ACYCLOVIR SODIUM INJECTION SOLUTION

Ülke: Kanada

Dil: İngilizce

Kaynak: Health Canada

Aktif bileşen:

ACYCLOVIR (ACYCLOVIR SODIUM)

Mevcut itibaren:

AURO PHARMA INC

ATC kodu:

J05AB01

INN (International Adı):

ACYCLOVIR

Doz:

50MG

Farmasötik formu:

SOLUTION

Kompozisyon:

ACYCLOVIR (ACYCLOVIR SODIUM) 50MG

Uygulama yolu:

INTRAVENOUS

Paketteki üniteler:

15G/50G

Reçete türü:

Prescription

Terapötik alanı:

NUCLEOSIDES AND NUCLEOTIDES

Ürün özeti:

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

Yetkilendirme durumu:

APPROVED

Yetkilendirme tarihi:

2019-12-03

Ürün özellikleri

PRODUCT MONOGRAPH
PR
ACYCLOVIR SODIUM INJECTION
(50 mg Acyclovir/mL)
House Standard
Antiviral Agent
AURO PHARMA INC.
Date of Preparation:
3700 Steeles Avenue West, Suite # 402
November 29, 2019
Woodbridge, Ontario, L4L 8K8
CANADA
Submission Control No.: 215417
PR ACYCLOVIR SODIUM INJECTION
50 mg Acyclovir/mL
House Standard
THERAPEUTIC CLASSIFICATION
Antiviral
ACTION AND CLINICAL PHARMACOLOGY
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, herpes virus-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
herpes virus-specified DNA polymerase. Acyclovir is selectively
converted to its active form in
herpes virus 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 herpes virus replication. No effect on latent
nonreplicating virus has been
demonstrated.
Inhibition of the virus reduces the period of viral shedding, limits
the degree of spread and level
of
pathology, and thereby facilitates healing. During suppression, there
is no eviden