Pharmacological Effects of Chrysin in Cancer Therapeutics

Chrysin, a naturally occurring flavonoid characterised by two hydroxyl groups on its flavone backbone, has emerged as a multifaceted agent in oncology research. Its principal anticancer actions include induction of apoptosis via both intrinsic and extrinsic pathways, inhibition of cell proliferation through cell-cycle arrest, and suppression of key survival signalling cascades such as PI3K/Akt, STAT3 and NF-κB. Chrysin exerts anti-angiogenic effects by downregulating vascular endothelial growth factor (VEGF) production and interfering with endothelial cell function. In the tumour microenvironment, it modulates immune cell activity, notably by attenuating pro-tumoural macrophage-driven autophagy and inflammatory cytokine release. Preclinical studies highlight its capacity to induce DNA damage responses, generate reactive oxygen species and stabilise G-quadruplex DNA structures, contributing to replication stress in malignant cells. Despite potent in vitro and in vivo efficacy, clinical translation has been hampered by poor water solubility, rapid metabolism and low systemic exposure. To address these limitations, structural derivatisation and nano-delivery platforms have been investigated, demonstrating improved bioavailability, targeted tumour accumulation and synergistic potential when combined with established chemotherapeutics. Collectively, the pharmacological profile of chrysin spans direct cytotoxicity, microenvironmental reprogramming and enhancement of chemosensitivity, positioning it as a promising adjunct in cancer therapeutics.

Research from Nature Portfolio

No recent Nature Portfolio content available.

Pharmacological Effects of Chrysin in Cancer Therapeutics publication trend

The graph below shows the total number of articles in pharmacological effects of chrysin in cancer therapeutics across all publications each year (not limited to Nature Index journals).

Technical terms

Flavonoid: A class of polyphenolic plant compounds with diverse biological activities, including antioxidant and anticancer effects.

Angiogenesis: The process by which new blood vessels form from pre-existing vasculature, critical for tumour growth and metastasis.

Autophagy: A cellular self-degradation mechanism that recycles organelles and proteins; can promote cancer cell survival under stress.

Tumour-associated macrophages (TAMs): Immune cells within the tumour microenvironment that often acquire a pro-tumoural phenotype, supporting growth and metastasis.

DNA damage response: A network of cellular pathways that detect and repair DNA lesions, whose overactivation can trigger cell death in cancer cells.

Bioavailability: The proportion of an administered substance that reaches systemic circulation in an active form, crucial for therapeutic efficacy.

References

1. Chrysin-Induced Regression of Angiogenesis via an Induction of DNA Damage Response and Oxidative Stress in In Vitro and In Vivo Models of Melanoma. Cells (2023).
2. Chrysin Inhibits TAMs-Mediated Autophagy Activation via CDK1/ULK1 Pathway and Reverses TAMs-Mediated Growth-Promoting Effects in Non-Small Cell Lung Cancer. Pharmaceuticals (2024).
3. Anticancer Activity of Ether Derivatives of Chrysin. Molecules (2025).
4. Broad-Spectrum Preclinical Antitumor Activity of Chrysin: Current Trends and Future Perspectives. Biomolecules (2020).