Lomeguatrib is a O6-methylguanine-DNA-methyl-transferase inhibitor which was developed by AstraZeneca for the treatment of cancer. It was tested in phase I and II of clinical trials for the treatment of colorectal cancer, melanoma and other solid tumors.

Vanoxerine, also known as GBR-12909, is a piperazine derivative exhibiting potent selective inhibition of sodium-dependent dopamine reuptake transporters. Vanoxerine has been in clinical trials for Parkinsonism, depression and cocaine addiction but lacked efficacy. Vanoxerine has also been observed as a potent blocker of the following channels: cardiac hERG/IKr potassium channel, Calcium channel, voltage-dependent, L type, alpha 1C subunit (also known as Cav1.2) and voltage-gated sodium channel Nav 1.5. Vanoxerine was studied as a potential treatment for atrial fibrillation. However, phase III clinical trials for this condition were terminated because of cardiac safety concerns. Research also indicates that vanoxerine may have additional mechanisms of action including antagonist action at nicotinic acetylcholine receptors (nAChRs).

Safingol, the synthetic L-threo-stereoisomer of endogenous (D-erythro-) sphinganine, is an inhibitor of protein kinase C and sphingosine kinase in vitro, and in some cell types has been implicated in ceramide generation and induction of apoptosis. Safingol inhibits enzymatic activity and 3H-phorbol dibutyrate binding of purified rat brain PKC (IC50 = 37.5 uM and 31uM, respectively). Inhibits human PKCα, the major overexpressed isoenzyme in MCF-7 DOXR cells (IC50 = 40 uM). Safingol enhances the cytotoxic effect of the chemotherapeutic agent Mitomycin C (MMC) in gastric cancer cells by promoting drug-induced apoptosis. Safingol is an inhibitor of SphK (Sphingosine kinase). Safingol has been shown to act synergistically with other chemotherapeutic agents and may potentiate chemotherapy drug-induced apoptosis in vitro and in vivo.

Pumaprazole is imidazopyridine derivative patented by Byk Gulden Lomberg Chemische Fabrik GmbH for the treatment of gastrointestinal diseases. Pumaprazole acts as a reversibly binding acid pump antagonist. Pumaprazole differs from covalently binding proton pump inhibitors (PPIs), such as omeprazole, both with respect to chemical structure and mode of interaction with the gastric H(+)/K(+)-ATPase. In preclinical models, the single dose of Pumaprazole is able to elevate intragastric pH in the dog with gastric fistula under pentagastrin or carbachol stimulation from pH 1 to about pH 7 while still displaying a dose-dependent, well-controllable duration of action of a few hours.

AstraZeneca developed disufenton (NXY-059), a free radical trapping agent, for the treatment of ischaemic stroke and other brain injuries. Nevertheless, large clinical trial (3306 versus 1722 patients) was neutral, providing no evidence for the efficacy of disufenton sodium in patients with stroke. One study using rat cortical brain slices concluded that NXY-059 improved neuronal survival. However, another study in mouse neuroblastoma cells reported no effect. Another study reported that NXY-059 restored endothelial blood-brain. Histological analyses revealed several therapeutic advantages associated with disufenton sodium treatment following acute acoustic trauma, including reductions in inner and outer hair cell loss; reductions in acute acoustic trauma-induced loss of calretinin-positive afferent nerve fibers in the spiral lamina; and reductions in fibrocyte loss within the spiral ligament. However, AstraZeneca terminated the development program.

Nicodicodine is a cough suppressant and analgesic. It was first synthesized in 1904. It is a Schedule III drug. Nicodicodine is metabolised in the liver to dihydromorphine. Since the final active metabolite is the slightly stronger opiate than morphine, nicodicodine can be expected to be more potent and longer acting than nicocodeine.

Indisulam (also known as E7070) is a sulfonamide derivative patented by Japanese pharmaceutical company Eisai Co. as antitumor agent. Indisulam inhibits cyclin-dependent kinases (CDK), which regulate cell cycle progression and are usually over-expressed in cancerous cells. Inhibition of CDK results in G1/S phase arrest of the cell cycle, and may lead to induction of apoptosis and inhibition of tumor cell proliferation. Preclinical and clinical studies have established the synergy of indisulam with nucleoside analogs as well as topoisomerase inhibitors. These combinations were tolerated with acceptable toxicities, including diarrhea, vomiting, and myelosuppression. In Phase II clinical trials Combination of indisulam with DNA‐damaging agent (idarubicin) and nucleoside analog (cytarabine) in patients with relapsed and refractory AML is effective and largely well tolerated.

Forodesine hydrochloride is the salt of the synthetic high-affinity transition-state analog forodesine (BCX-1777, immucillin-H), a substrate designed to mimic the properties or the geometry of the transition state of reaction. It is an anticancer drug that has been developed for the treatment of different hematologic malignancies. In December 2006, orphan designation (EU/3/06/421) was granted by the European Commission to Napp Pharmaceuticals Research Limited, United Kingdom, for forodesine hydrochloride for the treatment of acute lymphoblastic leukemia. Forodesine hydrochloride has been evaluated in Phase I/Phase II clinical trials for several cancer types including chronic lymphocytic leukemia (CLL), B-Cell acute lymphoblastic leukemia and refractory cutaneous T-cell lymphoma (CTCL). Forodesine is a potent purine nucleoside phosphorylase (PNP) inhibitor that acts by elevating plasma 2'-deoxyguanosine (dGuo) and intracellular deoxyguanosine triphosphate, which in turn affects deoxynucleotide-triphosphate pools and induces cell death by apoptosis. Forodesine in the presence of dGuo inhibited the proliferation of CEM-SS (T-acute lymphoblastic leukemia) cells with an IC50 of 0.015 uM. This inhibition by forodesine and dGuo was accompanied by a 154-fold and 8-fold elevation of endogenous dGuo triphosphate (dGTP) and deoxyadenosine triphosphate (dATP) pools, respectively. Cytotoxic activity of forodesine in the presence of dGuo was selective to T lymphocytes. It is a 10- to 100-fold more potent inhibitor of human lymphocyte proliferation than other known PNP inhibitors such as PD141955 and BCX-34.8