Table 2.
Summary of currently used ferroptosis-inducing agents across cancer types.
| Agent name | Mechanism of action | Applicable tumor types | References |
|---|---|---|---|
| Erastin | Inhibits System Xc- (SLC7A11/SLC3A2 complex), blocking cystine uptake → GSH depletion → GPX4 inactivation | Non-small cell lung cancer (NSCLC, cisplatin-resistant), triple-negative breast cancer (TNBC, paclitaxel-resistant) | (152, 153) |
| RSL3 | Covalently binds to the selenocysteine residue of GPX4 → irreversible inhibition of GPX4 activity | Hepatocellular carcinoma (HCC, TKI-resistant), pancreatic ductal adenocarcinoma (PDAC, drug-resistant) | (154–156) |
| Sulfasalazine | Competitively inhibits System Xc-, reducing cystine import → impaired GSH synthesis | Colorectal cancer (CRC, doxorubicin-resistant), NSCLC (immune checkpoint inhibitor-resistant) | (157, 158) |
| Dihydroartemisinin (DAT) | Triggers lysosomal ferritin degradation (non-autophagic pathway) → expands labile iron pool (LIP) → enhances Fenton reaction | Ovarian cancer (carboplatin-resistant), CRC (5-FU-resistant) | (159, 160) |
| Sorafenib | Indirectly upregulates ACSL4 → increases PUFA-PL accumulation; inhibits VEGFR signaling | Renal cell carcinoma (RCC, TKI-resistant), HCC (sorafenib-naive/resistant) | (54, 161) |
| ML210 | Directly binds to GPX4’s active site → suppresses lipid peroxide clearance | Melanoma (BRAF inhibitor-resistant), TNBC (platinum-resistant) | (162, 163) |