Carvedilol competitively blocks β1, β2 and α1 receptors. The drug lacks sympathomimetic activity and has vasodilating properties that are exerted primarily through α1-blockade. Animal models indicate that carvedilol confers protection against myocardial necrosis, arrhythmia and cell damage caused by oxidising free radicals, and the drug has no adverse effects on plasma lipid profiles. COREG® (carvedilol) is a racemic mixture in which nonselective β-adrenoreceptor blocking activity is present in the S(-) enantiomer and α1-adrenergic blocking activity is present in both R(+) and S(-) enantiomers at equal potency. Carvedilol is the first drug of its kind to be approved for the treatment of congestive heart failure, and is now the standard of care for this devastating disease. Carvedilol is also confirmed as effective in the management of mild to moderate hypertension and ischaemic heart disease.

(S)-carvedilol, an enantiomer of the drug carvedilol, which is used in the treatment of mild to moderate congestive heart failure. (S)-carvedilol is an alpha- and beta-adrenergic receptor blocker. It was shown, that only (S)-carvedilol caused beta-blockade. It was suggested, that the weak clinical net effect of beta-blockade of (R, S)-carvedilol at rest could be one reason why this drug causes fewer side effects than other beta-blockers, such as a reduction of nocturnal melatonin release.

(R)-carvedilol, an enantiomer of the drug carvedilol, which is used in the treatment of mild to moderate congestive heart failure. (R)-carvedilol is an alpha adrenergic receptor blocker. It was shown, that (R)-carvedilol increased sympathetic tone, presumably as a physiological reaction to the decrease in blood pressure caused by alpha-blockade. The weak clinical net effect of beta-blockade of (R, S)-carvedilol at rest might be one reason why this drug causes fewer side effects than other beta-blockers, such as a reduction of nocturnal melatonin release.