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.

Sibrafiban (G-7453) is the orally administered, nonpeptide, double-prodrug of Ro 44-3888 which is a selective glycoprotein IIb/IIIa receptor antagonist. Sibrafiban is a double prodrug that undergoes bioconversion to the inactive prodrug Ro 48-3656 and to the active IIb/IIIa antagonist, Ro 44-3888, after oral administration. Sibrafiban was undergoing clinical trials for secondary prevention of cardiac events in patients stabilised after acute coronary syndromes. Sibrafiban has been shown to have comparable efficacy to aspirin in preventing recurrent ischemic events in patients suffering from acute coronary syndromes. Sibrafiban was under development by Genentech and Hoffmann-La Roche, and in phase III trials as an antithrombotic. The development of sibrafiban was discontinued in 1999 following unfavorable Phase III efficacy data.

Rivenprost (ONO-4819) is a potent and selective EP4 receptor agonist. This compound can increase bone formation by stimulating osteoblast differentiation and function, possibly by modulating mesenchymal cell differentiation. Rivenprost has also been studied for its potential to prevent bone loss (in osteoporosis) and stabilize bone implants. Combined with risedronate, rivenprost may be an effective treatment for osteoporosis. A phase II study evaluating rivenprost in ulcerative colitis was terminated in 2009.

Tosedostat is a proprietary orally bioavailable inhibitor of the M1 family of aminopeptidases with potential antineoplastic activity. Tosedostat is converted intracellularly into a poorly membrane-permeable active metabolite (CHR-79888) which inhibits the M1 family of aminopeptidases, particularly puromycin-sensitive aminopeptidase (PuSA), and leukotriene A4 (LTA4) hydrolase; inhibition of these aminopeptidases in tumor cells may result in amino acid deprivation, inhibition of protein synthesis due to a decrease in the intracellular free amino acid pool, an increase in the level of the proapoptotic protein Noxa, and cell death. There are several ongoing Phase 2 cooperative group-sponsored trials and investigator-sponsored trials evaluating the clinical activity of Tosedostat in combination with standard agents in patients with acute myeloid leukemia (AML) or myelodysplastic syndrome (MDS).

Arhalofenate is a uricosuric drug which lowers serum urate by blocking its reabsorption by the proximal tubules of the kidney. Arhalofenate activity is mediated by inhibition of URAT1, OAT4 and OAT10. Additionally, arhalofenate has been suggested to exert potent anti-inflammatory activity. Arhalofenate has completed Phase 2 and is ready to advance to Phase 3 as a novel potential treatment for gout. The drug was also tested in patients with type 2 diabetes mellitus (phase III study), where it demonstrated its ability to lower glucose level, acting as a selective, partial PPAR-gamma agonist. However, the development of arhalofenate as an anti-diabetic drug was terminated.