LY377604 is a human β3-adrenergic receptor agonist and β1- and β2-adrenergic receptor antagonist with no sympathomimetic activity at the β1- and β2-adrenergic receptors. Combination of LY377604 and a norepinephrine-serotonin uptake inhibitor (sibutramine) was studied in the treatment of obesity. LY377604 would ameliorate side effect of sibutramine treatment (increase in blood pressure and heart rate due to activation of the sympathetic nervous system).

Acorafloxacin (JNJ-Q2) is a fluoroquinolone that was developed by Furiex Pharmaceuticals (a subsidiary of Forest Laboratories) for the treatment of complicated skin and and soft tissue infections. Acorafloxacin was originally developed by Janssen, then licensed to Furiex Pharmaceuticals (now a part of Actavis). JNJ-Q2 has excellent in vitro and in vivo activity against a variety of Gram-positive and Gram-negative organisms. In vitro studies indicate that JNJ-Q2 has potent activity against pathogens responsible for acute bacterial skin and skin structure infections (ABSSSI) and community-acquired bacterial pneumonia (CABP), such as Staphylococcus aureus and Streptococcus pneumoniae. JNJ-Q2 also has been shown to have a higher barrier to resistance compared to other agents in the class and it remains highly active against drug-resistant organisms, including methicillin-resistant S. aureus, ciprofloxacin-resistant methicillin-resistant S. aureus, and drug-resistant S. pneumoniae. In two Phase II studies, the efficacy of JNJ-Q2 was comparable to linezolid for ABSSSI and moxifloxacin for CABP. Furthermore, JNJ-Q2 was well tolerated, with adverse event rates similar to or less than other fluoroquinolones. Acorafloxacin inhibits MuRF enzyme, required for cell wall synthesis. Acorafloxacin directly inhibits bacterial DNA synthesis by halting the activity of DNA gyrase (responsible for negative helical supercoiling) and DNA topoisomerase IV (responsible for separating the nucleotide strands). Fast track designation and qualified infectious disease product designation (QIDP) was granted by FDA for the treatment of bacterial infections in 2013.

Trethinium is tetrahydroisoquinoline derivative. It is an antihypertensive agent.

Vidofludimus (SC12267; 4SC-101) is a novel oral immunomodulator inhibiting dihydroorotate dehydrogenase (DHODH) and the expression of proinflammatory cytokines including interleukin-17 (IL17A and IL17F) and interferon-gamma. This drug is in the clinical trial for the treatment of inflammatory bowel diseases and Rheumatoid arthritis.

Abbott Laboratories was developing the selective dopamine D3 receptor antagonist, ABT-925 (formerly A 437203), for the treatment of schizophrenia. ABT-925 is a selective dopamine D₃ receptor antagonist with an approximately 100-fold higher in vitro affinity for dopamine D₃ versus D₂ receptors. ABT 925 was undergoing phase II clinical development for the treatment of schizophrenia. However, development was discontinued in December 2007.

Bevenopran (also known as CB-5945), a peripherally acting mu-opioid receptor antagonist that was studied for the treatment of opioid-induced constipation. Due to difficulties with enrollment, phase III of clinical trials were terminated early.

ARQ-621 is a small-molecule inhibitor of the kinesin-related motor protein Eg5 with potential antineoplastic activity. Eg5 kinesin-related motor protein inhibitor ARQ 621 selectively inhibits the activity of Eg5, which may result in mitotic disruption, apoptosis and cell death. The ATP-dependent Eg5 kinesin-related motor protein (also known as KIF11 or kinesin spindle protein-5) is a plus-end directed kinesin motor protein involved in the regulation of spindle dynamics, including assembly and maintenance, during mitosis. In proliferation assays, ARQ-621 showed broad spectrum cytotoxicity against a panel of human cancer cell lines, with cell cycle analysis confirming a G2/M arrest followed by apoptosis. When administered intraperitoneally to nude mice bearing human pancreatic tumors (MIA PaCa-2), complete tumor stasis was achieved with a 6.25 mg/kg dose 3 times weekly for 4 weeks. At the completion of ARQ-621 dosing, the mice showed hematology profiles indistinguishable from untreated controls with no evidence of bone marrow toxicity. A phase I trial has been completed, however research has being discontinued.

E-3710 (Z-215) is a new proton pump inhibitor (PPI). E-3710 irreversibly inhibited H(+),K(+)-ATPase activity in pig gastric vesicles with an acidic internal environment. E-3710 is a long-acting inhibitor of gastric acid secretion and a promising novel therapy for acid-related diseases, such as gastroesophageal reflux disease. E-3710 is metabolized through oxidation, reduction and conjugation. Unchanged E-3710 was excreted in urine at trace levels but was not detected in faces. The major isozyme contributing to the oxidation of Z-215, including the formation of Z-215 sulphone, was CYP3A4. It is useful for treating gastroesophageal reflux disease in all CYP2C19 genotypes. E-3710 is in phase II clinical trial for the treatment of erosive esophagitis and gastro-esophageal reflux.