Thiothixene (trade mark Navane) belongs to a class of antipsychotics known as the first-generation antipsychotics, sometimes referred to as conventional or typical antipsychotics. Thiothixene is a thioxanthene antipsychotic which elicits antipsychotic activity by postsynaptic blockade of CNS dopamine receptors resulting in inhibition of dopamine-mediated effects; also has alpha-adrenergic blocking activity. Thiothixene is effective in the management of schizophrenia. Only cis isomer of thiothixene exerts clinical effectivity.

Dactinomycin (actinomycin D) was isolated from Streptomyces by Selman Waksman in 1940s. The antibiotic shows anti-cancer activity; it was approved by FDA for the treatment of different cancer conditions among which are Ewing's sarcoma, Wilm's tumor, gestational trophoblastic disease, etc. Dactinomycin exerts its action by binding to DNA (preferably to GC motif) and thus inhibiting transcription.

Lincomycin (LINCOCIN®) is an antibiotic produced by Streptomyces lincolnensis (Streptomycetaceae family). It has been used in the treatment of staphylococcal, streptococcal, and Bacteroides fragilis infections. Lincomycin (LINCOCIN®) inhibits protein synthesis in susceptible bacteria by binding to the 50S subunits of bacterial ribosomes and preventing peptide bond formation upon transcription. It is usually considered bacteriostatic, but may be bactericidal in high concentrations or when used against highly susceptible microorganisms.

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.

Chlorhexidine is a broad-spectrum biocide effective against Gram-positive bacteria, Gram-negative bacteria and fungi. It is used primarily as its salts (e.g., the dihydrochloride, diacetate, and digluconate). Chlorhexidine inactivates microorganisms with a broader spectrum than other antimicrobials (e.g. antibiotics) and has a quicker kill rate than other antimicrobials (e.g. povidone-iodine). It has both bacteriostatic (inhibits bacterial growth) and bactericidal (kills bacteria) mechanisms of action, depending on its concentration. Chlorhexidine kills by disrupting the cell membrane. The most common side effects associated with chlorhexidine gluconate oral rinses are: 1) an increase in staining of teeth and other oral surfaces; 2) an increase in calculus formation; and 3) an alteration in taste perception; 4) toothache; 5) upper respiratory tract infection; and 6) headache.

Fluorometholone is a glucocorticoid employed, usually as eye drops, in the treatment of allergic and inflammatory conditions of the eye. Corticosteroids such as fluorometholone inhibit the inflammatory response to a variety of inciting agents and probably delay or slow healing. There is no generally accepted explanation for the mechanism of action of ocular corticosteroids. However, corticosteroids are thought to act by the induction of phospholipase A2 inhibitory proteins, collectively called lipocortins. It is postulated that these proteins control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes by inhibiting the release of their common precursor, arachidonic acid. Arachidonic acid is released from membrane phospholipids by phospholipase A2. Corticosteroids are capable of producing a rise in intraocular pressure. In clinical studies of documented steroid-responders, fluorometholone demonstrated a significantly longer average time to produce a rise in intraocular pressure than dexamethasone phosphate.

Amphotericin B used to treat progressive, potentially life-threatening fungal infections, such as oral thrush, vaginal candidiasis and esophageal candidiasis in patients with normal neutrophil counts. Also, Amphotericin B is often used in otherwise-untreatable protozoan infections such as visceral leishmaniasis and primary amoebic meningoencephalitis. As with other polyene antifungals, amphotericin B binds with ergosterol, a component of fungal cell membranes, forming a transmembrane channel that leads to monovalent ion (K+, Na+, H+ and Cl−) leakage, which is the primary effect leading to fungal cell death. When administered concurrently, the following drugs may interact with amphotericin B: Antineoplastic agents, Corticosteroids and Corticotropin (ACTH); Digitalis glycosides; Flucytosine; Imidazoles (e.g., ketoconazole, miconazole, clotrimazole, fluconazole, etc.); Zidovudine; Skeletal muscle relaxants (tubocurarine); Rifabutin; Leukocyte transfusions. The adverse reactions most commonly observed are: fever; malaise; weight loss; hypotension; tachypnea; anorexia; nausea; vomiting; diarrhea; dyspepsia; cramping epigastric pain; normochromic, normocytic anemia; pain at the injection site with or without phlebitis or thrombophlebitis; generalized pain, including muscle and joint pains; headache; decreased renal function and renal function abnormalities.

Edetic acid (EDTA) is a chelating agent. The U.S. Food and Drug Administration (FDA) approved edetic acid chelation therapy as a treatment for lead and heavy metal poisoning. Edetic acid in form of disodium salt was withdrawn from the market due to death resulting from hypocalcemia during chelation.

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.

Isoniazid is a bactericidal agent active against organisms of the genus Mycobacterium, specifically M. tuberculosis, M. bovis and M. kansasii. Isoniazid is recommended for all forms of tuberculosis in which organisms are susceptible. Isoniazid is a prodrug and must be activated by bacterial catalase. Isoniazid inhibits InhA, the enoyl reductase from Mycobacterium tuberculosis, by forming a covalent adduct with the NAD cofactor. The most frequent adverse reactions to isoniazid are those affecting the nervous system and the liver.