Ropizone (SC-13504) is an anticonvulsant. This compound both enhances and inhibits [3H]dextromethorphan (DM) high-affinity binding to different areas of the guinea pig brain, suggesting distinct binding site types in the brain. Ropizone was shown to have limited anti-convulsant activity against chemically induced seizures. The drug may have anti-grand mal activity but lacked any anti-petit mal effect in Beagle dogs. No information on the current use of this compound is available.

Folitixorin, a thymidylate synthase inhibitor is a substrate used by the enzyme methylenetetrahydrofolate reductase (MTHFR) to generate 5-methyltetrahydrofolate. Folitixorin was studied in clinical trials for the treatment of breast cancer, metastatic colorectal cancer and for the treatment of advanced pancreatic cancer. Folitixorin had been granted orphan drug status for the treatment of pancreatic cancer in both the U.S. and EU. However, further development of this drug was discontinued.

Nifursemizone, a 5-nitrofuran derivative, is an antiprotozoal drug. It is used in the treatment of histomoniasis in poultry.

Verazide, which is related to Isoniazid has been developed in Australia for the treatment of pulmonary tuberculosis. It is equally effective as Isoniazid and less toxic.

Triapine (3-aminopyridine-2-carboxaldehyde thiosemcirbazone, (3-AP; NTO-1151; OCX-0191) is a novel small molecule ribonucleotide reductase inhibitor that acts on the M2 (R2) subunit. Ribonucleotide reductase is an enzyme involved in the de novo synthesis of deoxyribonucleotides, which are critical for DNA replication and DNA repair. Triapine has been used in trials phase II studying the treatment of Lung Cancer, Kidney Cancer, Prostate Cancer Pancreatic Cancer, among others. Recently was published the article describing, that the triple combination triapine-cisplatin-paclitaxel was safe and provided a rational basis for a follow-up phase II trial to evaluate the efficacy and progression-free survival in women with metastatic or recurrent uterine cervix cancer.

Tosagestin (Org 30659) is a synthetic 19-nortestosterone derived progestogen. It was under clinical development by NV Organon for use in oral contraceptive and hormone replacement therapy. After oral administration of [14C]-Org 30659 to postmenopausal women, the compound was extensively metabolized. The dosed radioactivity was predominantly excreted via urine. Org 30659 was to a large extent metabolized at the C3- and the C17-positions. Species comparison of the metabolic routes of Org 30659 after oral administration indicated that the monkey seems to be a better representative species than the rat for the metabolism of Org 30659 in humans. Daily oral administration of Org 30659 suppresses ovarian function to a level sufficient to inhibit ovulation. This effect is dose-dependent, and the suppressive effect is readily reversible at all doses tested. Tosagestin had been in phase II clinical trial for the treatment of the menopausal syndrome. However, this development was discontinued.

Semaxanib is a potent and selective vascular endothelial growth factor (VEGF) receptor protein tyrosine kinase 1/2 inhibitor that also inhibits other tyrosine kinases KIT, MET, FLT3, and RET. Semaxanib inhibited cell migration of human vascular endothelial cells expressing both Flt-1 and KDR in response to VEGF and also inhibited the cell migration in response to placenta growth factor (PIGF), a specific ligand for Flt-1. Chemotaxis of monocytes expressing only Flt-1 was also inhibited by SU5416 in a dose-dependent manner. Semaxanib targets the VEGF pathway, and both in vivo and in vitro studies have demonstrated antiangiogenic potential. On February 2002, Pharmacia, the then-parent of Sugen, prematurely ended Phase III clinical trials of Semaxinib in the treatment of advanced colorectal cancer due to discouraging results.

Ridogrel is a dual action drug used for the prevention of systemic thrombo-embolism and as an adjunctive agent to thrombolytic therapy in acute myocardial infarction. Ridogrel, a combined thromboxane synthase inhibitor, and receptor antagonist is used with streptokinase as an adjunctive therapy to reduce the formation and size of blood clots. Blood clots can cause ischemic cardiac events (heart attacks). Ridogrel has the dual property of inhibiting the synthesis of thromboxane and blocking the receptors of thromboxane/prostaglandin/endoperoxides. It has been shown to accelerate the speed of recanalization and to delay or prevent reocclusion during systemic thrombolysis with tissue plasminogen activator (streptokinase). Ridogrel is a more potent antiplatelet agent than aspirin and might offer an advantage over aspirin as an adjunct to thrombolysis in patients suffering from acute myocardial infarction. While aspirin inhibits cyclooxygenase, the enzyme responsible for producing thromboxane, ridogrel inhibits thromboxane synthesis directly. Ridogrel has been studied primarily as an adjunctive agent to thrombolytic therapy in acute MI (AMI). Despite positive results from initial pilot studies, the largest clinical study, the Ridogrel versus Aspirin Patency Trial (RAPT) failed to demonstrate any advantage with this agent over aspirin. In the study of 907 patients with AMI, there was no difference in the primary endpoint of infarct vessel patency rate between those randomized to ridogrel (72.2%) or aspirin (75.5%). Various mechanisms are likely responsible for the results seen with ridogrel in clinical trials, including potentially ineffective thromboxane receptor inhibition with the concentrations of ridogrel used in human studies. As such, there currently are no clinical indications for preferential use of ridogrel over aspirin.

BN-2629 (also known as SJG-136 and SG2000), a dimeric pyrrolobenzodiazepine that binds in the minor groove of DNA and produces G-G interstrand cross-links via reactive N(10)-C(11)/N(10')-C(ll') imine/carbinolamine moieties. This drug was investigated in phase II clinical trials in patients with epithelial ovarian, primary peritoneal, or fallopian tube cancer, however, these studied were terminated because of the slow accrual. In addition, BN-2629 participated in phase I/II trial in participants with advanced chronic lymphocytic leukemia and acute myeloid leukemia, but Spirogen also terminated these studies.

Icofungipen is a generic name of the compound, previously known as BAY 10-8888 or PLD-118. Icofungipen, a cyclic beta-amino acid was developed by PLIVA, under license from Bayer, for the potential oral treatment of fungal infection. The drug exerts its antifungal activity by inhibition of isoleucyl-tRNA synthetase activity and consequently disrupting protein biosynthesis. Phase II trials with an oral formulation of icofungipen were underway in Europe for Candida infection and for the treatment of vulvovaginal candidiasis in the USA, but these studies have been discontinued. In human toxicity studies, suppression of spermatogenesis in male volunteers was observed as a possible off-target adverse event.