Pleconaril (Picovir) is an antiviral drug that was being developed by Schering-Plough for prevention of asthma exacerbations and common cold symptoms in patients exposed to picornavirus respiratory infections. Pleconaril binds to a hydrophobic pocket in viral protein 1, the major protein which comprises the capsid (the outer "shell") of picornaviruses. In enteroviruses, this prevents the virus from exposing its RNA, and in rhinoviruses, it also prevents the virus from attaching itself to the host cell. The results of two randomized, double-blind, placebo studies found Pleconaril treatment could benefit patients suffering from colds due to picornaviruses. Participants in the studies were healthy adults from Canada and the United States, with self-diagnosed colds that had occurred within 24 hours of trial enrollment. Participants were randomly given a placebo or two 200 mg tablets to take three times daily for five days. To increase absorption it was recommended to be taken after a meal. To monitor the effectiveness of Pleconaril, Participants recorded the severity of their symptoms and nasal mucosal samples were obtained at enrollment, day 3, day 6 and day 18. The two studies had a total of 2096 participates and more than 90% (1945) completed the trial. The most common reason for a participant not finishing the trial was an adverse event. Pleconaril treatment showed a reduction in nose blowing, sleep disturbance, and less cold medication used. The U.S. Food and Drug Administration rejected pleconaril in 2002 due to the side effects. The most commonly reported side effects were mild to a moderate headache, diarrhea, and nausea.

Fipronil is a member of the phenyl pyrazole class of pesticides, which are principally chemicals with a herbicidal effect. Fipronil, however, acts as an insecticide with contact and stomach action. Fipronil is an extremely active molecule and is a potent disruptor of the insect central nervous system via the (-aminobutyric acid (GABA) regulated chloride channel. Fipronil is classed as a WHO Class II moderately hazardous pesticide. Cutaneous skin reactions appear to be the most common adverse drug experiences reported for fipronil in dogs and cats.Animals exposed to large doses of fipronil via accidental oral absorption are expected to display seizures, and neurological and hepatic function should be monitored. There appear to be no reported interactions between fipronil and approved companion animal drugs and ectoparasiticides.

Glurenorm is an anti-diabetic drug in the sulfonylurea class. It is used in the treatment of diabetes mellitus type 2. It is an ATP-dependent K+ (KATP) channel blocker. This block causes a depolarization which leads to activation of voltage-dependent Ca channels and Ca2+ influx, and eventually increases insulin release. Minor skin allergies, gastric upsets and other non-specific side effects have been reported. Hypoglycaemic reactions have been reported but they are infrequent. Glurenorm effect increase butadion, chloramphenicol, tetracycline, coumarin derivatives, cyclophosphamide, sulfonamides, MAO inhibitors, thiazide diuretics, beta-blockers, salicylates, alcohol.

Dequalinium is a quaternary ammonium cation commonly available as the dichloride salt. Dequalinium chloride has an antiseptic effect against a wide range of bacteria, yeasts, and some fungi and viruses. It kills the micro-organisms associated with various mild infections of the mouth and throat. Also, Dequalinium chloride is active against the bacteria which cause bacterial vaginosis. Dequalinium Chloride (DECA) is a PKC inhibitor and high-affinity blocker CNGA1 channel, and nearly as effective on heteromeric CNGA1+CNGB1 channels. Common side effects are: vaginal discharge; vaginal itching or vaginal burning; vaginal yeast infection (thrush); tender tongue.

Vernakalant is a new antiarrhythmic drug that acts selectively in the atrium, targeting atrial specific channels. Vernakalant is an anti-arrhythmic medicine that acts preferentially in the atria by prolonging atrial refractoriness and by rate-dependently slowing impulse conduction. These anti-fibrillatory actions on refractoriness and conduction are thought to suppress reentry, and are potentiated in the atria during atrial fibrillation. The preferential effects of vernakalant on the atria are postulated to result from its block of currents that are expressed in the atria (e.g., the ultra-rapid delayed rectifier potassium current; and the acetylcholine-activated potassium current), but not in the ventricles, as well as the unique electrophysiologic condition of the fibrillating atria. An oral formulation of vernakalant is in phase II development as a long-term maintenance therapy for patients with atrial fibrillation. An intravenous formulation of vernakalant has been launched in most countries in Europe and Latin America, and in Hong Kong, for the acute conversion of atrial fibrillation. The product has been approved for the acute conversion of atrial fibrillation in South Africa, Iceland, Turkey and is awaiting approval for the same indication in Canada. Phase III development of the IV formulation is ongoing at sites in Asia, and development is currently on hold in the US.

Cibenzoline is a class I sodium channel blocker antiarrhythmic drug available in a limited number of countries. Cibenzoline also has moderate calcium channel blocking (class IV) effects and prolongs the action potential duration through its potassium channel blocking (class III) effect. It is used for the treatment of supraventricular and ventricular arrhythmias, and in obstructive hypertrophic cardiomyopathy.

Aminoacridine derivative that is a potent intercalating antineoplastic agent. It is effective in the treatment of acute leukemias and malignant lymphomas, but has poor activity in the treatment of solid tumors. It is frequently used in combination with other antineoplastic agents in chemotherapy protocols. It produces consistent but acceptable myelosuppression and cardiotoxic effects. Although its mechanism of action is incompletely defined, amsacrine inhibits DNA synthesis by binding to and intercalating with DNA. Amsacrine also inhibits topoisomerase II activity and may exert an effect on cell membranes. This agent also possesses immunosuppressive and antiviral properties. While amsacrine is not cell cycle phase-specific, cytotoxicity is maximal during the G2 and S phases.

In the US, Ethaverine is a member of the drug class peripheral vasodilators. It’s an alkaloid prepared synthetically from opium with no narcotic properties. Directly relaxes all smooth muscles, especially when they have been spasmodically contracted. Action is especially pronounced when spasm is present on coronary, cerebral, pulmonary, and peripheral arteries. Acts directly on myocardium like quinidine; depresses conduction and irritability, and prolongs refractory period. Primarily for peripheral and cerebral vascular insufficiency associated with arterial spasm; also a smooth muscle spasmolytic in spastic conditions of the GI and GU tracts. Adverse Effects ( 1%) CNS: Vertigo, headache, drowsiness. CV: Hypotension, arrhythmias. GI: Nausea, anorexia, abdominal distress, dry throat. Other: Malaise, flushing, sweating, lassitude, respiratory depression. Ethaverine may decrease levodopa effectiveness; morphine may antagonize smooth muscle relaxation effect of ethaverine.

Nilvadipine (NIVADIL®) is a L-type calcium channel blocker for treatment of hypertension. It inhibits the influx of extracellular calcium through myocardial and vascular membrane pores by physically plugging the channel. The decrease in intracellular calcium inhibits the contractile processes of smooth muscle cells, causing dilation of the coronary and systemic arteries, increased oxygen delivery to the myocardial tissue, decreased total peripheral resistance, decreased systemic blood pressure, and decreased afterload.

Gallopamil is a L-type calcium channel blocker designed for the treatment of coronary heart diseases: angina pectoris, prinzmetal angina and hypertonia.