Source: Web Search
The bronchodilative action of procaterol hydrochloride hydrate was comparable to or more potent than that of isoproterenol and more potent than that of salbutamol sulfate and orciprenaline sulfate, as determined by inhibition on increased pulmonary resistance in dogs, cats, and guinea pigs.
Procaterol hydrochloride hydrate had a longer duration of action than isoproterenol, trimetoquinol, orciprenaline sulfate, and salbutamol sulfate in dogs, cats, and guinea pigs.
The selectivity of procaterol hydrochloride hydrate for β2-adrenergic receptors in the respiratory system was greater than that for such receptors in the cardiovascular system, as compared to isoproterenol, trimetoquinol, orciprenaline sulfate, and salbutamol sulfate in dogs, cats, and guinea pigs.
Procaterol hydrochloride hydrate exhibited a definite anti-allergic action by inhibiting antibody-induced increase in airway resistance, the PCAreaction, and histamine release from sensitized lung tissues in guinea pigs and rats, as well as allergen-induced skin reactions, and increases in asthmatic responses to antibody inhalation in bronchial asthma patients, as compared to isoproterenol, trimetoquinol, orciprenaline sulfate, and salbutamol sulfate. The drug also inhibited allergen-induced delayed-type and immediate-type bronchial responses.
Procaterol hydrochloride hydrate accelerated ciliary activity in airways of pigeons.
The results of treadmill or ergometer exercise or methacholine loading tests suggest that procaterol hydrochloride hydrate suppresses exercise-induced asthma attacks in patients with bronchial asthma.
Procaterol hydrochloride hydrate inhibited airway hypersensitivity accelerated by the inoculation of influenza virus C in dogs.
Procaterol hydrochloride hydrate inhibited vascular permeability increase and edema formation in dorsal subcutaneous air pouches induced by various inflammatory chemical agents in rats.
Its potency was similar to that of isoproterenol. Procaterol hydrochloride hydrate also inhibited pulmonary edema induced by histamin inhalation in guinea pigs, with greater potency than salbutamol sulfate.
Procaterol hydrochloride hydrate inhibited cough in acute bronchitis induces by the inhalation of substance P.
When Meptin Tablets 50 µg were administered orally to 8 healthy male subjects as single doses of 50µg/subjects as procaterol hydrochloride hydrate, the following plasma concentration curves and pharmacokinetic parameters were obtained.
Plasma kinetic data:
| tmax (hr) | Cmax (pg/mL) | t½ (hr) | AUC∞ (pg hr/mL) |
|---|---|---|---|
| 1.4 + 0.82 | 136.4 + 62.9 | 3.83 + 0.93 | 690.2 + 262.9 |
Following single oral administration of Meptin Tablets 50 µg at a dose of 50ìg/subject as procaterol hydrochloride hydrate, 15.7% of the administered dose was excreted as unchanged compound in the urine within 24 hours postdosing, and 23.6% was excreted as a glucuronide metabolite. Desisopropyl procaterol was also detected as a metabolite in the urine, accounting for 0.48% of the administered dose. It is believed that the main metabolic pathway in humans is glucuronide conjugation.
CYP3A4 is the main enzyme involved in the formation of desisopropyl procaterol (in vitro).
© All content on this website, including data entry, data processing, decision support tools, "RxReasoner" logo and graphics, is the intellectual property of RxReasoner and is protected by copyright laws. Unauthorized reproduction or distribution of any part of this content without explicit written permission from RxReasoner is strictly prohibited. Any third-party content used on this site is acknowledged and utilized under fair use principles.
