Esmolol (trade name Brevibloc) is a cardioselective beta1 receptor blocker with rapid onset, a very short duration of action, and no significant intrinsic sympathomimetic or membrane stabilizing activity at therapeutic dosages. Esmolol decreases the force and rate of heart contractions by blocking beta-adrenergic receptors of the sympathetic nervous system, which are found in the heart and other organs of the body. Esmolol prevents the action of two naturally occurring substances: epinephrine and norepinephrine. Esmolol predominantly blocks the beta-1 receptors in cardiac tissue. Used for the rapid control of ventricular rate in patients with atrial fibrillation or atrial flutter in perioperative, postoperative, or other emergent circumstances where short term control of ventricular rate with a short-acting agent is desirable. Also used in noncompensatory sinus tachycardia where the rapid heart rate requires specific intervention.

Etiguanfacine, also known as SSP-1871, is an α2-adrenoreceptor agonist.

Famotidine, a competitive histamine H2-receptor antagonist, is used to treat gastrointestinal disorders such as gastric or duodenal ulcer, gastroesophageal reflux disease, and pathological hypersecretory conditions. Famotidine inhibits many of the isoenzymes of the hepatic CYP450 enzyme system. Other actions of Famotidine include an increase in gastric bacterial flora such as nitrate-reducing organisms. Famotidine binds competitively to H2-receptors located on the basolateral membrane of the parietal cell, blocking histamine affects. This competitive inhibition results in reduced basal and nocturnal gastric acid secretion and a reduction in gastric volume, acidity, and amount of gastric acid released in response to stimuli including food, caffeine, insulin, betazole, or pentagastrin.

Buspirone is the first of a new class of anxioselective agents, the azaspirodecanediones. Animal studies have suggested antianxiety activity and the absence of abuse potential. Behavioural, electrophysiological and receptor binding experiments gradually led to the idea that buspirone owes much of its anxiolytic activity to its ability to attenuate central 5-hydroxytryptamine neurotransmission. In vitro preclinical studies have shown that buspirone has a high affinity for serotonin (5-HT1A) receptors. Some studies do suggest that buspirone may have indirect effects on other neurotransmitter systems. Buspirone differs from typical benzodiazepine anxiolytics in that it does not exert anticonvulsant or muscle relaxant effects. It also lacks the prominent sedative effect that is associated with more typical anxiolytics. The drug was approved by FDA for the treatment of anxiety.

Flurbiprofen, a propionic acid derivative, is a nonsteroidal anti-inflammatory drug that exhibits antiinflammatory, analgesic, and antipyretic activities in animal models. Flurbiprofen Tablets are indicated for relief of the signs and symptoms of rheumatoid arthritis and for relief of the signs and symptoms of osteoarthritis. It may also be used to treat pain associated with dysmenorrhea and mild to moderate pain accompanied by inflammation (e.g. bursitis, tendonitis, soft tissue trauma). Flurbiprofen may also be used topically prior to ocular surgery to prevent or reduce intraoperative miosis. Similar to other NSAIAs, the anti-inflammatory effect of flurbiprofen occurs via reversible inhibition of cyclooxygenase (COX), the enzyme responsible for the conversion of arachidonic acid to prostaglandin G2 (PGG2) and PGG2 to prostaglandin H2 (PGH2) in the prostaglandin synthesis pathway. This effectively decreases the concentration of prostaglandins involved in inflammation, pain, swelling and fever. Flurbiprofen is a non-selective COX inhibitor and inhibits the activity of both COX-1 and -2. It is also one of the most potent NSAIAs in terms of prostaglandin inhibitory activity.

Dexketoprofen is a nonsteroidal anti-inflammatory drug (NSAID), manufactured by Menarini under the tradename Keral. Dexketoprofen is indicated for short-term treatment of mild to moderate pain, including dysmenorrhoea. Dexketoprofen works by blocking the action of a substance in the body called cyclo-oxygenase, which is involved in the production of chemicals in the body called prostaglandins. Prostaglandins are produced in response to injury or certain diseases and would otherwise go on to cause swelling, inflammation, and pain. By blocking cyclo-oxygenase, dexketoprofen prevents the production of prostaglandins and therefore reduces inflammation and pain. Along with peripheral analgesic action, it possesses central analgesic action. Dexketoprofen may cause dizziness, and patients should not, therefore, drive or operate heavy machinery or vehicles until they are familiar with how dexketoprofen affects them. Concomitant use of alcohol and other sedatives may potentiate this effect. In a small subset of individuals, the dizziness may be intolerable and require the transition to an alternative treatment.

Aztreonam is the first monocyclic beta-lactam antibiotic (monobactam) originally isolated from Chromobacterium violaceum. Aztreonam has a high affinity for the protein-binding protein 3 (PBP-3) of aerobic gram-negative bacteria. Most of these organisms are inhibited and killed at low concentrations of the drug. Aztreonam must be administered as an intravenous or intramuscular injection (AZACTAM®), or inhaled (CAYSTON®). Aztreonam for injection is indicated for the treatment of the following infections caused by susceptible gram-negative microorganisms: urinary tract, lower respiratory tract, skin and skin-structure, intra-abdominal and gynecologic infections as well as for septicemia. Aztreonam for inhalation solution is indicated to improve respiratory symptoms in cystic fibrosis patients with Pseudomonas aeruginosa.

Flecainide is a potent anti-arrhythmia agent, effective in a wide range of ventricular and atrial arrhythmias and tachycardias. Flecainide has local anesthetic activity and belongs to the membrane stabilizing (Class 1) group of antiarrhythmic agents; it has electrophysiologic effects characteristic of the IC class of antiarrhythmics. Flecainide acts on sodium channels on the neuronal cell membrane, limiting the spread of seizure activity and reducing seizure propagation. The antiarrhythmic actions are mediated through effects on sodium channels in Purkinje fibers. Flecainide is a sodium channel blocker, binding to voltage gated sodium channels. It stabilizes the neuronal membrane by inhibiting the ionic fluxes required for the initiation and conduction of impulses. Ventricular excitability is depressed and the stimulation threshold of the ventricle is increased during diastole. Flecainide is sold under the trade name Tambocor (manufactured by 3M pharmaceuticals). Flecainide went off-patent on February 10, 2004. In addition to being marketed as Tambocor, it is also available in generic version and under the trade names Almarytm, Apocard, Ecrinal, and Flécaine.

Leuprolide acetate is a synthetic nonapeptide analog of naturally occurring gonadotropin-releasing hormone (GnRH or LH-RH). The analog possesses greater potency than the natural hormone. It acts primarily on the anterior pituitary, inducing a transient early rise in gonadotrophin release. With continued use, leuprorelin causes pituitary desensitisation and/or down-regulation, leading to suppressed circulating levels of gonadotrophins and sex hormones. Leuprolide acetate used to treat a wide range of sex hormone-related disorders including advanced prostatic cancer, uterine leiomyomata (fibroids), endometriosis and precocious puberty.

Levobunolol is a non-cardioselective beta-adrenoceptor blocking agent, equipotent at both beta1 and beta2 adrenergic receptors. Levobunolol is greater than 60 times more potent than its dextro isomer in its beta-blocking activity, yet equipotent in its potential for direct myocardial depression. Accordingly, the levo isomer, levobunolol, is used. Levobunolol does not have significant local anesthetic (membrane-stabilizing) or intrinsic sympathomimetic activity. Levobunolol, sold under the brand name Betagan, has been shown to be an active agent in lowering elevated as well as normal intraocular pressure (IOP) whether or not accompanied by glaucoma. Levobunolol is contraindicated in those individuals with bronchial asthma or with a history of bronchial asthma, or severe chronic obstructive pulmonary disease sinus bradycardia; second and third-degree atrioventricular block; overt cardiac failure cardiogenic shock; or hypersensitivity to any component of these products.