Results for Activators & Inhibitors ( 70851 )
MitoP (Legacy Tebubio ref. 282T37658). MitoP is a phenol product produced by the reaction of H2O2 with the ratiometric mass spectrometry probe MitoB . MitoB contains a triphenylphosphonium cation component that drives its accumulation in mitochondria where its arylboronic moiety selectively reacts with H2O2 to produce MitoP. Quantifying the MitoP/MitoB ratio by LC-MS/MS reflects the mitochondrial matrix H2O2 concentration.
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5-hydroxy Omeprazole (Legacy Tebubio ref. 282T37659). 5-hydroxy Omeprazole is a major metabolite of omeprazole , an inhibitor of the gastric H+/K+-ATPase pump.[1] 5-hydroxy Omeprazole is produced from omeprazole by the action of cytochrome P450 (CYP) isoform 2C19, a monooxygenase. [2][3] CYP2C19 polymorphisms significantly influence the metabolism of omeprazole, and individuals may be classified as homozygous extensive metabolizers, heterozygous extensive metabolizers, and poor metabolizers.[1]
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LY 2886721 Hydrochloride (Legacy Tebubio ref. 282T37661). Potent and selective β-secretase (BACE) inhibitor (IC50 values are 10.2 and 20.3 nM for human BACE2 and BACE1, respectively). Displays >5,000-fold selectivity for BACE over other proteases including cathepsin D, pepsin and renin. Inhibits Aβ1-40 and Aβ1-42 production in cells expressing mutated APP. Reduces hippocampal and cortical Aβ and sAPPβ levels in an Alzheimer's disease mouse model.
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Endosulfan I (Legacy Tebubio ref. 282T37665). Endosulfan I is an organochlorine insecticide and a stereoisomer of endosulfan II . It is active against a variety of insects, including bollworms (LD50 = 0.63 mg/g). Endosulfan I binds to GABA receptors in rat brain membranes with an IC50 value of 30 nM and is toxic to rats (LD50 = 18 mg/kg).
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Trihydroxycholestanoic Acid (Legacy Tebubio ref. 282T37666). Trihydroxycholestanoic acid is an intermediate in the biosynthesis of cholic acid .1 Elevated plasma levels of trihydroxycholestanoic acid have been found in patients with Zellweger syndrome, a neurological disorder characterized by mutations in PEX genes which result in defects in peroxisome formation.2,3