Evidence map›Paper›PMID 33532179›Full record

ReviewActa pharmaceutica Sinica. B2021

Selective inhibition of CDK4/6: A safe and effective strategy for developing anticancer drugs.

Kai Yuan, Xiao Wang, Haojie Dong, Wenjian Min, Haiping Hao, Peng Yang

Open access · diamondAbstract readReview
In one paragraph

Review in Acta pharmaceutica Sinica. B, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
65citing papers in PubMed, 1 pooled it
8.7field-weighted citation impact, top 2% 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

65 citing papers in PubMed, 1 synthesis or guideline pooled it, 139 citations in OpenAlex.

  1. Pooled it
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  5. Review
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  8. Article
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  13. Enhancer regulation in cancer: from epigenetics to mArchives of pharmacal research · 2025
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  18. Article
  19. MiRNA Dysregulation in Brain Injury: AnCurrent neuropharmacology · 2025
    Article
  20. Article

5 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

6 authors at 1 institution in 1 country.

Kai YuanState Key Laboratory of Natural Medicines and Jiangsu Key Laboratory of Drug Design and Optimization, China Pharmaceutical University, Nanjing 210009, China.
Xiao WangState Key Laboratory of Natural Medicines and Jiangsu Key Laboratory of Drug Design and Optimization, China Pharmaceutical University, Nanjing 210009, China.
Haojie DongState Key Laboratory of Natural Medicines and Jiangsu Key Laboratory of Drug Design and Optimization, China Pharmaceutical University, Nanjing 210009, China.
Wenjian MinState Key Laboratory of Natural Medicines and Jiangsu Key Laboratory of Drug Design and Optimization, China Pharmaceutical University, Nanjing 210009, China.
Haiping HaoState Key Laboratory of Natural Medicines and Jiangsu Key Laboratory of Drug Design and Optimization, China Pharmaceutical University, Nanjing 210009, China.
Peng YangState Key Laboratory of Natural Medicines and Jiangsu Key Laboratory of Drug Design and Optimization, China Pharmaceutical University, Nanjing 210009, China.
China Pharmaceutical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The sustained cell proliferation resulting from dysregulation of the cell cycle and activation of cyclin-dependent kinases (CDKs) is a hallmark of cancer. The inhibition of CDKs is a highly promising and attractive strategy for the development of anticancer drugs. In particular, third-generation CDK inhibitors can selectively inhibit CDK4/6 and regulate the cell cycle by suppressing the G1 to S phase transition, exhibiting a perfect balance between anticancer efficacy and general toxicity. To date, three selective CDK4/6 inhibitors have received approval from the U.S. Food and Drug Administration (FDA), and 15 CDK4/6 inhibitors are in clinical trials for the treatment of cancers. In this perspective, we discuss the crucial roles of CDK4/6 in regulating the cell cycle and cancer cells, analyze the rationale for selectively inhibiting CDK4/6 for cancer treatment, review the latest advances in highly selective CDK4/6 inhibitors with different chemical scaffolds, explain the mechanisms associated with CDK4/6 inhibitor resistance and describe solutions to overcome this issue, and briefly introduce proteolysis targeting chimera (PROTAC), a new and revolutionary technique used to degrade CDK4/6.

Indexed as

AKT, protein kinase BAML, acute myeloid leukemiaCancerCDK4/6CDKs, cyclin-dependent kinasesCell cycleCIP/KIP, cyclin-dependent kinase inhibitor 1/kinase inhibitory proteinCKIs, cyclin-dependent kinase inhibitorsCPU, China Pharmaceutical UniversityCRPC, castration-resistant prostate cancerDrug resistanceER, estrogen receptorERK, extracellular regulated protein kinasesFDA, U.S. Food and Drug AdministrationFLT, fms-like tyrosine kinaseHER2, human epidermal growth factor receptor 2INK4, inhibitors of CDK4JAK, janus kinaseMCL, mantle cell lymphomaMM, multiple myelomaNSCLC, non-small cell lung cancerORR, overall response ratesPDK1, 3-phosphoinositide-dependent protein kinase 1PFS, progression-free survivalPI3K, phosphatidylinositol 3-hydroxy kinasePROTACPROTAC, proteolysis targeting chimeraPR, progesterone receptorRB, retinoblastoma proteinSelectivitySPH, Shanghai Pharmaceuticals Holding Co., Ltd.STATs, signal transducers and activators of transcriptionUNISA, University of South Australia

Identifiers

PMID33532179
PMCPMC7838032
OpenAlexW3027057217

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.