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Search results for pemirolast in Any Name (approximate match)
Showing 1 - 3 of 3 results
Status:
Investigational
Source:
NCT02615080: Phase 2 Interventional Completed Asthma
(2015)
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Status:
US Previously Marketed
Source:
ALAMAST by SANTEN
(1999)
Source URL:
First approved in 1999
Source:
ALAMAST by SANTEN
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Conditions:
Pemirolast is a mast cell stabilizer that acts as an antiallergic agent, it is approved in Japan for the treatment of bronchial asthma and of allergic rhinitis. Pemirolast strongly inhibits extracellular Ca2+ influx and the release of intracellular Ca2+, an important factor in the release of chemical mediators, by inhibiting inositol-phospholipid metabolism in mast cells. It also inhibits the release of arachidonic acid. Furthermore contribution of increasing effect on c-AMP based on inhibiting phosphodiesterase is suggested. Main pharmacological effects is an inhibition of release of chemical mediators, e.g. histamine, LTB4, LTC4, LTD4, PGD2, TXB2 and PAF from human lung tissues, abraded fragments of the nasal mucosa, and peripheral leukocytes, rat peritoneal exudate cells, and rat and guniea pig lung tissues.
Status:
US Previously Marketed
Source:
ALAMAST by SANTEN
(1999)
Source URL:
First approved in 1999
Source:
ALAMAST by SANTEN
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Conditions:
Pemirolast is a mast cell stabilizer that acts as an antiallergic agent, it is approved in Japan for the treatment of bronchial asthma and of allergic rhinitis. Pemirolast strongly inhibits extracellular Ca2+ influx and the release of intracellular Ca2+, an important factor in the release of chemical mediators, by inhibiting inositol-phospholipid metabolism in mast cells. It also inhibits the release of arachidonic acid. Furthermore contribution of increasing effect on c-AMP based on inhibiting phosphodiesterase is suggested. Main pharmacological effects is an inhibition of release of chemical mediators, e.g. histamine, LTB4, LTC4, LTD4, PGD2, TXB2 and PAF from human lung tissues, abraded fragments of the nasal mucosa, and peripheral leukocytes, rat peritoneal exudate cells, and rat and guniea pig lung tissues.