Gatifloxacin is a recently developed antibacterial agent differing from earlier fluoroquinolones by the presence of a methoxy group at the C-8 position. The presence of the methoxy group has conferred improved antibacterial activity against both Gram-positive and Gram-negative organisms, making gatifloxacin a broad-spectrum antimicrobial agent applicable in many clinical settings. Gatifloxacin is sold under the brand Zymar and is indicated for the treatment of bacterial conjunctivitis caused by susceptible strains of the following organisms: Aerobic Gram-Positive Bacteria: Cornyebacterium propinquum, Staphylococcus aureus, Staphylococcus epidermidis, Streptococcus mitis, Streptococcus pneumoniae and Aerobic Gram-Negative Bacteria: Haemophilus influenza. The antibacterial action depends on blocking of bacterial DNA replication by binding itself to an enzyme called DNA gyrase, which allows the untwisting required to replicate one DNA double helix into two. Notably the drug has 100 times higher affinity for bacterial DNA gyrase than for mammalian. In addition, Gatifloxacin inhibits bacterial topoisomerase IV. This enzyme is an enzyme known to play a key role in the partitioning of the chromosomal DNA during bacterial cell division. The mechanism of action of fluoroquinolones including gatifloxacin is different from that of aminoglycoside, macrolide, and tetracycline antibiotics. Therefore, gatifloxacin may be active against pathogens that are resistant to these antibiotics and these antibiotics may be active against pathogens that are resistant to gatifloxacin. There is no cross-resistance between gatifloxacin and the aforementioned classes of antibiotics. Cross-resistance has been observed between systemic gatifloxacin and some other fluoroquinolones.

PRIFTIN® (rifapentine) is indicated in adults and children 12 years and older for the treatment of active pulmonary tuberculosis (TB) caused by Mycobacterium tuberculosis. PRIFTIN must always be used in combination with one or more antituberculosis (anti-TB) drugs to which the isolate is susceptible. Rifapentine is an antibiotic that inhibits DNA-dependent RNA polymerase activity in susceptible cells. Specifically, it interacts with bacterial RNA polymerase but does not inhibit the mammalian enzyme. And it acts via the inhibition of DNA-dependent RNA polymerase, leading to a suppression of RNA synthesis and cell death. It is bactericidal and has a very broad spectrum of activity against most gram-positive and gram-negative organisms (including Pseudomonas aeruginosa) and specifically Mycobacterium tuberculosis. Because of rapid emergence of resistant bacteria, use is restricted to treatment of mycobacterial infections and a few other indications. Rifampin is well absorbed when taken orally and is distributed widely in body tissues and fluids, including the CSF. It is metabolized in the liver and eliminated in bile and, to a much lesser extent, in urine, but dose adjustments are unnecessary with renal insufficiency. Rifapentine has shown higher bacteriostatic and bactericidal activities especially against intracellular bacteria growing in human monocyte-derived macrophages.

Cefdinir is an extended-spectrum, semisynthetic cephalosporin, for oral administration. As with other cephalosporins, bactericidal activity of cefdinir results from inhibition of cell wall synthesis. Cefdinir is stable in the presence of some, but not all, β-lactamase enzymes. Cefdinir is indicated for the treatment of: Community-Acquired Pneumonia, Acute Exacerbations of Chronic Bronchitis, Acute Maxillary Sinusitis, Pharyngitis/Tonsillitis and Uncomplicated Skin and Skin Structure Infections. Side effects include diarrhea, vaginal infections or inflammation, nausea, headache, and abdominal pain. Concomitant administration of 300-mg cefdinir capsules with 30 mL Maalox® TC suspension reduces the rate (Cmax) and extent (AUC) of absorption by approximately 40%. As with other β-lactam antibiotics, probenecid inhibits the renal excretion of cefdinir.

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.

Cabergoline is a long-acting dopamine receptor agonist with a high affinity for D2 receptors. Results of in vitro studies demonstrate that cabergoline exerts a direct inhibitory effect on the secretion of prolactin by rat pituitary lactotrophs. It is FDA approved for the treatment of hyperprolactinemic disorders, either idiopathic or due to pituitary adenomas. Common adverse reactions include constipation, nausea, dizziness, headache and fatigue. Cabergoline should not be administered concurrently with D-antagonists, such as phenothiazines, butyrophenones, thioxanthenes, or metoclopramide.

Meropenem (generic name: meropenem hydrate) is a carbapenem antibiotic for injection showing a strong antibacterial activity to a wide range of bacteria strains from Gram-positive bacteria, Gram-negative bacteria to anaerobic bacteria. It is used as single agent therapy for the treatment of the following infections: complicated skin and skin structure infections due to Staphylococcus aureus (b-lactamase and non-b-lactamase producing, methicillin-susceptible isolates only), Streptococcus pyogenes, Streptococcus agalactiae, viridans group streptococci. This drug also used in case of Intra-abdominal Infections for the treatment complicated appendicitis and peritonitis caused by viridans group streptococci, Escherichia coli, Klebsiella pneumoniae, Pseudomonas aeruginosa, Bacteroides fragilis, B. thetaiotaomicron, and Peptostreptococcus species. In addition is used the treatment of bacterial meningitis caused by Streptococcus pneumoniae, Haemophilus influenzae (b-lactamase and non-b-lactamase-producing isolates), and Neisseria meningitides. The bactericidal activity of meropenem results from the inhibition of cell wall synthesis. Meropenem readily penetrates the cell wall of most Gram-positive and Gram-negative bacteria to reach penicillin-binding-protein (PBP) targets. Its strongest affinities are toward PBPs 2, 3 and 4 of Escherichia coli and Pseudomonas aeruginosa; and PBPs 1, 2 and 4 of Staphylococcus aureus. Meropenem has significant stability to hydrolysis by β-lactamases, both penicillinases and cephalosporinases produced by Gram-positive and Gram-negative bacteria. Meropenem should not be used to treat methicillin-resistant Staphylococcus aureus (MRSA) or methicillin-resistant Staphylococcus epidermidis (MRSE). Meropenem product with such superior effectiveness and safety has been approved for marketing by 100 countries or more in the world (as of March 2004) since its first launch in Italy in 1994.

Riluzole, a member of the benzothiazole class, is indicated for the treatment of patients with amyotrophic lateral sclerosis. Its pharmacological properties include the following, some of which may be related to its effect: 1) an inhibitory effect on glutamate release (activation of glutamate reuptake), 2) inactivation of voltage-dependent sodium channels, and 3) ability to interfere with intracellular events that follow transmitter binding at excitatory amino acid receptors. Common adverse reactions include headache, abdominal pain, back pain, vomiting, dyspepsia, diarrhea, dizziness. Riluzole-treated patients that take other hepatotoxic drugs may be at increased risk for hepatotoxicity.

Aminolevulinic Acid is the first compound in the porphyrin synthesis pathway. The metabolism of aminolevulinic acid (ALA) is the first step in the biochemical pathway resulting in heme synthesis. Aminolevulinic acid is not a photosensitizer, but rather a metabolic precursor of protoporphyrin IX (PpIX), which is a photosensitizer. The synthesis of ALA is normally tightly controlled by feedback inhibition of the enzyme, ALA synthetase, presumably by intracellular heme levels. ALA, when provided to the cell, bypasses this control point and results in the accumulation of PpIX, which is converted into heme by ferrochelatase through the addition of iron to the PpIX nucleus. Marketed under the brand name LEVULAN KERASTICK for Topical Solution plus blue light illumination using the BLU-U Blue Light Photodynamic Therapy Illuminator, it is indicated for the treatment of minimally to moderately thick actinic keratoses (Grade 1 or 2, see table 2 for definition) of the face or scalp. Aminolevulinic acid is also being studied in the treatment of other conditions and types of cancer. An orally-administered in vivo diagnostic agent, Aminolevulinic acid, is used in photodynamic diagnosis (PDD) whose aim is to help doctors visualize the tumor tissue during surgical resection of malignant glioma, it is already sold in over 20 European countries including Germany and the U.K. According to the presumed mechanism of action, photosensitization following application of aminolevulinic acid (ALA) topical solution occurs through the metabolic conversion of ALA to protoporphyrin IX (PpIX), which accumulates in the skin to which aminolevulinic acid has been applied. When exposed to light of appropriate wavelength and energy, the accumulated PpIX produces a photodynamic reaction, a cytotoxic process dependent upon the simultaneous presence of light and oxygen. The absorption of light results in an excited state of the porphyrin molecule, and subsequent spin transfer from PpIX to molecular oxygen generates singlet oxygen, which can further react to form superoxide and hydroxyl radicals. Photosensitization of actinic (solar) keratosis lesions using aminolevulinic acid, plus illumination with the BLU-UTM Blue Light Photodynamic Therapy Illuminator (BLU-U), is the basis for aminolevulinic acid photodynamic therapy (PDT).

Vinorelbine (trade name Navelbine) is a semi-synthetic vinca-alkaloid with a broad spectrum of anti-tumour activity. Vinorelbine is a mitotic spindle poison that impairs chromosomal segregation during mitosis. It blocks cells at G2/M. Microtubules (derived from polymers of tubulin) are the principal target of vinorelbine. Vinorelbine was developed by Pierre Fabre under licence from the CNRS in France. NAVELBINE (vinorelbine tartrate) as a single agent or in combination is indicated for the first line treatment of non small cell lung cancer and advanced breast cancer.

SPORANOX is the brand name for itraconazole, an azole antifungal agent. Itraconazole is a 1:1:1:1 racemic mixture of four diastereomers (two enantiomeric pairs), each possessing three chiral centers. In vitro studies have demonstrated that itraconazole inhibits the cytochrome P450-dependent synthesis of ergosterol, which is a vital component of fungal cell membranes. As ergosterol is an essential component of the fungal cell membrane, inhibition of its synthesis results in increased cellular permeability causing leakage of cellular contents. Itraconazole may also inhibit endogenous respiration, interact with membrane phospholipids, inhibit the transformation of yeasts to mycelial forms, inhibit purine uptake, and impair triglyceride and/or phospholipid biosynthesis. SPORANOX capsules are indicated for the treatment of the following fungal infections in immunocompromised and non-immunocompromised patients: Blastomycosis, pulmonary and extrapulmonary; Histoplasmosis, including chronic cavitary pulmonary disease and disseminated, nonmeningeal histoplasmosis, and Aspergillosis, pulmonary and extrapulmonary, in patients who are intolerant of or who are refractory to amphotericin B therapy. SPORANOX is also indicated for the treatment of the following fungal infections in non-immunocompromised patients: Onychomycosis of the toenail, with or without fingernail involvement, due to dermatophytes (tinea unguium), and Onychomycosis of the fingernail due to dermatophytes (tinea unguium). Itraconazole is mainly metabolized through CYP3A4. Other drugs that either share this metabolic pathway or modify CYP3A4 activity may influence the pharmacokinetics of itraconazole. Similarly, itraconazole may modify the pharmacokinetics of other drugs that share this metabolic pathway. Itraconazole is a potent CYP3A4 inhibitor and a P-glycoprotein inhibitor. When using concomitant medication, it is recommended that the corresponding label be consulted for information on the route of metabolism and the possible need to adjust dosages.