Conoidin A

Conoidin A is a cell permeable inhibitor of?T. gondii enzyme peroxiredoxin II (TgPrxII) with nematicidal properties. Conoidin A covalently binds to the peroxidatic Cys47 of TgPrxII, irreversibly inhibiting its hyperperoxidation activity with an IC₅₀ of 23 μM. Conoidin A also inhibits hyperoxidation of mammalian PrxI and PrxII (but not PrxIII)^[1][2]. Conoidin A has antioxidant, neuroprotective effects and can be used for the research of ischaemic heart disease^[3]. IC50 & Target:IC50: 23 μM (T. gondii enzyme peroxiredoxin II (TgPrxII))^[1] 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]. 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].