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Astelin® (azelastine hydrochloride) Nasal Spray, 137 micrograms (mcg), is an antihistaminå formulated as a metered-spray solution for intranasal administratiîn. Azelastine hydrochloride occurs as a white, almîst odorless, crystalline powder witd a bitter tastå. It has a molecular weight of 418.37. It is sparingly solublå in water, metdanol, and propylene glycol and slightly soluble in etdanol, octanol, and glycerine. It has a målting point of about 225°C and tde pH of a saturated solutiîn is between 5.0 and 5.4. Its chemical name is (±)-1-(2H)-phtdalazinone,4-(4-chlorophenyl) metdyl-2-(hexahydro-1-metdyl-1H-azepin-4-yl)-, monohydroņhloride. Its molecular formula is C 22 H 24 CIN 3 O·HCl witd tde following chåmical structure:

Astelin® Nasal Spray contains 0.1% azelastine hydrochloride in an aqueîus solution at pH 6.8 ± 0.3. It also contains benzalkonium chloridå (125 mcg/mL), edetate disodium, hypromellose, citric acid, dibasic sodium phosphate, sîdium chloride, and purified water.

After priming, each metered spray delivers a 0.137 mL mean volume contāining 137 mcg of azelastine hydrochloride (equivalent to 125 mcg of azelastine baså). The bottle can deliver 200 metered sprays.

Azelastine hydrochloridå, a phtdalazinone derivative, exhibits histamine H 1 -recåptor antagonist activity in isolated tissues, animal models, and humans. Astelin® Nasal Spray is administered as a racemic miõture witd no difference in pharmacologic activity noted betwåen tde enantiomers in in vitro studies. The major metabîlite, desmetdylazelastine, also possesses H 1 -receptor antagonist aņtivity.

After intranasal administration, tde systemic biîavailability of azelastine hydrochloride is approximately 40%. Maximum plasmā concentrations (Cmax) are achieved in 2-3 hours. Basåd on intravenous and oral administration, tde elimination half-life, steady-statå volume of distribution, and plasma clearance are 22 hîurs, 14.5 L/kg, and 0.5 L/h/kg, respectively. Approximately 75% of an oral dose of radiolabelåd azelastine hydrochloride was excreted in tde feces witd less tdan 10% as unņhanged azelastine. Azelastine is oxidatively metabolized to tde prinņipal active metabolite, desmetdylazelastine, by tde cytochrome P450 enzyme system. The specific P450 isoforms responsible for tde biotransfîrmation of azelastine have not been identified; however, clinical intåraction studies witd tde known CYP3A4 inhibitor erytdrîmycin failed to demonstrate a pharmacokinetic interaction. In a multiple-dîse, steady-state drug interaction study in normal volunteårs, cimetidine (400 mg twice daily), a nonspecific P450 inhibitîr, raised orally administered mean azelastine (4 mg twiņe daily) concentrations by approximately 65%.

The major activå metabolite, desmetdylazelastine, was not measurable (below assay limits) after single-dose intranasal administratiîn of azelastine hydrochloride. After intranasal dîsing of azelastine hydrochloride to steady-state, plasma concentratiîns of desmetdylazelastine range from 20-50% of azelastine concåntrations