Pindolol was developed at Sandoz at 1960s. Pindolol is a nonselective beta-adrenergic antagonist (beta-blocker) which possesses intrinsic sympathomimetic activity (partial agonist activity) in therapeutic dosage ranges but does not possess quinidine-like membrane stabilizing activity. The partial beta-adrenergic agonistic activity of pindolol in the heart appears to be completely restricted to the sinoatrial pacemaker. In standard pharmacologic tests in man and animals, Pindolol attenuates increases in heart rate, systolic blood pressure, and cardiac output resulting from exercise and isoproterenol administration, thus confirming its beta-blocking properties. In addition to beta-adrenergic activity pindolol demonstrates mixed agonist-antagonist activity at central 5-HT receptors. Although in accordance with the hypothesis that pindolol increases the antidepressant effects of selective serotonin reuptake inhibitors by antagonism of 5-HT at inhibitory 5-HT1A autoreceptors, pindolol possesses partial agonist activity at 5-HT1A receptors. Pindolol tablets are indicated in the management of hypertension.

Yohimbine is a plant alkaloid with alpha-2-adrenergic blocking activity. Yohimbine has been used as a mydriatic and in the treatment of impotence. The exact mechanism for its use in impotence has not been fully elucidated. Yohimbine exerts antagonist actions at halpha(2A)-AR, h5-HT(1B), h5-HT(1D), and hD(2) sites, partial agonist actions at h5-HT(1A) sites. Yohimbine-mediated norepinephrine release at the level of the corporeal tissues may also be involved. In addition, beneficial effects may involve other neurotransmitters such as dopamine and serotonin and cholinergic receptors. Yohimbine has a mild anti-diuretic action, probably via stimulation of hypothalmic center and release of posterior pituitary hormone. Reportedly yohimbine exerts no significant influence on cardiac stimulation and other effects mediated by (beta)-adrenergic receptors. Its effect on blood pressure, if any, would be to lower it; however, no adequate studies are at hand to quantitate this effect in terms of Yohimbine dosage. Side effect of Yohimbine include anxiety, tremor, palpitations, diarrhea, and supine hypertension.

Terguride (INN), also known as trans-dihydrolisuride, is a serotonin receptor antagonist and dopamine receptor agonist of the ergoline family. Terguride is approved for and used in the treatment of hyperprolactinemia. Terguride is an oral, potent antagonist of 5-HT2B and 5-HT2A (serotonin) receptors. Serotonin stimulates the proliferation of pulmonary artery smooth muscle cells and induces fibrosis in the wall of pulmonary arteries. Together, this causes vascular remodeling and narrowing of the pulmonary arteries. These changes result in increased vascular resistance and PAH. Due to the potential anti-proliferative and anti-fibrotic activity of terguride, this potential medicine could offer the hope of achieving reversal of pulmonary artery vascular remodeling and attenuation of disease progression. In May 2008, terguride was granted orphan drug status for the treatment of pulmonary arterial hypertension. In May 2010 Pfizer purchased worldwide rights for the drug.

Oxitriptan is an aromatic amino acid with antidepressant activity. In vivo, oxitriptan is converted into 5-hydroxytryptamine (serotonin) as well as other neurotransmitters. Oxitriptan may exert its antidepressant activity via conversion to serotonin or directly by binding to serotonin receptors within the central nervous system. It is used as an antiepileptic and antidepressant. Oxitriptan is a worthwhile addition to the limited treatments available for obsessive-compulsive disorder and panic disorder, two psychiatric disorders which have previously been difficult to manage pharmacologically. Possible gastrointestinal side effects are: nausea, vomiting, abdominal pain, constipation or flatulence, which tend to disappear with continued treatment or, in any case, dose reduction. Other undesirable effects such as anorexia, xerostomia, tachycardia, extrasystoles, dizziness, headache, lightheadedness, tremor or myalgia may occur.

Pindolol was developed at Sandoz at 1960s. Pindolol is a nonselective beta-adrenergic antagonist (beta-blocker) which possesses intrinsic sympathomimetic activity (partial agonist activity) in therapeutic dosage ranges but does not possess quinidine-like membrane stabilizing activity. The partial beta-adrenergic agonistic activity of pindolol in the heart appears to be completely restricted to the sinoatrial pacemaker. In standard pharmacologic tests in man and animals, Pindolol attenuates increases in heart rate, systolic blood pressure, and cardiac output resulting from exercise and isoproterenol administration, thus confirming its beta-blocking properties. In addition to beta-adrenergic activity pindolol demonstrates mixed agonist-antagonist activity at central 5-HT receptors. Although in accordance with the hypothesis that pindolol increases the antidepressant effects of selective serotonin reuptake inhibitors by antagonism of 5-HT at inhibitory 5-HT1A autoreceptors, pindolol possesses partial agonist activity at 5-HT1A receptors. Pindolol tablets are indicated in the management of hypertension.

Yohimbine is a plant alkaloid with alpha-2-adrenergic blocking activity. Yohimbine has been used as a mydriatic and in the treatment of impotence. The exact mechanism for its use in impotence has not been fully elucidated. Yohimbine exerts antagonist actions at halpha(2A)-AR, h5-HT(1B), h5-HT(1D), and hD(2) sites, partial agonist actions at h5-HT(1A) sites. Yohimbine-mediated norepinephrine release at the level of the corporeal tissues may also be involved. In addition, beneficial effects may involve other neurotransmitters such as dopamine and serotonin and cholinergic receptors. Yohimbine has a mild anti-diuretic action, probably via stimulation of hypothalmic center and release of posterior pituitary hormone. Reportedly yohimbine exerts no significant influence on cardiac stimulation and other effects mediated by (beta)-adrenergic receptors. Its effect on blood pressure, if any, would be to lower it; however, no adequate studies are at hand to quantitate this effect in terms of Yohimbine dosage. Side effect of Yohimbine include anxiety, tremor, palpitations, diarrhea, and supine hypertension.

Terguride (INN), also known as trans-dihydrolisuride, is a serotonin receptor antagonist and dopamine receptor agonist of the ergoline family. Terguride is approved for and used in the treatment of hyperprolactinemia. Terguride is an oral, potent antagonist of 5-HT2B and 5-HT2A (serotonin) receptors. Serotonin stimulates the proliferation of pulmonary artery smooth muscle cells and induces fibrosis in the wall of pulmonary arteries. Together, this causes vascular remodeling and narrowing of the pulmonary arteries. These changes result in increased vascular resistance and PAH. Due to the potential anti-proliferative and anti-fibrotic activity of terguride, this potential medicine could offer the hope of achieving reversal of pulmonary artery vascular remodeling and attenuation of disease progression. In May 2008, terguride was granted orphan drug status for the treatment of pulmonary arterial hypertension. In May 2010 Pfizer purchased worldwide rights for the drug.

Terguride (INN), also known as trans-dihydrolisuride, is a serotonin receptor antagonist and dopamine receptor agonist of the ergoline family. Terguride is approved for and used in the treatment of hyperprolactinemia. Terguride is an oral, potent antagonist of 5-HT2B and 5-HT2A (serotonin) receptors. Serotonin stimulates the proliferation of pulmonary artery smooth muscle cells and induces fibrosis in the wall of pulmonary arteries. Together, this causes vascular remodeling and narrowing of the pulmonary arteries. These changes result in increased vascular resistance and PAH. Due to the potential anti-proliferative and anti-fibrotic activity of terguride, this potential medicine could offer the hope of achieving reversal of pulmonary artery vascular remodeling and attenuation of disease progression. In May 2008, terguride was granted orphan drug status for the treatment of pulmonary arterial hypertension. In May 2010 Pfizer purchased worldwide rights for the drug.