Dronabinol also known as (−)-trans-delta9-tetrahydrocannabinol is an active ingredient of cannabis. The drug was approved by FDA for the treatment of anorexia in patients with AIDS and chemotherapy-induced nausea and vomiting. Dronabinol exerts its action by activating CB1 and CB2 recepors which makes it a CNS active medicine.

Cefotetan is a semisynthetic cephamycin antibiotic that is administered intravenously or intramuscularly. The drug is highly resistant to a broad spectrum of beta-lactamases and is active against a wide range of both aerobic and anaerobic gram-positive and gram-negative microorganisms. It is FDA approved for the treatment of urinary tract infection, lower respiratory tract infection, skin and skin structure infections, gynecologic infection, intra-abdominal infection, and bone and joint infection; and for prophylaxis of postoperative infection. The bactericidal action of cefotetan results from inhibition of cell wall synthesis. The methoxy group in the 7-alpha position provides cefotetan with a high degree of stability in the presence of beta-lactamases including both penicillinases and cephalosporinase of gram-negative bacteria. Common adverse reactions include diarrhea and nausea. As with other cephalosporins, high concentrations of cefotetan may interfere with measurement of serum and urine creatinine levels.

Iopamidol is a nonionic, low-osmolar iodinated contrast agent. Iopamidol is indicated for angiography, pediatric angiocardiography, selective visceral arteriography and aortography, peripheral venography, and adult and pediatric intravenous excretory urography and intravenous adult and pediatric contrast enhancement of computed tomographic. Renal toxicity has been reported in a few patients with liver dysfunction who were given oral cholecystographic agents followed by intravascular contrast agents. Intravascular injection of contrast media is frequently associated with the sensation of warmth and pain especially in peripheral arteriography and venography. In angiocardiography the adverse reactions are: hot flashes, angina pectoris, flushing, bradycardia, hypotension, hives.

Labetalol is a blocker of both alpha- and beta-adrenergic receptors that is used as an antihypertensive. It may be used alone or in combination with other antihypertensive agents, especially thiazide and loop diuretics. The capacity of labetalol HCl to block alpha receptors in man has been demonstrated by attenuation of the pressor effect of phenylephrine and by a significant reduction of the pressor response caused by immersing the hand in ice-cold water ("cold-pressor test"). Labetalol HCl's beta1-receptor blockade in man was demonstrated by a small decrease in the resting heart rate, attenuation of tachycardia produced by isoproterenol or exercise, and by attenuation of the reflex tachycardia to the hypotension produced by amyl nitrite. Beta2-receptor blockade was demonstrated by inhibition of the isoproterenol-induced fall in diastolic blood pressure. Both the alpha- and beta-blocking actions of orally administered labetalol HCl contribute to a decrease in blood pressure in hypertensive patients. Labetalol HCl consistently, in dose-related fashion, blunted increases in exercise-induced blood pressure and heart rate, and in their double product. The pulmonary circulation during exercise was not affected by labetalol HCl dosing. Single oral doses of labetalol HCl administered to patients with coronary artery disease had no significant effect on sinus rate, intraventricular conduction, or QRS duration. The atrioventricular (A-V) conduction time was modestly prolonged in two of seven patients. In another study, IV labetalol HCl slightly prolonged A-V nodal conduction time and atrial effective refractory period with only small changes in heart rate. The metabolism of labetalol is mainly through conjugation to glucuronide metabolites. These metabolites are present in plasma and are excreted in the urine and, via the bile, into the feces. Approximately 55% to 60% of a dose appears in the urine as conjugates or unchanged labetalol within the first 24 hours of dosing. Labetalol has been shown to cross the placental barrier in humans. Only negligible amounts of the drug crossed the blood-brain barrier in animal studies. Labetalol is approximately 50% protein bound. Neither hemodialysis nor peritoneal dialysis removes a significant amount of labetalol HCl from the general circulation.

Inamrinone (Amrinone) is a positive inotropic cardiotonic with vasodilator properties, phosphodiesterase inhibitory activity, and the ability to stimulate calcium ion influx into the cardiac cell. Inamrinone is a phosphodiesterase inhibitor (PDE3), resulting in increased cAMP and cGMP which leads to an increase in the calcium influx like that caused by beta-agonists resulting in increased inotropic effect. Inamrinone is used in the treatment of congestive heart failure.

Naltrexone is marketed as its hydrochloride salt, naltrexone hydrochloride, under the trade names Revia and Depade. A once-monthly extended-release injectable formulation is marketed under the trade name Vivitrol. VIVITROL is indicated for the treatment of alcohol dependence in patients who are able to abstain from alcohol in an outpatient setting prior to initiation of treatment with VIVITROL. VIVITROL is indicated for the prevention of relapse to opioid dependence, following opioid detoxification. Naltrexone is a pure opiate antagonist and has little or no agonist activity. The mechanism of action of naltrexone in alcoholism is not understood; however, involvement of the endogenous opioid system is suggested by preclinical data. Naltrexone is thought to act as a competitive antagonist at mc, κ, and δ receptors in the CNS, with the highest affinity for the μ receptor. Naltrexone competitively binds to such receptors and may block the effects of endogenous opioids. This leads to the antagonization of most of the subjective and objective effects of opiates, including respiratory depression, miosis, euphoria, and drug craving. The major metabolite of naltrexone, 6-β-naltrexol, is also an opiate antagonist and may contribute to the antagonistic activity of the drug. Low dose naltrexone is an “off label” use of naltrexone. Normal naltrexone usage to break addictions is 50mg – 100mg. Usage of low dose naltrexone ranges in the area of 3 mg – 4.5 mg dosing and is prescribed in an oral pill form and is quite inexpensive. For people with multiple sclerosis, the dosage of LDN ranges from 1.5 to 4.5 ml per day.

Pimozide (Orap) is a diphenylbutylpiperidine that is effective as an antipsychotic agent and as an alternative to haloperidol for the suppression of vocal and motor tics in patients with Tourette syndrome. It is not intended as a treatment of first choice nor is it intended for the treatment of tics that are merely annoying or cosmetically troublesome. It should be reserved for use in Tourette’s Disorder patients whose development and/or daily life function is severely compromised by the presence of motor and phonic tics. Evidence supporting approval of pimozide for use in Tourette’s Disorder was obtained in two controlled clinical investigations, which enrolled patients between the ages of 8 and 53 years. Most subjects in the two trials were 12 or older. Pimozide is an orally active antipsychotic drug product, which shares with other antipsychotics the ability to blockade dopaminergic receptors on neurons in the central nervous system. Although its exact mode of action has not been established, the ability of pimozide to suppress motor and phonic tics in Tourette’s Disorder is thought to be a function of its dopaminergic blocking activity. However, receptor blockade is often accompanied by a series of secondary alterations in central dopamine metabolism and function which may contribute to both pimozide’s therapeutic and untoward effects. In addition, pimozide, in common with other antipsychotic drugs, has various effects on other central nervous system receptor systems which are not fully characterized.

Pentoxil (Pentoxifylline Extended-release Tablets, USP) is indicated for the treatment of patients with intermittent claudication based on chronic occlusive arterial disease of the limbs. Pentoxil can improve function and symptoms but is not intended to replace more definitive therapy, such as surgical bypass, or removal of arterial obstructions when treating peripheral vascular disease. Pentoxifylline and its metabolites improve the flow properties of blood by decreasing its viscosity. In patients with chronic peripheral arterial disease, this increases blood flow to the affected microcirculation and enhances tissue oxygenation. The precise mode of action of pentoxifylline and the sequence of events leading to clinical improvement are still to be defined. Pentoxifylline inhibits erythrocyte phosphodiesterase, resulting in an increase in erythrocyte cAMP activity. Subsequently, the erythrocyte membrane becomes more resistant to deformity. Along with erythrocyte activity, pentoxifylline also decreases blood viscosity by reducing plasma fibrinogen concentrations and increasing fibrinolytic activity. It is also a non-selective adenosine receptor antagonist. Pentoxifylline administration has been shown to produce dose-related hemorrheologic effects, lowering blood viscosity, and improving erythrocyte flexibility. Pentoxifylline has been shown to increase leukocyte deformability and to inhibit neutrophil adhesion and activation. Tissue oxygen levels have been shown to be significantly increased by therapeutic doses of pentoxifylline in patients with peripheral arterial disease. Clinical trials were conducted using either extended-release pentoxifylline tablets for up to 60 weeks or immediate-release pentoxifylline capsules for up to 24 weeks. Dosage ranges in the tablet studies were 400 mg bid to tid and in the capsule studies, 200-400 mg tid. The incidence of adverse reactions was higher in the capsule studies (where dose related increases were seen in digestive and nervous system side effects) than in the tablet studies. Studies with the capsule include domestic experience, whereas studies with the extended-release tablets were conducted outside the U.S.

Nicotine is a natural alkaloid obtained from the dried leaves and stems of the nightshade family of pants, such as Nicotiana tabacum and Nicotiana rustica, where it occurs in concentrations of 0.5-8%. Cigarette tobacco varies in its nicotine content, but common blends contain 15-25 mg per cigarette, with a current trend towards lower levels. Nicotine is highly addictive substance, it exhibits a stimulant effect when adsorbed at 2 mg. Administration of higher doses could be harmful. Action of nicotine is mediated by nicotinic cholinergic receptors. Nicotine binds to the interface between two subunits of the receptors, opens the channel and allows the entry of sodium or calcium. The principal mediator of nicotine dependence is α4β2 nicotine receptor.

Acebutolol is a cardioselective, beta-adrenoreceptor blocking agent, which possesses mild intrinsic sympathomimetic activity (ISA) in its therapeutically effective dose range. Acebutolol is marketed under the trade names Sectral, Prent. Acebutolol is indicated for the management of hypertension in adults. It may be used alone or in combination with other antihypertensive agents, especially thiazide-type diuretics. Acebutolol is also indicated in the management of ventricular premature beats; it reduces the total number of premature beats, as well as the number of paired and multiform ventricular ectopic beats, and R-on-T beats. Acebutolol is a selective β1-receptor antagonist. Activation of β1-receptors by epinephrine increases the heart rate and the blood pressure, and the heart consumes more oxygen. Acebutolol blocks these receptors, lowering the heart rate and blood pressure. This drug then has the reverse effect of epinephrine. In addition, beta blockers prevent the release of renin, which is a hormone produced by the kidneys which leads to constriction of blood vessels.