Daiichi Sankyo developed an inhibitor of acyl-coenzyme A:cholesterol acyltransferases (ACAT1 and ACAT2), pactimibe (also known as CS 505). Pactimibe has been used in trials phase II for reducing the progression of coronary artery disease and in patients with atherosclerosis. However, on October 26, 2005, the company made the decision to discontinue all ongoing clinical studies of pactimibe, because of the secondary endpoints that showed a lower effect of the drug on atherosclerosis than the standard of care alone and no beneficial effect on the frequency of cardiovascular events.

Nafagrel [DP 1904, SR 96325] is a thromboxane A2 synthetase inhibitor that was undergoing clinical trials with Daiichi Seiyaku, now Daiichi Pharmaceutical, for the diabetic angiopathies, lupus nephritis and Raynaud's disease in Japan. However the development of Nafagrel has been discontinued.

FLUBANILATE is a CNS stimulant.

Etiproston is a synthetic analog of prostaglandin F2α. Etiproston induces luteal regression. Etiproston is used in veterinary.

Esafloxacin (7-(3-amino-1-pyrrolidinyl)-1-ethyl-6-fluoro-1,4 -dihydro-4-oxo-1,8-naphthyridine-3-carboxylic acid) is an antibacterial agent.

Niometacin, an indometacin derivative, is a nonsteroidal anti-inflammatory drug.

Serfibrate, a clofibrate derivative, is a peroxisome proliferator activated receptor-α (PPAR-α) agonist. It is a hypolipidemic agent.

Ioprocemic Acid is hydrocinnamic acid derivative patented by Schering-Kahlbaum A.-G. as radiographic contrast medium for liver imaging

MK-0686 is a bradykinin B1 receptor antagonist patented by American multinational pharmaceutical company Merck & Co for the treatment of neuropathic pain and inflammation. MK-0686 demonstrates significantly reduced susceptibility to human P-gp mediated efflux and shows good potential for human CNS penetration based on brain levels in CF-1 mice and monkeys. Additionally, MK-0686 also exhibited good CNS bradykinin B1 receptor occupancy in the transgenic rat expressing the human B1 receptor and showed oral efficacy in reducing CFA-induced hyperalgesia in a humanized mouse. Unfortunately, in phase II clinical trials MK-0686 failed to demonstrate efficacy in phase II clinical trials.

CGP-36742 (3-Aminopropyl-n-butyl-phosphinic acid) is one of the first GABAB receptor antagonists that can penetrate the blood-brain barrier after peripheral administration. Although its affinity for GABA B binding sites labeled with a tritiated agonist is modest, being in the low micromolar range, it displays significant pharmacological activity when administered either orally or parenterally. CGP 36742 was effective in the learned helplessness paradigm in rats, dose-dependently improving the escape failures induced by the inescapable shocks, suggesting that it may have an antidepressant profile. CGP36742 displays pronounced cognition enhancing effects in Rhesus monkeys in active and passive avoidance paradigms, in an eight-arm radial maze and a Morris water maze and in a social learning task. CGP36742 blocks the late inhibitory postsynaptic potential and the paired-pulse inhibition of population spikes recorded from CA1 pyramidal neurons of the hippocampus of rats in vitro and in vivo. CGP36742 significantly enhances the release of glutamate, aspartate, glycine and somatostatin in vivo. Chronic administration of CGP36742 causes an up-regulation of GABA(B) receptors in the frontal cortex of rats. The effects of CGP36742 on cognition were investigated in a double-blind, placebo-controlled study undertaken as the first assessment of the efficacy of CGP36742 in 110 patients age 59–85 years with Mild cognitive impairment. The results showed significant improvement in working memory, psychomotor speed and attention with SGS742 as compared with placebo. SGS742 appeared to be safe and well tolerated in this study.