Tumor-targeting delivery of drugs has received much attention in the field of drug development. Traditional antitumor agents are often nonspecific for tumor cells; therefore, tumor-targeting drug-delivery design is a promising approach to improve the therapeutic efficacy of chemotherapy. Polyunsaturated fatty acids (PUFAs), such as linoleic acid, α-linolenic acid, arachidonic acid and docosahexaenoic acid, are naturally occurring essential substances which play important roles in cell growth. Due to their lipophilic nature, PUFAs are readily incorporated into the lipid bilayer of cells, especially tumor cells. Therefore, PUFAs can be used as an applicable carrier to increase the therapeutic efficacy of anticancer drugs. In this review, several PUFA–drug conjugates with potent antitumor activities are summarized, and the bright prospects of PUFAs in drug development are also proposed. A general design strategy of PUFA–drug conjugates is provided, as well as a discussion of the recent progress in PUFA–drug ...

Cell division in eukaryotes is a highly regulated process that is critical to the life of a cell. Dysregulated cell proliferation, often driven by anomalies in cell Cyclin-dependent kinase (CDK) activation, is a key pathological mechanism in cancer. Recently, selective CDK4/6 inhibitors have shown clinical success, particularly in treating advanced-stage estrogen receptor (ER)-positive and human epidermal growth factor receptor 2 (HER2)-negative breast cancer. This review provides an in-depth analysis of the action mechanism and recent advancements in CDK4/6 inhibitors, categorizing them based on their structural characteristics and origins. Furthermore, it explores proteolysis targeting chimers (PROTACs) targeting CDK4/6. We hope that this review could be of benefit for further research on CDK4/6 inhibitors and PROTACs.

A series of novel quinoxaline derivatives were synthesized and evaluated for their antiproliferative activity in three human cancer cell lines. Compound 12 exhibited the most potent antiproliferative activity with IC₅₀ in the range of 0.19–0.51 μM. The compound inhibited tubulin polymerization and disrupted the microtubule network, leading to G2/M phase arrest. Furthermore, compound 12 induced ROS production and malfunction of mitochondrial membrane potential. Compound 12 led to cancer cells apoptosis in a dose‐dependent manner. Western blot analysis showed that compound 12 induced up‐regulation of p21 and affected the expression of cell cycle‐related proteins. The binding mode was also probed by molecular docking.