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One hypothesis is that we observed a greater induction of NRF2 through liver-specific Gclc deletion as compared to KEAP1 inhibition with CDDO-me because CDDO-me is a weaker inhibitor of NRF2-KEAP1 interaction compared to the ROS generated following GSH depletion

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Biased Signaling : CT-868 has been designed as a biased agonist, which favors the activation of the cAMP pathway while not recruiting -arrestin to the receptors