Sultamicillin is the mutual prodrug of sulbactam and ampicillin. It is the tosylate salt of the double ester of sulbactam plus ampicillin. Sulbactam is a semisynthetic ß-lactamase inhibitor which, in combination with ampicillin, extends the antibacterial activity of the latter to include some ß-lactamase-producing strains of bacteria that would otherwise be resistant. The combination of sulbactam plus ampicillin for parenteral use has previously been shown to be clinically and bacteriologically effective in a variety of infections. Sultamicillin is marketed under a trade name Unasyn among others.

Dexibuprofen, S(+)-ibuprofen, is a non-steroidal anti-inflammatory drug and active dextrorotatory enantiomer of ibuprofen. Pharmacotherapeutic effects of dexibuprofen are more potent with lesser side effects than that of the racemic mixture of both isomers. In the acute and chronic treatment of osteoarthritis, it exhibits equivalent efficacy and tolerability as that of celecoxib. Dexibuprofen is a non-selective inhibitor of cyclooxygenase (COX), which is an enzyme involved in prostaglandin (mediators of pain and fever) and thromboxane (stimulators of blood clotting) synthesis via the arachidonic acid pathway. Dexibuprofen is a non-selective cyclooxygenase inhibitor and hence, it inhibits the activity of both COX-1 and COX-2. The inhibition of COX-2 activity decreases the synthesis of prostaglandins involved in mediating inflammation, pain, fever, and swelling while the inhibition of COX-1 is thought to cause some of the side effects of Dexibuprofen including GI ulceration. The major disadvantage of dexibuprofen is its low bioavailability, the account of its low solubility in physiological media.

Tenidap ([Z]-5-chloro-2,3-dihydro-3-[hydroxy-2-thienylmethylene]-2-oxo-1H-indole-1-carboxamide) is an oxindole derivative, a COX/5-LOX inhibitor and cytokine-modulating anti-inflammatory drug candidate that was under development by Pfizer as a promising potential treatment for rheumatoid arthritis. Tenidap shows potent inhibition of cyclooxygenase in vitro, that is of several magnitudes greater than 5-lipoxygenase inhibition. Lipoxygenase inhibition, however, has been difficult to document in vivo because Tenidap is highly protein bound and free drug concentrations are below those necessary for 5-lipoxygenase inhibition. However, several in-vitro activities distinguish Tenidap from conventional cyclooxygenase inhibitors. As shown with stimulated human neutrophils, tenidap inhibits activation of collagenase, lysosomal enzyme secretion, and superoxide generation, as well as aggregation and adhesion to endothelium. Furthermore, unlike Non-steroidal anti-inflammatory drugs (NSAIDs), it lowers circulating C-reactive protein (CRP) concentrations by a magnitude equivalent to hydroxychloroquine and auranofin. This result suggests an effect on the synthesis and/or release of the cytokines known to induce the acute-phase protein response-namely, IL-1, IL-6, and TNF-alpha. Tenidap, like existing second-line drugs, lowers serum IL-6 concentrations, a property not shared by NSAIDs The cytokine inhibitory effect also includes reduced in-vitro concentrations of TNF-alpha and IL-1 from both RA synovium and peripheral blood mononuclear cells. There is no immunosuppressive effect of Tenidap in either animal or clinical studies. In clinical studies. The comparisons between tenidap and other second-line agents show that Tenidap produced a faster reduction in CRP than Auranofin. The rate of withdrawal because of inefficacy was similar (18-20%) in Auranofin and Tenidap groups. The quality of life using the arthritis impact measurement scales has also been assessed Scores were better with tenidap than with NSAID monotherapy, but equivalent to the second line plus NSAID combinations. Tenidap is registered in the United States, Netherlands, and Italy but is not marketed because marketing approval was rejected by the FDA in 1996 due to liver and kidney toxicity, which was attributed to metabolites of the drug with a thiophene moiety that caused oxidative damage.

Fadrozole (CGS 16949A) is a tetrahydroimidazole-pyridine derivative is a non-steroidal inhibitor of aromatase. In the third phase of clinical trials it was shown, that this drug has good therapeutic effect as a second-line treatment in postmenopausal women with metastatic breast cancer.

Temocapril is a prodrug-type angiotensin-I converting enzyme (ACE) inhibitor not approved for use in the United States but is approved in Japan and South Korea. Temocapril can also be used in hemodialysis patients without risk of serious accumulation.

Velnacrine (9-amino-1,2,3,4-tetrahydroacridin-1-ol) is an inhibitor of acetylcholinesterase. It was studied for the treatment of Alzheimer's disease however development was discontinued. There has been no research into the use of velnacrine as a cognitive enhancer in the treatment of Alzheimer's disease since 1994. The FDA peripheral and CNS drug advisory board voted unanimously against recommending approval. This review shows the toxic nature of velnacrine, and provides no evidence of efficacy.

Gentamicin is an antibiotic of the aminoglycoside group, is derived from the growth of Micromonospora purpurea, an actinomycete. Gentamicin is a complex of three different closely related aminoglycoside sulfates, Gentamicins C1, C2, and C1a that have different patterns of methylation at the 69 position of the ring. Gentamicin C1a is a broad-spectrum antibiotic against Gram-positive and Gram-negative bacteria but may cause ear and kidney damage. Gentamicin C1a binds to the A-site RNA of the 30S bacterial ribosomal subunit. Adverse reactions include adverse renal effects, neurotoxicity (dizziness, vertigo, tinnitus, roaring in the ears, hearing loss, peripheral neuropathy or encephalopathy), respiratory depression, lethargy, confusion, depression, visual disturbances, etc.

Zorubicin is a benzoylhydrazone derivative of the anthracycline antineoplastic antibiotic daunorubicin, but it introduces lower cardiomyopathy and bone marrow toxicity. Zorubicin intercalates into DNA and interacts with topoisomerase II, thereby inhibiting DNA replication and repair as well as RNA and protein synthesis. The cytotoxic effect results from intercalation between DNA pairs. To minimize toxicity, individualized dose regimens are given preferentially over prolonged periods of time by carefully inspecting i.v. administration to prevent extravasation.

Medibazine (Vialibran) is a piperazine derivative. Medibazine is a coronary vasodilating agent. Although several non-controlled trials report favorable results with angina patients this medication certainly does not provide any outstanding results.

Tilarginine is L-N-monomethyl arginine (L -NMMA), a non-selective inhibitor of nitric oxide synthase (NOS), which has been studied in the treatment of septic shock and cardiogenic shock complicating myocardial infarction. Despite strong evidence that excessive nitric oxide (NO) production plays a pivotal role in the pathogenesis of septic shock and may contribute to the pathogenesis of cardiogenic shock complicating myocardial infarction, outcome studies in these two disorders have proved disappointing. Tilarginine therapy was associated with an excess mortality, particularly at doses > 5 mg/(kg h), in septic shock, whereas the effects of a lower dose (1 mg/(kg h)) in cardiogenic shock complicating myocardial infarction were neutral. The excess mortality in patients with septic shock was almost certainly the result of unfavorable hemodynamic changes induced by Tilarginine (decreased cardiac output, increased pulmonary vascular resistance and reduced tissue oxygen delivery) whereas the lack of benefit in patients with cardiogenic shock complicating myocardial infarction may have been because the dose of Tilarginine was too low.