Manidipine, (S)- is enantiomer of Manidipine a lipophilic, third-generation dihydropyridine calcium channel antagonist with a high degree of selectivity for the vasculature, thereby inducing marked peripheral vasodilation with negligible cardiodepression. Manidipine has different pharmacological effects and (S)-manidipine is shown to be about 30–80 times more potent than (R)-manidipine in its antihypertensive action and in the radioligand binding assay. Patch-clamp experiments revealed that the S-enantiomers of manidipine displayed a faster onset of action and produced a greater blockade than the R-enantiomer. Also, manidipine enantiomers have markedly different pharmacokinetics and the S/R ratio for (S)- and (R)-enantiomer concentrations is 2.0

Manidipine, (R)- is enantiomer of Manidipine a lipophilic, third-generation dihydropyridine calcium channel antagonist with a high degree of selectivity for the vasculature, thereby inducing marked peripheral vasodilation with negligible cardiodepression. Manidipine has different pharmacological effects and (S)-manidipine is shown to be about 30–80 times more potent than (R)-manidipine in its antihypertensive action and in the radioligand binding assay. Patch-clamp experiments revealed that the S-enantiomers of manidipine displayed a faster onset of action and produced a greater blockade than the R-enantiomer. Also, manidipine enantiomers have markedly different pharmacokinetics and the S/R ratio for (S)- and (R)-enantiomer concentrations is 2.0

Betaxolol is a competitive, beta(1)-selective (cardioselective) adrenergic antagonist. Betaxolol is used to treat hypertension, arrhythmias, coronary heart disease, glaucoma, and is also used to reduce non-fatal cardiac events in patients with heart failure. (R)-Betaxolol (Dextrobetaxolol) is the R-isomer of Betaxolol (B328000), a cardioselective β1-adrenergic blocker. It is also an antihypertensive and antiglaucoma agent. Dextrobetaxolol had a much weaker affinity at both b1 and b2 receptors than levobetaxolol. Levobetaxolol (Kb=6 nM at b1 and Kb=39 nM at b2 receptors) more potently inhibited functional activities in cells expressing human recombinant b1 and b2 receptors than dextrobetaxolol (Kb=350 and 278 nM, respectively). Likewise, levobetaxolol was a more potent antagonist in isolated tissues than dextrobetaxolol. In functional assays in cultured human NPE cells levobetaxolol (Ki =16.4 nM) was a potent antagonist of isoproterenol-induced cAMP production with dextrobetaxolol (Ki =2.9 uM) being considerably weaker than the latter antagonist. In ocular hypertensive cynomolgus monkeys, levobetaxolol was more effective at reducing IOP than dextrobetaxolol. The results of the study of the pharmacokinetic behavior of the R and S enantiomers of betaxolol following iv and oral administration of the racemate to healthy male subjects failed to reveal any important difference between the pharmacokinetics of the R and S enantiomer of betaxolol. Thus, the pharmacokinetic behavior of racemic betaxolol accurately reflects the behavior of betaxolol enantiomers in this subject group.

Azelnidipine is a dihydropyridine calcium channel antagonist being jointly developed by Daiichi Sankyo Inc (formerly Sankyo) and Ube Industries. Azelnidipine is a L-type calcium channel antagonist. Azelnidipine was approved by Pharmaceuticals and Medicals Devices Agency of Japan (PMDA) on Jan 31, 2003. Azelnidipine is indicated for the treatment of hypertension. Its trend name is Calblock. Azelnidipine has two enantiomers (R-(−)- and S-( )-enantiomers) due to an asymmetric carbon at the 4-position, and the (R)-(−) enantiomer of dihydropyridine calcium antagonists is considered to possess intrinsic pharmacological activity. The pharmacological action of azelnidipine resides in the (R)-enantiomer. This is in marked contrast to other calcium channel blocker (CCB) in which the (S)-enantiomer is responsible for the biological activity. There were no significant differences in the inhibitory effects on TGF-b1-induced expression of COL1A1 mRNA among vitamin E - pretreated LX-2 cells treated with azelnidipine (racemate), (R)-(-)-azelnidipine or (S)-( )-azelnidipine, although the L-type voltage-operated calcium channel blocking activity of (R)-(-)- enantiomer was more potent than that of the (S)-( )- enantiomer.

Azelnidipine is a dihydropyridine calcium channel antagonist being jointly developed by Daiichi Sankyo Inc (formerly Sankyo) and Ube Industries. Azelnidipine is a L-type calcium channel antagonist. Azelnidipine was approved by Pharmaceuticals and Medicals Devices Agency of Japan (PMDA) on Jan 31, 2003. Azelnidipine is indicated for the treatment of hypertension. Its trend name is Calblock. Azelnidipine has two enantiomers (R-(−)- and S-( )-enantiomers) due to an asymmetric carbon at the 4-position, and the (R)-(−) enantiomer of dihydropyridine calcium antagonists is considered to possess intrinsic pharmacological activity. The pharmacological action of azelnidipine resides in the (R)-enantiomer. This is in marked contrast to other calcium channel blocker (CCB) in which the (S)-enantiomer is responsible for the biological activity. There were no significant differences in the inhibitory effects on TGF-b1-induced expression of COL1A1 mRNA among vitamin E - pretreated LX-2 cells treated with azelnidipine (racemate), (R)-(-)-azelnidipine or (S)-( )-azelnidipine, although the L-type voltage-operated calcium channel blocking activity of (R)-(-)- enantiomer was more potent than that of the (S)-( )- enantiomer.

Talinolol (brand name Cordanurn) is the cardioselective beta-receptor antagonist which has been used for a long time in the treatment of various cardiovascular diseases and in tachyarrhythmia. The mean dosage is 10-20 mg intravenously administered over a period of 3-5 minutes, while the chronic oral dosage for this patient group amounts to 300mg/day. Cordanum eliminates the stimulating effect of catecholamines on the heart for physical and psychoemotional stress. The hypotensive effect is stabilized by the end of 2 weeks of course treatment. Reduces the frequency and severity of angina attacks; Contributes to the limitation of the heart attack zone and reduces the risk of arrhythmia in the presence of myocardial infarction, resulting in a decrease in mortality and the frequency of relapses. In average therapeutic doses, it has a less pronounced effect on the smooth muscles of the bronchi, myometrium, and peripheral arteries compared to non-selective beta-blockers. Talinolol is used in supraventricular (atrial fibrillation and flutter with high ventricular rate, paroxysmal supraventricular 1 tachycardia, sinus tachycardia) as well as ventricular extrasystoles and ventricular tachyarrhythmias. Patients with an increased tonus of the sympathetic nervous system related to sinus tachycardia, exercise-induced arrhythmias, hypertension, hyperthyroidism and coronary heart disease show a particularly positive reaction.

3-ISOPROPYLAMINO-1,2-PROPANEDIOL (Indenolol) is an antihypertensive agent, whose beta 1-adrenoceptor antagonist properties combined with beta 2-adrenoceptor agonist properties have been shown by experimental studies in animals. It was used for the treatment of angina pectoris, hypertension, arrhythmias

CAPOZIDE (captopril and hydrochlorothiazide tablets, USP) for oral administration combines two antihypertensive agents: captopril and hydrochlorothiazide. The mechanism of action of captopril has not yet been fully elucidated. Captopril prevents the conversion of angiotensin I to angiotensin II by inhibition of ACE, a peptidyldipeptide carboxy hydrolase. Hydrochlorothiazide belongs to thiazide class of diuretics. It reduces blood volume by acting on the kidneys to reduce sodium (Na+) reabsorption in the distal convoluted tubule. CAPOZIDE (captopril and hydrochlorothiazide tablets, USP) is indicated for the treatment of hypertension. The blood pressure lowering effects of captopril and thiazides are approximately additive. Major side effects are: Black, tarry stools; chest pain; chills; cough; fever; painful or difficult urination; shortness of breath; sore throat; sores, ulcers, or white spots on lips or in mouth; swollen glands; unusual bleeding or bruising; unusual tiredness or weakness. It has been reported that indomethacin may reduce the antihypertensive effect of captopril, especially in cases of low renin hypertension. Captopril’s effect will be augmented by antihypertensive agents that cause renin release. For example, diuretics (e.g., thiazides) may activate the renin-angiotensin-aldosterone system.

Penflutizide ‎is a thiazide diuretic drug, Na+-Cl- symport inhibitor. Penflutizide was shown to have high potency to photooxidize lipids. Penflutizide -photosensitized peroxidation of squalene was repressed by the presence of sodium azide or 2,5-dimethylfuran and was accelerated in a D2O suspension. These findings suggest the participation of singlet oxygen in Penflutizide photoperoxidation of squalene (type II mechanism). Penflutizide -photosensitized lysis of red blood cells (RBC) accompanied by formation of hydroperoxides in RBC membrane lipids was also noted. These results suggested that membrane lipids can be one of the target molecules of Penflutizide phototoxicity. Penflutizide ‎is an ingredient of the drug Praemenstron manufactured by Nordmark Arzneimittel and consisting of Flumedroxone, Meprobamate, Penflutizide.