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Vancomycin is a unique glycopeptide structurally unrelated to any currently available antibiotic. It also has a unique mode of action inhibiting the second stage of cell wall synthesis of susceptible bacteria. There is also evidence that vancomycin alters the permeability of the cell membrane and selectively inhibits ribonucleic acid synthesis. Induction of bacterial L-phase variants from susceptible organisms with vancomycin is extremely difficult, and such variants are unstable. Stable L-phase variants induced by other agents are susceptible to vancomycin. Vancomycin is active against a large number of species of Gram-positive bacteria, such as Staphylococcus aureus (including methicillin-resistant strains), Staph. epidermidis (including multiple-resistant strains), Streptococcus pneumoniae (including multiple-resistant strains), Str. pyogenes, Str. agalactiae, Str. bovis, Str. mutans, viridans streptococci, enterococci, Clostridium species, diphtheroids, Listeria monocytogenes, Actinomyces species and Lactobacillus species. There has been no increase in resistance to vancomycin during the past three decades. Enhancement of antimicrobial activity has been demonstrated with the combination of vancomycin and an aminoglycoside against Staph. aureus, Str. bovis, enterococci and viridans streptococci. The combination of vancomycin and rifampicin are antagonistic to most strains of Staph. aureus, though indifference and occasionally synergism have been shown, but is synergistic against strains of Staph. epidermidis. It shows indifference against enterococci. Vancomycin and fusidic acid are indifferent against Staph. aureus.

The novel bicyclic compound Wy-45,030 [1-2-(dimethylamino)-1-(4-methoxyphenyl)ethyl cyclohexanol, hydrochloride] exhibited a neurochemical profile predictive of antidepressant activity. Like the tricyclic antidepressants, it inhibited rat brain imipramine receptor binding and synaptosomal monoamine uptake (dopamine as well as norepinephrine and serotonin). It did not inhibit monoamine oxidase. Unlike the tricyclic antidepressants, it was not antimuscarinic in the guinea pig ileum, nor did it have any appreciable affinity for brain alpha-1 adrenergic or histamine-1 binding sites. Wy-45,030 was also without affinity for alpha-2 or beta adrenergic, benzodiazepine, serotonin-1, serotonin-2, dopamine-2, and opiate receptors. Such a profile is predictive of antidepressant activity devoid of the side-effects common to tricyclic therapy.