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|
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.
UAMC-3203 is an improved ferroptosis inhibitor, with an IC50 value of 10 nM in IMR-32 neuroblastoma cells.
ML162 is a covalent glutathione peroxidase 4 (GPX4) inhibitor that induces iron death and has shown cytotoxic effects against melanoma, lung adenocarcinoma, fibrosarcoma, and pancreatic cancer cell lines.
UAMC-3203 hydrochloride is a potent and selective Ferroptosis inhibitor, with an IC50 of 12 nM.
Products are for research use only. Not for human use. We do not sell to patients.
© Copyright 2010-2020 AbMole BioScience. All Rights Reserved.