Cloroperone (AHR 6134) is a derivative of butyrophenone with anxiolytic properties. In animals, cloroperone causes slight CNS depression in mice, prevents the lethal effects of d-amphetamine under crowded conditions in mice, suppresses emesis in dogs. The drug was investigated in the clinic for the treatment of psychotic patients. It was shown to be effective anxiolytic at low dosages without sedation, listlessness, drowsiness or neurologic reactions. Cloroperone is a selective binder to 5-HT2 receptors (Ki 4.5 nM).

Razaxaban (also known as BMS-561389 or DPC 906) is an oral factor Xa inhibitor that was being developed for the treatment of thrombosis. It showed excellent results in the lab for efficacy and bioavailability and was therefore selected for further development. In a phase 1 clinical trial with healthy subjects, Razaxaban was well tolerated with minor bleeding. However, higher bleeding was reported in thrombosis patients in a phase 2 clinical trial, and the development of this drug was therefore discontinued in 2005.

Delprostenate is a synthetic analogue of PGF2-alpha, which is the naturally occurring prostaglandin used in medicine to induce labor and as an abortifacient. It is a useful synchronizer for the sheep.

Bafetinib (NS-187, INNO-406) is a second-generation tyrosine kinase inhibitor in development by CytRx under license from Nippon Shinyaku for treating Bcr-Abl+ leukemia's, including chronic myelogenous leukemia (CML) and Philadelphia+ acute lymphoblastic leukemia. It is a rationally developed tyrosine kinase inhibitor based on the chemical structure of imatinib, with modifications added to improve binding and potency against Bcr-Abl kinase. Besides Abl, bafetinib targets the Src family kinase Lyn, which has been associated with resistance to imatinib in CML. In preclinical studies, bafetinib was 25- to 55-fold more potent than imatinib in vitro and ≥ 10-fold more potent in vivo. Bafetinibinhibits 12 of the 13 most frequent imatinib-resistant Bcr-Abl point mutations, but not a Thr315Ile mutation. A small fraction of bafetinib crosses the blood-brain barrier, reaching brain concentrations adequate for suppression of Bcr-Abl+ cells. Data from a phase I clinical trial conducted in patients with imatinib-resistant or -intolerant CML have confirmed that bafetinib has clinical activity in this setting, inducing a major cytogenetic response in 19% of those patients in chronic phase. Currently, bafetinib is being developed in two phase II clinical trials for patients with B-cell chronic lymphocytic leukemia and prostate cancer, and a trial is in progress for patients with brain tumors. In 2005, the compound was licensed to Innovive Pharmaceuticals (acquired by CytRx Oncology in 2008) by Nippon Shinyaku on a worldwide basis, with the exception of Japan, for the treatment of CML. Orphan drug designation was assigned to the compound for the treatment of CML in the U.S in 2007 and in the E.U. in 2010. Bafetinib is in phase II for the treatment of hormone-refractory prostate cancer and chronic lymphocytic leukemia.

Quiflapon Sodium (MK-0591; (3-[1-(4-chlorobenzyl)-3-(t-butylthio)-5-(quinolin-2-yl-methoxy)- indol-2-yl]-2,2-dimethyl propanoic acid, previously L-686,708) had been in phase II clinical studies for the treatment of inflammatory bowel disease, but the study was discontinued later, because in spite of MK-591 markedly inhibited Leukotrienes (LT) biosynthesis, it did not differ significantly from placebo in clinical efficacy. Also was discovered, that MK-0591 may modify the airway changes associated with bronchial hyper responsiveness, as well as offer symptomatic relief in asthma. MK-0591 is a selective and specific 5-Lipoxygenase-activating protein (FLAP) inhibitor with an IC50 value of 1.6 nM in a FLAP binding assay. In additional, recently was discovered, that MK591 possesses all major attributes of a standard anti-metastatic agent with significant cancer-selective effect, and suggest that MK591 may turn out to be an effective agent for therapy of castration-resistant, bone-metastatic prostate cancer. Though details of the molecular underpinnings of the anti-metastatic action of MK591 are unknown at this time, this finding gives an opportunity for further exploration to better understand the signaling mechanisms involved by in vitro and in vivo experiments.

Befiradol (also known as NLX-112) was initially developed by Pierre Fabre as a selective serotonin-1A receptor agonist for the treatment of cancer pain and neuropathic pain. However, these trials were discontinued. In 2013, the development and commercialization rights were licensed to Neurolixis. Neurolixis studied befiradol in Parkinson’s disease (PD) patients that exhibit dyskinesia. Dyskinesia is a side effect that appears after several years of action Levodopa, a drug that remains the gold standard treatment for PD. In 2019, FDA gave a positive response to Neurolixis’s befiradol to be tested in Phase 2 clinical in Parkinson's disease patients suffering from debilitating levodopa-induced dyskinesia.

Aprikalim [RP 52891, RPG 52891] is a potent, specific, and selective opener of ATP-sensitive K+ (KATP) channels. By virtue of this pharmacological property, aprikalim affords cardioprotection in experimental models of ischemia/reperfusion injury, and, at higher doses, also causes peripheral or coronary vasodilatation. It is undergoing phase II clinical trials with Aventis Pharma for the treatment of asthma; heart failure; hypertension; myocardial ischaemia.

Pemaglitazar was developed as a dual peroxisome proliferator-activated receptors alpha and gamma (PPAR- α,γ) agonist. Information about the further development of this drug is not available.

Ganstigmine is an orally active, carbamate-based acetylcholinesterase (AChE) inhibitor developed for the treatment of Alzheimer's disease. It is a newer generation AChE than BChE inhibitor, derived from genserine, and has a long duration of action in vivo. Studies have shown it significantly prevented the progressive neuronal cell death due to growth factor deprivation and decreased neurodegeneration. Ganstigmine may be a suitable candidate for the treatment of cholinergic deficit in Alzheimer's disease because it was found to significantly increase basal extracellular concentrations of acetylcholine in rat prefrontal cortex, and does not affect the concentrations of serotonin, noradrenaline and levels of dopamine and metabolites. It is safe and well tolerated at 5–10 mg doses as the study conducted in Phase I randomized, double-blind, placebo-controlled clinical trial. It was dropped from phase II trials because of its adverse effects reported in some patients.

Ilepatril, previously known as AVE7688, an inhibitor of neutral endopeptidase and angiotensin-converting enzyme (ACE), was initially being developed for cardiac failure. Ilepatril was in phase IIb/III clinical trials for hypertension and in phase II trials for diabetic nephropathy, however, studies were discontinued.