Table 2.

Old drugs used for proferroptotic anticancer therapy.

Old drugs	Target/function for ferroptosis
Acetaminophen	The combination of erastin and APAP can promote ferroptosis by NRF2 inhibition [89].
Artemisinin	Artemisinin compounds sensitize tumor cells to ferroptosis via impeding IRP/IRE-controlled iron homeostasis [91].
Auranofin	High dose of auranofin could induce lipid peroxidation and ferroptosis through TXNRD inhibition [45].
Cisplatin	Cisplatin promotes ferroptosis via GSH depletion and GPX4 inactivation [98].
Fenugreek	Fenugreek acts as an NRF2 inhibitor and sensitizes tumor cell to ferroptosis [99].
Haloperidol	Haloperidol treatment significantly increased the levels of intracellular free iron, facilitating GSH depletion and lipid peroxidation [101].
Neratinib	Neratinib promotes ferroptosis and inhibited brain metastasis in HER-2-positive breast cancer, but the underlying mechanism is still obscure [103].
Siramesine combined with lapatinib	The combination of siramesine and lapatinib synergistically induced ROS accumulation and ferroptosis, and this synergistic effect is mediated by lysosomes release iron and proteasomes degrade HO-1 [107, 108].
Sorafenib	Sorafenib induces ferroptosis via system Xc− inhibition and following GSH depletion [100].
Sulfasalazine	Sulfasalazine acts as a strong system Xc− inhibitor and induces ferroptosis by inhibiting GSH biosynthesis [1, 113].