Table 1.

List of antimicrobial agent and their mechanism of action.

Antibiotics Family	Mechanism of Action	Antibiotics
β-lactam	Binds to the serine active site of penicillin-binding proteins (PBPs) or the allosteric site in PBP2a to inhibit bacterial cell wall peptidoglycan transpeptidation [14,15].	Penicillins Cephalosporins Carbapenems Monocyclic β-lactams β-lactamase inhibitors (e.g., clavulanic acid) (Figure 1)
Glycopeptides	Interacts with the membrane-bound lipid II precursor of peptidogly and can prevent peptidoglycan from being incorporated into an essential structural cell wall component [16].	Vancomycin Teicoplanin Telavancin Dalbavancin Oritavancin (Figure 1)
Lipopeptide	Carries out their action by causing Gram-positive bacteria’s cell membrane integrity to be compromised, which results in cell death [17,18].	Polymyxins Daptomycin Amphomycin Friulimicin Ramoplanin Empedopeptin (Figure 2)
Rifamycins	RNA polymerase (RNAP) inhibitors are used to treat tuberculosis (TB) [19].	Rifampin Rifabutin Rifapentine (Figure 3)
Aminoglycoside	By attaching to the 30S ribosome’s A-site on the 16S ribosomal RNA, they inhibit protein synthesis [20].	Streptomycin Apramycin Tobramycin Gentamcin Amikacin Neomycin Arbekacin Plazomicin (Figure 3)
Fluoroquinolones	Target DNA gyrase, topoisomerase IV, and topoisomerase type II to prevent bacteria from synthesizing DNA [21].	Nalidixic acid Enoxacin Norfloxacin Ciprofloxacin Ofloxacin Lomefloxacin Sparfloxacin Grepafloxacin Clinafloxacin Gatifloxacin Moxifloxacin Gemifloxacin Trovafloxacin Garenoxacin (Figure 4)
Sulfonamides–Trimethoprim	Sulfonamides interfere with the activity of the dihydropteroate synthase enzyme by competing with p-aminobenzoic acid (PABA) in the process of dihydrofolate production.The dihydrofolate reductase enzyme is inhibited by trimethoprim because it competes directly with it [22].	Sulfamethoxazole Trimethoprim (Figure 4)
Macrolides	Target the nascent peptide exit tunnel (NPET) of the bacterial 50S ribosomal subunit, which is responsible for the release of newly synthesized protein from the ribosome, ultimately preventing protein synthesis [23,24].	Erythromycin Clarithromycin Azithromycin Fidaxomicin Telithromycin (Figure 4)
Tetracyclines	Bind to the small subunit’s decoding site and prevent bacterial protein synthesis [25,26].	Chlortetracycline Oxytetracycline Tetracycline Demeclocycline Doxycycline Minocycline Lymecycline Meclocycline Methacycline RolitetracyclineTigecycline Omadacycline Sarecycline Eravacycline (Figure 5)
Oxazolidinones	Block the translation sequence by interacting with the 50S subunit (A-site pocket) at the peptidyl transferase center (PTC) to inhibit protein synthesis [27].	Linezolid Sutezolid Eperezolid Delpazolid Tedizolid Tedizolid phosphate Radezolid TBI-223 (Figure 5)
Streptogramins	Inhibit protein synthesis during the elongation step by attaching to bacterial ribosomes [28]. The antibiotic has two unique structural groups (A and B) that cooperate to increase the affinity of group B in the nearby nascent peptide exit tunnel (NPET) when group A binds to the peptidyl transferase center (PTC) [29].	Quinupristin Pristinamycin Virginiamycin (Figure 6)
Phenicoles	Inhibit protein synthesis by binding to the 50S ribosomal subunit [30].	Chloramphenicol Thiamphenicol Florfenicol (Figure 6)
Lincosamides	Activate amino acid monomers by aminoacyl-tRNA, chain initiation, elongation, and termination of the formed polypeptides on the ribosome, which disrupts bacterial growth and death. These are only a few of the many processes that can be affected to prevent microbial protein synthesis [31].	Lincomycin Clindamycin (Figure 6)