Ubiquinone 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].

Signaling Pathways >> Immunology/Inflammation >> Interleukin Related

Signaling Pathways >> Protein Tyrosine Kinase/RTK >> EGFR

Signaling Pathways >> Autophagy >> Autophagy

Signaling Pathways >> Apoptosis >> Caspase

Signaling Pathways >> Cell Cycle/DNA Damage >> PARP

Signaling Pathways >> PI3K/Akt/mTOR >> mTOR

Signaling Pathways >> Apoptosis >> Bcl-2 Family

Signaling Pathways >> Apoptosis >> Apoptosis

Research Areas >> Cancer

Signaling Pathways >> JAK/STAT Signaling >> EGFR

Signaling Pathways >> Epigenetics >> PARP

Signaling Pathways >> Immunology/Inflammation >> NO Synthase

Signaling Pathways >> PI3K/Akt/mTOR >> Akt

Research Areas >> Inflammation/Immunology

Signaling Pathways >> Immunology/Inflammation >> COX

Signaling Pathways >> Metabolic Enzyme/Protease >> MMP

Research Areas >> Neurological Disease

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]. Cell Viability Assay[1] Cell Line: SKOV-3, A2780 and A2870/CP70 cells Concentration: 0, 10, 20, 30 and 40 µM Incubation Time: 24 hours Result: Decreased viability with the IC50 values of 26.6 µM, 27.3 µM and 28.4 µM for SKOV-3, A2780 and A2870/CP70 cells, respectively. Cell Cycle Analysis[1] Cell Line: SKOV-3, A2780 and A2870/CP70 cells Concentration: 0, 10, 20 and 30 µM Incubation Time: 24 hours Result: Arrested cell cycle at G2/M phase and reduced cell-cycle proteins in SKOV-3 cells. Apoptosis Analysis[1] Cell Line: SKOV-3, A2780 and A2870/CP70 cells Concentration: 0, 5, 15 and 30 µM Incubation Time: 24 hours Result: Promoted the conversion of LC3–1 to LC3-II and increased the LC3-II accumulation. Increased Bax/Bcl-2 ratio in a dose-dependent manner. Apoptosis Analysis[1] Cell Line: SKOV-3 cells Concentration: 0, 10, 20 and 30 µM Incubation Time: 24 hours Result: Had the percentage of early apoptotic cells are 25.1%, 34% and 36% for 10, 20 and 30 µM, respectively. Western Blot Analysis[1] Cell Line: SKOV-3 cells Concentration: 0, 5, 15 and 30 µM Incubation Time: 24 hours Result: Activated of caspase-3 and cleavaged of PARP. Increased the expressions of caspase-12, HSP-70 and Bax in a dose-dependent manner, decreased the expressions of Bcl-2. Western Blot Analysis[1] Cell Line: SKOV-3 cells Concentration: 30 µM Incubation Time: 24 hours Result: Decreased the phosphorylated HER-2 (Y1221) levels, p-AKT (Ser473) and p-mTOR (S2448) levels. Western Blot Analysis[2] Cell Line: RAW264.7 cells Concentration: 0, 2.5, 5 and 10 µM Incubation Time: 0.5-18 hours Result: Inhibited iNOS/COX-2 protein expressions with reductions of NO, PGE2, TNF-α and IL-1β secretions. Western Blot Analysis[3] Cell Line: EA.hy 926 cells Concentration: 5 µM Incubation Time: 0, 1, 3, 6 and 12 hours Result: Increased expressions of heme oxygenase-1 (HO-1) and γ-glutamylcysteine synthetase (γ-GCLC), inhibits protein expressions of matrix metalloproteinase-9 (MMP-9), reduces TNF-α-induced nuclear translocation and transcriptional activation of nuclear factor-κB (NF-κB).

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]. Animal Model: SKOV-3 xenografted nude mice[1] Dosage: 1.5 and 2.5 mg/kg Administration: Intraperitoneal injection; Once every four days, for 52 days Result: Inhibited the tumor growth at 1.5 and 2.5 mg/kg. Animal Model: LPS-treated female FVB mice[2] Dosage: 5 mg/kg Administration: Oral administration; for 4 hours Result: Down-regulates inflammatory genes in liver and spleen tissues of LPS injected mice.

[1]. Yang HL, et, al. Coenzyme Q0 regulates NFκB/AP-1 activation and enhances Nrf2 stabilization in attenuation of LPS-induced inflammation and redox imbalance: Evidence from in vitro and in vivo studies. Biochim Biophys Acta. 2016 Feb;1859(2):246-61.

[2]. Yang HL, et, al. Coenzyme Q0 regulates NFκB/AP-1 activation and enhances Nrf2 stabilization in attenuation of LPS-induced inflammation and redox imbalance: Evidence from in vitro and in vivo studies. Biochim Biophys Acta. 2016 Feb;1859(2):246-61.

[3]. Yang HL, et, al. Anti-angiogenic properties of coenzyme Q0 through downregulation of MMP-9/NF-κB and upregulation of HO-1 signaling in TNF-α-activated human endothelial cells. Biochem Pharmacol. 2015 Nov 1;98(1):144-56.