Artemisinin derivatives anticancer properties are remarkable and dynamic., They target cancer like a magnet.

How? Cancer cells uptake iron at a ferocious rate to maintain out of control cell division. Artemisinin binds selectively to cancer cells because of this. Upon binding, the molecule releases its payload – a type of peroxide that is toxic to cancer cells. This is its basic mode of anti-carcinogenic action, the cleavage of its endoperoxide bridge by free iron to release free radicals that induce toxicity to cancer. This process was revealed in its remarkable and safe antimalarial function. The method of action by which products like Artemene kill cancer is called FERROPTOSIS.

Malaria, like cancer has always been difficult to control without causing massive collateral damage. There are very few molecules like artemisinin, it is incredibly difficult to manufacture – almost a 100 million dollars have been spent trying. The plant sources remain the most viable. 

Artemisinin and compounds made with it, like Artemene have been shown to have vigorus anticancer properties against carcinoma of the gastric, colon, cervix and breast.

Human prostate cancer cells undergoing ferroptosis; captured with Nanolive cell imaging in the Lab of Priv.-Doz. Dr. med. Vivek Venkataramani, Institute for Pathology, University Hospital Göttingen, Germany

Ferroptosis in cancer treatment

Preliminary reports suggest that oxytosis/ferroptosis may be a means through which tumor cells can be killed. Oxytosis/ferroptosis has been implicated in several types of cancer, including:

These forms of cancer have been hypothesized to be highly sensitive to oxytosis/ferroptosis induction. An upregulation of iron levels has also been seen to induce oxytosis/ferroptosis in certain types of cancer, such as breast cancer (link to

The Role of Ferroptosis in Cancer Development and Treatment Response

Breast cancer cells have exhibited vulnerability to oxytosis/ferroptosis via a combination of siramesine and lapatinib. These cells also exhibited an autophagic cycle independent of ferroptotic activity, indicating that the two different forms of cell death could be controlled to activate at specific times following treatment.[2]