Vimenro 20% wv Oral Solution

Country: Malasía

Tungumál: enska

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

Virkt innihaldsefni:

ENROFLOXACIN

Fáanlegur frá:

Vemedim Sdn Bhd

INN (Alþjóðlegt nafn):

ENROFLOXACIN

Einingar í pakka:

1 L

Framleitt af:

VEMEDIM VETERINARY DRUGS AND PROBIOTICS CO., LTD (VEMEDIM ANIMAL HEALTH)

Vara einkenni

Vimenro
20%w/v
_Oral Solution_
COMPOSITION: Each ml contains:
Enrofloxacin….…………………..…… 200 mg
With Benzyl Alcohol 1% v/v as a preservative
Exp. Qs …………………….………………1 ml
DESCRIPTION
The
finished
product
is
yellowish
to
yellow
transparent
solution
PHARMACODYNAMICS
MODE OF ACTION
Two enzymes essential in DNA replication and transcription,
DNA gyrase and topoisomerase IV, have been identified as
the molecular targets of fluoroquinolones. They modulate
the topological state of DNA through cleaving and resealing
reactions. Initially, both strands of the DNA double helix are
cleaved. Then, a distant segment of DNA is passed through
this break before the strands are resealed. Target inhibition
is
caused
by
non-covalent
binding
of
fluroquinolone
molecules to an intermediate state in this sequence of
reactions, in which DNA is cleaved, but both strands are
retained covalently attached to the enzymes. Replication
forks and translational complexes cannot proceed beyond
such enzyme-DNA-fluroquinolone complexes, and inhibition
of DNA and mRNA synthesis triggers events resulting in a
rapid, drug concentration-dependant killing of pathogenic
bacteria.
ANTIBACTERIAL SPECTRUM
Enrofloxacin is active against many Gram-negative bacteria,
against Gram-positive bacteria and _Mycoplasma_ spp.
_In vitro _susceptibility has been shown in strains of (i) Gram-
negative
species
such
as,
_Pasteurella _
_multocida_
and
_Avibacterium _
_(Haemophilus) _
_paragallinarum_
and
(ii)
_Mycoplasma gallisepticum_ and_ Mycoplasma synoviae_.
TYPES AND MECHANISMS OF RESISTANCE
Resistance to fluoroquinolones has been reported to arise
from five sources, (i) point mutations in the genes encoding
for
DNA
gyrase
and/or
topoisomerase
IV
leading
to
alterations of the respective enzyme, (ii) alterations of drug
permeability
in
Gram-negative
bacteria,
(iii)
efflux
mechanisms,
(iv)
plasmid
mediated
resistance
and
(v)
gyrase
protecting
proteins.
All
mechanisms
lead
to
a
reduced susceptibility of the bacteria to fluoroqu