Anagrelide is an orally active quinazinolone derivative that was originally developed as an antiplatelet drug. The drug inhibits cyclic nucleotide phosphodiesterase III (PDEIII) and phopholipase A2, which is thought to cause the side effects of vasodilation, positive inotropism, reduced platelet aggregation. However, significant inhibition of platelet aggregation is observed only at doses of anagrelide higher than those required to reduce platelet count. It is indicated for the treatment of patients with thrombocythemia, secondary to myeloproliferative disorders. Commonly reported side effects of anagrelide include: abdominal pain, dizziness, headache, nausea, and palpitations. Other side effects include: back pain, fever, tachycardia, vomiting, and anorexia. There is a single case report, which suggests that sucralfate may interfere with anagrelide absorption. Anagrelide is an inhibitor of cyclic AMP PDE III. The effects of medicinal products with similar properties such as inotropes milrinone, enoximone, amrinone, olprinone and cilostazol may be exacerbated by anagrelide.

Acitretin is all-Trans-9-(4-methoxy-2, 3, 6¬ trimethylphenyl)-three, 7-dimethyl-2, 4, 6, 8-nonatetraenoic acid. It is a metabolite of exterminate and is related to both retinoic acid and retinol (vitamin A). It is taken orally, and is typically used for psoriasis. The mechanism of action of is unknown. However it is believed to work by targeting specific receptors (retinoid receptors such as RXR and RAR) in the skin, which help normalize the growth cycle of skin cells. Studies on nuclear retinoic acid receptors have shown that acitretin activates all 3 receptor subtypes (RAR-alpha, -beta, and -gamma) without measurable receptor binding; this paradox remains unexplained.

There is no information in the literature about pharmacological and biological application of definite isomer of valsatran, R – form (also known as VALSARTAN, D- or CGP-49309). However there were found, that in the tablets of valsartan, which are used to treat high blood pressure and to heart failure, the R-enantiomer was an impurity.

Cefepime is a fourth-generation cephalosporin antibiotic, which was developed in 1994. Cefepime has a broad spectrum in vitro activity that encompasses a wide range of Gram-positive and Gram-negative bacteria. Within bacterial cells, the molecular targets of cefepime are the penicillin binding proteins (PBP). It is FDA approved for the treatment of pneumonia, febrile neutropenia, uncomplicated UTI, uncomplicated skin infection and complicated intraabdominal infections. Common adverse reactions include rash, hypophosphatemia, diarrhea. Cefepime is metabolized to N-methylpyrrolidine (NMP) which is rapidly converted to the N-oxide (NMP-N-oxide). Urinary recovery of unchanged cefepime accounts for approximately 85% of the administered dose. Less than 1% of the administered dose is recovered from urine as NMP, 6.8% as NMP-N-oxide, and 2.5% as an epimer of cefepime. Because renal excretion is a significant pathway of elimination, patients with renal dysfunction and patients undergoing hemodialysis require dosage adjustment.

Atorvastatin calcium (LIPITOR®) is a pyrrole and heptanoic acid derivative, a synthetic lipid-lowering agent. Atorvastatin is a selective, competitive inhibitor of 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase. This enzyme catalyzes the conversion of HMG-CoA to mevalonate, an early and rate-limiting step in cholesterol biosynthesis. Atorvastatin is used to reduce serum levels of LDL(low-density lipoprotein)-cholesterol; apolipoprotein B; and triglycerides and to increase serum levels of HDL(high-density lipoprotein)-cholesterol in the treatment of hyperlipidemias and prevention of cardiovascular disease in patients with multiple risk factors.

Fosfomycin (marketed under the trade names Monurol and Monuril) is a broad-spectrum antibiotic. Monurol (fosfomycin tromethamine) sachet contains fosfomycin tromethamine, a synthetic, broad spectrum, bactericidal antibiotic for oral administration. Monurol is indicated only for the treatment of uncomplicated urinary tract infections (acute cystitis) in women due to susceptible strains of Escherichia coli and Enterococcus faecalis. Fosfomycin is a phosphoenolpyruvate analogue produced by Streptomyces that irreversibly inhibits enolpyruvate transferase (MurA), which prevents the formation of N-acetylmuramic acid, an essential element of the peptidoglycan cell wall.

Moexiprilat is the pharmacologically active metabolite of Moexipril. Formation of Moexiprilat is caused by hydrolysis of a Moexipril’s ethyl ester group. Moexiprilat competitively inhibits ACE, thereby blocking the conversion of angiotensin I to angiotensin II. This prevents the actions of the potent vasoconstrictor angiotensin II and leads to vasodilatation. This agent also prevents angiotensin II-induced aldosterone secretion by the adrenal cortex, thereby promoting diuresis and natriuresis. Moexiprilat showed an extended duration of action owing to a long terminal pharmacokinetic half-life and produced a persistent ACE inhibition.

Penciclovir (DENAVIR®) is a synthetic acyclic guanine derivative with antiviral activity, mainly used to treat infections from herpes simplex virus (HSV) types 1 and 2. In cells infected with HSV-1 or HSV-2, the viral thymidine kinase phosphorylates penciclovir to a monophosphate form that, in turn, is converted by cellular kinases to the active form penciclovir triphosphate. Biochemical studies demonstrate that penciclovir triphosphate inhibits HSV polymerase competitively with deoxyguanosine triphosphate. Consequently, herpes viral DNA synthesis and, therefore, replication are selectively inhibited. Famciclovir (FAMVIR®) is a prodrug form of penciclovir with improved oral bioavailability.

Histrelin is a gonadotropin releasing hormone (GnRH) agonist that acts as a potent inhibitor of gonadotropin when administered as an implant that delivers continuous therapeutic doses. Following an initial stimulatory phase with increased circulating levels of luteinizing hormone (LH) and follicle-stimulating hormone (FSH), leading to a transient increase in concentration of gonadal steroids (testosterone and dihydrotestosterone in males), continuous administration of histrelin acetate results in decreased levels of LH and FSH due to a reversible down-regulation of the GnRH receptors in the pituitary gland and desensitization of the pituitary gonadotropes. As the product Supprelin LA (FDA), histrelin is indicated for the treatment of children with central precocious puberty (CPP). As the product Vantas (FDA), histrelin is indicated for the palliative treatment of advanced prostate cancer.

Ondansetron (ZOFRAN®) is a selective 5-HT3 receptor antagonist. It is effective in the treatment of nausea and vomiting caused by radiotherapy, anesthesia, surgery or cytotoxic chemotherapy drugs, including cisplatin, and has reported anxiolytic and neuroleptic properties. While its mechanism of action has not been fully characterized, ondansetron is not a dopamine-receptor antagonist. It is not certain whether ondansetron's antiemetic action is mediated centrally, peripherally, or in both sites. However, cytotoxic chemotherapy appears to be associated with release of serotonin from the enterochromaffin cells of the small intestine. The released serotonin may stimulate the vagal afferents through the 5-HT3 receptors and initiate the vomiting reflex.