ZOVIRAX OINTMENT

Country: Canada

Language: English

Source: Health Canada

Active ingredient:

ACYCLOVIR

Available from:

BAUSCH HEALTH, CANADA INC.

ATC code:

D06BB03

INN (International Name):

ACICLOVIR

Dosage:

5%

Pharmaceutical form:

OINTMENT

Composition:

ACYCLOVIR 5%

Administration route:

TOPICAL

Units in package:

4G/30G

Prescription type:

Prescription

Therapeutic area:

ANTIVIRALS

Product summary:

Active ingredient group (AIG) number: 0115506007; AHFS:

Authorization status:

APPROVED

Authorization date:

2001-08-07

Summary of Product characteristics

PRODUCT MONOGRAPH
PR
ZOVIRAX
®
Acyclovir Cream, Mfr. Std.
Acyclovir Ointment, USP
5% w/w
ANTIVIRAL AGENT
BAUSCH HEALTH, CANADA INC.
DATE OF REVISION:
2150 St-Elzear Blvd. West
December 22, 2020
Laval, Quebec
H7L 4A8
Control #: 241907
ZOVIRAX
®
is a registered trademark of the GlaxoSmithKline group of companies
used under license.
_Pr_
_ZOVIRAX _
_®_
_ Product Monograph Page 2 of 32_
PRODUCT MONOGRAPH
PR
ZOVIRAX
®
Acyclovir Cream, Mfr. Std.
Acyclovir Ointment, USP
5% w/w
ACTIONS AND CLINICAL PHARMACOLOGY
ZOVIRAX (acyclovir), a synthetic acyclic purine nucleoside analog, is
a substrate with a high
degree of specificity for herpes simplex and varicella-zoster
specified thymidine kinase.
Acyclovir is a poor substrate for host cell-specified thymidine
kinase. Herpes simplex and
varicella-zoster specified thymidine kinase transform acyclovir to its
monophosphate which is
then transformed by a number of cellular enzymes to acyclovir
diphosphate and acyclovir
triphosphate. Acyclovir triphosphate is both an inhibitor of, and a
substrate for, herpesvirus-
specified DNA polymerase. Although the cellular α-DNA polymerase in
infected cells may also
be inhibited by acyclovir triphosphate, this occurs only at
concentrations of acyclovir triphosphate
which are higher than those which inhibit the herpesvirus-specified
DNA polymerase. Acyclovir
is selectively converted to its active form in herpesvirus-infected
cells and is thus preferentially
taken up by these cells.
Acyclovir has demonstrated a very much lower toxic potential _in
vitro_ for normal uninfected cells
because:
1)
less is taken up;
2)
less is converted to the active form;
3)
cellular α-DNA polymerase has a lower sensitivity to the action of
the active form of the
drug.
A combination of the thymidine kinase specificity, inhibition of DNA
polymerase and premature
termination of DNA synthesis results in inhibition of herpesvirus
replication. No effect on latent
non-replicating virus has been demonstrated. Inhibition of the virus
reduces the period of viral
sheddin