A-443654 is a potent and selective AKT inhibitor. A-443654 induces rapid Akt Ser-473 phosphorylation independent of mTORC1 inhibition. A-443654 interferes with mitotic progression by regulating aurora a kinase expression. A-443654 inhibits all three Akt isoforms in FL5.12 cells stably transfected with constitutively active myristoylated Akt1/2/3, and showed moderate selectivity when screened against related kinases in the AGC family, such as PKA and PKC20. A-443654 has being shown to extend survival in an intracranial glioma animal model. A-443654, either alone or in combination with existing drugs, may be a useful therapy for primary and drug-resistant T-ALL.

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.

Gantofiban (or EMD 122 347) is an oral double prodrug of the drug, EMD 132338 and is GPIIb/IIIa antagonist. The drug participated in phase II clinical trials in Japan in patients with thrombosis. However, in May 2004, Yamanouchi, the developing company, announced that the study was discontinued. Besides gantofiban was involved in phase II trials, like a treatment option in patients with the acute coronary syndrome. However, further information is not available.

Carafiban is orally active heterocyclic peptide mimetics fibrinogen IIb/IIIa receptor antagonist with antithrombotic activity. Carafiban is a prodrug, that underwent metabolic transformation to active metabolite des-ethyl- Carafiban, that inhibited dose-dependently and reversibly human platelet aggregation. In conscious dogs, Carafiban showed a high plasma availability of the active moiety of 42±8% and a plasma half-life of 9.9 h after oral administration as measured by bioassay. Carafiban may potentially be used for chronic treatment and prophylaxis of thrombotic diseases in humans.