Travoprost, an isopropyl ester prodrug, is a synthetic prostaglandin F2 alpha analogue that is rapidly hydrolyzed by esterases in the cornea to its biologically active free acid. The travoporst free acid is potent and highly selective for the FP prostanoid receptor. Travoprost free acid is a selective FP prostanoid receptor agonist and is believed to reduce intraocular pressure by increasing the drainage of aqueous humor, which is done primarily through increased uveoscleral outflow and to a lesser extent, trabecular outflow facility. Travoprost ophthalmic solution is used for the reduction of elevated intraocular pressure in patients with open-angle glaucoma or ocular hypertension who are intolerant of other intraocular pressure lowering medications or insufficiently responsive (failed to achieve target IOP determined after multiple measurements over time) to another intraocular pressure lowering medication. Travoprost is known by the brand names of Travatan and Travatan Z, manufactured by Alcon.

Ertapenem is a carbapenem antibiotic marketed by Merck as Invanz. The bactericidal activity of ertapenem results from the inhibition of cell wall synthesis and is mediated through ertapenem binding to penicillin binding proteins (PBPs). In Escherichia coli, it has strong affinity toward PBPs 1a, 1b, 2, 3, 4 and 5 with preference for PBPs 2 and 3. Ertapenem has been designed to be effective against Gram-negative and Gram-positive bacteria. The most common drug-related adverse experiences in patients treated with INVANZ, including those who were switched to therapy with an oral antimicrobial, were diarrhea (5.5%), infused vein complication (3.7%), nausea (3.1%), headache (2.2%), vaginitis in females (2.1%), phlebitis/thrombophlebitis (1.3%), and vomiting (1.1%). The coadministration with probenecid to extend the half-life of ertapenem is not recommended.

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.

Montelukast (SINGULAIR®) is a selective and orally active leukotriene D4 (LTD4) receptor antagonist that inhibits the cysteinyl leukotriene CysLT1 receptor. It is indicated for the prophylaxis and chronic treatment of asthma, for prevention of exercise-induced bronchoconstriction, and for the relief of symptoms of seasonal allergic rhinitis. LTD4 is a product of arachidonic acid metabolism and is released from various cells, including mast cells and eosinophils. This eicosanoid binds to CysLT1 receptor found in the human airway (including airway smooth muscle cells and airway macrophages) and on other pro-inflammatory cells (including eosinophils and certain myeloid stem cells). Cysteinyl leukotriene receptors (CysLTs) have been correlated with the pathophysiology of asthma and allergic rhinitis. In asthma, leukotriene-mediated effects include airway edema, smooth muscle contraction, and altered cellular activity associated with the inflammatory process. In allergic rhinitis, CysLTs are released from the nasal mucosa after allergen exposure during both earlyand late-phase reactions and are associated with symptoms of allergic rhinitis. Montelukast (SINGULAIR®) binds with high affinity and selectivity to the CysLT1 (in preference to other pharmacologically important airway receptors, such as the prostanoid, cholinergic, or beta-adrenergic receptor). It inhibits physiologic actions of LTD4 at the CysLT1 receptor without any agonist activity.

Tramadol (sold under the brand name Ultram) is a narcotic analgesic proposed for moderate to severe pain. Tramadol and its O-desmethyl metabolite (M1) are selective, weak OP3-receptor agonists. Opiate receptors are coupled with G-protein receptors and function as both positive and negative regulators of synaptic transmission via G-proteins that activate effector proteins. As the effector system is adenylate cyclase and cAMP located at the inner surface of the plasma membrane, opioids decrease intracellular cAMP by inhibiting adenylate cyclase. Subsequently, the release of nociceptive neurotransmitters such as substance P, GABA, dopamine, acetylcholine, and noradrenaline is inhibited. The analgesic properties of Tramadol can be attributed to norepinephrine and serotonin reuptake blockade in the CNS, which inhibits pain transmission in the spinal cord. The (+) enantiomer has the higher affinity for the OP3 receptor and preferentially inhibits serotonin uptake and enhances serotonin release. The (-) enantiomer preferentially inhibits norepinephrine reuptake by stimulating alpha(2)-adrenergic receptors. Tramadol is used primarily to treat mild-severe pain, both acute and chronic. Its analgesic effects take about one hour to come into effect and 2 h to 4 h to peak after oral administration with an immediate-release formulation. On a dose-by-dose basis, tramadol has about one-tenth the potency of morphine and is approximately equally potent when compared to pethidine and codeine. The most common adverse effects of tramadol include nausea, dizziness, dry mouth, indigestion, abdominal pain, vertigo, vomiting, constipation, drowsiness, and headache. Compared to other opioids, respiratory depression and constipation are considered less of a problem with tramadol.

Nefazodone hydrochloride (trade name Serzone) is an antidepressant drug marketed by Bristol-Myers Squibb. Its sale was discontinued in 2003 in some countries, due to the small possibility of hepatic (liver) injury, which could lead to the need for a liver transplant, or even death. The incidence of severe liver damage is approximately 1 in 250,000 to 300,000 patient-years. On May 20, 2004, Bristol-Myers Squibb discontinued the sale of Serzone in the United States. Within the serotonergic system, nefazodone acts as an antagonist at type 2 serotonin (5-HT2) post-synaptic receptors and, like fluoxetine-type antidepressants, inhibits pre-synaptic serotonin (5-HT) reuptake. These mechanisms increase the amount of serotonin available to interact with 5-HT receptors. Within the noradrenergic system, nefazodone inhibits norepinephrine uptake minimally. Nefazodone also antagonizes alpha(1)-adrenergic receptors, producing sedation, muscle relaxation, and a variety of cardiovascular effects. Nefazodone's affinity for benzodiazepine, cholinergic, dopaminergic, histaminic, and beta or alpha(2)-adrenergic receptors is not significant.

Salmeterol is a long-acting beta2-adrenergic agonist. Although beta2-adrenoceptors are the predominant adrenergic receptors in bronchial smooth muscle and beta1-adrenoceptors are the predominant receptors in the heart, there are also beta2-adrenoceptors in the human heart comprising 10% to 50% of the total beta-adrenoceptors. The precise function of these is not yet established, but they raise the possibility that even highly selective beta2-agonists may have cardiac effects. It is FDA approved for the treatment of asthma, prevention of exercise-induced bronchospasm, maintenance treatment of chronic obstructive pulmonary disease. Common adverse reactions include musculoskeletal pain, headache, influenza, nasal/sinus congestion, pharyngitis, rhinitis, tracheitis/bronchitis, cough, throat irritation, viral respiratory infection. Salmeterol should be administered with extreme caution to patients being treated with monoamine oxidase inhibitors or tricyclic antidepressants, or within 2 weeks of discontinuation of such agents, because the action of salmeterol on the vascular system may be potentiated by these agents. Coadministration of salmeterol and ketoconazole was associated with more frequent increases in QTc duration compared with salmeterol and placebo administration.

Lodoxamide is a mast-cell stabilizer for topical administration into the eye. This compound belongs to the class of organic compounds known as alpha amino acids and derivatives. Lodoxamide inhibits the in vivo Type I immediate hypersensitivity reaction. In vitro, Lodoxamide stabilizes mast cells and prevents antigen-stimulated release of histamine. In addition, Lodoxamide prevents the release of other mast cell inflammatory mediators and inhibits eosinophil chemotaxis. Although Lodoxamide's precise mechanism of action is unknown, the drug has been reported to prevent calcium influx into mast cells upon antigen stimulation. Among side effects to Lodoxamide, the most frequently reported ocular adverse experiences were transient burning, stinging, or discomfort upon instillation. Nonocular events reported were headache and heat sensation, dizziness, somnolence, nausea, stomach discomfort, sneezing, dry nose, and rash.

Nicardipine is a potent calcium channel blockader with marked vasodilator action used to treat high blood pressure and angina. By deforming the channel, inhibiting ion-control gating mechanisms, and/or interfering with the release of calcium from the sarcoplasmic reticulum, nicardipine inhibits the influx of extracellular calcium across the myocardial and vascular smooth muscle cell membranes The decrease in intracellular calcium inhibits the contractile processes of the myocardial smooth muscle cells, causing dilation of the coronary and systemic arteries, increased oxygen delivery to the myocardial tissue, decreased total peripheral resistance, decreased systemic blood pressure, and decreased afterload.

Mesna is an organosulfur compound used as an adjuvant in cancer chemotherapy involving cyclophosphamide and ifosfamide. No clinical drug interaction studies have been conducted with mesna. Mesna concentrates in the bladder where acrolein accumulates after administration of chemotherapy and through a Michael addition, forms a conjugate with acrolein and other urotoxic metabolites. This conjugation reaction inactivates the urotoxic compounds to harmless metabolites. The most common adverse reactions (> 10%) when MESNEX is given with ifosfamide are nausea, vomiting, constipation, leukopenia, fatigue, fever, anorexia, thrombocytopenia, anemia, granulocytopenia, diarrhea, asthenia, abdominal pain, headache, alopecia, and somnolence.