Furodazole, a benzimidazole derivative was studied as an anthelmintic drug. Information about the current use of this compound is not available.

Amustaline (S-303) is a quinacrine mustard compound with potential antineoplastic activity. Amustaline binds to, intercalates and crosslinks DNA and RNA. This agent is mainly used for ex vivo purposes, specifically for the inactivation of pathogens such as viruses, protozoa and bacteria in red blood cells (RBCs). When S-303 is added to red blood cells, the compound rapidly passes through membranes, including those of cells and viral envelopes, due to its amphipathic character, and intercalates into helical regions of the nucleic acids of pathogens and white blood cells. TERCEPTTMBlood System usingamustaline (S-303) and glutathione (GSH) was able to inactivate high levels of DENV and ZIKV in RBCs. S-303 system has been shown to effectively inactivate a broad spectrum of pathogens, while maintaining RBC quality.

FENPRINAST is a cromotyn-like bronchodilator used for the treatment of allergy and exercise-induced asthma.

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.

Ruboxistaurin is an orally bioavailable, selective, potent inhibitor of protein kinase C β developed for treating diabetic retinopathy. In vitro and in vivo non-clinical models have demonstrated that Ruboxistaurin decreases PKC β activity and ameliorates many of the effects of PKC β on pathologic processes in the retina. Ruboxistaurin prevents the slowing of retinal blood flow that is observed by fluorescein video angiography in the eyes of diabetic rats. It is also reported to cause regression of retinal neovascularization produced by laser-induced major branch vein occlusions in a porcine model. Ruboxistaurin positively affected the diabetes-induced retinal blood flow abnormalities in a Phase Ib study in diabetic patients. Ruboxistaurin is in phase III clinical trials for the treatment of diabetic nephropathy and diabetic macular edema. Eli Lilly had submitted Ruboxistaurin for approval in the US and the EU; however, the company subsequently discontinued development as it was unable to demonstrate sufficient efficacy

Inocoterone acetate (USAN) (also known as RU-38882, RU-882) is the acetate ester of inocoterone a steroid-like nonsteroidal antiandrogen (NSAA) that was developed for topical administration to treat acne but was never marketed. Inocoterone acetate is actually not a silent antagonist of the androgen receptor but rather a weak partial agonist, similarly to steroidal antiandrogens like cyproterone acetate. In this double-blind study of 126 male subjects with acne, a topical solution of the antiandrogen inocoterone produced a modest but statistically significant reduction in the number of inflammatory acne lesions.

Eprociclovir (A5021, 9-[[cis-1', 2'-bis(hydroxymethyl)cycloprop-1'-yl]methyl]guanine) is a nucleoside analog with antiviral activity. Antiviral activity of eprociclovir appears to depend rapid and stable accumulation of its triphosphate in infected cells and on inhibition of viral DNA polymerase by its triphosphate. Eprociclovir was shown to be a potent inhibitor of the replication of herpes simplex virus type 1, 2, 6, Epstein-Barr virus and varicella zoster virus, both in vitro and in vivo. Eprociclovir development has been discontinued.

Vadimezan (5,6-dimethyl(xanthenone-4-acetic acid), ASA404, DMXAA) is a fused tricyclic analogue of flavone acetic acid with potential antineoplastic activity. In pre-clinical mouse tumour models it was demonstrated that administration of Vadimezan rapidly leads to disruption of the existing vasculature in the tumour and consequent haemorrhagic necrosis of the tumour. This was consistent with the finding that a single dose of Vadimezan induced a prolonged reduction in the growth of xenografted tumours in animal models. The ability to disrupt the vasculature in these pre-clinical models has been attributed to a rapid induction of cytokines, particularly TNFα (tumour necrosis factor α), serotonin and nitric oxide, resulting in hemorrhagic necrosis and a decrease in angiogenesis. Despite the fact that the molecular targets for the drug remained unknown, the promising pre-clinical results led to Vadimezan being selected for clinical development. Results of Phase I trials showed some restriction of tumour blood flow within 24 h of treatment, although this was not as dramatic as seen in pre-clinical models. Unlike the animal models, there was also very little evidence for the rapid death of blood vessels or for increases in TNFα levels in human tumors. No difference in antitumour activity, cytokine induction or toxicity was observed between two parallel Phase I trials, one dosed weekly and the other dosed every 3 weeks. Therefore the drug proceeded to Phase II clinical trials, dosed every 21 days in combination with chemotherapeutic agents. These trials indicated the drug had small benefits in the treatment of non-small-cell lung cancer and prostate cancer. However, a subsequent Phase III clinical trial was not able to reproduce this response and clinical development was halted.

MLN8054 is a reversible, ATP competitive inhibitor of recombinant Aurora A, developed by Millennium Pharmaceuticals. MLN8054 was tested in phase I clinical trials against advanced solid tumors. Reversible somnolence probably due to off-target inhibition of alpha-1 subunit of GABA-A receptor was dose limiting and prevented achievement of plasma concentrations predicted necessary for target modulation.