ArticleCancer medicine2026
Artesunate Induces G0/G1 Phase Arrest in Tumor Cells and Associates With Cyclin-Dependent Kinase 4 (CDK4).
Article in Cancer medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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6 authors.
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Abstract
backgroundNon-small cell lung cancer (NSCLC) is the leading cause of cancer-related death worldwide. Cyclin-dependent kinase 4 (CDK4) is a well-validated oncogenic driver in NSCLC, yet current CDK4 inhibitors-predominantly based on the aminopyrimidine scaffold-are limited by structural homogeneity and the rapid emergence of acquired resistance, underscoring the need for novel chemotypes.
methodsWe employed a HuProt human proteome microarray to screen for direct cellular targets of artesunate, an FDA-approved artemisinin derivative. Candidate interactions were validated by molecular docking, surface plasmon resonance (SPR), and in vitro kinase assays. Functional effects were assessed in A549 and H1299 NSCLC cell lines using flow cytometry and Western blotting.
resultsArtesunate was identified as a direct binder of CDK4, with molecular docking revealing a strong binding affinity (-7.069 kcal/mol). SPR analysis confirmed this interaction with a K
conclusionOur findings establish artesunate as a structurally distinct, non-aminopyrimidine CDK4 inhibitor with potent biochemical and cellular activity in NSCLC models. This work provides a promising therapeutic strategy to circumvent resistance associated with current CDK4 inhibitors and supports the repurposing of artesunate for CDK4-driven cancers.
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