Valovir (Valaciclovir Tablet 500mg)

Country: Malaysia

Bahasa: Inggeris

Sumber: NPRA (National Pharmaceutical Regulatory Agency, Bahagian Regulatori Farmasi Negara)

Beli sekarang

Ciri produk Ciri produk (SPC)
08-07-2021

Bahan aktif:

VALACICLOVIR HYDROCHLORIDE

Boleh didapati daripada:

CAMBER LABORATORIES SDN. BHD.

INN (Nama Antarabangsa):

VALACICLOVIR HYDROCHLORIDE

Unit dalam pakej:

100Tablet Tablets; 100Tablet Tablets; 100Tablet Tablets

Dikeluarkan oleh:

Hetero Labs Limited

Ciri produk

                                VALOVIR
Valaciclovir Tablet 500 mg
DESCRIPTION AND COMPOSITION:
White to off-white, film coated, caplet shaped tablets,
debossed with 'V' on one side and '500' on other side.
Each film coated tablet contains: Valaciclovir Hydor-
chloride 556mg equivalent to Valaciclovir 500mg
PHARMACODYNAMIC PROPERTIES:
Valaclovir an antiviral, is the L-valine ester of acyclovir.
Aciclovir is a purine (guanine) nucleoside analogue.
MODE OF ACTION:
Valaciclovir is rapidly and almost completely converted
in man to acyclovir and valine, probably by the enzyme
referred to as valaciclovir hydrolase.
Aciclovir is a specific inhibitor of the herpes viruses with in vitro
activity against herpes simplex viruses (HSV) type 1 and type 2,
varicella zoster virus (VZV), cytomegalvorus (CMV), Epstein-
Bair Virus (EBV) and human herpes virus 6 (HHV-6). Aciclovir
inhibits herpes virus DNA synthesis once it has been
phosphorylated to the active triphosphate form. The first stage of
phosphorylation requires the activity of a virus-specific enzyme.
In the case of HSV, VZV and EBV this enzyme is the viral
thymidine kinase (TK), which is only present in virus infected
cells. Selectivity is maintained in CMV with phosphorylation,
at least in part, being mediated through the phosphotransferase
gene product of UL97.
This requirement for activation of acyclovir by a virus specific
enzyme largely explains its selectivity. The phosphorylation
process is completed conversion from mono to triphosphate by
cellular kinases. Aciclovir triphosphate competitively inhibits the
virus DNA polymerase and incorporation of this nucleoside
analogue results in obligate chain termination, halting virus DNA
synthesis and this blocking virus replication. Extensive monitoring
of clinical HSV and VZV isolates
from patients receiving
acyclovir therapy or prophylaxis has revealed that virus with
reduced sensitivity to acyclovir is extremely rare in the
immunocomptetent and is only found infrequently in severely
immuno compromised individuals e.g. organ or bone marrow
transplant 
                                
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