JKE-1674 is an inhibitor of glutathione peroxidase 4 (GPX4) and an active metabolite of the GPX4 inhibitor ML-210. JKE-1674 reduces viability of LOX-IMVI cancer cells and in a panel of additional cancer cell lines, an effect that can be blocked by the ferroptosis inhibitor ferrostatin-1. JKE-1674 forms a nitrile-oxide electrophile in cells. JKE-1674 dehydration yields a nitrile-oxide electrophile that binds GPX4. JKE-1674 exhibits far greater stability than chloroacetamide inhibitors.
|Body Surface Area (m2)||0.007||0.025||0.15||0.05||0.02||0.5|
|Animal A (mg/kg) = Animal B (mg/kg) multiplied by||Animal B Km|
|Animal A Km|
For example, to modify the dose of Compound A used for a mouse (20 mg/kg) to a dose based on the BSA for a rat, multiply 20 mg/kg by the Km factor for a mouse and then divide by the Km factor for a rat. This calculation results in a rat equivalent dose for Compound A of 10 mg/kg.
|Solubility||DMSO 90 mg/mL|
|Storage||2-8°C, protect from light, sealed|
|Related Ferroptosis Products|
|Ethylenediaminetetraacetic acid trisodium salt
Ethylenediaminetetraacetic acid trisodium salt (EDTA trisodium salt) is used to bind metal ions in the practice of chelation therapy, for treating mercury and lead poisoning, used in a similar manner to remove excess iron from the body, for treating the complication of repeated blood transfusions, as would be applied to treat thalassaemia.
DL-Buthionine-(S,R)-sulfoximine is a potent inhibitor of glutamylcysteine synthetase biosynthesis.
|Ammonium iron(III) citrate
Ammonium iron(III) citrate (Ammonium ferric citrate), a physiological form of nonetransferrin-bound iron, induces intracellular iron overload to cause ferroptosis. Ammonium iron(III) citrate can enhance protein production.
IFSP1 is an effective, selective and glutathione-independent inhibitor of ferroptosis Suppressor protein 1 (FSP1/AIFM2) with an EC50 value of 103 nM. IFSP1 can selectively induce iron death in Pfa1 cells and HT1080 cells with GPX4 knockout gene overexpressing FSP1.
SRS16-86 is a potent inhibitor of ferroptosis. SRS16-86 is more metabolically and plasma-stable in vivo than Ferrostatin-1. SRS16-86 can be used for renal ischemia-reperfusion injury (IRI) and spinal cord injury (SCI) studies.
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