||Properties of R-enantiomer
||Properties of S-enantiomer
||Unichiral drugs approved for use
||Inhibits the elimination of S-ketamine in the racemate
||Two to three times more potent than racemic 2,3 ketamine. Eliminated more rapidly as a single enantiomer than as a component of the racemate. Incidence of psychotomimetic phenomena is negligibly less with Sketamine
in comparison to racemic ketamine.
||Inactive as bronchodilator but not completely inert and can induce airway hyper-reactivity, eventually contributing to
increased morbidity and mortality in patients with asthma.
||More propensity for anticholinergic effects.
||More active than R-zopiclone at the benzodiazepine receptor complex and is responsible for most of the hypnotic activity
of the racemic compound. Shorter duration of action, which could minimize or prevent
residual hangover effects.
||Smaller volume of distribution, smaller even than that of cetirizine - confers improved
safety because of low hemato-encephalic barrier passage and low cerebral receptor binding. Enhanced peripheral receptor
binding and improved overall selectivity specific to the H1 receptor than the racemate. Pharmacokinetic studies
indicate improved safety profile.
||Inactive nature (large-scale comparative studies are however, warranted to address the issue).
||Inactive as a calcium channel blocker but may not be completely inert. Mainly responsible for blunting of precapillary
postural vasoconstrictor reflex and for other local changes responsible for peripheral edema due to racemic amlodipine.
||Only vasoactive enantiomer of amlodipine Longer plasma half-life. Lesser intersubject variability in the clearance. Negligible
incidence of peripheral oedema than the racemate.
||Relatively stronger activity in blocking beta-2 receptors than beta-1 receptors. Responsible for loss of cardioselectivity at
higher doses of racemate
||Predominantly responsible for cardiac beta-blocking activity.
||Relatively stronger activity in blocking beta-2 receptors than beta-1 receptors. Responsible for loss of cardioselectivity at higher doses of racemate. Clearance is slower than S-metoprolol in poor metabolizers, resulting in higher concentrations of the non-selective R-enantiomer if a racemate is administered.
||Predominantly responsible for cardiac beta-blocking activity. Ensures cardioselectivity even in poor metabolizers as concentrations of only the beta-1-selective component would be increased. Avoids some harmful drug-interactions with some drugs like paroxetine, cimetidine, ciprofloxacin and verapamil, which selectively increase the
concentrations of non-selective R-metoprolol.
||Exhibits greater variability than S-isomer in poor versus extensive metabolizers of CYP2C19 substrates.More dependent on CYP2C19. This results in the less active Renantiomer achieving higher concentrations in poor metabolizers, which may in the long term cause adverse effects like gastric carcinoids and enterochromaffin-like cell hyperplasia.
||Could be metabolized by alternative pathways like CYP3A4 and sulfotransferases. Clinically more effective than the racemate.
||Exhibits greater variability than their Sisomers in poor versus extensive metabolizers of CYP2C19 substrates. More dependent on CYP2C19. This results in the less active R-enantiomer achieving higher concentrations in poor metabolizers, which may in the long term cause adverse effects like gastric carcinoids and enterochromaffin-
like cell hyperplasia.
||Could be metabolized by alternative path ways like CYP3A4 and sulfotransferases Clinically more effective
than the racemate.
||No QTc prolongation.29 Less cardiotoxic than ei ther S-ondanset ron or racemic ondansetron. More potent than the Sisomer.
||Causes QTc prolongation.
||Cardiotoxic effects and toxic effects on the CNS.
||Less cardiotoxic effects and less toxic effects on the CNS in comparison with both dextrobupivacaine and bupivacaine itself. Wider safety margin than the racemate.