Berubicin, an anthracycline derivative, is a DNA binding agent and potent topoisomerase II poison. Reata Pharmaceuticals were developing it as a treatment for brain cancer as it can breach the blood-brain barrier. It had also been in early clinical trials for the treatment of lung cancer and malignant gliomas. However, studies have been terminated. In October 2006, it was granted orphan drug designation from the FDA for the treatment of malignant gliomas. According to a CNS Pharmaceuticals media release in April 2018, berubicin will be studied for glioblastoma patients, these investigations will be funded in part by an equity crowdfunding campaign.

Odanacatib is a potent, selective, and neutral cathepsin K inhibitor, an enzyme involved in bone resorption. Merck & Co was developing odanacatib, a once-weekly, oral Odanacatib, for the treatment of postmenopausal osteoporosis and osteoporosis in men. Merck & Co. has discontinued development of its cathepsin K inhibitor odanacatib, citing an increased risk of cardiovascular events for the osteoporosis drug.

Wyeth was developing the small molecule plasminogen activator inhibitor-1 (PAI-1) antagonist aleplasinin for the treatment of Alzheimer's disease in the US. PAZ-417 inhibits PAI-I (Plasminogen activator inhibitor-1), thereby increasing the activation of plasminogen to form plasmin. There is some evidence that plasmin can increase the cleavage of amyloid precursor protein at the alpha cleavage site, which could reduce the formation or increase the clearance of amyloid beta, a suspected culprit in Alzheimer's disease. However, it`s development for Alzheimer's disease treatment was discontinued.

Budiodarone is a chemical analog of amiodarone with mixed ion channel electrophysiological activity. Budiodarone was developed to capitalize on the proven efficacy of amiodarone and to avoid its side effects. Budiodarone has a short plasma half-life (7 h) and a lower volume of distribution (13 L/kg). It is cleared from the body in 48 h. Like amiodarone, Budiodarone has balanced, multiple cardiac ion channel inhibiting activity, giving it properties of all four Vaughan Williams antiarrhythmic drug classes. Budiodarone, unlike amiodarone, undergoes rapid metabolism by plasma and tissue esterases. In clinical trials, Budiodarone effectively reduces the number and duration of atrial tachycardia/atrial fibrillation episodes.

Camphramine is biologically active salt of N-methylcoramine and 2-oxo-3-Bornanesulfonic acid. N-methylcoramine is a potent stimulant of gastrin release present in alcoholic beverages produced by alcoholic fermentation, but not by distillation.

Elucaine is local anesthetic and anti-ulcerative agent, acting as a gastric muscarinic acetylcholine receptor antagonist.

Butinoline (also known as azulone) was used as an antispasmodic drug to treat gastritis.

Eflucimibe is a new and potent Acyl coenzyme A:cholesterol acyltransferases inhibitor. Eflucimibe effectively decreased plasma cholesterol in cholesterol-fed animals. In animal models, drug restores normolipodemia in endogenous hypercholesterolemic rabbits and prevents the progression of atherosclerosis by decreasing the number of macrophages in the foam cells. Eflucimibe has been in phase II clinical trials for the treatment of atherosclerosis and hyperlipidemia. However, this research has been discontinued.

Edifolone (SC-35135) is a structurally unique class Ia antiarrhythmic agent. It acts as a sodium channel antagonist. Edifolone development has been discontinued.

Mozenavir is a non-peptidomimetic, water soluble, cyclic urea that is a selective inhibitor of HIV-1 protease. Mozenavir is active against the virus with the signature D30N nelfinavir resistance-associated mutation and the L90M mutants with decreased susceptibility to a number of other protease inhibitors. In a dose-ranging study assessing Mozenavir, in doses of 750 mg 3 times a day, 1250 mg twice daily, or 1250 mg 3 times a day, compared with standard doses of indinavir, both in combination with lamivudine and stavudine, plasma HIV-1 RNA levels were reduced to below 50 copies/mL in 75% to 80% of patients receiving Mozenavir-based treatment and in 70% of those receiving indinavir-based treatment. Mozenavir-based regimens were generally well tolerated. However, the virus was able to mount considerable resistance against this compound, which was not further developed, also because of poor oral bioavailability in humans and highly variable blood levels.