Ceftobiprole is a fifth-generation cephalosporin antibiotic. It was discovered by Basilea Pharmaceutica and was developed by Johnson & Johnson Pharmaceutical Research and Development. The drug is demonstrates activity against clinically important gram-positive pathogens, including methicillin-resistant Staphylococcus aureus, penicilliin-resistant Staphylococcus pneumoniae, and Enterococcus faecalis. The drug also has demonstrated activity against gram-negative bacteria including Citrobacter spp., Escherichia coli, Enterobacter spp., Klebsiella spp., Serratia marcescens, and Pseudomonas aeruginosa. The drug has gained regulatory authorization from European states for the treatment of hospital-acquired pneumonia (HAP, excluding ventilator-associated pneumonia, VAP) and community-acquired pneumonia (CAP).

Rifamycin SV is a derivative of antibiotic rifamycin B (the natural fermentation product of S. mediterranei broths). The primary target of rifampicin on whole bacteria is the synthesis of RNA. Rifamycin belongs to the ansamycin class of antibacterial drugs and acts by inhibiting the beta subunit of the bacterial DNA-dependent RNA polymerase, blocking one of the steps in DNA transcription. This results in inhibition of bacterial synthesis and consequently growth of bacteria. Rifampicin exhibits bactericidal activity on Gram-positive and Gram-negative bacteria and on mycobacteria. Rifamycin SV MMX® (AEMCOLO), a non-absorbable rifamycin antibiotic formulated using the multi-matrix system, was designed to exhibit its pharmacological action on the distal small intestine and colon. AEMCOLO is indicated for the treatment of travelers’ diarrhea (TD) caused by non-invasive strains of Escherichia coli in adults.

Methicillin sodium anhydrous is a sodium salt of methicillin (methicillin). Methicillin is an antibiotic formerly used in the treatment of bacterial infections caused by organisms of the genus Staphylococcus. Methicillin is a semisynthetic derivative of penicillin. It was first produced in the late 1950s and was developed as a type of antibiotic called penicillinase-resistant penicillin—it contained a modification to the original penicillin structure that made it resistant to a bacterial enzyme called penicillinase (beta-lactamase). Compared to other penicillins that face antimicrobial resistance due to β-lactamase, it is less active, can be administered only parenterally, and has a higher frequency of interstitial nephritis, an otherwise-rare adverse effect of penicillins. However, the selection of meticillin depended on the outcome of susceptibility testing of the sampled infection, and since it is no longer produced, it is also not routinely tested for anymore.

Chloramphenicol is a broad-spectrum antibiotic that was first isolated from Streptomyces venezuelae in 1947. The drug was subsequently chemically synthesized. It has both a bacteriostatic and bactericidal effect; in the usual therapeutic concentrations it is bacteriostatic. Chloramphenicol is used for the treatment of serious gram-negative, gram-positive, and anaerobic infections. It is especially useful in the treatment of meningitis, typhoid fever, and cystic fibrosis. It should be reserved for infections for which other drugs are ineffective or contraindicated. Chloramphenicol, a small inhibitor of bacterial protein synthesis, is active against a variety of bacteria and readily enters the CSF. It has been used extensively in the last decades for the treatment of bacterial meningitis. In industrialized countries, chloramphenicol is restricted mostly to topical uses because of the risk of induction of aplastic anemia. However, it remains a valuable reserve antibiotic for patients with allergy to β-lactam antibiotics or with CNS infections caused by multiresistant pathogens.

Garenoxacin is an antibacterial agent active against a range of aerobic Gram-positive and Gram-negative bacteria. It exerts its action by inhibiting bacterial DNA gyrase and topoisomerase IV. The drug was withdrawn from the market in Europe and was never approved in the USA. Garenoxacin is still marketed in Japan under the name Geninax.

Iclaprim is an investigational broad-spectrum diaminopyrimidine antibiotic in development for the treatment of acute bacterial skin and skin structure infections (ABSSSIs). Iclaprim acts on bacterial cells by competitively inhibiting dihydrofolate reductase (DHFR), a key enzyme in the folate cycle; the same mode of inhibition is exerted by trimethoprim. Iclaprim resistance is mainly determined by point mutations in the dfr gene as studied in S. aureus and S. pneumoniae. Surveillance studies demonstrate that the spectrum of activity of iclaprim includes many organisms indicated in cSSSI including S. aureus and S. pyogenes. Iclaprim is bactericidal in vitro, generally at concentrations equal to the MIC that are maintained in human plasma for several hours after a therapeutic dose. Bactericidal activity is primarily time-dependent and concentration independent. Due to its structural similarity with trimethoprim, iclaprim is synergistic with sulfonamides against a broad spectrum of bacterial species. The antimicrobial mechanism of action of iclaprim is mediated by competitive inhibition of bacterial DHFR, the same mode of inhibition exerted by TMP. The activity of iclaprim against TMP-R mutants of S. aureus and S. pneumoniae is attributable to additional hydrophobic interaction between iclaprim and the enzyme. The same mechanism of action of iclaprim, competitive inhibition with the natural substrate DHF, is seen against both TMP-S and -R enzymes. Iclaprim is well suited for use as a first-line empiric monotherapy in patients with ABSSSI who are comorbid with renal impairment for the following reasons. n July 2015, the U.S. Food and Drug Administration, or FDA, designated the IV formulation of iclaprim as a Qualified Infectious Disease Product (QIDP) for ABSSSI and HABP. QIDP status grants iclaprim regulatory Fast Track designation, Priority Review and, if approved, a five-year extension to the statutory market exclusivity period in the United States, resulting in 10 years of market exclusivity from the date of approval.

Nemonoxacin is a non-fluorinated quinolone antibiotic in clinical development in an oral and intravenous formulation. It exhibits potent antibacterial activities against Gram-positive, Gram-negative, and atypical pathogens, especially methicillin-resistant Staphylococcus aureus. The molecule inhibits bacterial DNA synthesis by forming a ternary complex with a DNA molecule and gyrase and topoisomerase IV enzymes, thus blocking bacterial DNA supercoiling. Nemonoxacin is developed by TaiGen Biotechnology Company and has reached worldwide approval in 2014 and is marketed under the name Taigexyn®.

Olanexidine [1-(3,4-dichlorobenzyl)-5-octylbiguanide] (formerly OPB-2045), an antimicrobial agent exhibited antimicrobial activity against a wide range of bacteria, especially Gram-positive bacteria, was synthesized in 1997. To optimize its use as a topical antiseptic, olanexidine was converted to the gluconate salt. The resulting formulation (OPB) had more potent bactericidal activity against methicillin-resistant S. aureus and vancomycin-resistant enterococci in both in vitro and in vivo animal models than chlorhexidine and PVP-I. The mechanism of action was considered to be follows: olanexidine binds to the cell membrane, disrupts membrane integrity, and exerts its bacteriostatic and bactericidal activities by causing the irreversible leakage of intracellular components. At relatively high concentrations, olanexidine aggregates the cells through a protein-denaturing effect.

Dalbavancin is a second-generation lipoglycopeptide antibiotic that was designed to improve on the natural glycopeptides currently available, such as vancomycin and teicoplanin. Modifications from these older glycoprotein classes allowed a similar mechanism of action with increased activity and once weekly dosing. Its use is indicated for the treatment of acute bacterial skin and skin structure infections (ABSSSI) caused by the following gram-positive microorganisms: Staphylococcus aureus (including methicillin-susceptible and methicillin-resistant strains), S. pyogenes, S. agalactiae, and S. anginosus group (including S. anginosus, S. intermedius, and S. constellatus). Under the brand name DALVANCE Dalbavancin is indicated for acute bacterial skin and skin structure infections (ABSSSI) caused by designated susceptible strains of Gram-positive microorganisms. The bactericidal action of dalbavancin results primarily from inhibition of cell-wall biosynthesis. Specifically, dalbavancin prevents 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, which is normally a five-point interaction. Binding of dalbavancin to the D-Ala-D-Ala prevents the incorporation of the NAM/NAG-peptide subunits into the peptidoglycan matrix. In addition, dalbavancin alters bacterial-cell-membrane permeability and RNA synthesis.