IC50: 23 µM (T. gondii enzyme peroxiredoxin II (TgPrxII))[1]
In Vivo
Conoidin A (intraperitoneal injection; 5 mg/kg; for three successive days before MI/R injury) blocks the effect of Luteolin (HY-N0162) on the ST‐segment elevation. Furthermore, an increase in the infarct size presented of the MI/R group can be reduced by Luteolin. But pre‐treatment with conoidin A abolishs the effect of Luteolin. Pre‐treatment with conoidin A also prevents Luteolin-reduced activities of CK‐MB, AST and LDH in vivo[3]. Animal Model: Rat myocardial I/R model[3] Dosage: 5 mg/kg Administration: Intraperitoneal injection; 5 mg/kg; for three successive days before MI/R injury Result: Significantly reversed the antioxidative effect of Luteolin. Impaired the protective effects of luteolin.
In Vitro
Peroxiredoxins are a widely conserved family of enzymes that function in antioxidant defense and signal transduction. And the changes in PrxII expression are associated with a variety of human diseases, including cancer[1]. Conoidin A binds to the peroxidatic cysteine of TgPrxII, inhibiting its enzymatic activity in vitro. Conoidin A also shown to alkylate or crosslink catalytic cysteines of wild type AcePrx-1 in Ancylostoma ceylanicum and human PrxII and PrxIV with similar efficiency. But it is ineffective to mitochondrial hPrxIII[2]. Conoidin A (5 µM) can inhibit the glucose oxidase-mediated hyperoxidation of mammalian peroxiredoxin I and II[2].
Kinase Assay
Cell Assay
Animal Administration
References
[1]. Jeralyn D Haraldsen, et al. IDENTIFICATION OF CONOIDIN A AS A COVALENT INHIBITOR OF PEROXIREDOXIN II. Org Biomol Chem. 2009;7:3040-3048.
[2]. Gu Liu, et al. Optimisation of conoidin A, a peroxiredoxin inhibitor. ChemMedChem. 2010 Jan;5(1):41-5.
[3]. Bo Wei, et al. Luteolin ameliorates rat myocardial ischaemia-reperfusion injury through activation of peroxiredoxin II. Br J Pharmacol
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