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Ferroptosis Research Reagents ― for iron-dependent programmed cell death ―

(Modified from Reference 1)


Ferroptosis is a recently recognized form of regulated cell death characterized by the accumulation of lipid peroxidation products and lethal reactive oxygen species (ROS) derived from iron metabolism. Activation of mitochondrial voltage-dependent anion channels and mitogen-activated protein kinases, upregulation of endoplasmic reticulum stress, and inhibition of cystine/glutamate antiporter is involved in the induction of ferroptosis.
Morphologically, it is characterized by the presence of smaller than normal mitochondria with condensed mitochondrial membrane densities, reduction or vanishing of mitochondria crista, and outer mitochondrial membrane rupture.

Ferroptosis Inhibitors

H0726
Trolox
Inhibitor of ferroptosis; antioxidant
T2721
Baicalein
Inhibitor of ferroptosis; 5- and 1-lipoxygenase inhibitor
C1971
Coenzyme Q10 (= CoQ10)
Inhibitor of ferroptosis; antioxidant
E0946
Ebselen
Inhibitor of ferroptosis; Inhibits lipoxygenase, cyclooxygenase nitric oxide synthase, protein kinase C and H+/K+-ATPase activity. Inhibits the hepatic carcinogenic effects of aflatoxin B1.
I0848
Idebenone
Inhibitor of ferroptosis; blocks glutamate neurotoxicity in vitro and in vivo
F1302
Ferrostatin-1
Inhibitor of ferroptosis

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Ferroptosis Activators

G0059
L-Glutamic Acid
Induces ferroptosis; endogenous, non-selective agonist
S0509
Simvasatin
Induces ferroptosis; HMG-CoA reductase inhibitor
S0580
Sulfasalazine
Induces ferroptosis; cystine-glutamate antiporter inhibitor and inhibitor of NF-κB activation

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Reference

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