Clominorex is an appetite suppressant, developed in the 1950s by McNeil Laboratories. The compound is claimed to possess the central nervous system stimulant action. Administration of clominorex to mice led to a strong increase in activity and decrease in food intake.

Amcinafal is an anti-inflammatory agent. It is glucocorticoid corticosteroid.

Streptonigrin is an antibiotic produced by Streptomyces flocculus. Streptonigrin exhibits activity as a broad spectrum antibiotic against both Gram-positive and Gram-negative bacteria. Streptonigrin shows antitumor activity against sarcomas, carcinomas, leukemias and lymphomas in vivo and in vitro. Due to its high toxicity, streptonigrin has not recieved widespread clinical use.

Iodocetylic Acid I-123 is a radiolabeled derivative of cetylic acid. Iodocetylic Acid I-123 was studied as for in vivo diagnosis of the myocardium.

Puromycin dihydrochloride belongs to the aminonucleoside family of antibiotics and is isolated from Streptomyces alboniger. Since the partial structure of this antibiotic showed it to be a purine derivative, puromycin was assigned as its generic name. Puromycin is a broad spectrum antibiotic and antibacterial agent. It is active against Gram-positive microorganisms, less active against acid-fast bacilli, and weakly active against Gram-negative microorganisms. It acts very quickly and can kill 99% of the cells within 2 days. It also exhibits antitumor activity in studies on brain tumor cells. Puromycin is a protein synthesis inhibitor that causes premature chain termination by acting as an analog of the 3’-terminal end of aminoacyl-tRNA. It has been used to study transcriptional regulatory mechanisms that control the sequential and coordinate expression of genes during cell differentiation.

Phorbol 12-myristate 13-acetate (PMA) also commonly known as 12-O-Tetradecanoylphorbol-13-acetate (TPA) is a phorbol ester that is commonly used to activate phospholipid-dependent protein kinase (protein kinase C). PMA/ TPA possesses potential antineoplastic effects and was studied in phase II clinical trials together with dexamethasone in patients with relapsed or refractory acute myeloid leukemia. In addition, PMA/ TPA participated in phase I trial for treating patients with hematologic cancer or bone marrow disorder that has not responded to previous treatment. Nevertheless, both clinical trials were terminated. Besides, PMA/ TPA was studied in patients with solid tumors, which had depressed white blood cell and neutrophil counts because of prior treatment with cytotoxic cancer chemotherapeutic drugs. It was shown, that the drug increased the low white blood cell and neutrophil counts toward the normal range.

Tetrachloroethylene is a nonflammable colorless liquid. Other names for tetrachloroethylene include perchloroethylene, PCE, PERC, tetrachloroethene, and perchlor. Tetrachloroethylene is used as a dry cleaning agent and metal degreasing solvent. It is also used as a starting material (building block) for making other chemicals and is used in some consumer products. It has also been used in water repellants, paint removers, printing inks, glues, sealants, polishes, and lubricants. Tetrachloroethylene has been in commercial use since the early 1900s. Tetrachlorethylene has been suspected of causing some types of cancer, based on both human and animal evidence. Laboratory studies have found that ingesting or inhaling tetrachlorethylene increased the risk of liver cancer in mice. In rats, inhaling tetrachloethylene was linked to kidney cancer and a rare type of leukemia. EPA has classified tetrachloroethylene as likely to be carcinogenic to humans by all routes of exposurebased on suggestive evidence in epidemiological studies and conclusive evidence in rats (mononuclear cellleukemia) and mice (increased incidence of liver tumors). The International Agency for Research on Cancer(IARC) has classified tetrachloroethylene as probably carcinogenic to humans (Group 2A).

Ceronapril is a phosphonate angiotensin-converting enzyme inhibitor that was being developed by Bristol-Myers Squibb for the treatment of hypertension. In spontaneously hypertensive rats, Ceronapril narrowed the autoregulatory range and shifted it to lower pressures. In in vitro experiments, Ceronapril inhibited ACE in slices of the brain with an IC50 of approximately 34 nM, as measured by in vitro autoradiography. In C.S.F. ACE was inhibited with an IC50 of approximately 34 nM, as assessed by a fluorimetric enzyme assay. Ceronapril (100 mg/kg, p.o.) inhibited ACE in plasma, kidney, and lung rapidly (3 hr) after administration. Inhibition of ACE in kidney lasted up to 48 hr after administration of Ceronapril, whereas the activity of ACE in plasma and lung recovered rapidly (8 hr). In lung and plasma ACE was increased at 72 hr after administration. Therefore, induction of ACE in plasma and lung by the drug may partly obscure the acute inhibition and may contribute to the different time-course of inhibition of ACE from the kidney. Ceronapril inhibited ACE in the vascular organ of the lamina terminals (OVLT) and subfornical organ (SFO) of the brain slowly (onset at 8 hr) but persistently (from 24 to 48 hr). However, the drug did not inhibit ACE in structures of the brain within the blood-brain barrier, such as the caudate-putamen, choroid plexus, globus pallidus, supraoptic nucleus and paraventricular nucleus of the hypothalamus.