Detail of "58581-89-8"

Reference

Inhibitory effects of various drugs on phorbol myristate acetate and n-formyl-methionyl-leucyl-phenylalanine-induced superoxide production in polymorphonuclear leukocytes

Inhibitory effects of various drugs on phorbol myristate acetate and n-formyl-methionyl-leucyl-phenylalanine-induced superoxide production in polymorphonuclear leukocytes. Taniguchi, Katsuhiko; Takanaka, Koichiro (Dep. Toxicol., Niigata Coll. Pharm., Niigata, Japan). Biochem. Pharmacol., 33(20), 3165-9 (English) 1984. CODEN: BCPCA6. ISSN: 0006-2952. DOCUMENT TYPE: Journal CA Section: 4 (Toxicology) Section cross-reference(s): 1 To clarify the mechanisms of superoxide (O2-) formation by polymorphonuclear leukocytes (PMNs), the effects of clin. employed drugs on PMNs were investigated by measuring changes in membrane potential and rates of O2- prodn. These variables were effectively diminished with antihistaminic agents, adrenergic b-antagonists, and antiarrhythmic drugs when guinea pig peritoneal PMNs were stimulated by phorbol myristate acetate (PMA)(I) [16561-29-8] or n-formyl-methionyl-leucyl-phenylalanine (FMLP) [59880-97-6]. The order of potency of the inhibitory effects of these chems. on the PMA-induced O2- formation was as follows: azelastine [58581-89-8] (IC50 = 4.1 mM) < clemastine [15686-51-8] < DL-propranolol [13013-17-7] < chloropheniramine [132-22-9] < dichlorisoproterenol [59-61-0] < quinidine [56-54-2] < diphenylhydramine [58-73-1] < indomethacin [53-86-1] (IC50 >400 mM). Similar phenomena were obsd. when FMLP was employed instead of PMA, but the FMLP-stimulated O2- prodn. was effectively inhibited by indomethacin. Changes in membrane potential also indicated that most of these drugs cancelled functional changes of the plasma membrane of PMNs. Thus, changes in membrane potential by the stimuli were essential for the initiation of O2- generation from plasma membrane of PMNs, although the initiation mechanisms were not identical for the 2 stimuli.

Azelastine eye drops in the treatment of perennial allergic conjunctivitis

Azelastine eye drops in the treatment of perennial allergic conjunctivitis. Nazarov, Ozod; Petzold, Ursula; Haasec, Hans; Nguyen, Duc Tung; Ellers-Lenz, Barbara; Hermann, Robert (Scientific Center for Allergy of Uzbekistan, Tashkent, Uzbekistan). Arzneimittel-Forschung, 53(3), 167-173 (English) 2003 Editio Cantor Verlag. CODEN: ARZNAD. ISSN: 0004-4172. DOCUMENT TYPE: Journal CA Section: 1 (Pharmacology) Section cross-reference(s): 63 Azelastine (CAS 58581-89-8) is a selective H1-receptor antagonist that inhibits histamine release and interferes with activation of other mediators of allergic inflammation. The present double-blind study aimed to evaluate azelastine eye drops (Allergodil) in patients with perennial allergic conjunctivitis compared to placebo. A total of 116 patients with an ocular symptoms score for itching and conjunctival redness 33 (0-6 scale) were randomized to twice-daily 0.05% azelastine eye drops treatment (n = 58) or placebo. Patients maintained daily logs and were clin. evaluated after 7, 21 and 42 days of treatment. Azelastine significantly improved itching and conjunctival redness vs. placebo (p < 0.001). Tolerability was rated good or better by 97% of patients with only bitter taste and application site reaction notable adverse experiences. On Day 7, ocular symptoms score improved by 1.5±0.9 (vs. 0.5±0.8 placebo) with score improvement 32 in 55% with azelastine (vs. 14% placebo). Itching and redness further improved at Day 42 (score improvement 32 in 95% with azelastine vs. 33% placebo) and completely resolved for 47% azelastine patients (vs. 10% placebo). Daily patient logs confirmed the clin. assessed scores. Topical azelastine progressively improved itching and conjunctival redness in patients with moderate to severe perennial allergic conjunctivitis. Continued improvement with prolonged use is consistent with mechanisms other than H1-receptor blockade, such as possible down regulation of adhesion mol. receptors.