FLUCETOREX is a substituted amphetamine with anorectic activity.

Temurtide was developed as an immune adjuvant. Information about the current application of this drug is not available.

Intiquinatine is a quinolone derivative patented by Wayne State University as antineoplastic agent. Intiquinatine exhibited efficacy against early stage mammary cancer (Mam-17/Adr) and showed none of the neuromuscular toxicity.

Icoduline (previously known as CBS-113 A) is a dual inhibitor of 5-lipoxygenase and cyclo-oxygenase with anti-inflammatory properties. This drug was potentially useful in ophthalmology and as an alternative to glucocorticoids. In addition, icoduline was useful to treat skin disorders. The drug participated in the clinical trial for eye disorders in France; however, this study was discontinued.

Nanafrocin (nanaomycin A) belongs to the class of quinone antibiotics isolated from a strain OS-3966 of Streptomyces rosa var. notoensis. Nanafrocin (nanaomycin A) mode of action is dependent on its reduction by the respiratory chain-linked NADH or flavin dehydrogenase of the organism. The reduced form of nanafrocin (nanaomycin A) is quickly auto-oxidized by molecular oxygen producing singlet molecular oxygen (O2−). The ability to produce O2− is related to the antimicrobial activity of nanafrocin (nanaomycin A).

Naminterol [VAL 479], a phenethanolamine derivative, is a β2 adrenoceptor agonist with bronchodilatory properties. The compound was undergoing phase II clinical trials for asthma in Italy.

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.