5-carboxamidotryptamine (5-CT) is a 5-HT1 agonist with high affinity at 5-HT1A, 5-HT1B, 5-HT1D, 5-HT5 and 5-HT7 receptors. As one of the first compounds reported active at 5-HT1B, 5-carboxamidotryptamine was originally investigated as a potential treatment for migraine. During preclinical studies, 5-CT was found to cause vasodilatation of carotid circulation and hypotension in animals, effects that were later attributed to potent agonist activity at 5-HT7. Subsequent structural modifications of 5-CT led to the discovery of the anti-migraine drug sumatriptan. 5-CT is primarily used as a pharmacological tool for study of 5-HT1 and 5-HT7 mediated functional responses.

Vortioxetine DL-lactate is a lactate salt of vortioxetine and its chemical name is 1-[2-(2,4-dimethylphenylsulfanyl)-phenyl]-piperazine (RS)-2-hydroxypropanoate. Vortioxetine DL-lactate is manufactured from the milled Vortioxetine hydrobromide via the nonisolated free base. One site is involved in the manufacture of the lactate salt of Vortioxetine. Vortioxetine is an antidepressant for the treatment of major depressive disorder. Unlike the film-coated tablets where a hydrobromide salt of the active substance is used, the oral drops formulation contains vortioxetine DL-lactate as the active substance which shows higher solubility in polar solvents. Vortioxetine is a novel multimodal antidepressant that acts as a serotonin (5-HT)3, 5-HT7, and 5-HT1D receptor antagonist; 5-HT1B receptor partial agonist; 5-HT1A receptor agonist; and 5-HT transporter inhibitor in vitro.

Anpirtoline [D 16949] is a dichloropyridine derivative with antinociceptive and antidepressant activity. Anpirtoline has been described as an agonist at 5-HT1B and 5-HT1D receptors with a relatively high potency. It also acts as an agonist at 5-HT1A receptors, but has a lower potency than at the 5-HT1B sites. In addition, Anpirtoline acts as an antagonist at 5-HT3 receptors. The drug was in phase I clinical trials with ASTA Medica in Germany for the treatment of pain and depression, but development was suspended.

(-)-Propranolol is a small molecule β-adrenergic receptor antagonist and the active isomer of (±)-Propranolol preparations. (-)-Propranolol blocks the binding of epinephrine, norepinephrine, and other endogenous catecholamines to the β-adrenergic receptor, impeding increases in cardiac flow velocity and general stimulation of the sympathetic nervous system signaled by the association of these molecules to the β-adrenergic receptor. In addition to blockade of agonist binding, antagonism of the β-adrenergic receptor by (-)-Propranolol produces negative chronotropic and inotropic action, effectively dampening the force and rate of cardiac contraction. These negative chronotropic and inotropic effects correlate to a demonstrated suppression of adrenaline-induced cardiac arrhythmia by (-)-Propranolol. Suppression of β-adrenergic receptor activation by (-)-Propranolol has been widely exploited in counteracting situations sensitive to heightened cardiac activity including hypertension, angina pectoris, and cardiac ischemia.

Frovatriptan succinate (trade name Frova) is a selective 5-hydroxytryptamine1 (5-HT1B/1D) receptor subtype agonist, and is used for the treatment of migraine attacks with or without aura in adults. Frovatriptan has no significant effects on GABAA mediated channel activity and has no significant affinity for benzodiazepine binding sites. Frovatriptan is believed to act on extracerebral, intracranial arteries and to inhibit excessive dilation of these vessels in migraine. Serious but rare cardiac events have been reported in patients with risk factors predictive of coronary artery disease (CAD). These include coronary artery vasospasm, transient myocardial ischemia, myocardial infarction, ventricular tachycardia and ventricular fibrillation.

Frovatriptan succinate (trade name Frova) is a selective 5-hydroxytryptamine1 (5-HT1B/1D) receptor subtype agonist, and is used for the treatment of migraine attacks with or without aura in adults. Frovatriptan has no significant effects on GABAA mediated channel activity and has no significant affinity for benzodiazepine binding sites. Frovatriptan is believed to act on extracerebral, intracranial arteries and to inhibit excessive dilation of these vessels in migraine. Serious but rare cardiac events have been reported in patients with risk factors predictive of coronary artery disease (CAD). These include coronary artery vasospasm, transient myocardial ischemia, myocardial infarction, ventricular tachycardia and ventricular fibrillation.