BLOKTIENE

Valsts: Indonēzija

Valoda: indonēziešu

Klimata pārmaiņas: Badan Pengawas Obat dan Makanan RI - Indonesian Food and Drug Supervisory Agency

Aktīvā sastāvdaļa:

MONTELUKAST SODIUM

Pieejams no:

ACTAVIS INDONESIA - Indonesia

SNN (starptautisko nepatentēto nosaukumu):

MONTELUKAST SODIUM

Deva:

10.40 MG

Zāļu forma:

TABLET SALUT SELAPUT

Vienības iepakojumā:

DUS, 3 BLISTER @ 10 TABLET SALUT SELAPUT

Ražojis:

TEVA OPERATIONS POLAND SP. Z O.O. - Poland

Autorizācija datums:

2022-01-03

Produkta apraksts

BLOKTIENE
FILM‐COATED
TAB
L
ET
COMPOSITION
Each film‐coated tablet contains montelukast sodium equivalent to 10
mg montelukast
PHARMACODYNAMIC PROPERTIES
PHARMACOTHERAPEUTIC GROUP: Leukotriene receptor antagonists
ATC‐CODE: R03D C03
The cysteinyl leukotrienes (LTC
4
, LTD
4
, LTE
4
) are potent inflammatory eicosanoids released from various
cells including mast cells and eosinophils. These important
pro‐asthmatic mediators bind to cysteinyl
leukotriene (CysLT) receptors. The CysLT type‐1 (CysLT
1
) receptor is found in the human
airway
(including
airway smooth muscle cells and airway macrophages) and on other
pro‐inflammatory cells
(including eosinophils and certain myeloid stem cells). CysLTs have
been correlated with the
pathophysiology of asthma and allergic rhinitis. In asthma,
leukotriene‐mediated effects include
bronchoconstriction, mucous secretion, vascular permeability, and
eosinophil recruitment. In allergic
rhinitis, CysLTs are released from the nasal mucosa after allergen
exposure during both early‐ and late‐
phase reactions and are associated with symptoms of allergic rhinitis.
Intranasal challenge with CysLTs
has been shown to increase nasal airway resistance and symptoms of
nasal obstruction.
Montelukast is an orally active compound which binds with high
affinity and selectivity to the CysLT
1
receptor. In clinical studies, montelukast inhibits
bronchoconstriction due to inhaled LTD
4
at doses as
low as 5 mg. Bronchodilation was observed within 2 hours of oral
administration. The bronchodilation
effect caused by a β‐agonist was additive to that caused by
montelukast. Treatment with montelukast
inhibited both early‐ and late‐phase bronchoconstriction due to
antigen challenge. Montelukast,
compared with placebo, decreased peripheral blood eosinophils in adult
and paediatric patients. In a
separate study, treatment with montelukast significantly decreased
eosinophils in the airways (as
measured in sputum) and in peripheral blood while improving clinical
asthma control.
PHARMAC