Exemestane is an oral steroidal aromatase inhibitor used in the adjuvant treatment of hormonally-responsive (also called hormone-receptor-positive, estrogen-responsive) breast cancer in postmenopausal women. It acts as a false substrate for the aromatase enzyme, and is processed to an intermediate that binds irreversibly to the active site of the enzyme causing its inactivation. Breast cancer cell growth may be estrogen-dependent. Aromatase (exemestane) is the principal enzyme that converts androgens to estrogens both in pre- and postmenopausal women. While the main source of estrogen (primarily estradiol) is the ovary in premenopausal women, the principal source of circulating estrogens in postmenopausal women is from conversion of adrenal and ovarian androgens (androstenedione and testosterone) to estrogens (estrone and estradiol) by the aromatase enzyme in peripheral tissues. Estrogen deprivation through aromatase inhibition is an effective and selective treatment for some postmenopausal patients with hormone-dependent breast cancer. Exemestane is an irreversible, steroidal aromatase inactivator, structurally related to the natural substrate androstenedione. It acts as a false substrate for the aromatase enzyme, and is processed to an intermediate that binds irreversibly to the active site of the enzyme causing its inactivation, an effect also known as "suicide inhibition". Exemestane significantly lowers circulating estrogen concentrations in postmenopausal women, but has no detectable effect on the adrenal biosynthesis of corticosteroids or aldosterone. This reduction in serum and tumor concentrations of estrogen delays tumor growth and disease progression. Exemestane has no effect on other enzymes involved in the steroidogenic pathway up to a concentration at least 600 times higher than that inhibiting the aromatase enzyme. Exemestane is marketed under the trade name Aromasin.

Moxifloxacin is a synthetic antibacterial agent developed by Bayer AG (initially called BAY 12-8039) for oral and intravenous administration. Moxifloxacin, a fluoroquinolone, is available as the monohydrochloride salt of 1-cyclopropyl-7-[(S,S)-2,8diazabicyclo[4.3.0]non-8-yl]-6-fluoro-8-methoxy-1,4-dihydro-4-oxo-3 quinoline carboxylic acid. Moxifloxacin is marketed worldwide (as the hydrochloride) under the brand names Avelox, Avalox, and Avalon for oral treatment. In most countries, the drug is also available in the parenteral form for intravenous infusion. Moxifloxacin is also sold in an ophthalmic solution (eye drops) under the brand names Vigamox, and Moxeza for the treatment of conjunctivitis (pink eye). Its antibacterial spectrum includes enteric Gram-(−) rods (Escherichia coli, Proteus species, Klebsiella species), Haemophilus influenzae, atypical bacteria (Mycoplasma, Chlamydia, Legionella), and Streptococcus pneumoniae, and anaerobic bacteria. It differs from earlier antibacterials of the fluoroquinolone class such as levofloxacin and ciprofloxacin in having greater activity against Gram-positive bacteria and anaerobes.

Oseltamivir phosphate is an ethyl ester prodrug requiring ester hydrolysis for conversion to the active form, oseltamivir carboxylate. Oseltamivir carboxylate is an inhibitor of influenza virus neuraminidase affecting release of viral particles. Oseltamivir is a well tolerated orally active neuraminidase inhibitor which significantly reduces the duration of symptomatic illness and hastens the return to normal levels of activity when initiated promptly in patients with naturally acquired influenza.

Orlistat or tetrahydrolipstatin (Xenical, Hoffmann-La Roche) is a saturated derivative of lipstatin originally isolated from Streptomyces toxytricini. Orlistat (Xenical, Hoffmann-La Roche) is a powerful inhibitor of gastrointestinal lipase and as such, reduces fat absorption. Orlistat acts by binding covalently to the serine residue of the active site of gastric and pancreatic lipases. When administered with fat-containing foods, orlistat partially inhibits hydrolysis of triglycerides, thus reducing the subsequent absorption of monoaclglycerides and free fatty acids. Unlike other weight-reducing drugs it is minimally absorbed and has no effects in the CNS. Xenical is indicated for obesity management including weight loss and weight maintenance when used in conjunction witha reduced-calorie diet. XENICAL is also indicated to reduce the risk for weight regain after prior weight loss. XENICAL is indicated for obese patients with an initial body mass index (BMI) ≥ 30 kg/m2 or ≥ 27 kg/m2 in the presence of other risk factors (eg, hypertension, diabetes, dyslipidemia). In addition to its well established efficacy in achieving modest weight loss, orlistat has been shown to improve glycaemic parameters in obese adults with type 2 diabetes mellitus as well as some features of the metabolic syndrome.

Zanamivir, an antiviral agent, is a neuraminidase inhibitor indicated for treatment of uncomplicated acute illness due to influenza A and B virus in adults and pediatric patients 7 years and older who have been symptomatic for no more than 2 days. Zanamivir has also been shown to significantly inhibit the human sialidases NEU3 and NEU2 in the micromolar range (Ki 3.7 +/-0.48 and 12.9+/-0.07 uM, respectively), which could account for some of the rare side effects of zanamivir. The proposed mechanism of action of zanamivir is via inhibition of influenza virus neuraminidase with the possibility of alteration of virus particle aggregation and release. By binding and inhibiting the neuraminidase protein, the drug renders the influenza virus unable to escape its host cell and infect others. Zanamivir was the first neuraminidase inhibitor commercially developed. It is currently marketed by GlaxoSmithKline under the trade name Relenza as a powder for oral inhalation.

Epirubicin is an anthracycline cytotoxic agent, is a 4'-epi-isomer of doxorubicin. The compound is marketed by Pfizer under the trade name Ellence in the US. It is indicated as a component of adjuvant therapy in patients with evidence of axillary node tumor involvement following resection of primary breast cancer. Although it is known that anthracyclines can interfere with a number of biochemical and biological functions within eukaryotic cells, the precise mechanisms of epirubicin’s cytotoxic and/or antiproliferative properties have not been completely elucidated. It is known, that epirubicin forms a complex with DNA by intercalation of its planar rings between nucleotide base pairs, with consequent inhibition of nucleic acid (DNA and RNA) and protein synthesis. Such intercalation triggers DNA cleavage by topoisomerase II, resulting in cytocidal activity. Epirubicin also inhibits DNA helicase activity, preventing the enzymatic separation of double-stranded DNA and interfering with replication and transcription. Epirubicin is also involved in oxidation/reduction reactions by generating cytotoxic free radicals.

Amprenavir is an inhibitor of HIV-1 protease. Amprenavir binds to the active site of HIV-1 protease and thereby prevents the processing of viral gag and gag-pol polyprotein precursors, resulting in the formation of immature non-infectious viral particles. Amprenavir-containing combination regimens have shown virological efficacy, and have generally been well tolerated, in patients with HIV infection (primarily treatment-naive or protease inhibitor-naive). Fosamprenavir (GW433908, Lexiva, Telzir) is an oral prodrug of amprenavir, with a reduced daily pill burden. The use of protease inhibitors has also been associated with dyslipidemia and an increased risk of cardiovascular disease. Amprenavir activates Pregnane X receptor to mediate dyslipidemia.

Quinupristin is an antibiotic compound and a semisynthetic derivative of pristinamycin Ia. Quinupristin is a combination of three peptide macrolactones. Quinupristin is used in combination with dalfopristin, another antibiotic, under the trade name Synercid. Synercid is indicated for treatment of complicated skin and skin structure infections caused by methicillin-susceptible Staphylococcus aureus or Streptococcus pyogenes. The mechanism of action of quinupristin is inhibition of the late phase of protein synthesis in the bacterial ribosome. Quinupristin binds to 23S rRNA within the 50S ribosomal subunit and prevents elongation of the polypeptide as well as causing incomplete chains to be released. Adverse reactions to Synercid include inflammation at infusion site, rash, nausea, vomiting and others.

Levalbuterol is the (R)-enantiomer of the drug substance racemic albuterol (salbutamol). Binding studies have demonstrated that (R)-albuterol binds to the beta2-adrenergic receptor with a high affinity, whereas (S)-albuterol binds with 100-fold less affinity than (R)-albuterol. Other evaluations have suggested that (R)-albuterol possesses the bronchodilatory, bronchoprotective, and ciliary-stimulatory properties of racemic albuterol, while (S)-albuterol does not contribute beneficially to the therapeutic effects of the racemate and was originally assumed to be inert. Xopenex (levalbuterol HCl) Inhalation Solution is indicated for the treatment or prevention of bronchospasm in adults, adolescents, and children 6 years of age and older with reversible obstructive airway disease.

Rabeprazole sodium was discovered by Eisai Co., Ltd. Janssen Pharmaceutica N.V. and Eisai Co., Ltd. have a strategic alliance in which Eisai and Janssen-Cilag co-promote the drug in Germany and the U.K. In the US rabeprazole sodium is co-promoted under the brand name AcipHex by Eisai Inc. and Janssen Pharmaceutica Inc. Pariet is available through Janssen-Cilag in most other countries excluding Japan and some Asian countries. Rabeprazole is an antiulcer drug in the class of proton pump inhibitors. Rabeprazole is a prodrug and is converted to the active sulphenamide form in the acid environment of the parietal cells. Rabeprazole is used to heal and maintain the healing of Erosive or Ulcerative Gastroesophageal Reflux Disease (GERD), for healing Duodenal Ulcers, and for treatment of pathological hypersecretory conditions such as Zollinger-Ellison Syndrome. Rabeprazole suppresses gastric acid secretion by inhibiting the gastric H+, K+ATPase at the secretory surface of the gastric parietal cell and does not exhibit anticholinergic or histamine H2-receptor antagonist properties. Because this enzyme is regarded as the acid (proton) pump within the parietal cell, rabeprazole has been characterized as a gastric proton-pump inhibitor which blocks the final step of gastric acid secretion. In gastric parietal cells, rabeprazole is protonated, accumulates, and is transformed to an active sulfonamide.