Ferroptosis is a non-apoptotic form of regulated cell death. It is distinct from other regulated cell death phenotypes, such as apoptosis and necroptosis. Ferroptosis is characterized by extensive lipid peroxidation, which can be suppressed by iron chelators or lipophilic antioxidants. Mechanistically, Ferroptosis inducers are divided into two classes: (1) inhibitors of cystine import via system xc− (e.g., Erastin), which subsequently causes depletion of glutathione (GSH), and (2) covalent inhibitors (e.g., (1S, 3R)-RSL3) of glutathione peroxidase 4 (GPX4). Since GPX4 reduces lipid hydroperoxides using GSH as a co-substrate, both compound classes ultimately result in loss of GPX4 activity, followed by elevated levels of lipid reactive oxygen species (ROS) and consequent cell death.
Ferroptosis is an iron- and ROS-dependent form of regulated cell death (RCD). Misregulated Ferroptosis has been implicated in multiple physiological and pathological processes, including cancer cell death, neurotoxicity, neurodegenerative diseases, acute renal failure, drug-induced hepatotoxicity, hepatic and heart ischemia/reperfusion injury, and T-cell immunity.
|Cat. No.||Product Name||CAS No.||Information|
Erastin is a ferroptosis inducer. Erastin binds and inhibits voltage-dependent anion channels (VDAC2/VDAC3)
Liproxstatin-1 is a specific small molecule ferroptosis inhibitor (IC50=22 nM) via inactivation of the ferroptosis regulator Gpx4 (glutathione peroxidase 4), shows no activity on necroptosis; prevents BODIPY 581/591 C11 oxidation in Gpx4−/− cells, does not interfere with other classical types of cell death, such as TNFα-induced apoptosis and H2O2-induced necrosis; suppresses ferroptosis in Gpx4(-/-) mice, and in a pre-clinical model of ischaemia/reperfusion-induced hepatic damage.
A potent and specific Ferroptosis inducer that promotes the degradation of the lipid-repair enzyme GPX4; also binds to and activates squalene synthase, an enzyme involved in the cholesterol synthesis, to suppress non-steroidogenic metabolites-most likely coenzyme Q10; the mechanism involves two distinct pathways: one pathway is degradation of GPX4, which requires the enzymatic activity of ACC; the other pathway is activation of SQS, which leads to coenzyme Q10 depletion.
Piperazine Erastin is an analog of Erastin, which can induces ferroptosis in cancer cells, an iron-dependent form of nonapoptotic cell death.
UAMC-3203 is a novel potent, drug-like ferroptosis inhibitor with IC50 of 12 nM, inhibit erastin-induced ferroptotic cell death more potently than Ferrostatin-1; shows an improved protection compared to Fer-1 against multi-organ injury in mice, represents novel lead compounds with therapeutic potential in relevant ferroptosis-driven disease models.
SRS11-92 (SRS 11-92) is a small molecule inhibitor of Ferroptosis and a derivative of Ferrostatin-1 (Fer-1), inhibits ferroptotic cell death induced by erastin in HT-1080 human fibrosarcoma cells with EC50 of 6 nM; inhibits iron-induced cell death in isolated mouse kidney proximal tubules at 2 uM, and fully protects rat oligodendrocytes from cystine deprivation-induced cell death in an in vitro model of periventricular leukomalacia when used at a concentration of 100 nM; also increases survival of medium spiny neurons in rat corticostriatal brain slices in an in vitro model of Huntington’s disease in a concentration-dependent manner.
Imidazole ketone erastin
Imidazole ketone erastin (IKE, Ferroptosis inducer IKE) is a potent, metabolically stable inhibitor of system xc- and inducer of ferroptosis potentially suitable for in vivo applications; potently reduces DLBCL cell number with IC50 of <100 nM (SUDHL6 cell IC50=1 nM); exerts antitumor effect by inhibiting system xc-, leading to glutathione depletion (GSH depletion IC50=34 nM, SUDHL6 cells), lipid peroxidation, and the induction of ferroptosis biomarkers both in vitro and in vivo, induced lipid peroxidation in tumor tissue.
YAP1 inhibitor CA3 (CA3;CIL56) is a small molecule that has remarkable inhibitory activity on YAP1/Tead transcriptional activity; also demonstrates strong inhibitory effects on esophageal adenocarcinoma cell growth especially on YAP1 high-expressing esophageal adenocarcinoma cells both in vitro and in vivo; can effectively suppress radiation-resistant cancer stem cell (CSC) properties and aggressive phenotype by inhibiting proliferation, inducing apoptosis, reducing tumor sphere formation; synergistically inhibits cancer cell growth combined with 5-FU; triggers nonapoptotic cell death, a potent and selective probe of ferroptosis; stimulates the activity of ACC1, inhibits the normal breakdown of fatty acids by mitochondrial β-oxidation.
Ferrostatin-1 is a potent ferroptosis inhibitor with IC50 of 33 nM, inhibits erastin-induced ferroptosis in HT-1080 cells with EC50 of 60 nM; prevents erastin-induced accumulation of cytosolic and lipid ROS, does not inhibit ERK phosphorylation or arrest the proliferation of HT-1080 cells.
RSL-3 is an oncogenic RAS-selective lethal compound that actvates iron-dependent, nonapoptotic cell death in oncogenic-RAS-harboring cancer cells, inhibits glutathione peroxidase (GPX4) and induces ferroptosis in BJeLR cells (EC50=10 nM); increases PTGS2 expression and significantly inhibits tumor growth in a xenograft mouse model (100 mg/kg).
No.1378 West Wenyi Road, Yuhang District, HangZhou, Zhejiang, China