Artemisinin-Based Therapeutics in Cancer Treatment

Artemisinin and its semi-synthetic derivatives, notably artesunate and dihydroartemisinin, have emerged from antimalarial agents to promising anticancer compounds. Their characteristic endoperoxide bridge reacts with intracellular iron to yield reactive oxygen species, triggering a cascade of molecular events including lipid peroxidation, DNA damage and organelle dysfunction. These effects converge on regulated cell death pathways such as apoptosis, ferroptosis and necroptosis, selectively targeting cancer cells with elevated iron metabolism. Preclinical studies have revealed inhibition of signalling pathways involved in proliferation, angiogenesis and metastasis, while also overcoming multidrug resistance by modulating efflux pumps and DNA repair mechanisms. Advances in nanoparticle formulations and targeted delivery systems are enhancing bioavailability and tumour specificity, and early clinical case reports suggest that artemisinin derivatives can augment standard chemotherapy regimens with manageable toxicity profiles. This body of work underscores the global significance of artemisinin-based therapeutics as cost-effective adjuncts or alternatives in oncology, with active exploration across solid tumours, haematological malignancies and cancer stem cell populations.

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Artemisinin-Based Therapeutics in Cancer Treatment publication trend

The graph below shows the total number of articles in artemisinin-based therapeutics in cancer treatment across all publications each year (not limited to Nature Index journals).

Technical terms

Endoperoxide bridge: A cyclic peroxide moiety within artemisinin that reacts with ferrous iron to generate cytotoxic radicals.

Reactive oxygen species: Chemically reactive molecules containing oxygen that can inflict damage on DNA, proteins and lipids.

Apoptosis: Programmed cell death characterised by membrane blebbing, chromatin condensation and caspase activation.

Ferroptosis: Iron-dependent regulated cell death driven by lipid peroxidation and glutathione depletion.

Necroptosis: A form of programmed necrosis mediated by receptor-interacting protein kinases, leading to cell swelling and membrane rupture.

DNA double-strand break: A critical lesion involving simultaneous breaks in both strands of the DNA helix, often triggering repair pathways or cell death if unrepaired.

References

1. Artesunate in glioblastoma therapy: Case reports and review of clinical studies. Phytomedicine (2023).
2. Medicinal and mechanistic overview of artemisinin in the treatment of human diseases. Biomedicine & Pharmacotherapy (2023).
3. Naturally occurring anti-cancer compounds: shining from Chinese herbal medicine. Chinese Medicine (2019).