Coenzyme Q0

Coenzyme Q0 (CoQ0) is a potent, oral active ubiquinone compound can be derived from Antrodia cinnamomea. Coenzyme Q0 induces apoptosis and autophagy, suppresses of HER-2/AKT/mTOR signaling to potentiate the apoptosis and autophagy mechanisms. Coenzyme Q0 regulates NFκB/AP-1 activation and enhances Nrf2 stabilization in attenuation of inflammation and redox imbalance. Coenzyme Q0 has anti-angiogenic activity through downregulation of MMP-9/NF-κB and upregulation of HO-1 signaling^[1][2][3]. In Vitro:Coenzyme Q0 (0-40 µM; 24 h) and inhibits viability and growth of human ovarian carcinoma cells^[1].
Coenzyme Q0 (CoQ0) (0-30 µM; 24 h; SKOV-3 cells) has anti-proliferative activity through induction of G2/M cell-cycle arrest and reduction of cell-cycle regulatory proteins^[1].
Coenzyme Q0 (CoQ0) (0-30 µM; 0-30 min; SKOV-3 cells) increases intracellular ROS levels to promote SKOV-3 cell death^[1].
Coenzyme Q0 (CoQ0) (0-30 µM; 24 h; SKOV-3 cells) induces autophagy by increase accumulation of LC3-II, GFP-LC3 puncta, AVOs formation and Beclin-1/Bcl-2 dysregulation^[1].
Coenzyme Q0 (CoQ0) (0-30 µM; 24 h; SKOV-3 cells) induces apoptosis by mitochondrial (caspase-3, PARP and Bax/Bcl-2 dysregulation) and ER stress (caspase-12 and Hsp70) signals^[1].
Coenzyme Q0 (CoQ0) (30 µM; 24 h; SKOV-3 cells) suppresses of HER-2/AKT/mTOR signaling to potentiate the apoptosis and autophagy mechanisms^[1].
Coenzyme Q0 (CoQ0) (0-10 µM; 0.5-18 h; RAW264.7 cells) regulates NFκB/AP-1 activation and enhances Nrf2 stabilization^[2].
Coenzyme Q0 (CoQ0) (5 µM; 0-12 h; EA.hy 926 cells) has anti-angiogenic activity in EA.hy 926 cells^[3]. In Vivo:Coenzyme Q0 (CoQ0) (1.5 and 2.5 mg/kg; i.p.; once every four days, for 52 d) suppresses tumor growth in SKOV-3 xenografted nude mice^[1].
Coenzyme Q0(CoQ0) (5 mg/kg; p.o.; for 4 h) has anti-inflammatory activities through Nrf2 activation and NFκB inhibition in liver and spleen of LPS-treated mice^[2].