Iobenguane I-131 is a radioactive therapeutic agent. The drug contains radioactive isotope I-131, which decays by electron emission with a half-life of about 8 days. By the chemical structure, iobenguane is similar to the neurotransmitter norepinephrine and is subject to the same uptake and regulation pathways. After intravenous administration, iobenguane I-131 accumulates within pheochromocytoma and paraganglioma cells, and radiation from the radioactive decay causes cell death and tumor necrosis. Iobenguane I-131 was approved by the FDA for the treatment of adult and pediatric patients with iobenguane scan positive, unresectable, locally advanced or metastatic pheochromocytoma or paraganglioma who require systemic anticancer therapy. Iobenguane I-131 is investigated in clinical trials as a treatment of neuroblastoma, ganglioneuroblastoma and other tumors of neuroendocrinal origin.

Trimetrexate, a second-generation folate antagonist which was used under brand name NEUTREXIN with concurrent leucovorin administration (leucovorin protection) was indicated as an alternative therapy for the treatment of moderate-to-severe Pneumocystis carinii pneumonia (PCP) in immunocompromised patients, including patients with the acquired immunodeficiency syndrome (AIDS). Nevertheless, this product was discontinued. In present time, trimetrexate with a different combinations is in the phase II of clinical trial for the treatment the following cancer diseases: pancreatic cancer and colorectal cancer (in combination with fluorouracil and leucovorin) and to treat a refractory acute leukemia in combination with leucovorin. Trimetrexate is a competitive inhibitor of dihydrofolate reductase (DHFR) from bacterial, protozoan, and mammalian sources. DHFR catalyzes the reduction of intracellular dihydrofolate to the active coenzyme tetrahydrofolate. Inhibition of DHFR results in the depletion of this coenzyme, leading directly to interference with thymidylate biosynthesis, as well as inhibition of folate-dependent formyltransferases, and indirectly to inhibition of purine biosynthesis. The result is disruption of DNA, RNA, and protein synthesis, with consequent cell death.

Trimetrexate, a second-generation folate antagonist which was used under brand name NEUTREXIN with concurrent leucovorin administration (leucovorin protection) was indicated as an alternative therapy for the treatment of moderate-to-severe Pneumocystis carinii pneumonia (PCP) in immunocompromised patients, including patients with the acquired immunodeficiency syndrome (AIDS). Nevertheless, this product was discontinued. In present time, trimetrexate with a different combinations is in the phase II of clinical trial for the treatment the following cancer diseases: pancreatic cancer and colorectal cancer (in combination with fluorouracil and leucovorin) and to treat a refractory acute leukemia in combination with leucovorin. Trimetrexate is a competitive inhibitor of dihydrofolate reductase (DHFR) from bacterial, protozoan, and mammalian sources. DHFR catalyzes the reduction of intracellular dihydrofolate to the active coenzyme tetrahydrofolate. Inhibition of DHFR results in the depletion of this coenzyme, leading directly to interference with thymidylate biosynthesis, as well as inhibition of folate-dependent formyltransferases, and indirectly to inhibition of purine biosynthesis. The result is disruption of DNA, RNA, and protein synthesis, with consequent cell death.

Metipranolol is a beta-adrenergic antagonist effective for both beta-1 and beta-2 receptors. It is used as an antiarrhythmic, antihypertensive, and antiglaucoma agent. Metipranolol blocks beta1 and beta2 (non-selective) adrenergic receptors. It does not have significant intrinsic sympathomimetic activity, and has only weak local anesthetic (membrane-stabilizing) and myocardial depressant activity. Orally administered beta-adrenergic blocking agents reduce cardiac output in both healthy subjects and patients with heart disease. In patients with severe impairment of myocardial function, beta-adrenergic receptor antagonists may inhibit the sympathetic stimulatory effect necessary to maintain adequate cardiac output. Metipranolol when applied topically in the eye, has the action of reducing elevated as well as normal intraocular pressure (IOP), whether or not accompanied by glaucoma. Elevated intraocular pressure is a major risk factor in the pathogenesis of glaucomatous visual field loss. The higher the level of intraocular pressure, the greater the likelihood of glaucomatous visual field loss and optic nerve damage. The primary mechanism of the ocular hypotensive action of Metipranolol is most likely due to reduction in aqueous humor production. A slight increase in outflow may be an additional mechanism. Metipranolol reduces IOP with little or no effect on pupil size or accommodation. Metipranolol is known as the brand OptiPranolol. Brand-name OptiPranolol is manufactured by Bausch & Lomb Incorporated. However, the patents for OptiPranolol have expired, and this medication is currently available in generic form. Generic OptiPranolol eye drops are available in one strength -- metipranolol 0.3 percent solution. It is made by Falcon Pharmaceuticals.

Methylparaben (E number E218) is preservative in the food, cosmetic, and pharmaceutical industries. It is completely absorbed through the skin or after ingestion and and it is hydrolyzed to para-hydroxybenzoic acid, and metabolites are rapidly excreted in the urine. Methylparaben is on the FDA generally regarded as safe list.

Pirbuterol (trade name Maxair) is a short-acting β2 adrenoreceptor agonist with bronchodilating action used in the treatment of asthma. The pharmacologic effects of beta-adrenergic agonist drugs, including pirbuterol, are at least in proof attributable to stimulation through beta-adrenergic receptors of intracellular adenyl cyclase, the enzyme which catalyzes the conversion of adenosine triphosphate (ATP) to cyclic-adenosine monophosphate (c-AMP). Increased c-AMP levels are associated with relaxation of bronchial smooth muscle and inhibition of release of mediators of immediate hypersensitivity from cells, especially from mast cells. Pirbuterol is used in asthma for reversal of acute bronchospasm, and also as a maintenance medication to prevent future attacks. It should be used in patients 12 years of age and older with or without concurrent theophylline and/or inhaled corticosteroid. After inhalation of doses up to 800 μg (twice the maximum recommended dose) systemic blood levels of pirbuterol are below the limit of assay sensitivity (2–5 ng/ml). A mean of 51% of the dose is recovered in urine as pirbuterol plus its sulfate conjugate following administration by aerosol. Pirbuterol is not metabolized by catechol-O-methyltransferase.

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.

Guanabenz, an antihypertensive agent for oral administration-, is an aminoguanidine derivative, 2,'6-dichlorobenzylideneamina-guanidine acetate. It is white to an almost white powder having not more than a slight odor. Sparingly soluble in water and in 0.1 N hydrochloric acid; soluble in alcohol and in propylene glycol. Guanabenz is an orally active central alpha-2 adrenergic agonist. Its antihypertensive action appears to be mediated via stimulation of central alpha-adrenergic receptors, resulting in a decrease of sympathetic outflow from the brain at the bulbar level to the peripheral circulatory system. In clinical trials, guanabenz acetate, given orally to hypertensive patients, effectively controlled blood pressure without any significant effect on glomerular filtration rate, renal blood flow, body fluid volume or body weight. The Myelin Repair Foundation and the National Institutes of Health (National Institute of Neurological Disorders and Stroke) are developing guanabenz for the treatment of multiple sclerosis. Unlike the currently available treatment for multiple sclerosis that suppresses the immune system, guanabenz, an FDA approved the drug for the treatment of high blood pressure, has a potential to reduce the loss of myelin by protecting and repairing myelin-producing cells in the brain from damage. Phase I development is underway in the US.

Saralasin is an angiotensin II analogue which was developed for the treatment of hypertension in 1970s. For many years saralasin was supposed to be angiotensin receptors blocker, but recent studies have revealed that its pharmacological action can be explained by agonistic behavior toward angiotensin II receptor. The drug was approved by FDA under the name Sarenin, however, it is no longer available on the market.

Cefotaxime sodium is a semisynthetic, broad spectrum cephalosporin antibiotic for parenteral administration. It’s a 3rd Generation Cephalosporin that is FDA approved for the treatment of lower respiratory tract infections, genitourinary infections, gynecologic infections, bacteremia/septicemia, skin and skin structure infections, intra-abdominal infections, bone and/or joint infections and central nervous system infections. The bactericidal activity of cefotaxime sodium results from inhibition of cell wall synthesis. Cefotaxime sodium has in vitro activity against a wide range of gram-positive and gram-negative organisms. Cefotaxime sodium has a high degree of stability in the presence of ß-lactamases, both penicillinases and cephalosporinases, of gram-negative and gram-positive bacteria. Increased nephrotoxicity has been reported following concomitant administration of cephalosporins and aminoglycoside antibiotics. Common adverse reactions include injection site pain, injection site phlebitis, rash, diarrhea, vomiting. Increased nephrotoxicity has been reported following concomitant administration of cephalosporins and aminoglycoside antibiotics.