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MedChemExpress - Model Coenzyme Q0 - ...

MedChemExpress - Model Coenzyme Q0 - 605-94-7

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].

Coenzyme Q0

MCE China：Coenzyme Q0

Brand：MedChemExpress (MCE)

Cat. No.HY-W016412

CAS：605-94-7

Synonyms：CoQ0

Purity：99.88%

Storage：Powder -20°C 3 years 4°C 2 years In solvent -80°C 6 months -20°C 1 month

Shipping：Room temperature in continental US; may vary elsewhere.

Description：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.

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].

References：

[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. [Content Brief]

[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. [Content Brief]

[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. [Content Brief]

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