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.

Licofelone (ML 3000) is a pyrrolizine derivative originally discovered by Merckle GmbH and developed by EuroAllaince with a unique pharmacological profile, which comprises optimal gastrointestinal tolerability and high analgesic and anti-inflammatory activity. These effects are due to balanced and selective inhibition of both cyclo-oxygenase and 5-lipoxygenase. Inhibition of 5-lipoxygenase may reduce the gastrointestinal toxicity associated with other non steroidal anti-inflammatory drugs, which only inhibit cyclooxygenase. Licofelone also has antipyretic and antiaggregatory properties. Clinical and preclinical trials were also undertaken for osteoarthritis, rheumatoid arthritis, asthma, pain and inflammation. However, development for these indications appear to have been discontinued.

Cytochalasin B is a cell-permeable alkaloid, isolated from a fungus Helminthosporium dematioideum. Cytochalasin B is an inhibitor of actin polymerization through binding to the fast-growing (barbed) end of F-actin filaments. Cytochalasin is used in studies of actin polymerization, cell division, and cell movement. The compound also inhibits glucose transporters GLUT1,3 and 4 and was investigated in a clinical trial to prevent restenosis after angioplasty surgery.

Eperezolid is an antibiotic agent developed for the treatment of a wide range of bacterial infections. The drug exerts its action by binding to 50 S ribosome subunit causing the inhibition of protein synthesis in bacterias. Eperezolid was tested in preclinical in vivo models of different becterial diseases in which it was shown to be active.

Erbulozole (R 55104) is a water soluble congener of the microtubule inhibitor tubulozole, which has proven to possess anti-invasive, antitumoral and radiosensitizing capacities. Erbulozole development for the treatment of cancer has been discontinued.

Trifenagrel is a potent inhibitor of arachidonate (AA)- and collagen-induced aggregation of platelets from several animal species and humans. When trifenagrel was administered p.o. to guinea pigs, there was a sustained (greater than 3 hr) inhibition of AA- and collagen-induced platelet aggregation ex vivo. In humans, trifenagrel inhibited the second phase of ADP-induced aggregation ex vivo up to 6 hr after a single dose of 100 to 300 mg p.o. The mechanism of action of trifenagrel appears to be a reversible inhibition of platelet AA cyclooxygenase. Although trifenagrel caused gastrointestinal irritation in dogs and humans, the nature of the damage suggests that the compound may have acted as a local irritant in these species. Furthermore, compared to aspirin trifenagrel produced significantly less gastric irritation and fecal blood loss in humans. Trifenagrel was developed for the treatment of ischemic heart disorders. However, this development was discontinued.

Ramifenazone is pyrazolone derivative with analgesic, antipyretic, and anti-inflammatory activity. In preclinical studies, Ramifenazone shows potent inhibition of prostaglandin production, carrageenan edema, and yeast fever.

CC-401 is a potent inhibitor of all three forms of c-Jun N-terminal Kinase (JNK) (Ki of 25 to 50 nM) and has at least 40-fold selectivity for JNK compared with other related kinases. Celgene was developing CC 401 for the treatment of cancer and inflammatory disorders. CC 401 was being developed in an IV formulation and was in a phase I trial in patients with refractory acute myelogenous leukaemia. However, trials have ended and the company is not pursuing CC 401, but will advance other JNK inhibitors.

Elzasonan (CP 448187) is a serotonin 1B/1D receptor antagonist. Elzasonan was primarily metabolized via oxidative N‐demethylation, N‐oxidation, and aryl hydroxylation. Pfizer was developing elzasonan for the treatment of anxiety and affective disorders however development has been discontinued.