Volpristin is an antibiotic. Information about the current use of this agent is not available.

EF5 [2-(2-nitro-1H-imidazol-1-yl)-N-(2,2,3,3,3-pentafluoropropyl) acetamide] is a 2-nitroimidazole-based hypoxia marker that selectively binds hypoxic cells. It is a compound developed at the University of Pennsylvania by Dr. Cameron Koch and Dr. Sydney Evans. Upon injection into animal tissues, EF5 selectively binds to hypoxic cells and forms adducts. 2-(2-Nitro-1H-imidazol-1-yl)-N-(2,2,3,3,3-pentafluoropropyl) acetamide ([18F]EF5) is a specific positron emission tomography tracer approved by the US Food and Drug Administration for in vivo detection of hypoxia. EF5 has been used to detect hypoxia in rodent and human tumors, and it has shown good correlation with other hypoxia markers, such as hypoxia-inducible transcription factor. EF5 undergoes a biochemical reduction by nitroreductases in viable cells and forms covalent adducts to intracellular macromolecules in the absence of oxygen Therefore, only viable hypoxic cells are detectable with EF5. EF5 is a lipophilic compound and has better pharmacokinetic properties than other nitroimidazole compounds. [18F]EF5 positron emission tomography imaging has been introduced as a promising tool for the detection of hypoxia in tumor tissues in patients and in experimental models. Large atherosclerotic plaques in mice contained hypoxic areas and showed uptake of [18F]EF5. Despite its slow blood clearance, the high uptake of [18F]EF5 in plaques suggested that plaque hypoxia is a potential target for identifying high-risk plaques noninvasively.

5-Fluoro-2-deoxycytidine is a fluorinated pyrimidine analog antimetabolite with potential antineoplastic activity. As a prodrug, 5-fluoro-2-deoxycytidine is converted by intracellular deaminases to the cytotoxic agent 5-fluorouracil (5-FU). 5-FU is subsequently metabolized to active metabolites including 5-fluoro-2-deoxyuridine monophosphate (FdUMP) and 5-fluorouridine triphosphate (FUTP). FdUMP binds to and inhibits thymidylate synthase, thereby reducing the production of thymidine monophosphate, which leads to depletion of thymidine triphosphate and the inhibition of DNA synthesis and cell division. FUTP competes with uridine triphosphate (UTP) for incorporation into the RNA strand, which results in the inhibition of RNA and protein synthesis and cell proliferation. 5-Fluoro-2-deoxycytidine undergoing trials to test its effectiveness in treating cancer that has not responded to standard therapies.

N-Methyl Buzepide is diphenylpropane derivative with antisecretory activity.

Sufugolix (TAK-013 or 5-(N-benzyl-N-methylaminomethyl)-1-(2,6-difluorobenzyl)-6-[4-(3-methoxyureido)phenyl]-3-phenylthieno[2,3-d]pyrimidine-2,4(1H,3H)-dione) is a highly potent and orally active non-peptide antagonist of luteinizing hormone-releasing hormone (LHRH) receptor. Sufugolix by oral administration suppresses a pituitary-ovarian axis continuously and reversibly in cynomolgus monkeys. Takeda studied Sufugolix in the trials for the treatment of endometriosis and uterine leiomyoma however development was discontinued.

FENOCINOL, a diarylmethane derivative, is a choleretic agent.

IPRAMIDIL, a furoxan compound, revealed marked dilator activity in the coronary circulation of isolated working guinea pig hearts.

Halofuginone is a low molecular weight quinazolinone alkaloid, and a potent inhibitor of collagen alpha1(I) and matrix metalloproteinase 2 (MMP-2) gene expression. Halofuginone also effectively suppresses tumor progression and metastasis in mice. Halofuginone is a potent inhibitor of collagen a1(I) and matrix metalloproteinase 2 (MMP-2) gene expression. Halofuginone also suppresses extracellular matrix deposition and cell proliferation. Also was shown that halofuginone increased apoptosis in α smooth muscle actin- and prolyl 4-hydroxylase β-expressing cells in mdx diaphragm and in myofibroblasts, the major source of extracellular matrix. The profound antitumoral effect of halofuginone is attributed to its combined inhibition of tumour-stromal support, vascularization, invasiveness, and cell proliferation. HT-100 (delayed-release halofuginone), currently in clinical phase 1b/2a in five U.S. hospitals, is a small molecule drug candidate taken orally for the treatment of Duchenne muscular dystrophy (DMD) patients primarily through its ability to reduce fibrosis and inflammation and promote muscle fiber regeneration. The medicine candidate has been granted orphan drug designation in the U.S. and the EU — meaning it has been commercially undeveloped due to its limited profitability — and fast-track designation in the U.S. — an FDA process that aims to facilitate the development and patients’ reach to novel therapies for unmet medical needs.

Oxazafone was studied as an anticonvulsant and anxiolytic agent. Information about the further development of this compound is not available.