Neocinchophen is an analgesic and uricosuric. Cinchophen and neocinchophen (introduced by Chemische Fabrik auf Aktien as Atophan and Novatophan) were being advertised as superior substitutes for salicylates in the treatment of rheumatic fever. Chemically, cinchophen is phenylcinchoninic acid, and neocinchophen is the ethyl ester of its methyl derivative.

KW-2449, a multikinase inhibitor of FLT3, ABL, ABL-T315I, and Aurora kinase, is under investigation to treat leukaemia patients. KW-2449 is a multikinase inhibitor of FLT3, ABL, ABL-T315I, and Aurora kinase with IC50 values of 6.6nM, 14nM, 4nM and 48nM, respectively. KW-2449 has potent growth inhibitory activity against various types of leukaemia by several mechanisms of action. Kyowa Hakko Kirin Pharma Inc. (a US subsidiary of Kyowa Hakko Kirin Co) was developing KW-2449 for the treatment of acute lymphoblastic leukaemia; acute myeloid leukaemia; chronic myeloid leukaemia; myelodysplastic syndromes, but later these studies were discontinued.

Doliracetam possesses activity on the central nervous system. It has cognition enhancing properties and might be useful in the treatment of Alzheimer’s disease and epilepsy

Vicriviroc or SCH 417690 is a potent and selective antagonist of the CCR5 receptor. vicriviroc binds specifically to the CCR5 receptor and prevents infection of target cells by CCR5-tropic HIV-1 isolates. In antiviral assays, vicriviroc showed potent, broad-spectrum activity against genetically diverse and drug-resistant HIV-1 isolates and was consistently more active than SCH-C in inhibiting viral replication. This compound demonstrated synergistic anti-HIV activity in combination with drugs from all other classes of approved antiretrovirals. Competition binding assays revealed that vicriviroc binds with higher affinity to CCR5 than SCH-C. Functional assays, including inhibition of calcium flux, guanosine 5'-[35S]triphosphate exchange, and chemotaxis, confirmed that vicriviroc acts as a receptor antagonist by inhibiting signaling of CCR5 by chemokines. Finally, vicriviroc demonstrated diminished affinity for the human ether a-go-go related gene transcript ion channel compared to SCH-C, suggesting a reduced potential for cardiac effects. Vicriviroc represented a promising new candidate for the treatment of HIV-1 infection. Vicriviroc for HIV treatment was previously in Phase III studies but has since been discontinued.

Clotioxone is a fungicide compound for the use in agriculture, developed by a French company Rhone-Poulenc in the 1960s.

Delfaprazine is an antidepressant drug, synthesized at the Spanish Centro de Investigacion, Grupo Ferrer S.A. Toxicological study in rats, rabbits, and dogs have shown that delfaprazine has less cardiotoxic side effects.

Enviradene (LY 127123) is a benzimidazole antiviral compound. It inhibited picornavirus replication and infection in vitro.

CYC-116 is a novel, ATP-competitive, pyrimidine drug that is taken by mouth as a capsule. The drug is a selective agent that potently inhibits the enzymes Aurora kinases and VEGFR-2 kinase at comparable levels with a range of 19 to 69 nanomolar. Median potency of CYC-116 in cancer cells is approximately 300 nanomolar. CYC-116 has demonstrated a broad spectrum of potent cytotoxic activity against human tumor cell types. Non-clinical efficacy of CYC-116 has been demonstrated by the oral route using mouse leukemia models, in which increased survival was observed, and human solid tumor xenograft models, in which reductions in tumor growth were observed. Cancer cell types that appear to be particularly sensitive to CYC-116 are leukemia, non-small cell lung cancer and pancreatic cancer. CYC-116 works by affecting the cell cycle progression of cancer cells before they enter mitosis or divide to create daughter cancer cells. The mechanism of action of CYC-116 affects cancer cells in several ways. CYC-116-treated cells display delayed entry into mitosis; defective polymerization of tubulins, or proteins that make up microtubules which are the target of the taxane drugs; changes in the function of the centrosome, or the cell's microtubule organizing center; and formation of the mitotic spindle, or the highway along which chromosomes and cellular materials are transported from the mother cell to the daughter cells. After cancer cells are treated with CYC-116, their spindle checkpoint is inactivated resulting in inhibition of cytokinesis or the process by which a mother cell divides. These defects result in the generation of polyploidy or cells with more than two chromosome sets, multinucleated cells or cells with multiple cores and apoptosis or cancer cell death. In a mouse model of leukemia CYC116-treatment induced decreases in tumor cell volume and infiltration of leukemic cells in the bone marrow and resulted in an increase in life span. No significant effects on body weight or normal bone marrow cells were observed at effective doses of CYC-116. Tumor neovascularization, or creation of new blood vessels around a tumor, was significantly reduced in a dose dependent manner. The data confirm that CYC-116 acts as a dual mitotic and angiogenesis inhibitor, a combination of anti-cancer mechanisms which could have therapeutic benefit in the clinic. CYC-116 is currently being studied in a Phase 1 trial in patients with solid tumors at Roswell Park Cancer Institute in Buffalo, New York, and South Texas Accelerated Research Therapeutics (START) in San Antonio. The study is designed to identify the maximum tolerated dose of CYC-116 and evaluate its pharmacokinetic, pharmacodynamic and anti-tumor effects.

Modipafant is a dihydropyridine derivative patented by American multinational pharmaceutical corporation Pfizer Ltd. as platelet-activating factor antagonist for bronchoconstriction and asthma treatment. Platelet-activating factor, proposed as an important inflammatory mediator in asthma, reproduces several of the features of asthma, such as microvascular leakage, mucus secretion, bronchoconstriction, and possibly increased airway responsiveness. Unfortunately, in clinical trials, Modipafant failed to demonstrate superior efficacy compared to placebo.

Fosbretabulin (Combretastatin A4 phosphate, CA4P) is the lead compound of a relatively new class of agents termed vascular disrupting agents that target existing tumor blood vessels. Rapid tumor blood flow shutdown has been demonstrated in preclinical models and patients by various techniques such as dynamic contrast-enhanced MRI, perfusion computed tomography and PET scans following CA4P infusion. CA4P typically induces rapid tumor necrosis in the center of the tumor and leaves a rim of viable cells in the periphery. In oncology, CA4P does not appear to be that active by itself, but may be more efficacious when combined with chemotherapy, antiangiogenic therapy and radiation therapy. Combretastatin was initially isolated from the root bark of the South African Bush willow Combretum caffrum in 1982 by Pettit and colleagues at the Arizona State University (AZ, USA). Combretastatin A4 phosphate binds avidly to tubulin at the colchicine-binding site to inhibit microtubule assembly and destabilize the cytoskeleton. CA4P is a tubulin-binding agent that binds at or near the colchicine binding site of β-tubulin (Kd = 0.40 uM), inhibits tubulin assembly with IC50 of 2.4 uM. Fosbretabulin has orphan drug status in the EU and the US for the treatment of ATC (Anaplastic Thyroid Cancer). Later the development of this drug was discontinued.