AZD5672 was developed by AstraZeneca for the treatment of rheumatoid arthritis. It was found that the drug inhibits P-glycoprotein and is a CCR5 antagonist. Exists hypothesis that inhibition of CCR5 can bring benefits in the treatment of rheumatoid arthritis. In July 2009, Phase-II for Rheumatoid arthritis was discontinued.

AZD-1981, developed by AstraZeneca, is a potent (binding IC50 of 4nM), fully reversible, functionally non-competitive antagonist of human CRTh2. It blocks agonist-induced human eosinophil CD11b expression, shape change (including in whole blood), and chemotaxis as well as an basophil shape change and Th2-cell chemotaxis at IC50's of 8.5-50nM. Potency is similar across species as is plasma protein binding (~97%). AZD-1981 is a weak (10s of μM) inhibitor in vitro of CYP2C9, OATP1B1 and UGT1A1 as well as an inducer of CYP3A4. AZD-1981 was well tolerated and no safety concerns were identified.There was no beneficial clinical effect of AZD-1981, at a dose of 1000 mg twice daily for 4 weeks, in patients with moderate to severe COPD. AZD-1981 has being discontinued for asthma and chronic obstructive pulmonary disease. AstraZeneca is collaborating with Johns Hopkins University for the development of AZD-1981 in the treatment of chronic idiopathic urticaria. It is in phase II clinicals studies for the treatment of Urticaria.

Granotapide (JTT-130) has been studied for use in treatment of diabetes mellitus type II. This intestine-specific microsomal transfer protein inhibitor has hypoglycemic effects. Granotapide is thought to block fat absorption, which results in enhanced glucose-stimulated insulin secretion and enhanced insulin sensitivity. In an animal study, granotapide improved hyperglycemia and dyslipidemia via a mechanism independent of suppression of food intake. Granotapide enhances glucagon-like peptide-1 secretion and reduces lipotoxicity. A phase 2 study has been conducted to evaluate the effect of JTT-130 on diabetes as well as the safety and tolerability of JTT-130 in obese Type 2 diabetic patients.

Saniona was developing seridopidine (also known as ACR343), a modulator of dopaminergic activity, as an orally administered therapy for schizophrenia, Tourette's syndrome and parkinson's disease. Seridopidine is a modulator of dopaminergic activity.

Bisegliptin (also known as KRP-104) was developed as an orally active dipeptidyl peptidase IV (DPPIV) inhibitor. It is known, that DPPIV inhibition reduces blood glucose through suppression of the degradation of the insulin-releasing hormone. Bisegliptin successfully completed the phase II clinical trials for patients with type 2 diabetes. However, further development of the drug has been discontinued for business reason. The company wasn’t able to find a tie-up partner to co-develop.

Dexniguldipine (B8509-035, (-)-(R)-niguldipine) is a new dihydropyridine derivative, that exerts selective antiproliferative activity in a variety of tumor models and, in addition, has a high potency in overcoming multidrug resistance. Dexniguldipine is ( - )-(R)-enantiomer of niguldipine, of which the ( )-(S)-enantiomer shows pronounced cardiovascular hypotensive activity due to its high affinity for the voltage-dependent Ca2 channel. As compared with the (S)-enantiomer, the (R)-enantiomer has a 40-fold lower affinity for the Ca 2 channel and, accordingly, only minimal hypotensive activity in animal pharmacology models. Dexniguldipine have shown antiproliferative activity in several tumor cell lines, but the concentrations necessary to inhibit growth have varied by several orders of magnitude between cell lines. Initial results of preclinical investigations for the evaluation of the mechanism of its antiproliferative activity demonstrate that dexniguldipine interferes with intracellular signal transduction by affecting phosphoinositol pathways, protein kinase C expression, and intracellular Ca 2 metabolism. In a series of human tumor xenografts in vitro, dexniguldipine demonstrated selective antiproliferative activity against several tumor types, e.g., melanoma and renal-cell carcinoma. Striking results were obtained in a hamster model, in which neuroendocrine lung tumors could be completely eradicated by 20 weeks of oral treatment with 32.5mg/kg dexniguldipine, whereas Clara-cell-type lung tumors were not affected. In in vitro studies, dexniguldipine has been found to bind to P-glycoprotein (P-gp) and to enhance the cytotoxicity of chemotherapeutic agents such as doxorubicin and etoposide in several cell lines The synergistic effect may well be associated with the reversal of multidrug resistance (MDR) related to the activity of P-gp. In the clinical therapy of cancer, resistance to many cytostatic drugs is a major cause of treatment failure. However, the high potency of dexniguldipine (about 10-fold as compared with that of verapamil in vitro) and its low cardiovascular activity provide the opportunity to achieve blood or tumor concentrations that might be high enough to overcome Mdr 1 resistance in patients without producing dose-limiting cardiovascular effects.

Mirfentanil was developed as CNS analgesic with a short duration of action. It induced antinociception predominately through mu opioid receptors. It was shown that at doses larger than those, which exert opioid effects, mirfentanil had nonopioid analgesic effects. The drug was successfully encapsulated in liposomes having a variety of compositions. The lipid composition of the formulation was varied to optimize the stabilization of liposomes and the encapsulation of solutes. Mirfentanil participated in phase II clinical trials for the treatment of pain. However, this study was discontinued.

Metergotamine (MY-25 or 1-methyl-ergotamine-bitartrate) is a derivative of ergotamine and belongs to peptide alkaloids. It exerts a dampening effect on vessels, in that relaxation is brought about in contracted vessels, whereas contraction is brought in dilated vessels. Metergotamine was being studied in migraine prophylaxis.

Dexsotalol is an isomer of antiarrhythmic drug d,l-sotalol, but in opposite to drug, it increases the incidence of arrhythmias