ATC Group: J01D Other beta-lactam antibacterials

Aztreonam exhibits activity in vitro against gram-negative aerobic pathogens, including P. aeruginosa. Aztreonam binds to penicillin-binding proteins of susceptible bacteria, which leads to inhibition of bacterial cell wall synthesis, followed by filamentation and cell lysis.

Aztreonam inhibits bacterial peptidoglycan cell wall synthesis following binding to penicillin-binding proteins (PBPs), which leads to bacterial cell lysis and death. Avibactam is a non β-lactam, β-lactamase inhibitor that acts by forming a covalent adduct with the enzyme that is stable to hydrolysis. Avibactam inhibits both Ambler class A and class C β-lactamases and some class D enzymes, including extended-spectrum β-lactamases (ESBLs), Klebsiella pneumoniae carbapenemase (KPC) and OXA-48 carbapenemases, and AmpC enzymes.

Cefaclor is a second-generation cephalosporin antibiotic. Cefaclor has no activity against Pseudomonas species or Acinetobacter species. Methicillin-resistant staphylococci and most strains of enterococci (eg, Str. faecalis) are resistant to cefaclor.

Cefadroxil is a cephalosporin for oral administration which inhibits bacterial wall synthesis of actively dividing cells by binding to one or more penicillin-binding proteins.

Cefalexin is an antibacterial agent of the cephalosporin class. Like other cephalosporins cefalexin exerts antibacterial activity by binding to and inhibiting the action of penicillin-binding proteins involved in the synthesis of bacterial cell walls. This leads to bacterial cell lysis and cell death.

Cephalothin is a first generation, semisynthetic analogue of natural cephalosporin antibiotic. The in-vitro bactericidal action of cephalothin results from inhibition of cell-wall synthesis. In general, cephalothin has higher activity against Gram positive than Gram negative organisms. Cephalothin is primarily indicated in conditions like bone and joint infection, genitourinary tract infections, respiratory tract infections, soft tissue and skin infections and others.

Cefatrizine is a broad-spectrum, semisynthetic, first-generation cephalosporin with antibacterial activity. Cefatrizine binds to and inactivates penicillin-binding proteins (PBPs) located on the inner membrane of the bacterial cell wall. PBPs are enzymes involved in the terminal stages of assembling the bacterial cell wall and in reshaping the cell wall during growth and division. Inactivation of PBPs interferes with the cross-linkage of peptidoglycan chains necessary for bacterial cell wall strength and rigidity. This results in the weakening of the bacterial cell wall and causes cell lysis.

Cefazolin is a bactericidal cephalosporin antibiotic of the first generation for parenteral administration. Cephalosporins inhibit cell wall synthesis (in the growth stage) through blocking the penicillin-binding proteins (PBPs) like transpeptidases. The outcome is a bactericidal action.

Cefditoren is a cephalosporin with antibacterial activity against gram-positive and gram-negative pathogens. The bactericidal activity of cefditoren results from the inhibition of cell wall synthesis via affinity for penicillin-binding proteins (PBPs).

Cefepime is a broad-spectrum, bactericidal antibiotic, with activity against a wide range of Gram-positive and Gram-negative bacteria, including many strains resistant to aminoglycosides or third generation cephalosporins. It has a reduced affinity for beta-lactamases.

Cefepime exerts bactericidal activity by inhibiting peptidoglycan cell wall synthesis as a result of binding to and inhibition of penicillin-binding proteins (PBPs). Enmetazobactam is a penicillanic acid sulfone beta-lactamase inhibitor structurally related to penicillin. Enmetazobactam binds to β-lactamases and prevents the hydrolysis of cefepime. It is active against class A ESBLs.

Cefiderocol is a siderophore cephalosporin. In addition to passive diffusion through outer membrane porin channels, cefiderocol is able to bind to extracellular free iron via its siderophore side chain, allowing active transport into the periplasmic space of Gram-negative bacteria through siderophore uptake systems. Cefiderocol subsequently binds to penicillin binding proteins (PBPs), inhibiting bacterial peptidoglycan cell wall synthesis which leads to cell lysis and death.

Cefixime is an oral third generation cephalosporin which has marked in vitro bactericidal activity against a wide variety of Gram-positive and Gram-negative organisms.

Cefoperazone, a third-generation cephalosporin, interferes with cell wall synthesis by binding to the penicillin-binding proteins (PBPs), thus preventing cross-linking of nascent peptidoglycan. Cefoperazone is stable to penicillinases and has a high degree of stability to many beta-lactamases produced by gram-negative bacteria.

Cefotaxime exerts its action by binding to one or more of the penicillin-binding proteins (PBPs) which in turn inhibits the final transpeptidation step of peptidoglycan synthesis in bacterial cell walls, thereby inhibiting cell wall synthesis.

Cefotetan is a bactericidal agent that acts by inhibition of bacterial cell wall synthesis. Cefotetan has activity in the presence of some beta-lactamases, both penicillinases and cephalosporinases, of gram-negative and gram-positive bacteria.

Cefoxitin is a beta-lactam antibiotic of the group of the second-generation cephalosporins.

Like other beta-lactam drugs, cefpodoxime exerts antibacterial activity by binding to and inhibiting the action of certain bacterial cell wall synthetic enzymes, namely the penicillin binding proteins.

Cefprozil is a semi synthetic broad-spectrum cephalosporin antibiotic intended for oral administration. The bactericidal action of cefprozil results from inhibition of cell-wall synthesis.

Cefradine is a broad-spectrum, bactericidal first generation cephalosporin antibiotic active against both Gram-positive and Gram-negative bacteria. It is also highly active against most strains of penicillinase producing Staphylococci. The anti-bacterial action of cefradine is through inhibition of bacterial cell wall synthesis.

In vitro studies have shown that ceftaroline is bactericidal and able to inhibit bacterial cell wall synthesis in methicillin-resistant Staphylococcus aureus (MRSA) and penicillin non-susceptible Streptococcus pneumoniae (PNSP) due to its affinity for the altered penicillin-binding proteins (PBPs) found in these organisms. As a result, minimum inhibitory concentrations (MICs) of ceftaroline against a proportion of these organisms tested fall into the susceptible range.

Ceftazidime inhibits bacterial cell wall synthesis following attachment to penicillin binding proteins (PBPs). This results in the interruption of cell wall (peptidoglycan) biosynthesis, which leads to bacterial cell lysis and death.

Ceftibuten is a semisynthetic, beta-lactamase-stable, third-generation cephalosporin with antibacterial activity. Ceftibuten binds to and inactivates penicillin-binding proteins (PBPs) located on the inner membrane of the bacterial cell wall. This results in the weakening of the bacterial cell wall and causes cell lysis.

Ceftobiprole exerts bactericidal activity through binding to important penicillin-binding proteins (PBPs) in susceptible species.

Ceftriaxone is an antibacterial for systemic use, a third-generation cephalosporin. It inhibits bacterial cell wall synthesis following attachment to penicillin binding proteins (PBPs) leading to bacterial cell lysis and death.

Cefuroxime inhibits bacterial cell wall synthesis following attachment to penicillin binding proteins (PBPs). This results in the interruption of cell wall (peptidoglycan) biosynthesis, which leads to bacterial cell lysis and death.

Doripenem is a synthetic carbapenem antibacterial agent. Doripenem exerts its bactericidal activity by inhibiting bacterial cell wall biosynthesis. Doripenem inactivates multiple essential penicillin-binding proteins (PBPs) resulting in inhibition of cell wall synthesis with subsequent cell death.

Ertapenem inhibits bacterial cell wall synthesis following attachment to penicillin binding proteins (PBPs). In Escherichia coli, affinity is strongest to PBPs 2 and 3.

Faropenem is an orally active beta-lactam antibiotic belonging to the penem group. Like other beta-lactam antibiotics, faropenem acts by inhibiting the synthesis of bacterial cell walls. It inhibits cross-linkage between the linear peptidoglycan polymer chains that make up a major component of the cell wall of Gram-positive bacteria. It does this by binding to and competitively inhibiting the transpeptidase enzyme used by bacteria to cross-link the peptide (D-alanyl-alanine) used in peptidogylcan synthesis.

Imipenem is a semi-synthetic derivative of thienamycin, the parent compound produced by the filamentous bacterium Streptomyces cattleya. Imipenem exerts its bactericidal activity by inhibiting bacterial cell wall synthesis in Gram-positive and Gram-negative bacteria through binding to penicillin-binding proteins (PBPs).

Imipenem, also referred to as N-formimidoyl-thienamycin, is a semi-synthetic derivative of thienamycin, the parent compound produced by the filamentous bacterium Streptomyces cattleya. Imipenem exerts its bactericidal activity by inhibiting bacterial cell wall synthesis in Gram-positive and Gram-negative bacteria through binding to penicillin-binding proteins (PBPs). Cilastatin sodium is a competitive, reversible and specific inhibitor of dehydropeptidase-I, the renal enzyme which metabolizes and inactivates imipenem. It is devoid of intrinsic antibacterial activity and does not affect the antibacterial activity of imipenem.

The bactericidal activity of imipenem results from the inhibition of penicillin binding proteins (PBPs) leading to inhibition of peptidoglycan cell wall synthesis. Cilastatin limits the renal metabolism of imipenem and does not have antibacterial activity. Relebactam is a non-beta lactam inhibitor of Ambler class A and class C beta-lactamases, including class A Klebsiella pneumoniae carbapenemase (KPC) and extended-spectrum beta-lactamases (ESBLs), and class C (AmpC-type) beta-lactamases including Pseudomonas-Derived Cephalosporinase (PDC). Relebactam does not inhibit class B enzymes (metallo-beta-lactamases) or class D carbapenemases. Relebactam has no antibacterial activity.

Meropenem exerts its bactericidal activity by inhibiting bacterial cell wall synthesis in Gram-positive and Gram-negative bacteria through binding to penicillin-binding proteins (PBPs).

Meropenem exerts bactericidal activity by inhibiting peptidoglycan cell wall synthesis as a result of binding to and inhibition of activity of essential penicillin-binding proteins (PBPs). Vaborbactam is a non-beta-lactam inhibitor of class A and class C serine beta-lactamases, including Klebsiella pneumoniae carbapenemase, KPC. It acts by forming a covalent adduct with beta-lactamases and is stable to beta-lactamase-mediated hydrolysis.