JKE-1674 is an orally active glutathione peroxidase 4 ( GPX4 ) inhibitor and an active metabolite of GPX4 inhibitor ML-210. JKE-1674, an analog of ML-210 in which the nitroisoxazole ring is replaced with an α-nitroketoxime. JKE-1674 can convert into a nitrile oxide JKE-1777. JKE-1674 kills LOX-IMVI cells in a manner that is equipotent to ML-210 and is completely rescued by ferroptosis inhibitors In Vitro JKE-1674 exhibits activity indistinguishable from that of ML210 in cellular target engagement assays including yielding the same +434Da GPX4 adduct in cells. JKE-1674 kills LOX-IMVI cells in a manner that is equipotent to ML210 and is completely rescued by ferroptosis inhibitors. 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. MCE has not independently confirmed the accuracy of these methods. They are for reference only. In Vivo JKE-1674 (50 mg/kg; p.o.) can be detected in the serum of mice dosed orally with the compound . MCE has not independently confirmed the accuracy of these methods. They are for reference only. Animal Model: SCID mice Dosage: 50 mg/kg (Pharmacokinetic Analysis) Administration: P.o. Result: Could be detected in the serum of mice dosed orally with the compound. Form:Solid IC50& Target:GPX4