Furadantin (nitrofurantoin), a synthetic chemical, is a stable, yellow, crystalline compound. Furadantin is an antibacterial agent for specific urinary tract infections. Orally administered Furadantin is readily absorbed and rapidly excreted in urine. Blood concentrations at therapeutic dosage are usually low. Unlike many drugs, the presence of food or agents delaying gastric emptying can increase the bioavailability of Furadantin, presumably by allowing better dissolution in gastric juices. Nitrofurantoin is active against some gram positive organisms such as S. aureus, S. epidermidis, S. saprophyticus, Enterococcus faecalis, S. agalactiae, group D streptococci, viridians streptococci and Corynebacterium. Its spectrum of activity against gram negative organisms includes E. coli, Enterobacter, Neisseria, Salmonella and Shigella. It may be used as an alternative to trimethoprim/sulfamethoxazole for treating urinary tract infections though it may be less effective at eradicating vaginal bacteria. May also be used in females as prophylaxis against recurrent cystitis related to coitus. Nitrofurantoin is highly stable to the development of bacterial resistance, a property thought to be due to its multiplicity of mechanisms of action. Nitrofurantoin is activated by bacterial flavoproteins (nitrofuran reductase) to active reduced reactive intermediates that are thought to modulate and damage ribosomal proteins or other macromolecules, especially DNA, causing inhibition of DNA, RNA, protein, and cell wall synthesis. The overall effect is inhibition of bacterial growth or cell death.

Erythromycin cyclocarbonate (Davercin) is a first generation semi-synthetic erythromycin. It is active against Gram-positive and some Gram-negative microorganisms. Davercin shows comparable or better in vitro potency, low host toxicity and improved pharmacokinetics compared with erythromycin. It is approved for the treatment of acne, atypical pneumonia (caused by Mycoplasma pneumoniae, Chlamydia pneumoniae, Legionella pneumophila), whooping cough (treatment and prevention), urethritis (caused by Ureaplasma urealyticum and Chlamydia trachomatis), gastrointestinal infection caused by Campylobacter spp., short-term infections of the skin and soft tissues (e.g. acne, staphylococcal dermatitis). In streptococcal infections, diphtheria, gonorrhea, early syphilis in patients who are allergic to penicillin, and in the prevention of bacterial endocarditis before the planned dental procedures. Adverse effects are: nausea, vomiting, abdominal pain, diarrhea, skin allergic reactions.

Streptomycin is a water-soluble aminoglycoside derived from Streptomyces griseus. Aminoglycosides work by binding to the bacterial 30S ribosomal subunit, causing misreading of t-RNA, leaving the bacterium unable to synthesize proteins vital to its growth. Aminoglycosides are useful primarily in infections involving aerobic, Gram-negative bacteria, such as Pseudomonas, Acinetobacter, and Enterobacter. In addition, some mycobacteria, including the bacteria that cause tuberculosis, are susceptible to aminoglycosides. Infections caused by Gram-positive bacteria can also be treated with aminoglycosides, but other types of antibiotics are more potent and less damaging to the host. In the past the aminoglycosides have been used in conjunction with penicillin-related antibiotics in streptococcal infections for their synergistic effects, particularly in endocarditis. Aminoglycosides are mostly ineffective against anaerobic bacteria, fungi and viruses. Aminoglycosides like Streptomycin "irreversibly" bind to specific 30S-subunit proteins and 16S rRNA. Specifically Streptomycin binds to four nucleotides of 16S rRNA and a single amino acid of protein S12. This interferes with decoding site in the vicinity of nucleotide 1400 in 16S rRNA of 30S subunit. This region interacts with the wobble base in the anticodon of tRNA. This leads to interference with the initiation complex, misreading of mRNA so incorrect amino acids are inserted into the polypeptide leading to nonfunctional or toxic peptides and the breakup of polysomes into nonfunctional monosomes. Streptomycin is indicated for the treatment of tuberculosis. May also be used in combination with other drugs to treat tularemia (Francisella tularensis), plague (Yersia pestis), severe M. avium complex, brucellosis, and enterococcal endocarditis (e.g. E. faecalis, E. faecium).

Penicillin G, also known as benzylpenicillin, is a penicillin derivative commonly used in the form of its sodium or potassium salts in the treatment of a variety of infections. It is effective against most gram-positive bacteria and against gram-negative cocci. It is administered intravenously or intramuscularly due to poor oral absorption. Penicillin G may also be used in some cases as prophylaxis against susceptible organisms. Microbiology Penicillin G is bactericidal against penicillin-susceptible microorganisms during the stage of active multiplication. It acts by inhibiting biosynthesis of cell-wall mucopeptide. It is not active against the penicillinase-producing bacteria, which include many strains of staphylococci. Penicillin G is highly active in vitro against staphylococci (except penicillinase-producing strains), streptococci (groups A, B, C, G, H, L and M), pneumococci and Neisseria meningitidis. Other organisms susceptible in vitro to penicillin G are Neisseria gonorrhoeae, Corynebacterium diphtheriae, Bacillus anthracis, clostridia, Actinomyces species, Spirillum minus, Streptobacillus monillformis, Listeria monocytogenes, and leptospira; Treponema pallidum is extremely susceptible. Adverse effects can include hypersensitivity reactions including urticaria, fever, joint pains, rashes, angioedema, anaphylaxis, serum sickness-like reaction.

Sulfadiazine is a sulfonamide antibiotic. The sulfonamides are synthetic bacteriostatic antibiotics with a wide spectrum against most gram-positive and many gram-negative organisms. However, many strains of an individual species may be resistant. Sulfonamides inhibit multiplication of bacteria by acting as competitive inhibitors of p-aminobenzoic acid in the folic acid metabolism cycle. Bacterial sensitivity is the same for the various sulfonamides, and resistance to one sulfonamide indicates resistance to all. Most sulfonamides are readily absorbed orally. However, parenteral administration is difficult, since the soluble sulfonamide salts are highly alkaline and irritating to the tissues. The sulfonamides are widely distributed throughout all tissues. High levels are achieved in pleural, peritoneal, synovial, and ocular fluids. Although these drugs are no longer used to treat meningitis, CSF levels are high in meningeal infections. Their antibacterial action is inhibited by pus. Sulfadiazine is a competitive inhibitor of the bacterial enzyme dihydropteroate synthetase. This enzyme is needed for the proper processing of para-aminobenzoic acid (PABA) which is essential for folic acid synthesis. The inhibited reaction is necessary in these organisms for the synthesis of folic acid. Used for the treatment of rheumatic fever and meningococcal meningitis.

Methenamine is an antibacterial agent for preventing recurrent urinary tract infection. It can be used as methenamine hippurate or methenamine mandelate preparations and is United States Food and Drug Administration-approved. Methenamine exerts its activity because it is hydrolyzed to formaldehyde in acid urine.

Oxytetracycline, a tetracycline analog isolated from the actinomycete streptomyces rimosus, was the second of the broad-spectrum tetracycline group of antibiotics to be discovered The drug is used for the prophylaxis and local treatment of superficial ocular infections due to oxytetracycline- and polymyxin-sensitive organisms for animal use only. These infections include the following: Ocular infections due to streptococci, rickettsiae E. coli, and A. aerogenes (such as conjunctivitis, keratitis, pinkeye, corneal ulcer, and blepharitis in dogs); ocular infections due to secondary bacterial complications associated with distemper in dogs; and ocular infections due to bacterial inflammatory conditions which may occur secondary to other diseases in dogs. Allergic reactions may occasionally occur. Treatment should be discontinued if reactions are severe. If new infections due to nonsensitive bacteria or fungi appear during therapy, appropriate measures should be taken. Oxytetracycline inhibits cell growth by inhibiting translation. It binds to the 30S ribosomal subunit and prevents the amino-acyl tRNA from binding to the A site of the ribosome. The binding is reversible in nature. Oxytetracycline is lipophilic and can easily pass through the cell membrane or passively diffuses through porin channels in the bacterial membrane.

Chlortetracycline (trade name Aureomycin, Lederle) is a tetracycline antibiotic, the first tetracycline to be identified. It was discovered in 1945 by Benjamin Minge Duggar working at Lederle Laboratories under the supervision of Yellapragada Subbarow. Duggar identified the antibiotic as the product of an actinomycete he cultured from a soil sample collected from Sanborn Field at the University of Missouri. The organism was named Streptomyces aureofaciens and the isolated drug, Aureomycin, because of their golden color. Chlortetracycline inhibits cell growth by inhibiting translation. It binds to the 16S part of the 30S ribosomal subunit and prevents the amino-acyl tRNA from binding to the A site of the ribosome. In veterinary medicine, chlortetracycline is commonly used to treat conjunctivitis in cats.

Doripenem is a synthetic carbapenem that has broad antibacterial potency against aerobic and anaerobic gram-positive and gram-negative bacteria. Doripenem is structurally related to beta-lactam antibiotics and shares the bactericidal mode of action of other β-lactam antibiotics by targeting penicillin-binding proteins (PBPs) to inhibit the biosynthesis of the bacterial cell wall. Doripenem is resistant to hydrolysis by most β-lactamases and is resistant to inactivation by renal dehydropeptidases. Doripenem has many similarities to the other carbapenems, as well as some important differences, such as greater potency against Pseudomonas aeruginosa. It was found to be similar to comparator agents. The most common adverse effects related to doripenem therapy were headache, nausea, diarrhea, rash, and phlebitis.

French pharmaceutical company Hoechst Marion Roussel (later Sanofi-Aventis) began phase II/III clinical trials of telithromycin (HMR-3647) in 1998. Telithromycin was approved by the European Commission in July 2001 and subsequently went on sale in October 2001. In the US, telithromycin received U.S. Food and Drug Administration (FDA) approval on April 1, 2004 Telithromycin is the first ketolide antibiotic to enter clinical use and is sold under the brand name of Ketek. After significant controversy regarding safety and research fraud, the US Food and Drug Administration sharply curtailed the approved uses of the drug in 2007. Telithromycin is a semi-synthetic erythromycin derivative. It is created by substituting a ketogroup for the cladinose sugar and adding a carbamate ring in the lactone ring. An alkyl-aryl moiety is attached to this carbamate ring. Furthermore, the carbon at position 6 has been methylated, as is the case in clarithromycin, to achieve better acid-stability. For the treatment of Pneumococcal infection, acute sinusitis, acute bacterial tonsillitis, acute bronchitis and bronchiolitis, lower respiratory tract infection and lobar (pneumococcal) pneumonia. KETEK tablets contain telithromycin, a semisynthetic antibacterial in the ketolide class for oral administration. Telithromycin blocks protein synthesis by binding to domains II and V of 23S rRNA of the 50S ribosomal subunit. By binding at domain II, telithromycin retains activity against gram-positive cocci (e.g., Streptococcus pneumoniae) in the presence of resistance mediated by methylases (erm genes) that alter the domain V binding site of telithromycin. Telithromycin may also inhibit the assembly of nascent ribosomal units.