Sulforidazine (Imagotan (Sandoz); Inofal (Sandoz)) is a typical piperidine-type phenothiazine antipsychotic agent. It is dopamine receptor blocker. Being the second active metabolite of thioridazine (converted from mesoridazine), Sulforidazine is significantly more potent than the parent drug.

Cycloguanil is a dihydrofolate reductase inhibitor and is a metabolite of the antimalarial drug proguanil. The parent drug proguanil was suggested to contribute to the antimalarial activity as well, but the mechanism of action is unknown. Proguanil is a prodrug that is metabolized to its main active metabolite, cycloguanil, mostly via CYP2C19. There is significant variation in proguanil pharmacokinetics.12 CYP2C19 is the predominant enzyme catalyzing the bioactivation of proguanil to cycloguanil. Cycloguanil is one of the few antimalarial drugs that act on both the erythrocytic and on the pre-erythrocytic (hepatic) forms of the malaria parasites. Although cycloguanil is not currently in general use as an antimalarial, the continuing development of resistance to current antimalarial drugs has led to renewed interest in studying the use of cycloguanil in combination with other drugs.

Prednimustine is chlorambucil ester of prednisolone. Prednimustine is a cytostatic agent. Prednimustine is active against a wide variety of experimental tumors both in vivo and in vitro. In many of these tumor systems, prednimustine exhibits distinct advantages over a mixture of its constituents, chlorambucil and prednisolone. In vitro, a higher cell kill is obtained, and in vivo, at doses that are equally effective, prednimustine is less toxic. It has been used in the treatment of various malignancies, including chronic lymphatic leukaemia and non-Hodgkin's lymphomas. It has also been tested for use in the treatment of breast cancer

Azosemide is a monosulfamyl belonging to the class of loop diuretics, used to treat hypertension, edema, and ascites. Azosemide inhibits sodium and chloride reabsorption throughout the thick ascending limb of the loop of Henle. The exact mechanism of action is not fully understood, but it mainly acts on both the medullary and cortical segments of the thick ascending limb of the loop of Henle. Delayed tolerance was demonstrated in humans by homeostatic mechanisms (principally an increase in aldosterone secretion and perhaps also an increase in the reabsorption of solute in the proximal tubule). After oral administration to healthy humans in the fasting state, the plasma concentration of azosemide reached its peak at 3–4 h with an absorption lag time of approximately 1 h and a terminal half-life of 2–3 h. The estimated extent of absolute oral bioavailability in humans was approximately 20.4%. After oral administration of the same dose of azosemide and furosemide, the diuretic effect was similar between the two drugs, but after intravenous administration, the effect of azosemide was 5.5–8 times greater than that in furosemide. This could be due to the considerable first-pass effect of azosemide. Azosemide is actively secreted in the renal proximal tubule possibly via nonspecific organic acid secretory pathway in humans. Thus, the amount of azosemide that reaches its site of action could be significantly modified by changes in the capacity of this transport system. This capacity, in turn, could be predictably changed in disease states, resulting in decreased delivery of the diuretic to the transport site, as well as in the presence of other organic acids such as nonsteroidal anti-inflammatory drugs which could compete for active transport of azosemide.

AMFLUTIZOLE is a xanthine oxidase inhibitor used for the treatment of gout.

Glibornuride is sulphonylurea derivative used as an oral hypoglycemic drug in patients with diabetes. The drug was marketed under the name Glutril, however, it is no longer available.

A-escin (Escin Ia) and isoescin Ia have been traditionally used clinically as the chief active ingredients of escin, a major triterpene saponin isolated from horse chestnut (Aesculus hippocastanum) seeds for the treatment of chronic venous insufficiency, hemorrhoids, inflammation and edema. A-escin administration to prednisolone-treated rats slightly reduced the unfavorable effects of prednisolone on width of periosteal and endosteal osteoid and periosteal transverse growth in the tibia. A-escin suppresses the metastasis of triple-negative breast cancer by inhibiting epithelial-mesenchymal transition via down-regulating LOXL2 expression. Escin Ia has being shown to inhibit pancreatic lipase.

Aclarubicin (INN) or aclacinomycin A is an anthracycline drug is primarily indicated in conditions like Acute non-lymphoblastic leukemia, Breast cancer, Gastric cancer, Lymphoma, Ovarian coma, Small cell lung cancer, Thyroid cancer. Soil bacteria Streptomyces galilaeus can produce aclarubicin. Aclarubicin (HCl) is used in combination with different anticancerous drugs to obtain best therapeutic results and to reduce toxicity or side effects. Aclarubicin (HCl) is administered intravenously. Aclarubicin is antagonistic to other agents that inhibit topoisomerase II, such as etoposide, teniposide and amsacrine. This agent is less cardiotoxic than doxorubicin and daunorubicin.

Alloxan, a compound for evoking experimental diabetes, preferentially accumulate in pancreatic beta cells via the GLUT2 glucose transporter. Alloxan is a proteasome inhibitor, and its specific toxicity toward β-cell is at least in part through proteasome inhibition. It was found that human beta cells were relatively resistant to this toxin.

MOTRETINIDE is a retinoic acid derivative. It is used as a topical agent in the treatment of mild to moderate acne.