Metronidazole was synthesized by France's Rhone-Poulenc laboratories and introduced in the mid-1950s under the brand name Flagel in the US, while Sanofi-Aventis markets metronidazole globally under the same trade name, Flagyl, and also by various generic manufacturers. Metronidazole is one of the rare examples of a drug developed as ant parasitic, which has since gained broad use as an antibacterial agent. Metronidazole, a nitroimidazole, exerts antibacterial effects in an anaerobic environment against most obligate anaerobes. Metronidazole is indicated for the treatment of the following infections due to susceptible strains of sensitive organisms: Trichomoniasis: symptomatic, asymptomatic, asymptomatic consorts; Amebiasis: acute intestinal amebiasis (amebic dysentery) and amebic liver abscess; Anaerobic bacterial infections; Intra-abdominal infections, including peritonitis, intra-abdominal abscess, and liver abscess; Skin and skin structure infections; Gynecologic infections, including endometritis, endomyometritis, tubo-ovarian abscess, and postsurgical vaginal cuff infection; Bacterial septicemia; Bone and joint infections, as adjunctive therapy; Central Nervous System infections, including meningitis and brain abscess; Lower Respiratory Tract infections, including pneumonia, empyema, and lung abscess; Endocarditis. Metronidazole is NOT effective for infections caused by aerobic bacteria that can survive in the presence of oxygen. Metronidazole is only effective against anaerobic bacterial infections because the presence of oxygen will inhibit the nitrogen-reduction process that is crucial to the drug's mechanism of action. Once metronidazole enters the organism by passive diffusion and activated in the cytoplasm of susceptible anaerobic bacteria, it is reduced; this process includes intracellular electron transport proteins such as ferredoxin, transfer of an electron to the nitro group of the metronidazole, and formation of a short-lived nitroso free radical. Because of this alteration of the metronidazole molecule, a concentration gradient is created and maintained which promotes the drug’s intracellular transport. The reduced form of metronidazole and free radicals can interact with DNA leading to inhibition of DNA synthesis and DNA degradation leading to death of the bacteria. The precise mechanism of action of metronidazole is unknown. Metronidazole has a limited spectrum of activity that encompasses various protozoans and most Gram-negative and Gram-positive anaerobic bacteria. Metronidazole has activity against protozoans like Entamoeba histolytica, Giardia lamblia and Trichomonas vaginalis, for which the drug was first approved as an effective treatment.

Ampicillin is a penicillin beta-lactam antibiotic. The following gram-negative and gram-positive bacteria have been shown in in vitro studies to be susceptible to ampicillin: Hemolytic and nonhemolytic streptococci, Streptococcus pneumoniae, Nonpenicillinase-producing staphylococci, Clostridium spp., B. anthracis, Listeria monocytogenes, most strains of enterococci, H. influenzae, N. gonorrhoeae, N. meningitidis, Proteus mirabilis, many strains of Salmonella, Shigella, and E. coli. Ampicillin is indicated in the treatment of bacterial meningitis, septicemia, endocarditis, urinary tract, gastrointestinal, respiratory tract infections caused by susceptible strains of the designated organisms.

Ampicillin is a penicillin beta-lactam antibiotic. The following gram-negative and gram-positive bacteria have been shown in in vitro studies to be susceptible to ampicillin: Hemolytic and nonhemolytic streptococci, Streptococcus pneumoniae, Nonpenicillinase-producing staphylococci, Clostridium spp., B. anthracis, Listeria monocytogenes, most strains of enterococci, H. influenzae, N. gonorrhoeae, N. meningitidis, Proteus mirabilis, many strains of Salmonella, Shigella, and E. coli. Ampicillin is indicated in the treatment of bacterial meningitis, septicemia, endocarditis, urinary tract, gastrointestinal, respiratory tract infections caused by susceptible strains of the designated organisms.

Ampicillin is a penicillin beta-lactam antibiotic. The following gram-negative and gram-positive bacteria have been shown in in vitro studies to be susceptible to ampicillin: Hemolytic and nonhemolytic streptococci, Streptococcus pneumoniae, Nonpenicillinase-producing staphylococci, Clostridium spp., B. anthracis, Listeria monocytogenes, most strains of enterococci, H. influenzae, N. gonorrhoeae, N. meningitidis, Proteus mirabilis, many strains of Salmonella, Shigella, and E. coli. Ampicillin is indicated in the treatment of bacterial meningitis, septicemia, endocarditis, urinary tract, gastrointestinal, respiratory tract infections caused by susceptible strains of the designated organisms.

Ampicillin is a penicillin beta-lactam antibiotic. The following gram-negative and gram-positive bacteria have been shown in in vitro studies to be susceptible to ampicillin: Hemolytic and nonhemolytic streptococci, Streptococcus pneumoniae, Nonpenicillinase-producing staphylococci, Clostridium spp., B. anthracis, Listeria monocytogenes, most strains of enterococci, H. influenzae, N. gonorrhoeae, N. meningitidis, Proteus mirabilis, many strains of Salmonella, Shigella, and E. coli. Ampicillin is indicated in the treatment of bacterial meningitis, septicemia, endocarditis, urinary tract, gastrointestinal, respiratory tract infections caused by susceptible strains of the designated organisms.

Ampicillin is a penicillin beta-lactam antibiotic. The following gram-negative and gram-positive bacteria have been shown in in vitro studies to be susceptible to ampicillin: Hemolytic and nonhemolytic streptococci, Streptococcus pneumoniae, Nonpenicillinase-producing staphylococci, Clostridium spp., B. anthracis, Listeria monocytogenes, most strains of enterococci, H. influenzae, N. gonorrhoeae, N. meningitidis, Proteus mirabilis, many strains of Salmonella, Shigella, and E. coli. Ampicillin is indicated in the treatment of bacterial meningitis, septicemia, endocarditis, urinary tract, gastrointestinal, respiratory tract infections caused by susceptible strains of the designated organisms.

Ampicillin is a penicillin beta-lactam antibiotic. The following gram-negative and gram-positive bacteria have been shown in in vitro studies to be susceptible to ampicillin: Hemolytic and nonhemolytic streptococci, Streptococcus pneumoniae, Nonpenicillinase-producing staphylococci, Clostridium spp., B. anthracis, Listeria monocytogenes, most strains of enterococci, H. influenzae, N. gonorrhoeae, N. meningitidis, Proteus mirabilis, many strains of Salmonella, Shigella, and E. coli. Ampicillin is indicated in the treatment of bacterial meningitis, septicemia, endocarditis, urinary tract, gastrointestinal, respiratory tract infections caused by susceptible strains of the designated organisms.

Tegafur (INN, BAN, USAN) is a chemotherapeutic fluorouracil prodrug used in the treatment of cancers. It is a component of the combination drugs tegafur/uracil and tegafur/gimeracil/oteracil. UFT is an anticancer medication composed of a fixed molar ration (1:4) of tegafur and uracil. This drug is commonly used in the treatment of head and neck cancer, gastric cancer, colorectal cancer, hepatic cancer, gallbladder cancer, bile-duct cancer, pancreatic cancer, lung cancer, breast cancer, bladder cancer, prostatic cancer, or uterine cervical cancer. In the body, tegafur is converted into 5-fluorouracil (5-FU), the active antineoplastic metabolite. The mechanism of cytotoxicity of 5-FU is thought to be derived from the fact that 5-fluoro-deoxyuridine-monophosphate (FdUMP), the active metabolite of 5-FU, competes with deoxyuridine-monophosphate (dUMP), thereby inhibiting thymidylate synthase and subsequently DNA synthesis. Another active metabolite of 5-FU, 5-fluorouridine-triphosphate (FUTP) is integrated into cellular RNA, inhibiting RNA function. Uracil, when combined with tegafur, enhances the antitumor activity of 5-FU due to higher 5-FU concentrations in the tumor tissue versus normal surrounding tissue compared with tegafur alone. Uracil inhibits degradation of the released 5-FU. The combination of these two drugs enhances the antitumor activity of Tegafur.

Tegafur (INN, BAN, USAN) is a chemotherapeutic fluorouracil prodrug used in the treatment of cancers. It is a component of the combination drugs tegafur/uracil and tegafur/gimeracil/oteracil. UFT is an anticancer medication composed of a fixed molar ration (1:4) of tegafur and uracil. This drug is commonly used in the treatment of head and neck cancer, gastric cancer, colorectal cancer, hepatic cancer, gallbladder cancer, bile-duct cancer, pancreatic cancer, lung cancer, breast cancer, bladder cancer, prostatic cancer, or uterine cervical cancer. In the body, tegafur is converted into 5-fluorouracil (5-FU), the active antineoplastic metabolite. The mechanism of cytotoxicity of 5-FU is thought to be derived from the fact that 5-fluoro-deoxyuridine-monophosphate (FdUMP), the active metabolite of 5-FU, competes with deoxyuridine-monophosphate (dUMP), thereby inhibiting thymidylate synthase and subsequently DNA synthesis. Another active metabolite of 5-FU, 5-fluorouridine-triphosphate (FUTP) is integrated into cellular RNA, inhibiting RNA function. Uracil, when combined with tegafur, enhances the antitumor activity of 5-FU due to higher 5-FU concentrations in the tumor tissue versus normal surrounding tissue compared with tegafur alone. Uracil inhibits degradation of the released 5-FU. The combination of these two drugs enhances the antitumor activity of Tegafur.

Tegafur (INN, BAN, USAN) is a chemotherapeutic fluorouracil prodrug used in the treatment of cancers. It is a component of the combination drugs tegafur/uracil and tegafur/gimeracil/oteracil. UFT is an anticancer medication composed of a fixed molar ration (1:4) of tegafur and uracil. This drug is commonly used in the treatment of head and neck cancer, gastric cancer, colorectal cancer, hepatic cancer, gallbladder cancer, bile-duct cancer, pancreatic cancer, lung cancer, breast cancer, bladder cancer, prostatic cancer, or uterine cervical cancer. In the body, tegafur is converted into 5-fluorouracil (5-FU), the active antineoplastic metabolite. The mechanism of cytotoxicity of 5-FU is thought to be derived from the fact that 5-fluoro-deoxyuridine-monophosphate (FdUMP), the active metabolite of 5-FU, competes with deoxyuridine-monophosphate (dUMP), thereby inhibiting thymidylate synthase and subsequently DNA synthesis. Another active metabolite of 5-FU, 5-fluorouridine-triphosphate (FUTP) is integrated into cellular RNA, inhibiting RNA function. Uracil, when combined with tegafur, enhances the antitumor activity of 5-FU due to higher 5-FU concentrations in the tumor tissue versus normal surrounding tissue compared with tegafur alone. Uracil inhibits degradation of the released 5-FU. The combination of these two drugs enhances the antitumor activity of Tegafur.