Deserpidine is an ester alkaloid drug isolated from Rauwolfia canescens (family Apocynaceae) with antipsychotic and antihypertensive properties that has been used for the control of high blood pressure and for the relief of psychotic behavior. Rauwolfia alkaloids work by controlling nerve impulses along certain nerve pathways. As a result, they act on the heart and blood vessels to lower blood pressure. Deserpidine's mechanism of action is through inhibition of the ATP/Mg2+ pump responsible for the sequestering of neurotransmitters into storage vesicles located in the presynaptic neuron. The neurotransmitters that are not sequestered in the storage vesicle are readily metabolized by monoamine oxidase (MAO) causing a reduction in catecholamines.

Reserpine is an alkaloid, isolated from the Rauwolfia serpentina plant and developed by Ciba pharma. Reserpine was approved by FDA for the treatment of hypertension and psychotic disorders. The drug exerts its effect by blocking two vesicular monoamine transporters, VMAT1 and VMAT2. The blockade results in vesicles that lose their ability to store neurotransmitter molecules. Neurotransmitters, thus retained in cytosol, are then neutralized by MAO.

Monobenzone is a topical drug used for medical depigmentation. The mechanism of action of monobenzone is not fully understood. Monobenzone is oxidized by tyrosinase from melanocytes to a toxic quinones which induce non-apoptotic melanocyte cell death.

Mephenytoin is an antiepileptic drug which can be useful in the treatment of epilepsy. The primary site of action appears to be the motor cortex where spread of seizure activity is inhibited. Possibly by promoting sodium efflux from neurons, mephenytoin tends to stabilize the threshold against hyperexcitability caused by excessive stimulation or environmental changes capable of reducing membrane sodium gradient. This includes the reduction of posttetanic potentiation at synapses. Loss of posttetanic potentiation prevents cortical seizure foci from detonating adjacent cortical areas. Mephenytoin reduces the maximal activity of brain stem centers responsible for the tonic phase of tonic-clonic (grand mal) seizures. The mechanism of action of mephenytoin is not definitely known, but extensive research strongly suggests that its main mechanism is to block frequency-, use- and voltage-dependent neuronal sodium channels, and therefore limit repetitive firing of action potentials. Mephenytoin is no longer available in the US or the UK. It is still studied largely because of its interesting hydroxylation polymorphism.

Trimethadione (brand name is TRIDIONE) is an oxazolidinedione compound that was developed as an antiepileptic agent for control of petit mal seizures that are refractory to treatment with other drugs. Tridione does not modify the maximal seizure pattern in patients undergoing electroconvulsive therapy and has a sedative effect that may increase to the point of ataxia when excessive doses are used. Trimethadione acts as a voltage-activated T-type Ca2+ channel blocker. Trimethadione is rapidly absorbed from the gastrointestinal tract. It is demethylated by liver microsomes to the active metabolite, dimethadione. Approximately 3% of a daily dose of tridione is recovered in the urine as the unchanged drug. The majority of trimethadione is excreted slowly by the kidney in the form of dimethadione.

Guanidine is a small basic compound. Guanidine stimulates the neuromuscular junction presynaptically by inhibiting voltage-gated potassium (Kv) channels, leading to the enhanced release of acetylcholine in the synaptic cleft. This stimulatory effect of guanidine underlies its use in the therapy for the neuromuscular diseases. The hydrochloride salt of guanidine was approved by FDA for the reduction of the symptoms of muscle weakness and easy fatigability associated with the myasthenic syndrome of Eaton-Lambert.

Monoethanolamine is both a primary amine and a primary alcohol. It is an olamine derivative. Monoethanolamine occurs in every cell in the human body as the head group of Phosphatidylethanolamine. Monoethanolamine is a component of glycosylphosphatidylinositol-anchored proteins, which are essential for viability. Other sources of monoethanolamine or phosphoethanolamine in the human body are the degradation of sphingosine phosphate by sphingosine phosphate lyase and the degradation of the endocannabinoid anandamide by the fatty acid amine hydrolase. Monoethanolamine stimulates the rapid growth of mammalian cells in culture. Monoethanolamine has a cardioprotective role against ischemia/reperfusion injury via activation of the transcription factor STAT-3. Monoethanolamine is a chemical intermediate in the manufacture of cosmetics, surface-active agents, emulsifiers, pharmaceuticals, and plasticizing agents.

Verteporfin (trade name Visudyne), a benzoporphyrin derivative, is a medication used for the treatment of patients with predominantly classic subfoveal choroidal neovascularization due to age-related macular degeneration, pathologic myopia or presumed ocular histoplasmosis syndrome. Verteporfin can also be used to destroy tumors. Verteporfin is a 1:1 mixture of two regioisomers (I and II), VISUDYNE therapy is a two-stage process requiring administration of both verteporfin for injection and nonthermal red light. Verteporfin accumulates in these abnormal blood vessels and, when stimulated by nonthermal red light with a wavelength of 689 nm in the presence of oxygen, produces highly reactive short-lived singlet oxygen and other reactive oxygen radicals, resulting in local damage to the endothelium and blockage of the vessels. Verteporfin is also used off-label for the treatment of central serous retinopathy. Verteporfin is given intravenously, 15 minutes before laser treatment. Light activation of verteporfin results in local damage to neovascular endothelium, resulting in vessel occlusion. Damaged endothelium is known to release procoagulant and vasoactive factors through the lipo-oxygenase (leukotriene) and cyclo-oxygenase (eicosanoids such as thromboxane) pathways, resulting in platelet aggregation, fibrin clot formation and vasoconstriction. Verteporfin appears to somewhat preferentially accumulate in neovasculature, including choroidal neovasculature. However, animal models indicate that the drug is also present in the retina. Therefore, there may be collateral damage to retinal structures following photoactivation including the retinal pigmented epithelium and outer nuclear layer of the retina. The temporary occlusion of choroidal neovascularization (CNV) following VISUDYNE therapy has been confirmed in humans by fluorescein angiography.