorHumansMiceProteolysisUbiquitinMYC protein, humanProto-Oncogene Proteins c-mycUbiquitinUbiquitin-Protein Ligasescancerc-Myc oncoproteinproteolysis targeting moleculetargeted therapyWBC100

Identifiers

PMID35048559
PMCPMC8922104
OpenAlexW4205773749

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.