NQO2 Inhibitors

Benzo[a]pyrene is a polycyclic aromatic hydrocarbon found in tobacco smoke and other combustion products. It induces oxidative stress and activates the aryl hydrocarbon receptor (AhR) pathway, potentially influencing NQO2 through AhR-mediated signaling, as NQO2 has been reported to be regulated by the AhR pathway.

Dicoumarol is a coumarin derivative that inhibits NQO2 by competing with its natural substrate, menadione. Dicoumarol disrupts the electron transfer process in the NQO2 enzymatic reaction, directly inhibiting the enzyme's activity and leading to modulation of cellular redox processes associated with NQO2 function.

Ellagic Acid is a polyphenolic compound with antioxidant properties. It inhibits NQO2 by binding to its active site, interfering with the enzyme's catalytic activity. This direct inhibition impacts cellular redox homeostasis, as NQO2 is a key player in the regulation of intracellular redox balance and cellular responses to oxidative stress.

Streptonigrin is an antibiotic that induces DNA damage and activates the ataxia-telangiectasia mutated (ATM) pathway. Its action on the ATM pathway can indirectly influence NQO2, as NQO2 has been reported to be involved in cellular responses to DNA damage. The modulation of ATM signaling by Streptonigrin can impact NQO2 function and cellular redox regulation.

β-Lapachone is a natural quinone that undergoes futile redox cycling with NQO2, leading to the formation of reactive oxygen species. This direct interaction with NQO2 disrupts cellular redox processes, as β-Lapachone-induced oxidative stress modulates NQO2 function. The compound's redox cycling with NQO2 contributes to its inhibitory effects on the enzyme.

Trifluoperazine is an antipsychotic drug that inhibits NQO2 by binding to its active site. This direct inhibition disrupts the enzymatic activity of NQO2, leading to alterations in cellular redox homeostasis. Trifluoperazine's impact on NQO2 function may be associated with its broader effects on cellular processes related to oxidative stress and redox regulation.

Mitomycin C is an antitumor antibiotic that induces DNA crosslinking and activates the ATM pathway. Its action on ATM signaling can indirectly influence NQO2, as NQO2 has been linked to cellular responses to DNA damage. The modulation of ATM signaling by Mitomycin C can impact NQO2 function and cellular redox regulation.

Acetaminophen, a widely used analgesic and antipyretic, undergoes redox cycling and generates reactive oxygen species. Its interaction with cellular redox processes can indirectly influence NQO2, as NQO2 plays a role in cellular responses to oxidative stress. Acetaminophen-induced oxidative stress can impact NQO2 function and its role in maintaining redox balance.

Lapatinib is a dual tyrosine kinase inhibitor targeting epidermal growth factor receptor (EGFR) and human epidermal growth factor receptor 2 (HER2). Its impact on EGFR signaling can potentially influence NQO2, as EGFR has been linked to redox regulation. Lapatinib's modulation of EGFR signaling may indirectly affect NQO2 function and cellular redox processes.

Juglone is a natural naphthoquinone that undergoes redox cycling with NQO2, leading to the generation of reactive oxygen species. This direct interaction with NQO2 disrupts cellular redox processes, impacting NQO2 function. Juglone's redox cycling with NQO2 contributes to its inhibitory effects on the enzyme and its role in cellular redox regulation.