Penbutolol is a new beta-adrenergic blocking drug approved for the treatment of hypertension. It is a noncardioselective beta-blocker and has intrinsic sympathomimetic activity. Penbutolol is marketed under the trade names Levatol, Levatolol, Lobeta, Paginol, Hostabloc, Betapressin. Penbutolol acts on the β1 adrenergic receptors in both the heart and the kidney. When β1 receptors are activated by catecholamines, they stimulate a coupled G protein that leads to the conversion of adenosine triphosphate (ATP) to cyclic adenosine monophosphate (cAMP). The increase in cAMP leads to activation of protein kinase A (PKA), which alters the movement of calcium ions in heart muscle and increases the heart rate. Penbutolol blocks the catecholamine activation of β1 adrenergic receptors and decreases heart rate, which lowers blood pressure. Levatol (Penbutolol) is indicated in the treatment of mild to moderate arterial hypertension. It may be used alone or in combination with other antihypertensive agents, especially thiazide-type diuretics.

Encainide is an antiarrhythmic drug, developed by Bristol Myers Co supplied 25 and 35 mg capsules for oral administration. Encainide is no longer used because of its frequent proarrhythmic side effects. The mechanisms of the antiarrhythmic effects of Enkaid are unknown but probably are the result of its ability to slow conduction, reduce membrane responsiveness, inhibit automaticity, and increase the ratio of the effective refractory period to action potential duration. Enkaid produces a differentially greater effect on the ischemic zone as compared with normal cells in the myocardium. This could result in the elimination of the disparity in the electrophysiologic properties between these two zones and eliminate pathways of abnormal impulse conduction, development of boundary currents and/or sites of abnormal impulse generation. The absorption of Enkaid after oral administration is nearly complete with peak plasma levels present 30 to 90 minutes after dosing. There are two major genetically determined patterns of encainide metabolism. In over 90% of patients, the drug is rapidly and extensively metabolized with an elimination half-life of 1 to 2 hours. These patients convert encainide to two active metabolites, O-demethylencainide (ODE) and 3-methoxy-O-demethylencainide (MODE), that are more active (on a per mg basis) than encainide itself. In less than 10% of patients, metabolism of encainide is slower and the estimated encainide elimination half-life is 6 to 11 hours. Slow metabolism of encainide is associated with a diminished ability to metabolize debrisoquin. Enkaid should be administered only after appropriate clinical assessment and the dosage of Enkaid must be individualized for each patient on the basis of therapeutic response and tolerance. The recommended initial dosing schedule for adults is one 25 mg Enkaid capsule t.i.d. at approximately 8-hour intervals.

Niclosamide is an antihelminth used against tapeworm infections. It may act by the uncoupling of the electron transport chain to ATP synthase. The disturbance of this crucial metabolic pathway prevents creation of adenosine tri-phosphate (ATP), an essential molecule that supplies energy for metabolism. Niclosamide works by killing tapeworms on contact. Adult worms (but not ova) are rapidly killed, presumably due to uncoupling of oxidative phosphorylation or stimulation of ATPase activity. The killed worms are then passed in the stool or sometimes destroyed in the intestine. Niclosamide may work as a molluscicide by binding to and damaging DNA. Niclosamide is used for the treatment of tapeworm and intestinal fluke infections: Taenia saginata (Beef Tapeworm), Taenia solium (Pork Tapeworm), Diphyllobothrium latum (Fish Tapeworm), Fasciolopsis buski (large intestinal fluke). Niclosamide is also used as a molluscicide in the control of schistosomiasis. Niclosamide was marketed under the trade name Niclocide, now discontinued.

Zomepirac Sodium (Zomax) is a pyrrole-acetic acid structurally related to tolmetin sodium. Zomepirac is a prostaglandin synthetase inhibitor and is not an opioid, an opioid antagonist, or a salicylate. Zomepirac was approved by the Food and Drug Administration for marketing in the United States as an analgesic. It was indicated for all forms of mild to moderately severe pain, and was being promoted as a "comprehensive, non-addicting analgesic." Later Zomepirac was found to be associated with fatal and near-fatal anaphylactoid reactions. The manufacturer voluntarily removed Zomax tablets from the Canadian, US, and UK markets in March 1983.

Maprotiline is a tetracyclic antidepressant with similar pharmacological properties to tricyclic antidepressants (TCAs). Similar to TCAs, maprotiline inhibits neuronal norepinephrine reuptake, possesses some anticholinergic activity, and does not affect monoamine oxidase activity. It differs from TCAs in that it does not appear to block serotonin reuptake. Maprotiline may be used to treat depressive affective disorders, including dysthymic disorder (depressive neurosis) and major depressive disorder. Maprotiline is effective at reducing symptoms of anxiety associated with depression. The mechanism of action of maprotiline is not precisely known. It does not act primarily by stimulation of the central nervous system and is not a monoamine oxidase inhibitor. The postulated mechanism of maprotiline is that it acts primarily by potentiation of central adrenergic synapses by blocking reuptake of norepinephrine at nerve endings. This pharmacologic action is thought to be responsible for the drug’s antidepressant and anxiolytic effects. The mean time to peak is 12 hours. The half-life of elimination averages 51 hours.

Triclosan was used as a hospital scrub in the 1970s. Since then, it has expanded commercially and is now prevalent in soaps (0.10-1.00%), shampoos, deodorants, toothpastes, mouth washes, cleaning supplies and pesticides. It is part of consumer products, including kitchen utensils, toys, bedding, socks and trash bags. In healthcare, triclosan is used in surgical scrubs and hand washes. Use in surgical units is effective with a minimum contact time of approximately two minutes. More recently, showering with 2% triclosan has become a recommended regimen in surgical units for the decolonization of patients whose skin carries methicillin-resistant Staphylococcus aureus (MRSA). Triclosan is also used in the coatings for some surgical sutures. Triclosan has been employed as a selective agent in molecular cloning. At high concentrations, triclosan acts as a biocide with multiple cytoplasmic and membrane targets. However, at the lower concentrations seen in commercial products, triclosan appears bacteriostatic, and it targets bacteria primarily by inhibiting fatty acid synthesis. Triclosan binds to bacterial enoyl-acyl carrier protein reductase (ENR) enzyme, which is encoded by the gene FabI. This binding increases the enzyme's affinity for nicotinamide adenine dinucleotide (NAD+). This results in the formation of a stable, ternary complex of ENR-NAD+-triclosan, which is unable to participate in fatty acid synthesis. Fatty acids are necessary for building and reproducing cell membranes. Humans do not have an ENR enzyme and thus are not affected.

Butaperazine is an antipsychotic phenothiazine. As shown in animal studies butaperazine increases striatal and mesolimbic dopamine turnover. Butaperazine is effective in the management of schizophrenia. Extrapyramidal symptoms and drowsiness are the most common adverse effects.

Levomepromazine (also known as methotrimeprazine) is a phenothiazine neuroleptic drug. It is sold in many countries under the generic name (levomepromazine) or under brand names such as Nozinan, Detenler and many more. Levomepromazine is an antipsychotic drug is commonly used as an antiemetic to alleviate nausea and vomiting in palliative care settings particularly in terminal illness. Levomepromazine is a phenothiazine with pharmacological activity similar to that of both chlorpromazine and promethazine. It has the histamine-antagonist properties of the antihistamines together with central nervous system effects resembling those of chlorpromazine. Levomepromazine's antipsychotic effect is largely due to its antagonism of dopamine receptors in the brain. In addition, it can block 5HT2 receptors and some others, like histamine, serotonin.

Dydrogesterone is an orally active progestogen which acts directly on the uterus, producing a complete secretory endometrium in an estrogen-primed uterus. At therapeutic levels, dydrogesterone has no contraceptive effect as it does not inhibit or interfere with ovulation or the corpus luteum. Furthermore, dydrogesterone is non-androgenic, non-estrogenic, non-corticoid, non-anabolic and is not excreted as pregnanediol. Dydrogesterone helps to regulate the healthy growth and normal shedding of the uterus lining. Therefore, it may be useful in the treatment of menstrual disorders such as absent, irregular or painful menstrual periods, infertility, premenstrual syndrome and endometriosis. Dydrogesterone works by regulating the healthy growth and normal shedding of the womb lining by acting on progesterone receptors in the uterus. Used to treat irregular duration of cycles and irregular occurrence and duration of periods caused by progesterone deficiency. Also used to prevent natural abortion in patients who have a history of habitual abortions. Dydrogesterone was first introduced to the market in 1961, and is currently approved in over 100 countries world-wide. Banned in the USA and wthdrawn from the UK, but still used in other countries.

Chlorprothixene (Taractan, Tarasan, Truxal) is a thioxanthine derivative developed by Lundbeck for the treatment of psychotic disorders. The drug exerts its activity by binding to and inhibiting serotonin receptors, dopamine receptors, muscarinic acetylcholine receptor, histamine H1 receptor and alpha1-adrenergic receptor.