Indirin Mechanism of Action

Pharmacology: Pharmacodynamics: Propranolol Hydrochloride (Indirin) is a competitive antagonist at both the β-1 and β-2 adrenoceptors. It has no agonist activity at the beta-adrenoceptor, but has membrane stabilizing activity at concentrations exceeding 1-3 mg/liter, though such concentrations are rarely achieved during oral therapy. Competitive beta-adrenoceptor blockade has been demonstrated in man by a parallel shift to the right in the dose-heart rate response curve to beta agonists such as Isoprenaline.
Propranolol Hydrochloride (Indirin), as with other beta-blockers, has negative inotropic effects, and is therefore contraindicated in uncontrolled heart failure (see Precautions).
Propranolol is a racemic mixture and the active form is the S (-) isomer of propranolol. With the exception of inhibition of the conversion of thyroxine to triiodothyronine, it is unlikely that any additional ancillary properties possessed by R (+) propranolol in comparison with racemic mixture will give rise to different therapeutic effects.
Propranolol Hydrochloride (Indirin) is effective and well-tolerated in most ethnic populations, although the response may be less in black patients.
Pharmacokinetics: Propranolol is completely absorbed after oral administration and peak plasma concentrations occur 1-2 hours after dosing in fasting patients. The liver removes up to 90% of an oral dose with an elimination half-time of 3 to 6 hours. Propranolol is widely and rapidly distributed throughout the body with the highest levels occurring in the lungs, liver, kidney, brain and heart. Propranolol is highly protein bound (80-95%).
Toxicology: Preclinical Safety Data: Non-clinical data reveal no special hazard for humans based on conventional studies of safety pharmacology, repeated dose toxicity, local tolerance, genotoxicity, carcinogenic potential and toxicity to reproduction.