Actions of Butrin in details
Pharmacology: Pharmacodynamics: Mechanism of Action and Pharmacodynamic Effects: Butrin, the sole active ingredients of Sinecod, is a cough suppressant which is neither chemically, nor pharmacologically related to opium alkaloids.
The substance is thought to have central effect. However the exact mechanism of action is unknown. Butrin possesses non-specific anticholinergic and bronchospasmolytic effects, which facilitate the respiratory function. Butrin (Sinecod) does not induce habit-forming effects or dependence.
Butrin has a broad therapeutic margin; thus it is well tolerated, even at high doses, and well suited for cough relief in adults and children.
Pharmacokinetics: Absorption: Based on available data, it can be assumed that the ester Butrin is well and rapidly absorbed and that it is hydrolyzed into phenyl-2-butyric acid and diethylaminoethoxyethanol. The influence of food ingestion has not been investigated. Exposure to 2-phenylbutyric acid and diethylaminoethoxyethanol is fully proportional across the dose range of 22.5 mg-90 mg.
Syrup: Butrin is rapidly absorbed following oral administration, with measurable concentrations being detected in the blood within 5 to 10 minutes of administration of the 22.5 mg, 45 mg, 67.5 mg and 90 mg dose levels. Maximum plasma concentrations are reached within 1 hour for all four dose levels with a mean value of 16.1 nanogram/mL at the dose of 90 mg.
The mean plasma concentration of 2-phenylbutyric acid is reached within 1.5 hours with the greatest exposure being observed after 90 mg (3052 nanogram/mL). The mean plasma concentration of diethylaminoethoxyethanol is reached within 0.67 hour with greatest exposure again being observed after 90 mg (160 nanogram/mL).
Tablet: The mean maximum plasma concentration of the principal metabolite phenyl-2-butyric acid is 1.4 microgam/mL (with considerable scatter) following the administration of one 50 mg modified-release film-coated tablet, and is reached after 9 hours.
Distribution: Butrin has a high volume of distribution ranging between 81 and 112 L (adjusted for body weight in kg) as well as a high degree of protein binding. 2-phenylbutyric acid is highly protein bound in plasma across all dose levels (22.5-90 mg) with mean values of 89.3%-91.6%. Diethylaminoethoxyethanol exhibits some degree of protein binding with mean values ranging between 28.8%-45.7%. It is not known whether Butrin crosses the placenta or whether it is secreted into breast milk.
Metabolism: The hydrolysis of Butrin, which leads mainly to phenyl-2-butyric acid and diethylaminoethoxyethanol, takes place quickly. Based on studies in various species, is assumed that both principal metabolites have a cough-relieving effect. There are no human data on the alcoholic metabolite. Phenyl-2-butyric acid undergoes further partial metabolism through hydroxylation in the para-position.
Elimination: Excretion of the three metabolites takes place primarily via the kidneys; following conjugation in the liver, the acid metabolites undergo large-scale binding to glucuronic acid. Urinary 2-phenylbutyric acid conjugate levels are much higher than in plasma. Butrin is detectable in the urine up to 48 hours and the amount of Butrin excreted in urine over the 96-hour sampling period, accounts for approximately 0.02, 0.02, 0.03 and 0.03% of the 22.5 mg, 45 mg, 67.5 mg and 90 mg dose levels, respectively. A greater percentage of the Butrin dose is excreted in the urine as diethylaminoethoxyethanol than Butrin, or unconjugated 2-phenylbutyric acid. The measured eliminaiton half-life mean values for 2-phenylbutyric acid, Butrin, and diethylaminoethoxyethanol are 23.26-24.42, 1.48-1.93, and 2.72-2.90 hours, respectively.
Kinetics in Specific Patient Groups: It is known whether disorders of hepatic or renal function influence the pharmacokinetic parameters of Butrin.
Toxicology: Pre-Clinical Safety Data: Non-clinical data reveal no special hazard for humans based on conventional studies of safety pharmacology, repeated dose toxicity, genotoxicity, carcinogenic potential, toxicity to reproduction and development.
Butrin pharmacology
Sulfonylureas lower blood glucose in patients with type 2 diabetes by directly stimulating the acute release of insulin from functioning beta cells of pancreatic islet tissue by an unknown process that involves a sulfonylurea receptor (receptor 1) on the beta cell. Sulfonylureas inhibit the ATP-potassium channels on the beta cell membrane and potassium efflux, which results in depolarization and calcium influx, calcium-calmodulin binding, kinase activation, and release of insulin-containing granules by exocytosis, an effect similar to that of glucose.
Reviews
The results of a survey conducted on ndrugs.com for Butrin are given in detail below. The results of the survey conducted are based on the impressions and views of the website users and consumers taking Butrin. We implore you to kindly base your medical condition or therapeutic choices on the result or test conducted by a physician or licensed medical practitioners.User reports
Consumer reported administration
No survey data has been collected yetConsumer reviews
There are no reviews yet. Be the first to write one! |
Information checked by Dr. Sachin Kumar, MD Pharmacology
