Warfarin is an anticoagulant drug normally used to prevent blood clot formation as well as migration. Warfarin is marketed under the brand name Coumadin among others. Coumadin (crystalline warfarin sodium) is an anticoagulant which acts by inhibiting vitamin K-dependent coagulation factors. Chemically, it is 3-(α-acetonylbenzyl)-4-hydroxycoumarin and is a racemic mixture of the R- and S-enantiomers. Coumadin is indicated for the prophylaxis and/or treatment of venous thrombosis and its extension, and pulmonary embolism. It is also indicated for the prophylaxis and/or treatment of the thromboembolic complications associated with atrial fibrillation and/or cardiac valve replacement. Warfarin is thought to interfere with clotting factor synthesis by inhibition of the C1 subunit of the vitamin K epoxide reductase (VKORC1) enzyme complex, thereby reducing the regeneration of vitamin K1 epoxide. The degree of depression is dependent upon the dosage administered and, in part, by the patient’s VKORC1 genotype. Therapeutic doses of warfarin decrease the total amount of the active form of each vitamin K dependent clotting factor made by the liver by approximately 30% to 50%.

Hydralazine is a direct-acting vasodilator that is used as an antihypertensive agent. Hydralazine works by relaxing blood vessels (arterioles more than venules) and increasing the supply of blood and oxygen to the heart while reducing its workload. It also functions as an antioxidant. It inhibits membrane-bound enzymes that form reactive oxygen species, such as superoxides. Excessive superoxide counteracts NO-induced vasodilation. Hydralazine is used for the treatment of essential hypertension, alone or as an adjunct. Also for the management of severe hypertension when the drug cannot be given orally or when blood pressure must be lowered immediately, congestive heart failure (in combination with cardiac glycosides and diuretics and/or with isosorbide dinitrate), and hypertension secondary to pre-eclampsia/eclampsia.

Erythromycin cyclocarbonate (Davercin) is a first generation semi-synthetic erythromycin. It is active against Gram-positive and some Gram-negative microorganisms. Davercin shows comparable or better in vitro potency, low host toxicity and improved pharmacokinetics compared with erythromycin. It is approved for the treatment of acne, atypical pneumonia (caused by Mycoplasma pneumoniae, Chlamydia pneumoniae, Legionella pneumophila), whooping cough (treatment and prevention), urethritis (caused by Ureaplasma urealyticum and Chlamydia trachomatis), gastrointestinal infection caused by Campylobacter spp., short-term infections of the skin and soft tissues (e.g. acne, staphylococcal dermatitis). In streptococcal infections, diphtheria, gonorrhea, early syphilis in patients who are allergic to penicillin, and in the prevention of bacterial endocarditis before the planned dental procedures. Adverse effects are: nausea, vomiting, abdominal pain, diarrhea, skin allergic reactions.

Ergoalcifediol (Vitamin D2) is a fat soluble steroid hormone precursor of vitamin D. The principal biologic function of vitamin D is the maintenance of normal levels of serum calcium and phosphorus in the bloodstream by enhancing the efficacy of the small intestine to absorb these minerals from the diet. Cholecalciferol is synthesized within our bodies naturally, but if UV exposure is inadequate or the metabolism of cholecalciferol is abnormal, then an exogenous source is required. Vitamin D2 is converted to 25-hydroxyvitamin D (25OHD) in the liver, and then to the active form, 1,25-dihydroxyvitamin D (1,25(OH)2D), in the kidney. Once transformed, it binds to the vitamin D receptor, which leads to a variety of regulatory roles. Vitamin D plays an important role in maintaining calcium balance and in the regulation of parathyroid hormone (PTH). It promotes renal reabsorption of calcium, increases intestinal absorption of calcium and phosphorus, and increases calcium and phosphorus mobilization from bone to plasma. Very few foods naturally contain vitamin D. Sources that contain the vitamin include fatty fish, the liver and fat of aquatic mammals (e.g., seals, polar bears), and eggs from chickens fed vitamin D-fortified feed. As such, many countries have instituted policies to fortify certain foods with vitamin D to compensate for the potentially low exposures of skin to sunlight. Vitamin D deficiency results in inadequate mineralization of bone or compensatory skeletal demineralization and causes decreased ionized calcium concentrations in blood and a resultant increase in the production and secretion of PTH. Increase in PTH stimulates the mobilization of skeletal calcium, inhibits renal excretion of calcium, and stimulates renal excretion of phosphorus. This results in normal fasting serum calcium concentrations and low or near-normal serum phosphorus. The enhanced mobilization of skeletal calcium induced by this secondary hyperparathyroidism leads porotic bone. Ergoalcifediol is used for use in the management of hypocalcemia and its clinical manifestations in patients with hypoparathyroidism, as well as for the treatment of familial hypophosphatemia (vitamin D resistant rickets). This drug has also been used in the treatment of nutritional rickets or osteomalacia, vitamin D dependent rickets, rickets or osteomalacia secondary to long-term high dose anticonvulsant therapy, early renal osteodystrophy, osteoporosis (in conjunction with calcium), and hypophosphatemia associated with Fanconi syndrome (with treatment of acidosis). Ergocalciferol is manufactured and marketed under various names, including Deltalin (Eli Lilly and Company), Drisdol (Sanofi-Synthelabo) and Calcidol (Patrin Pharma).

Tetraamminecopper sulfate is a dark blue crystalline solid with a faint odor of ammonia. The primary hazard is the threat to the environment. Immediate steps should be taken to limit its spread to the environment. Used as a pesticide and fungicide, to print fabrics (especially in calico finishing), and to make other copper compounds.

Racepinephrine or racemic epinephrine is a mixture of levo and dextro isomers of epinephrine act as a nonselective agonist at adrenergic receptors. It is a bronchodilator used in the temporary relief of mild symptoms of intermittent asthma including wheezing, shortness of breath. Inhaled racepinephrine became available in September 2012 as a nonprescription treatment for bronchospasm based on a 1986 US Food and Drug Administration rule. Besides, racemic epinephrine relieves respiratory distress in hospitalized infants with bronchiolitis and is safe but does not abbreviate hospital stay. Morbidity associated with bronchiolitis as identified by parents persists for at least one week after hospital discharge in most infants.

Dalvastatin is a synthetic HMG-CoA reductase inhibitor developed by Rhône-Poulenc Rorer. Dalvastatin is a prodrug and is itself an inactive lactone. After oral ingestion, the drug is hydrolyzed in vivo to the corresponding beta-hydroxy acid, which is the pharmacologically active form. HMG-CoA reductase is the rate-limiting enzyme in the cholesterol biosynthetic pathway. An active form of dalvastatin inhibits HMG-CoA reductase with IC50 of 3.4 nM. In ex vivo assay, orally administered dalvastatin inhibited cholesterol biosynthesis in rat liver slices with an ED50 value of 0.9. The efficacy of dalvastatin to lower cholesterol was investigated in the clinical trials in the 1990s, but no results were reported.

Tosedostat is a proprietary orally bioavailable inhibitor of the M1 family of aminopeptidases with potential antineoplastic activity. Tosedostat is converted intracellularly into a poorly membrane-permeable active metabolite (CHR-79888) which inhibits the M1 family of aminopeptidases, particularly puromycin-sensitive aminopeptidase (PuSA), and leukotriene A4 (LTA4) hydrolase; inhibition of these aminopeptidases in tumor cells may result in amino acid deprivation, inhibition of protein synthesis due to a decrease in the intracellular free amino acid pool, an increase in the level of the proapoptotic protein Noxa, and cell death. There are several ongoing Phase 2 cooperative group-sponsored trials and investigator-sponsored trials evaluating the clinical activity of Tosedostat in combination with standard agents in patients with acute myeloid leukemia (AML) or myelodysplastic syndrome (MDS).

MK-5108 is a small molecule inhibitor of AuroraA kinase with high selectivity versus Aurora-B and C. It was tested in phase I study against advanced or refractory solid tumors both as a monotherapy or in combination with docetaxel, but this study was terminated early due to toxicities at MK-5108 doses below the anticipated PK exposure target.