TELAVANCIN (VIBATIV®) is a lipoglycopeptide antibacterial that is a synthetic derivative of vancomycin. It exerts concentration-dependent, bactericidal activity against Gram-positive organisms in vitro. TELAVANCIN (VIBATIV®) inhibits cell wall biosynthesis by binding to late-stage peptidoglycan precursors, including lipid II. It also binds to the bacterial membrane and disrupts membrane barrier function. TELAVANCIN (VIBATIV®) is indicated for the treatment of adult patients with complicated skin and skin structure infections caused by susceptible isolates of the following Gram-positive microorganisms: Staphylococcus aureus (including methicillin-susceptible and -resistant isolates), Streptococcus pyogenes, Streptococcus agalactiae, Streptococcus anginosus group (includes S. anginosus, S. intermedius, and S. constellatus), or Enterococcus faecalis (vancomycin-susceptible isolates only). It is also indicated for the treatment of adult patients with hospital-acquired and ventilator-associated bacterial pneumonia (HABP/VABP), caused by susceptible isolates of Staphylococcus aureus (both methicillin-susceptible and -resistant isolates). It should be reserved for use when alternative treatments are not suitable.

Linezolid is an antibiotic used for the treatment of infections caused by Gram-positive bacteria that are resistant to other antibiotics. Linezolid appears to be unique in that it blocks the initiation of protein production. Most common adverse reactions include diarrhea, vomiting, headache, nausea, and anemia. Linezolid has the potential for interaction with adrenergic and serotonergic agents. And with monoamine oxidase inhibitors because it’s nonselective inhibitor of monoamine oxidase.

Tobramycin, an aminoglycoside antibiotic obtained from cultures of Streptomyces tenebrarius, it is effective against gram-negative bacteria, especially the pseudomonas species. Tobramycin is used in combination with other antibiotics to treat urinary tract infections, gynecologic infections, peritonitis, endocarditis, pneumonia, bacteremia and sepsis, respiratory infections including those associated with cystic fibrosis, osteomyelitis, and diabetic foot and other soft-tissue infections. It acts primarily by disrupting protein synthesis, leading to altered cell membrane permeability, progressive disruption of the cell envelope, and eventual cell death. Tobramycin has in vitro activity against a wide range of gram-negative organisms including Pseudomonas aeruginosa. Tobramycin binds irreversibly to one of two aminoglycoside binding sites on the 30 S ribosomal subunit, inhibiting bacterial protein synthesis. Tobramycin may also destabilize bacterial memebrane by binding to 16 S 16 S r-RNA. An active transport mechanism for aminoglycoside uptake is necessary in the bacteria in order to attain a significant intracellular concentration of tobramycin. KITABIS PAK (co-packaging of tobramycin inhalation solution and PARI LC PLUS Reusable Nebulizer) is indicated for the management of cystic fibrosis in adults and pediatric patients 6 years of age and older with P. aeruginosa.

Vancomycin is a branched tricyclic glycosylated nonribosomal peptide produced by the fermentation of the Actinobacteria species Amycolatopsis orientalis (formerly Nocardia orientalis). Vancomycin became available for clinical use >50 years ago. It is often reserved as the "drug of last resort", used only after treatment with other antibiotics had failed. Vancomycin has been shown to be active against most strains of the following microorganisms, both in vitro and in clinical infections: Listeria monocytogenes, Streptococcus pyogenes, Streptococcus pneumoniae (including penicillin-resistant strains), Streptococcus agalactiae, Actinomyces species, and Lactobacillus species. The combination of vancomycin and an aminoglycoside acts synergistically in vitro against many strains of Staphylococcus aureus, Streptococcus bovis, enterococci, and the viridans group streptococci. The bactericidal action of vancomycin results primarily from inhibition of cell-wall biosynthesis. Specifically, vancomycin prevents the incorporation of N-acetylmuramic acid (NAM)- and N-acetylglucosamine (NAG)-peptide subunits from being incorporated into the peptidoglycan matrix; which forms the major structural component of Gram-positive cell walls. The large hydrophilic molecule is able to form hydrogen bond interactions with the terminal D-alanyl-D-alanine moieties of the NAM/NAG-peptides. Normally this is a five-point interaction. This binding of vancomycin to the D-Ala-D-Ala prevents the incorporation of the NAM/NAG-peptide subunits into the peptidoglycan matrix. In addition, vancomycin alters bacterial-cell-membrane permeability and RNA synthesis. There is no cross-resistance between vancomycin and other antibiotics. Vancomycin is not active in vitro against gram-negative bacilli, mycobacteria, or fungi.

Norvancomycin is an analog of glycopeptide antibiotic vancomycin. It was first found to be produced by a soil microorganisms such Nocardia orientalis and Amycolatopsis orientalis and recently was found in actinomycete Amycolatopsis orientalis CPCC200066. Norvancomycin can be derived by demethylation at N-terminus of vancomycin. It has significant inhibitory activity against Gram-positive cocci and bacilli. The mode of action of norvancomycin is based on its ability to bind to the cell-wall peptidoglycan of Gram-positive bacteria terminating tripeptide -L-Lys-D-Ala-D-Ala. Similar to vancomycin in terms of antibacterial activity, spectrum and clinical efficacy norvancomycin has more potent antibiotic activity against Staphylococcus aureus and higher affinity for bacteria cell wall analogue DALAA than vancomycin. Norvancomycin has been widely used in China to treat endocarditis, osteomyelitis and other severe infections caused by Staphylococcus aureus (including methicillin-resistant strains). The adverse drug reactions of norvancomycin are like vancomycin, such as nephrotoxicity, ototoxicity, rash and itching. Norvancomycin is not available therapeutically outside of China.