Vincristine is a vinca alkaloid antineoplastic agent used as a treatment for various cancers including breast cancer, Hodgkin's disease, Kaposi's sarcoma, and testicular cancer. The vinca alkaloids are structurally similar compounds comprised of 2 multiringed units, vindoline and catharanthine. The vinca alkaloids have become clinically useful since the discovery of their antitumour properties in 1959. Initially, extracts of the periwinkle plant (Catharanthus roseus) were investigated because of putative hypoglycemic properties, but were noted to cause marrow suppression in rats and antileukemic effects in vitro. Vincristine binds to the microtubular proteins of the mitotic spindle, leading to crystallization of the microtubule and mitotic arrest or cell death. Vincristine has some immunosuppressant effect. The vinca alkaloids are considered to be cell cycle phase-specific. The antitumor activity of Vincristine is thought to be due primarily to inhibition of mitosis at metaphase through its interaction with tubulin. Like other vinca alkaloids, Vincristine may also interfere with: 1) amino acid, cyclic AMP, and glutathione metabolism, 2) calmodulin-dependent Ca2+-transport ATPase activity, 3) cellular respiration, and 4) nucleic acid and lipid biosynthesis.Vincristine was marketed under the brand name Oncovin, but was discontinued. In 2012 the FDA approved a Liposomal formulation of Vincristine, named MARQIBO KIT.

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.

Acetylcysteine (also known as N-acetylcysteine or N-acetyl-L-cysteine or NAC) is primarily used as a mucolytic agent and in the management of acetaminophen poisoning. Acetylcysteine likely protects the liver by maintaining or restoring the glutathione levels, or by acting as an alternate substrate for conjugation with, and thus detoxification of, the reactive metabolite. Nacystelyn (NAL), a recently-developed lysine salt of N-acetylcysteine (NAC) is known to have excellent mucolytic capabilities and is used to treat cystic fibrosis (CF) lung disease. NAC as a precursor to the antioxidant glutathione modulates glutamatergic, neurotrophic, and inflammatory pathways. The potential applications of NAC to facilitate recovery after traumatic brain injury, cerebral ischemia, and in treatment of cerebrovascular vasospasm after subarachnoid hemorrhage. Acetylcysteine serves as a prodrug to L-cysteine, which is a precursor to the biologic antioxidant, glutathione, and hence administration of acetylcysteine replenishes glutathione stores. L-cysteine also serves as a precursor to cystine, which in turn serves as a substrate for the cystine-glutamate antiporter on astrocytes hence increasing glutamate release into the extracellular space. Acetylcysteine also possesses some anti-inflammatory effects possibly via inhibiting NF-κB through redox activation of the nuclear factor kappa kinases thereby modulating cytokine synthesis. NAC is associated with reduced levels of inflammatory cytokines and acts as a substrate for glutathione synthesis. These actions are believed to converge upon mechanisms promoting cell survival and growth factor synthesis, leading to increased neurite sprouting.

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.

Amitriptyline is a derivative of dibenzocycloheptadiene and a tricyclic antidepressant (TCA) and is mainly used to treat symptoms of depression. It works on the central nervous system (CNS) by inhibiting the membrane pump mechanism responsible for uptake of norepinephrine and serotonin in adrenergic and serotonergic neurons. Amitriptyline has been frequently used as an active comparator in clinical trials on newer antidepressants. It is rarely used as a first-line antidepressant nowadays due to its high degree of toxicity in overdose and generally poorer tolerability than the newer antidepressants.

Sulfamethoxazole is a synthetic antibacterial drug,which is used in combination with trimethoprim (Bactrim, Septra) for the treatment or prevention of infections that are proven or strongly suspected to be caused by bacteria. Sulfamethoxazole acts by inhibiting folic acid synthesis via enzyme called dihydropteroate synthase.

Vinblastine is a Vinca alkaloid obtained from the Madagascar periwinkle plant. Vinca alkaloids were found out in the 1950's by Canadian scientists, Robert Noble and Charles Beer for the first time. Medicinal applications of this plant lead to the monitoring of these compounds for their hypoglycemic activity, which is of little importance compared to their cytotoxic effects. They have been used to treat diabetes, high blood pressure and the drugs have even been used as disinfectants. Nevertheless, the vinca alkaloids are so important for being cancer fighters. The mechanism of action of vinblastine sulfate has been related to the inhibition of microtubule formation in the mitotic spindle, resulting in an arrest of dividing cells at the metaphase stage. Vinblastine is an antineoplastic agent used to treat Hodgkin's disease, non-Hodgkin's lymphomas, mycosis fungoides, cancer of the testis, Kaposi's sarcoma, Letterer-Siwe disease, as well as other cancers.

Betamethasone and its derivatives, betamethasone sodium phosphate and betamethasone acetate, are synthetic glucocorticoids. Used for its antiinflammatory or immunosuppressive properties, betamethasone is combined with a mineralocorticoid to manage adrenal insufficiency and is used in the form of betamethasone benzoate, betamethasone dipropionate, or betamethasone valerate for the treatment of inflammation due to corticosteroid-responsive dermatoses. Betamethasone and clotrimazole are used together to treat cutaneous tinea infections. Betamethasone is a glucocorticoid receptor agonist. This leads to changes in genetic expression once this complex binds to the GRE. The antiinflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. The immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding. Betamethasone binds to plasma transcortin, and it becomes active when it is not bound to transcortin.Betamethasone is used for: treating certain conditions associated with decreased adrenal gland function. It is used to treat severe inflammation caused by certain conditions, including severe asthma, severe allergies, rheumatoid arthritis, ulcerative colitis, certain blood disorders, lupus, multiple sclerosis, and certain eye and skin conditions.

Spironolactone is a synthetic 17-lactone steroid which is a renal competitive aldosterone antagonist in a class of pharmaceuticals called potassium-sparing diuretics. On its own, spironolactone is only a weak diuretic, but it can be combined with other diuretics. Due to its anti-androgen effect, it can also be used to treat hirsutism, and is a common component in hormone therapy for male-to-female transgendered people. Spironolactone inhibits the effect of aldosterone by competing for intracellular aldosterone receptor in the distal tubule cells. This increases the secretion of water and sodium, while decreasing the excretion of potassium. Spironolactone has a fairly slow onset of action, taking several days to develop and similarly the effect diminishes slowly. Spironolactone is a specific pharmacologic antagonist of aldosterone, acting primarily through competitive binding of receptors at the aldosterone-dependent sodium-potassium exchange site in the distal convoluted renal tubule. Spironolactone causes increased amounts of sodium and water to be excreted, while potassium is retained. Spironolactone acts both as a diuretic and as an antihypertensive drug by this mechanism. It may be given alone or with other diuretic agents which act more proximally in the renal tubule. Aldosterone interacts with a cytoplasmic mineralocorticoid receptor to enhance the expression of the Na+, K+-ATPase and the Na+ channel involved in a Na+ K+ transport in the distal tubule . Spironolactone bind to this mineralcorticoid receptor, blocking the actions of aldosterone on gene expression. Aldosterone is a hormone; its primary function is to retain sodium and excrete potassium in the kidneys. Spironolactone is used primarily to treat low-renin hypertension, hypokalemia, and Conn's syndrome.