Semagacestat (LY-450139) was a gamma secretase inhibitor being developed as a treatment for Alzheimer's disease by Eli Lilly. It was hoped that the drug would help to delay the onset of severe Alzheimer's disease, and thereby help preserve cognitive and executive functioning and in turn improve patient quality of life. Semagacestat (LY-450139) is designed to inhibit gamma secretase, an enzyme that is involved in the cleavage of APP to beta-amyloid. By decreasing production of beta-amyloid, it is hoped that gamma secretase inhibitors will exert a disease-modifying effect in Alzheimer's disease and thus slow or halt the destruction of nerve cells – the final stage in the amyloid cascade hypothesis. In March 2008 semagacestat (LY-450139) advanced to Phase III development, where it was evaluated in the IDENTITY (Interrupting Alzheimer's Dementia by EvaluatiNg Treatment of AmyloId PaThologY) trial, the first Phase III trial for this new anti-dementia drug. In August 2010, Eli Lilly announced its decision to halt the development of Semagacestat. The decision was taken after analysing the preliminary results of the second Phase III clinical trial of the drug, which indicated that semagacestat failed to slow disease progression. The drug, in fact, worsened cognition and the ability to perform day-to-day activities.

Cicarperone is decahydroquinoline derivative with local anesthetic action. In ex vivo models Cicarperone protected anesthetized guinea-pigs against ouabain-induced ventricular fibrillation and increased the lethal dose of ouabain. Unlike most drugs with local anesthetic properties, Cicarperone did not depress contractions in isolated atria but increased them. Cicarperone reduces the spontaneous frequency, maximum follow frequency and conduction velocity of rabbit isolated atria. Cicarperone had no blocking action on the chronotropic or positive inotropic actions of isoprenaline on isolated atrial muscle. In vivo evaluation of Cicarperone in anesthetized dogs shows that Cicarperone caused small dose-related bradycardia and a large dose-related decrease in peripheral vascular resistance. Ciclactate has never been marketed in the US and EU.

Ciamexon is an aziridine derivative with potent immuno-modulating activity developed by German pharmaceutical company Boehringer Mannheim G.m.b.H. for autoimmune diseases treatment. Ciamexon shows promising effects in experimental models of rheumatoid arthritis, diabetes, and obesity without toxic side effects. In animal studies, Ciamexon inhibits the proliferation of autoreactive lymphocytes dose-dependently, without affecting the reaction against foreign antigens. Clinical efficacy evaluation of the Ciamexon in patients with rheumatoid arthritis shows significant, dose-dependent improvement in both the clinical and the biochemical disease activity indexes. The major adverse effects of Ciamexon were hepatotoxicity, diarrhea, and rash.

Cicaprost is a prostacyclin receptor (IP) agonist and orally active prostacyclin analog with potent systemic and pulmonary vasodilatation and anti-inflammatory activity. In preclinical models, Cicaprost treatment largely prevented the hypercholesterolemia-related impairment of coronary vasodilation and nitric oxide release in Isolated Langendorff-hearts. Cicaprost inhibits proinflammatory chemokines production not only from lipopolysaccharides (LPS) or (tumor necrosis factor-alpha) induced primary human monocyte-derived macrophages but also from LPS-stimulated monocyte-derived dendritic cells. Besides that Cicapost strongly inhibits lymph node and organ metastases of spontaneously metastasizing mammary tumors with a mode of action different from cytostatic or antihormonal drugs. In animal models, Cicaprost prevents metastasis if given continuously from the day of tumor implantation, and is effective in reducing metastasis if treatment is begun following surgical removal of the primary tumor when micrometastases are already present. Clinical trials of Cicaprost in healthy male volunteers demonstrate significant anti-platelet and vasodilatory effects.

Chromocarb is benzo-γ-pyrone derivative with vasoprotection activity used to eliminate lipoperoxidation post-vitrectomy. Peroral treatment of rats with chromocarb significantly reduced the degradation of the vascular wall by intravenous collagenase, as demonstrated by a lesser permeability increase of the blood-brain barrier, a shorter recovery time, lower hydroxyproline levels in the cerebrospinal fluid and a lesser decrease of the collagen content of the brain capillary basal lamina.

Carsalam is a nonsteroidal anti-inflammatory compound and platelet aggregation inhibitor.

Cartasteine is thioether derivative patented by Beijing Beipeng Technology Co. for resisting platelet aggregation and preventing or treating cardiovascular and cerebrovascular diseases

Eflumast (RP42068; N-(2-hydroxy-3-acetyl-5-fluorophenyl)-5-carboxamido-1H tetrazole) is an antiallergic agent. It was under development as an orally active antiasthmatic.

Clociguanil (BRL 50216, WR 38839) is an antimalarial compound, a derivative of N-benzyloxydihydrotriazine, developed by Beecham Pharmaceuticals. Mode of action studies indicated that clociguanil is a dihydrofolate reductase inhibitor of Plasmodium and is capable of marked potentiation with a selected sulphonamide against both the sensitive N strain and the cycloguanil-resistant B line of P. berghei. A combination of clociguanil and sulphadiazine prevented the development of parasitemia caused by P. falciparum in humans. The subsequent development of clociguanil was discontinued because of a relatively short half-life in man and lack of suppression of pre-erythrocytic schizogony of a strain of P. falciparum resistant to chloroquine, pyrimethamine, and proguanil.