Coenzyme Q0 targets the mitochondrial electron transport chain and participates in redox reactions as a quinone. As a precursor to coenzyme Q10, it is involved in the biosynthesis of this essential mitochondrial electron carrier. CoQ0 can accept and donate electrons, functioning as a mobile electron carrier in the mitochondrial respiratory chain. The compound also targets cellular redox pathways and can modulate oxidative stress levels. At low concentrations, CoQ0 acts as an antioxidant, scavenging free radicals and protecting cells from oxidative damage. At higher concentrations, it can undergo redox cycling and generate reactive oxygen species (ROS), which may contribute to its anticancer effects. CoQ0 has been shown to modulate various signaling pathways involved in inflammation, apoptosis, and cell proliferation. The compound's redox properties make it a valuable tool for studying oxidative stress and mitochondrial function in research settings.

Coenzyme Q0 (0–40 μM; 24 h) prevents the growth and viability of human ovaries [1]. Coenzyme Q0 (CoQ0) (0-30 μM; 24 h; SKOV-3 cells) inhibits cell division by lowering cell cycle regulatory proteins and inducing G2/M cell cycle induction [1]. Coenzyme Q0 (CoQ0) (0-30 μM; 0-30 minutes; SKOV-3 cells) raises intracellular ROS levels to encourage the death of SKOV-3 cells [1]; via increasing the accumulation of LC3-II, GFP-LC3 pigment, AVO formation, and Beclin-1/Bcl-2 repair, Coenzyme Q0 (CoQ0) (0-30 μM; 24 hours; SKOV-3 cells) induces self-repair. Coenzyme Q0 (CoQ0) (0-30 μM; 24 hours; SKOV-3 cells) inhibits HER-2/AKT/mTOR signaling to improve cytochrome and autophagy mechanisms. Coenzyme Q0 (CoQ0) signals through mitochondria (caspase-3, PARP, and Bax/Bcl-2 corrector) and ER intermediates (caspase-12 and Hsp70) [1]. Q0 (CoQ0) (0-10 μM; 0.5-18 hours; RAW264.7 cells) improves Nrf2 stability and controls NFκB/AP-1 activation [2]. 5 μM Coenzyme Q0 (CoQ0); 0–12 hours;
In vitro, Coenzyme Q0 has demonstrated various biological activities including antioxidant, anti-inflammatory, and anticancer effects. The compound acts as a redox-active molecule that can both scavenge free radicals and generate ROS depending on concentration. In cancer cell lines, CoQ0 has been shown to induce apoptosis and inhibit cell proliferation through mechanisms involving ROS generation, mitochondrial dysfunction, and activation of caspases. The compound also exhibits anti-inflammatory activity by inhibiting the production of pro-inflammatory cytokines and modulating NF-κB signaling. In neuronal cells, CoQ0 has demonstrated neuroprotective effects by reducing oxidative stress and mitochondrial dysfunction. The compound's antioxidant properties have been studied in various cell-based models of oxidative stress. CoQ0 has also been shown to modulate the expression of genes involved in antioxidant defense and mitochondrial biogenesis.

In SKOV-3 xenografted nude mice, intraperitoneal administration of Coenzyme Q0 (CoQ0) at 1.5 and 2.5 mg/kg every four days for 52 days inhibits the growth of tumors [1]. Through Nrf2 activation and NFκB inhibition, Coenzyme Q0 (CoQ0) (5 mg/kg; lateral wall; duration: 4 hours) has anti-inflammatory activity in the liver and the liver of mice treated with lipopolysaccharide (LPS) [2].
In vivo, Coenzyme Q0 has been studied in animal models for its potential therapeutic effects. The compound has demonstrated neuroprotective effects in models of neurodegenerative diseases, reducing oxidative stress and improving mitochondrial function. In models of inflammation, CoQ0 has shown anti-inflammatory activity by reducing the production of pro-inflammatory mediators. The compound has also been studied for its anticancer effects in tumor-bearing animals, showing inhibition of tumor growth through mechanisms involving ROS generation and apoptosis induction. CoQ0 has been shown to improve mitochondrial function and reduce oxidative damage in various tissues. The compound's ability to modulate redox balance and mitochondrial function makes it a potential therapeutic agent for conditions associated with oxidative stress and mitochondrial dysfunction. However, CoQ0 is primarily used as a research tool and is not approved for clinical use.

In vitro assays for Coenzyme Q0 typically involve measuring its redox activity, antioxidant capacity, and effects on cellular function. For antioxidant assays, CoQ0 is dissolved in appropriate solvents and its ability to scavenge free radicals is measured using DPPH, ABTS, or other radical-scavenging assays. For cell-based assays, CoQ0 is dissolved in DMSO and diluted in cell culture medium at concentrations ranging from 1-100 μM. Cells are treated with CoQ0 for 24-72 hours, and cell viability is assessed using MTT or CCK-8 assays. Apoptosis is measured using annexin V/PI staining or caspase activity assays. ROS levels are measured using fluorescent probes such as DCFH-DA. Mitochondrial membrane potential is assessed using JC-1 or TMRE staining. Western blot analysis is used to measure the expression of proteins involved in apoptosis, inflammation, and antioxidant defense. The compound is typically stored as a powder at -20°C and protected from light.

Cell Viability Assay[1]
Cell Types: SKOV-3, A2780 and A2870/CP70 cells
Tested Concentrations: 0, 10, 20, 30 EA.hy 926 cells) in EA Anti-angiogenic activity in .hy 926 cells [3]. and 40 µM
Incubation Duration: 24 hrs (hours)
Experimental Results: The viability of SKOV-3, A2780 and A2870/CP70 cells was diminished, with IC50 values of 26.6 µM, 27.3 µM and 28.4 µM respectively.

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Cell cycle analysis[1]
Cell Types: SKOV-3, A2780 and A2870/CP70 Cell
Tested Concentrations: 0, 10, 20 and 30 µM
Incubation Duration: 24 hrs (hours)
Experimental Results: Cell cycle arrest in G2/M phase and diminished cyclin expression in in SKOV-3 cells.

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Apoptosis analysis[1]
Cell Types: SKOV-3, A2780 and A2870/CP70 Cell
Tested Concentrations: 0, 5, 15 and 30 µM
Incubation Duration: 24 hrs (hours)
Experimental Results: Promoted conversion of LC3–1 to LC3-II and increased LC3 -II accumulation. The Bax/Bcl-2 ratio increased in a dose-dependent manner.

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Apoptosis analysis[1]
Cell Types: SKOV-3 Cell
Tested Concentrations: 0, 10, 20 and 30 µM
Incubation Duration: 24 hrs (hours)
Experimental Results: Had the percentage of early apoptotic cells are 25.1%, 34% and 36% for 10, 20 and 30 µM, respectively.

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Western Blot Analysis[1]
Cell Types: SKOV-3 cells
Tested Concentrations: 0, 5, 15 and 30 µM
Incubation Duration: 24 hrs (hours)
Experimental Results: Activated of caspase-3 and cleavaged of PARP. Increased the expressions of caspase-12, HSP-70 and Bax in a dose-dependent manner, diminished the expressions of Bcl-2.

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Western Blot Analysis[1]
Cell Types: SKOV-3 cells
Tested Concentrations: 30 µM
Incubation Duration: 24 hrs (hours)
Experimental Results: diminished the phosphorylated HER-2 (Y1221) levels, p-AKT (Ser473) and p-mTOR (S2448) levels.

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Western Blot Analysis[2]
Cell Types: RAW264.7 cells
Tested Concentrations: 0, 2.5, 5 and 10 µM
Incubation Duration: 0.5-18 hrs (hours)
Experimental Results: Inhibited iNOS/COX-2 protein expressions with reductions of NO, PGE2, TNF-α and IL-1β secretions.

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Western Blot Analysis[3]
Cell Types: EA.hy 926 cells
Tested Concentrations: 5 µM
Incubation Duration: 0, 1, 3, 6 and 12 hrs (hours)
Experimental Results: 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).
In vitro cell-based assays using Coenzyme Q0 are conducted in various cell lines including cancer cells, neuronal cells, and immune cells. Cells are seeded in multi-well plates and treated with CoQ0 at concentrations ranging from 1-100 μM for 24-72 hours. After treatment, cell viability is assessed using MTT, CCK-8, or other cell viability assays. Apoptosis is measured using annexin V/PI staining followed by flow cytometry, or by measuring caspase-3/7 activity. ROS levels are measured using fluorescent probes such as DCFH-DA. Mitochondrial membrane potential is assessed using JC-1 or TMRE staining. For mechanistic studies, cells are harvested for Western blot analysis to measure the expression of proteins involved in apoptosis (Bax, Bcl-2, caspases), inflammation (NF-κB, COX-2, iNOS), and antioxidant defense (Nrf2, HO-1, SOD). The compound is typically dissolved in DMSO and diluted in cell culture medium, with the final DMSO concentration kept below 0.1%.

Animal/Disease Models: SKOV-3 xenograft nude mice [1]
Doses: 1.5 and 2.5 mg/kg
Route of Administration: intraperitoneal (ip) injection; once every four days for 52 days
Experimental Results: 1.5 and 2.5 mg/kg inhibited tumor growth.

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Animal/Disease Models: LPS-treated female FVB mice [2]
Doses: 5 mg/kg
Route of Administration: po (po (oral gavage)) 4 hrs (hrs (hours))
Experimental Results: Down-regulated inflammatory genes in the liver and spleen tissues of LPS-injected mice.
In vivo animal experiments with Coenzyme Q0 are conducted in various disease models including neurodegenerative diseases, inflammatory conditions, and cancer. The compound is typically administered orally, intraperitoneally, or intravenously at doses ranging from 1-50 mg/kg depending on the study. In models of neurodegeneration, CoQ0 is administered daily for several weeks, and neurological function is assessed using behavioral tests. Brain tissues are collected for analysis of oxidative stress markers, mitochondrial function, and protein expression. In models of inflammation, CoQ0 is administered before or after induction of inflammation, and inflammatory markers are measured in tissues and serum. In tumor models, CoQ0 is administered to tumor-bearing animals, and tumor growth is monitored. Tissue samples are collected for histopathological examination and biochemical analysis. The compound is formulated in appropriate vehicles such as DMSO, PEG, or saline for administration.

Dosing formulations for Coenzyme Q0 in animal studies typically involve dissolving the compound in appropriate vehicles such as DMSO, PEG300, Tween 80, and saline or PBS. The compound is administered orally, intraperitoneally, or intravenously at doses ranging from 1-50 mg/kg depending on the study design. Pharmacokinetic parameters including Cmax, Tmax, half-life, and AUC are determined from plasma concentration-time profiles. The compound's bioavailability is calculated by comparing oral and intravenous administration. Tissue distribution studies may be conducted to assess compound accumulation in target organs. Metabolism studies identify the major metabolites and pathways of elimination. The compound's redox properties may affect its stability in biological fluids. For long-term storage, the powder is kept at -20°C and protected from light. In solvent, the compound is stored at -80°C for up to 6 months.

The toxicity of Coenzyme Q0 has been evaluated in preclinical studies. In animal models, the compound is generally well-tolerated at therapeutic doses (1-50 mg/kg), with no significant adverse effects observed at lower doses. At higher doses, the compound's pro-oxidant activity may lead to toxicity due to excessive ROS generation. The compound's toxicity is likely related to its redox cycling properties and the generation of reactive oxygen species. Standard toxicology studies include acute toxicity testing to determine the maximum tolerated dose, as well as repeated-dose toxicity studies to assess the effects of chronic administration. Histopathological examination of major organs (liver, kidney, heart, lung, and spleen) is performed to identify any target organ toxicity. Hematological parameters are monitored to assess any effects on blood cells. The compound is intended for research use only and is not approved for clinical use. Safety data sheets recommend standard handling procedures for research chemicals.

[1]. 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]. 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]. 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.

Ubiquinone-0 is a derivative of benzoquinone, with a methyl substituent at the 5-position and methoxy substituents at the 2- and 3-positions. It is the core structure of ubiquinone compounds. Ubiquinone-0 is a metabolite of Escherichia coli and humans. Ubiquinone-0 is a metabolite found or produced in Escherichia coli (K12 strain, MG1655 strain). 2,3-Dimethoxy-5-methyl-1,4-benzoquinone has been reported in Antrodia camphorata, Salmonella formosanus, and Antrodia cinnamomea, and relevant data are available.
Coenzyme Q0 (CAS 605-94-7) is a ubiquinone derivative and a precursor in the biosynthesis of coenzyme Q10. It has the molecular formula C9H8O4 and a molecular weight of 180.16 g/mol. The compound is also known as 2,3-dimethoxy-5-methyl-1,4-benzoquinone. CoQ0 is a redox-active molecule that participates in electron transport and has antioxidant properties. It has been studied for its potential anticancer, anti-inflammatory, and neuroprotective activities. The compound is a quinone derivative that can undergo redox cycling, generating ROS at high concentrations while acting as an antioxidant at lower concentrations. CoQ0 is found naturally in small amounts in various organisms and is used in research to study mitochondrial function, oxidative stress, and the biosynthesis of coenzyme Q10. The compound is typically stored as a yellow crystalline powder at -20°C and protected from light. CoQ0 is intended for research use only and is not approved for clinical use. It is soluble in DMSO and other organic solvents.

C9H10O4

182.1733

182.057

605-94-7

69068

Brown to red solid powder

1.2±0.1 g/cm3

331.4±42.0 °C at 760 mmHg

58-60 °C(lit.)

148.6±27.9 °C

0.0±0.7 mmHg at 25°C

1.498

0.12

0

4

2

13

323

0

2934.99.9001

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)

DMSO : ~50 mg/mL (~274.45 mM)

Solubility in Formulation 1: ≥ 1.67 mg/mL (9.17 mM) (saturation unknown) in 10% DMSO + 40% PEG300 + 5% Tween80 + 45% Saline (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 16.7 mg/mL clear DMSO stock solution to 400 μL PEG300 and mix evenly; then add 50 μL Tween-80 to the above solution and mix evenly; then add 450 μL normal saline to adjust the volume to 1 mL.
Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH₂ O to obtain a clear solution.

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Solubility in Formulation 2: ≥ 1.67 mg/mL (9.17 mM) (saturation unknown) in 10% DMSO + 90% (20% SBE-β-CD in Saline) (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 16.7 mg/mL clear DMSO stock solution to 900 μL of 20% SBE-β-CD physiological saline solution and mix evenly.
Preparation of 20% SBE-β-CD in Saline (4°C，1 week): Dissolve 2 g SBE-β-CD in 10 mL saline to obtain a clear solution.

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 (Please use freshly prepared in vivo formulations for optimal results.)