Apaziquone (EOquin, EO9) is an indolequinone that is a bioreductive prodrug and a chemical analog of the older chemotherapeutic agent mitomycin C. In hypoxic cells, such as those on the inner surface of the urinary bladder, apaziquone is converted to active metabolites by intracellular reductases (such as NQO1). The active metabolites alkylate DNA and lead to apoptosis. In animal tumour models, EO9 was inactive against the P388 murine leukaemia but exhibited anti-tumour activity against human tumour xenografts and the generally chemo-resistant murine adenocarcinomas of the colon (MAC) tumours. Initial evidence that in vivo response correlated with NQO1 activity. Apaziquone was selected for clinical evaluation based upon its novel mechanism of action (which was distinct from MMC), its preferential activity against cells derived from solid tumours in vitro and in vivo, its ability to target both aerobic and hypoxic cells and the lack of myelosuppression in mice and rats. Apaziquone has been applied in clinical studies sponsored by Spectrum Pharmaceuticals and Allergan, Inc. for the treatment of superficial (non-muscle invasive) bladder cancer. However, the US-FDA determined that it was not statistically effective.

Roxifiban (also known as DMP754), a potent antiplatelet agent in inhibiting platelet aggregation, and has a high specificity and affinity for human platelet glycoprotein IIb/IIIa complex (GPIIb/IIIa) receptors. Roxifiban participated in clinical trials phase III for the treatment of peripheral arterial disorders. This drug was also well tolerated in patients with chronic stable angina pectoris and was studied in the treatment of heparin-induced thrombocytopenia, and thrombosis. However, the development of this drug appears to have been discontinued.