Art. -Nr.: HY-118075

Coenzyme Q2

Name: Coenzyme Q2
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Coenzyme Q2 is a benzoquinone electron carrier in the mitochondrial electron transport chain and a p53-dependent apoptosis inducer. Coenzyme Q2 induces p53 phosphorylation at Ser15, promoting p53 accumulation and functional activation. Coenzyme Q2 induces ROS generation, caspase-3 activation, DNA fragmentation, phosphatidylserine externalization, mitochondrial permeability transition pore opening, and oxidative phosphorylation uncoupling. Coenzyme Q2 inhibits Complex I, Complex III, and Complex IV activities, disrupting electron transport and membrane potential generation. Coenzyme Q2 induces excessive mitochondrial proton leak in forebrain mitochondria. Coenzyme Q2 causes loss of righting reflex in mice, accompanied by slow-wave delta EEG activity and reversible loss of wakefulness. Coenzyme Q2 inhibits lipid peroxidation and scavenges superoxide radicals. Coenzyme Q2 is used in research on leukemia, myocardial ischemia-reperfusion injury, and mitochondrial encephalomyopathy.

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CAS. Nr.: 606-06-4
Formel: C₁₉H₂₆O₄
Molecular Weight:318.41

Speicherung:

Please store the product under the recommended conditions in the Certificate of Analysis.

Coenzyme Q2 Chemical Structure

CAS. Nr.: 606-06-4

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Strong Fluorescence Signal / Multi-Disciplinary Applications / High Fluorescence Specificity

Biologische Aktivität
- Beschreibung
- IC₅₀ & Target
- Cellular Effect
- In Vitro
- In Vivo
Chemical Information
Reinheit & Dokumentation
Verweise
Calculators
Help & FAQs
Classifications
Bioz

Biologische Aktivität

Beschreibung

IC₅₀ & Target

^[1]

Caspase-3

Alle Caspase Isoform-spezifische Produkte anzeigen :

Cellular Effect

Cell Line	Type	Value	Description	References
BALL-1	IC50	20 μM	Inhibition of human leukemia BALL-1 cell growth assessed as reduction in cell viability incubated for 24 hrs by MTT assay. Inhibition of human leukemia BALL-1 cell growth assessed as reduction in cell viability incubated for 24 hrs by MTT assay.	15905035

In Vitro

ApoptosisAnti-cancerOxidative StressMitochondrial Function

Apoptosis

Coenzyme Q2 (60 μM; 24 h) induces p53-dependent apoptosis in BALL-1 cells, but not in MOLT-4F or HL-60 cells^[1].
Coenzyme Q2 (20 μM; 6 h)-induced cell death depends on caspase-3 in BALL-1 cells^[1].
Coenzyme Q2 (60 μM; 2-6 h) induces p53 phosphorylation at Ser15 in BALL-1 cells^[1].

Anti-cancer

Coenzyme Q2 (20-100 μM; 6-24 h) inhibits BALL-1 cell growth with an IC₅₀ of 20 μM, induces DNA fragmentation, and induces phosphatidylserine externalization^[1].

Oxidative Stress

Coenzyme Q2 (60 μM; 30 min) induces ROS generation in BALL-1 cells^[1].
Coenzyme Q2 (23 μM) uncouples oxidative phosphorylation in isolated rabbit heart and rat liver mitochondria by increasing state 4 respiration and decreasing the respiratory control index^[3].

Mitochondrial Function

Oxidative Stress

Coenzyme Q2 (5-46 μM) decreases calcium retention capacity in isolated rabbit heart mitochondria, thereby favoring mPTP opening^[3].
Coenzyme Q2 (23 μM) increases calcium retention capacity in isolated rat liver mitochondria, thereby inhibiting mPTP opening^[3].
Coenzyme Q2 (23 μM) significantly decreases NADH DUb-reductase activity in isolated rabbit heart and rat liver mitochondria^[3].

Oxidative Stress

Mitochondrial Function

Coenzyme Q2 (23 μM) antagonizes the inhibition of complex I respiration by Rotenone (HY-B1756) in isolated rat liver mitochondria, but only slightly affects its action at low concentrations of Rotenone in isolated rabbit heart mitochondria^[3].
Coenzyme Q2 (23 μM) increases H₂O₂ production in isolated rabbit heart mitochondria, but does not significantly alter H₂O₂ production in isolated rat liver mitochondria under basal conditions^[3].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Apoptosis Analysis^[1]

Cell Line:

BALL-1, MOLT-4F, HL-60
Concentration:

60 μM
Incubation Time:

24 h
Result:

Killed BALL-1 cells at a high rate (approximately 92% cell death), but barely killed MOLT-4F (approximately 13% cell death) or HL-60 (approximately 10% cell death) cells.
Increased caspase-3 activity approximately 30-fold in BALL-1 cells, while MOLT-4F and HL-60 cells showed little caspase-3 activation.

Cell Viability Assay^[1]

Cell Line:

HepG2, HuH-7, Hep3B
Concentration:

100 μM
Incubation Time:

24 h
Result:

Induced cell death strongly in HuH-7 cells (approximately 40% cell death) and induced a lower level of cell death in HepG2 cells (approximately 28% cell death).
Hep3B cells were not affected by CoQ2 (approximately 0% cell death).
Increased caspase-3 activity approximately 2-fold in HuH-7 cells and approximately 1-fold in HepG2 cells, while Hep3B showed no increase.

Cell Viability Assay^[1]

Cell Line:

BALL-1
Concentration:

0, 20, 40, 60, 80, 100 μM
Incubation Time:

24 h
Result:

Decreased cell viability dose-dependently with an IC₅₀ of 20 μM.

Apoptosis Analysis^[1]

Cell Line:

BALL-1
Concentration:

20 μM
Incubation Time:

6 h
Result:

Induced the externalization of phosphatidylserine in a time-dependent manner.\nCaspase-3 activation in BALL-1 cells was observed.
A caspase-3 specific inhibitor, Ac-DEVD-CHO, dramatically blocked CoQ2-induced cell death.
Caspase-8 and -9 were little activated by CoQ2.

Western Blot Analysis^[1]

Cell Line:

BALL-1
Concentration:

60 μM
Incubation Time:

2, 4, or 6 h
Result:

Phosphorylated the Ser15 site of p53, but not the Ser9, Ser20, Ser46, or Ser392 site.

Cell Viability Assay^[1]

Cell Line:

BALL-1
Concentration:

60 μM
Incubation Time:

4 h
Result:

Induced cell death (approximately 67% viability), caspase-3 activation (approximately 22-fold increase), and p53 Ser15 phosphorylation, which were suppressed by treatment with L-ascorbic acid (approximately 98% viability, approximately 1-fold caspase-3 activity).

In Vivo

Coenzyme Q2 (20 mg/mL; i.v.; single injection) exhibits sedative-hypnotic properties with an ED₅₀ of approximately 100 mg/kg, inducing transient and reversible loss of consciousness in mice^[2].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Animal Model:

C57Bl/6 N (male, 6-8 weeks old, 20-25 grams)^[2]
Dosage:

20 mg/mL (various doses); 200 mg/kg (EEG assessment)
Administration:

i.v.; single injection
Result:

Induced short-lived loss of righting reflex (LORR) across a range of doses.
Mice regained righting reflex within approximately 8 minutes.
Latency to return of righting reflex (RORR) showed a significant positive correlation with dose.
Mean latency to LORR was 95.0 s (95% CI: 23.3-166.7).
ED50 was approximately 100 mg/kg.

Related Protocols :

Chemical Information

CAS. Nr. 606-06-4
Appearance Liquid
Molecular Weight 318.41
Formel C₁₉H₂₆O₄
Color Light yellow to yellow
SMILES

O=C(C(C)=C(C1=O)C/C=C(C)/CC/C=C(C)\C)C(OC)=C1OC
Versand

Room temperature in continental US; may vary elsewhere.
Speicherung

Please store the product under the recommended conditions in the Certificate of Analysis.

Reinheit & Dokumentation

Select Batch:

Reinheit: 99.98%

Assay: 99.98%

ee.: 99.98%

Data Sheet (284 KB)
SDS (393 KB)
- English - EN (393 KB)
- Français - FR (393 KB)
- Deutsch - DE (393 KB)
- Norwegian - NO (393 KB)
- Español - ES (393 KB)
- Swedish - SV (393 KB)
- Italian - IT (393 KB)
- Korean - KR (393 KB)
- Portuguese - PT (393 KB)
COA (2659 KB)
Elemental Analysis Report (2659 KB)
HNMR (2659 KB)
CNMR (2659 KB)
RP-HPLC (2659 KB)
NP-HPLC (2659 KB)
MS (2659 KB)
LCMS (2659 KB)
IR (2659 KB)
GC (2659 KB)
OR (2659 KB)
SDS-PAGE (2659 KB)
SEC-HPLC (2659 KB)
Other Report (2659 KB)
Handling Instructions (2659 KB)

Verweise

[1]. Esaka Y, et al. Coenzyme Q2 induced p53-dependent apoptosis. Biochimica et biophysica acta. 2005 Jun 20;1724(1-2):49-58.

[2]. Lim H, et al. Sedative-hypnotic properties and mitochondrial effects of coenzyme Q2 in mice. Current molecular pharmacology. 2025;18(1):100-107.

[3]. Gharib A, et al. Opposite and tissue-specific effects of coenzyme Q2 on mPTP opening and ROS production between heart and liver mitochondria: role of complex I. Journal of molecular and cellular cardiology. 2012 May;52(5):1091-5.

[4]. Beyer RE, et al. The participation of coenzyme Q in free radical production and antioxidation. Free radical biology & medicine. 1990;8(6):545-65.

Calculators

Molaritätsrechner

Mass (g) = Concentration (mol/L) × Volume (L) × Molecular Weight (g/mol)

Mass Mass

Konzentration Konzentration

Volumen Volumen

Molecular Weight Molecular Weight

Verdünnungsrechner

Konzentration _{(Stammlösung)} × Volumen _{(Stammlösung)} = Konzentration _{(Ziellösung)} × Volumen _{(Ziellösung)}

Konzentration _{(Stammlösung)} Konzentration _{(Stammlösung)}

Volumen _{(Stammlösung)} Volumen _{(Stammlösung)}

Konzentration _{(Ziellösung)} Konzentration _{(Ziellösung)}

Volumen _{(Ziellösung)} Volumen _{(Ziellösung)}

Help & FAQs

How should lyophilized recombinant proteins be reconstituted and stored?

1. Before opening the cap, centrifuge the vial at 13000 rpm for 20-30 seconds. This step will ensure that any lyophilized powder that may have adhered to the cap or walls is collected at the bottom of the vial, minimizing the risk of product loss.

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Coenzyme Q2

Alle Caspase Isoform-spezifische Produkte anzeigen