Ifosfamide (IF) is a widely used antitumor prodrug. It is in the oxazaphosphorine class of alkylating agents, and it is effective against solid tumors. Ifosfamide mechanism of crosslinking DNA plays a major role in preventing cancer cells from proliferating. Ifosfamide is approved by FDA for the treatment of germ cell testicular cancer.

Mitoxantrone (NOVANTRONE) is a synthetic antineoplastic anthracenedione. Mitoxantrone, a DNA-reactive agent that intercalates into deoxyribonucleic acid (DNA) through hydrogen bonding, causes crosslinks and strand breaks. Mitoxantrone also interferes with ribonucleic acid (RNA) and is a potent inhibitor of topoisomerase II, an enzyme responsible for uncoiling and repairing damaged DNA. It has a cytocidal effect on both proliferating and nonproliferating cultured human cells, suggesting lack of cell cycle phase specificity. Mitoxantrone has been shown in vitro to inhibit B cell, T cell, and macrophage proliferation and impair antigen pre sentation, as well as the secretion of interferon gamma, TNFα, and IL-2. NOVANTRONE is indicated for reducing neurologic disability and/or the frequency of clinical relapses in patients with secondary (chronic) progressive, progressive relapsing, or worsening relapsing-remitting multiple sclerosis (i.e., patients whose neurologic status is significantly abnormal between relapses). NOVANTRONE in combination with corticosteroids is indicated as initial chemotherapy for the treatment of patients with pain related to advanced hormone-refractory prostate cancer. NOVANTRONE in combination with other approved drug(s) is indicated in the initial therapy of acute nonlymphocytic leukemia (ANLL) in adults. This category includes myelogenous, promyelocytic, monocytic, and erythroid acute leukemias.

Amlodipine is a dihydropyridine calcium antagonist (calcium ion antagonist or slow-channel blocker) that inhibits the transmembrane influx of calcium ions into vascular smooth muscle and cardiac muscle. Experimental data suggest that amlodipine binds to both dihydropyridine and nondihydropyridine binding sites. The contractile processes of cardiac muscle and vascular smooth muscle are dependent upon the movement of extracellular calcium ions into these cells through specific ion channels. Amlodipine inhibits calcium ion influx across cell membranes selectively, with a greater effect on vascular mooth muscle cells than on cardiac muscle cells. Amlodipine is indicated for the treatment of hypertension and coronary artery disease.

Alfentanil is an opioid analgesic with a rapid onset of action. Alfentanil interacts predominately with the opioid mu-receptor. These mu-binding sites are discretely distributed in the human brain, spinal cord, and other tissues. In clinical settings, alfentanil exerts its principal pharmacologic effects on the central nervous system. Its primary actions of therapeutic value are analgesia and sedation. Alfentanil may increase the patient's tolerance for pain and decrease the perception of suffering, although the presence of the pain itself may still be recognized. In addition to analgesia, alterations in mood, euphoria and dysphoria, and drowsiness commonly occur. Alfentanil depresses the respiratory centers, depresses the cough reflex, and constricts the pupils. Alfentanil, marketed under the trade name Alfenta, Rapifen in Australia is indicated for the management of postoperative pain and the maintenance of general anesthesia.

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.

Sulconazole (trade name Exelderm) is an antifungal medication of the imidazole class. Sulconazole has a broad spectrum of antifungal activity in vitro and has been shown to be an effective topical antifungal agent for the management of superficial fungal infections of the skin, particularly dermatophytosis and tinea versicolor. Sulconazole inhibits the cytochrome P-450 isoenzyme, C-14-alpha-demethylase by binding to the heme iron of the enzyme. This results in a largely fungistatic effect. The selectivity of azole antifungal agents for pathogenic organisms compared with mammalian cells appears to depend on a preferred affinity of these drugs for fungal versus mammalian cytochrome P-450 sterol demethylases. Enzyme inhibition by sulconazole prevents the synthesis of ergosterol, a sterol found in fungal cell membranes but, in general, not in mammalian cell membranes. Additionally, lanosterol accumulates, which changes membrane permeability, cell volume, secondary metabolic effects, and causes defective cell division and growth inhibition. As sulconazole is primarily fungistatic, an intact immune system may be needed for infection resolution.In selected situations, sulconazole may have growth phase-dependent fungicidal activity against very susceptible organisms. The 1% concentration of sulconazole may greatly exceed the minimum inhibitory concentration and exert a direct physiochemical effect on the fungal cell membrane. The fungicidal effect may be due to hydrophobic interactions between sulconazole and unsaturated fatty acids in the membrane. Mammalian cells generally have little or no unsaturated fatty acids. Sulconazole may also prevent DNA and RNA synthesis and increase their degradation.Sulconazole has activity against many dermatophytes and yeast. One measure of the drug's antifungal activity is the relative inhibition factor (RIF). The RIF approaches 0% for a drug to which a fungus is highly sensitive and 100% for a drug that is non-inhibitory. The RIF values of sulconazole for Candida species, Aspergillus species, and dermatophytes are broadly similar to those of clotrimazole, econazole, ketoconazole, miconazole, and tioconazole. The mean RIF values were 69% (30—98%) for Candida species, 71% (61—82%) for Aspergillus species, and 12% (5—18%) for dermatophytes. Sulconazole is available as a cream or solution to treat skin infections such as athlete's foot, ringworm, jock itch, and sun fungus.

Ceftazidime is a semisynthetic, broad-spectrum, beta-lactam antibiotic, used especially for Pseudomonas and other gram-negative infections in debilitated patients. Ceftazidime is used to treat lower respiratory tract, skin, urinary tract, blood-stream, joint, and abdominal infections, and meningitis. The drug is given intravenously (IV) or intramuscularly (IM) every 8–12 hours (two or three times a day), with dose and frequency varying by the type of infection, severity, and/or renal function of the patient. Injectable formulations of ceftazidime are currently nebulized "off-label" to manage Cystic Fibrosis, non-Cystic Fibrosis bronchiectasis, drug-resistant nontuberculous mycobacterial infections, ventilator-associated pneumonia, and post-transplant airway infections. Ceftazidime is generally well-tolerated. When side effects do occur, they are most commonly local effects from the intravenous line site, allergic reactions, and gastrointestinal symptoms. According to one manufacturer, in clinical trials, allergic reactions including itching, rash, and fever, happened in fewer than 2% of patients. Rare but more serious allergic reactions, such as toxic epidermal necrolysis, Stevens-Johnson syndrome, and erythema multiforme, have been reported with this class of antibiotics, including ceftazidime. Gastrointestinal symptoms, including diarrhea, nausea, vomiting, and abdominal pain, were reported in fewer than 2% of patients.

Enalapril (marketed as Vasotec in the US, Enaladex and Renitec in some other countries) is an angiotensin-converting-enzyme (ACE) inhibitor used in the treatment of hypertension, diabetic nephropathy, and some types of chronic heart failure. Enalapril, after hydrolysis to enalaprilat, inhibits angiotensin-converting enzyme (ACE) in human subjects and animals. ACE is a peptidyl dipeptidase that catalyzes the conversion of angiotensin I to the vasoconstrictor substance, angiotensin II. Angiotensin II also stimulates aldosterone secretion by the adrenal cortex. The beneficial effects of enalapril in hypertension and heart failure appear to result primarily from suppression of the renin-angiotensin-aldosterone system. Inhibition of ACE results in decreased plasma angiotensin II, which leads to decreased vasopressor activity and to decrease aldosterone secretion.

Imipenem is a beta-lactam antibiotic belongings to the subgroup of carbapenems. Imipenem has a broad spectrum of activity against aerobic and anaerobic Gram positive as well as Gram negative bacteria. It is particularly important for its activity against Pseudomonas aeruginosa and the Enterococcus species. Imipenem is rapidly degraded by the renal enzyme dehydropeptidase when administered alone, and is always co-administered with cilastatin to prevent this inactivation. The bactericidal activity of imipenem results from the inhibition of cell wall synthesis. Its greatest affinity is for penicillin binding proteins (PBPs) 1A, 1B, 2, 4, 5 and 6 of Escherichia coli, and 1A, 1B, 2, 4 and 5 of Pseudomonas aeruginosa. The lethal effect is related to binding to PBP 2 and PBP 1B. Imipenem is marketed under the brand name Primaxin. PRIMAXIN I.M. (Imipenem and Cilastatin for Injectable Suspension) is a formulation of imipenem (a thienamycin antibiotic) and cilastatin sodium (the inhibitor of the renal dipeptidase, dehydropeptidase I). PRIMAXIN I.M. is a potent broad spectrum antibacterial agent for intramuscular administration.

Auranofin (brand name Ridaura) is an organogold compound classified by the World Health Organization as an antirheumatic agent. Ridaura is indicated in the management of adults with active classical or definite rheumatoid arthritis (ARA criteria) who have had an insufficient therapeutic response to, or are intolerant of, an adequate trial of full doses of one or more nonsteroidal anti-inflammatory drugs. The mechanism of action of is not understood. In patients with adult rheumatoid arthritis, it may modify disease activity as manifested by synovitis and associated symptoms, and reflected by laboratory parameters such as ESR. There is no substantial evidence, however, that gold-containing compounds induce remission of rheumatoid arthritis. It may act as an inhibitor of kappab kinase and thioredoxin reductase, which would lead to a decreased immune response and decreased free radical production, respectively. In patients with inflammatory arthritis, such as adult and juvenile rheumatoid arthritis, gold salts can decrease the inflammation of the joint lining. This effect can prevent destruction of bone and cartilage. Ridaura should be added to a comprehensive baseline program, including non-drug therapies. Unlike anti-inflammatory drugs, RIDAURA does not produce an immediate response. Therapeutic effects may be seen after three to four months of treatment, although improvement has not been seen in some patients before six months.