Muhammad Aiyaz Sharif

Product Manager
PharmEvo Pvt. Ltd
 What is Co-enzyme Q10?
Coenzyme Q10, also known as ubiquinone, coenzyme Q, and
abbreviated at times to CoQ10 .
This oil-soluble, vitamin-like substance is present in most
eukaryotic cells, primarily in the mitochondria.
It is a component of the electron transport chain and
participates in aerobic cellular respiration, generating
energy in the form of ATP.
Ninety-five percent of the human body’s energy is
generated this way.1,2
1.Ernster, L; Dallner, G (1995). "Biochemical, physiological and medical aspects of ubiquinone function". Biochimica et
Biophysica Acta 1271 (1): 195–204.
2.Dutton, PL; Ohnishi, T; Darrouzet, E; Leonard, MA; Sharp, RE; Cibney, BR; Daldal, F; Moser, CC (2000). "4 Coenzyme Q
oxidation reduction reactions in mitochondrial electron transport". In Kagan, VE; Quinn, PJ. Coenzyme Q: Molecular
mechanisms in health and disease. Boca Raton: CRC Press. pp. 65–82
 Who discovered it?
CoQ10 was first discovered by Professor Fredrick L. Crane
and colleagues at the University of Wisconsin–Madison
Enzyme Institute in 1957.3,4
In 1958, its chemical structure was reported by Dr. Karl
Folkers and coworkers at Merck.
In 1961 Peter Mitchell proposed the electron transport
chain (which includes the vital proton motive role of CoQ 10)
and he received a Nobel Prize for the same in 1978.

3.Crane, F; Hatefi, Y; Lester, R; Widmer, C (1957). "Isolation of a quinone from beef heart mitochondria".
Biochimica et Biophysica Acta 25 (1): 220–1
4.Peter H. Langsjoen,"Introduction of Coezyme Q10“
What is the role of NeoQ10
 How is it synthesized?
Starting from acetyl-CoA, a
multistep process of mevalonate
pathway produces farnesyl-PP
(FPP), the precursor for
cholesterol and CoQ10.
 Causes of CoQ10 decrease
1. Age Dependent Decrease.
2. Use Of Statin.
 Why use along with statin?

Statin Use

So reduction in cholesterol
leads to reduction in CoQ10
which results in myalgia and
reduced cardio protection

Add
What to do?
 Pharmacokinetics
Absorption:
Following ingestion of 100 mg of CoQ, peak
plasma levels occur between 5 and 10 hours.
T max is approximately 6.5 hours
 Pharmacokinetics
Distribution:
The plasma half-life of CoQ in different tissues
varies between 49-125 hours.
Following absorption from the GI tract, CoQ is
taken up by chylomicrons. The major portion of
an exogenous dose of CoQ is deposited in the
liver and packaged into VLDL lipoprotein.
 Pharmacodynamics
Metabolism/Excretion:
It is assumed that metabolism and excretion of
exogenous CoQ is analogous to endogenously
produced CoQ. The excretion of CoQ is
predominantly via the biliary tract.
 Pharmacodynamics
Drug interaction:
Warfarin: CoQ may antagonize the effects of
warfarin. CoQ is structurally similar to vitamin K.

Chemotherapy: Theoretically, CoQ may

decrease the efficacy of chemotherapy due to
antioxidant activity.
 Dosage and Indication

Dosage:
• One capsule twice daily.

Indication:
• Statin Induced Myalgia.
• Age dependent depletion of CO-Q10.
• In Patients with major cardiovascular events.
• Chronic Fatigue syndrome
Clinical Studies
Am J Clin Nutr 2013;97:233–4
Cell Number: 0333-2292231
 Conclusion
These patients, steadily worsening and expected to die
within 2 years under conventional therapy, generally
showed an extraordinary clinical improvement, indicating
that CoQ10 therapy might extend the lives of such patients.
This improvement could be due to correction of a
myocardial deficiency of CoQ10 and to enhanced synthesis
of CoQ10-requiring enzymes.
Response of patients in classes III and IV of cardiomyopathy to
therapy in a blind and crossover trial with coenzyme Q10
Proc. Nati. Acad. Sci. USA
Vol. 82, pp. 4240-4244, June 1985
Medical Sciences

A double-blind and double-crossover trial has been

conducted by administering CoQ10 and a matching placebo
orally to two groups of patients having class I or IV
cardiomyopathy (classification according to criteria of the
New York Heart Association).
Group A received CoQ10 and then placebo; group B
received placebo and then CoQ10. Blood levels of CoQ1o
and cardiac function were determined at 0 and 4 weeks
(control stabilization period) and at 16 and 28 weeks (after
the 12-week CoQ/placebo-treatment periods).
 Results
• For group A, significant increases in CoQ10 blood levels
and cardiac function (SV and EF) occurred during CoQ10
treatment and then decreased during crossover to
placebo.
• For group B, there was no change in CoQ10 blood levels
and cardiac function (SV and EF) during placebo
treatment, but increases in both parameters occurred in
crossover to CoQ10