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.

Icofungipen is a generic name of the compound, previously known as BAY 10-8888 or PLD-118. Icofungipen, a cyclic beta-amino acid was developed by PLIVA, under license from Bayer, for the potential oral treatment of fungal infection. The drug exerts its antifungal activity by inhibition of isoleucyl-tRNA synthetase activity and consequently disrupting protein biosynthesis. Phase II trials with an oral formulation of icofungipen were underway in Europe for Candida infection and for the treatment of vulvovaginal candidiasis in the USA, but these studies have been discontinued. In human toxicity studies, suppression of spermatogenesis in male volunteers was observed as a possible off-target adverse event.

Elsibucol (AGI-1096) is a phenolic intracellular antioxidant with anti-inflammatory and antiproliferative properties. In vitro, elsibucol inhibited the inducible expression of vascular cell adhesion molecule (VCAM)-1, E-selectin, and monocyte chemoattractant protein (MCP)-1 in endothelial cells and tumor necrosis factor (TNF)-alpha and interleukin (IL)-1beta secretion from lipopolysaccharide (LPS)-stimulated peripheral blood mononuclear cells. It also inhibited serum-stimulated proliferation of aortic smooth-muscle cells. In vivo, elsibucol demonstrated anti-inflammatory properties in a murine delayed-type hypersensitivity model. In hypercholesterolemic animals, elsibucol inhibits atherosclerosis and preserves endothelial healing following arterial injury. Elsibucol development for the prevention of transplant rejection has been discontinued.

Prenisteine is an enylhomocysteine derivative used as reagent in organic synthesis

Elarofiban is a novel nonpeptide glycoprotein IIb/IIIa (GPIIb/IIIa) antagonist. It inhibits thrombin-induced platelet aggregation in human gel-filtered platelets and platelet aggregation in human platelet-rich plasma (PRP) in response to collagen, arachidonic acid, ADP, and SFLLRN-NH(2). Elarofiban had adequate oral pharmacokinetics in dogs and excellent oral pharmacodynamics. Elarofiban has been in phase II clinical trials for the treatment of myocardial infarction and thrombosis. However, this research has been discontinued.

Etomoxir is an irreversible inhibitor of carnitine O-palmitoyltransferase (CPT) I. It inhibits fatty acid oxidation and fatty acid and cholesterol synthesis in an enantiomer-selective manner: only the R-enantiomer of etomoxir inhibits fatty acid oxidation, S-enantiomer inhibits fatty acid and cholesterol synthesis but not fatty acid oxidation. Etomoxir was studied for the treatment of congestive heart failure and type II diabetes, however, its development was discontinued.

Triclazate is an anticholinergic agent.