FERROTRENINE is a hematinic agent.

AstraZeneca was developing AZD-2066, a metabotropic glutamate receptor 5 (mGLUR5) antagonist, for the oral treatment of pain indications (e.g. chronic neuropathic pain and painful diabetic neuropathies), depressive disorders and gastro-oesophageal reflux disease. AZD-2066 had been in phase II clinical trials by AstraZeneca for the treatment of diabetic neuropathic pain and phase I for the treatment of gastrooesophageal reflux disease (GERD). However, this reasearch had being discontinued.

Rebastinib (DCC-20) is a TIE2 kinase inhibitor currently in Phase 1 clinical development to treat breast cancer and Chronic Myeloid Leukemia. Rebastinib potently inhibited TIE2 kinase in cellular assays and blocked primary tumor growth by 75% as a single agent and by 90% in combination with the standard chemotherapeutic agent paclitaxel. Furthermore, rebastinib therapy significantly reduced the presence of tumor-promoting macrophages in tumor biopsies by 80%. This blockade of tumor macrophages correlated with inhibition of breast cancer lung metastases.

MK-8776 (SCH900776) is inhibitor of CHK1. It was tested in clinical trials against acute myeloid leukaemia, solid tumors and lymphoma.

Miransertib (ARQ 092) is a selective, pan-AKT (protein kinase B) inhibitor that potently inhibits AKT1, 2 and 3 isoforms. Miransertib binds inactive AKT, preventing membrane localization and subsequent AKT activation, and binds active AKT, resulting in direct inhibition. Miransertib participates in Phase 1/2 of clinical trials to treat patients at least 2 years of age with PIK3CA-related Overgrowth Spectrum (PROS) and Proteus syndrome (PS). In addition, the drug is involved in the phase I trial in patients with lymphoma, endometrial cancer, and AKT1 E17K mutations. Recently was shown that miransertib could be an excellent lead compound for the development of new oral drug therapy for visceral and cutaneous leishmaniasis.

AZD-1208 is an orally available, potent and highly selective Pim inhibitor that effectively inhibits all three isoforms. AZD-1208 inhibits the growth of several AML cell lines and sensitivity correlates with the level of Pim-1 expression, STAT5 activation and presence of protein tyrosine kinase mutation. AZD-1208 causes cell cycle arrest and apoptosis in MOLM-16 cells in culture. This is accompanied by a dose-dependent reduction in phosphorylation of BAD, 4EBP1 and p70S6K. In addition, AZD-1208 leads to potent inhibition of colony growth of primary AML cells from bone marrow aspirates and downregulates phosphorylation of Pim targets. AZD-1208 was in Phase 1 trials to evaluate the safety and tolerability profile and to determine the maximum tolerated dose (MTD). There were two trials where AZD-1208 had been administered orally in AML and solid tumour (of all types) patients. The studies had being discontinued due to safety reasons.

Trepirium is a ganglion-blocking agent. During clinical testing of the administration of ganglion-blocking agent by inhalation it was established that drug aerosol of trepirium possesses high effectiveness, acts rapidly, and is relatively safe. Trepirium does not cause any local irritating effect. It blocks the n-cholinergic receptors of the autonomic ganglia (it inhibits the transmission of excitation from the preganglionic to the postganglionic fibers of the autonomic nerves) of the adrenal medulla and the sinocarotid region. Reduces the flow of vasoconstrictor impulses to the vessels and adrenaline secretion by the adrenal glands, weakens reflex pressor reactions, and lowers blood pressure. Trepirium is used for the treatment of cerebral or pulmonary edema, hypertensive crisis, nephropathy and eclampsia (in obstetric practice), for the hypotension control in anesthesia practice.

Trazium is a putative antidepressant compound with special pharmacological effects on the catecholaminergic systems. Trazium esilate (EGYT-3615) is structurally an as-triazino isoquinolinium salt which showed considerable activity in pharmacological tests characteristic for antidepressants (antagonism of tetrabenazine, potentiation of yohimbine, behavioral despair). The compound exhibited the minimal sedative effect. The drug potentiated actions of amphetamine such as stereotypy and hypermotility. It differentially blocked the hypothermic and the stereotypy inducing action of apomorphine. Trazium esilate also inhibited the cataleptic state provoked by bulbocapnine in mice. In higher dose it decreased the plasma prolactin level in rats. Trazium esilate is a weak displacer on a1-, a2- and D2-receptors, however, it induced a2-receptor desenzitization after repeated treatment. Trazium bounds to the serum proteins and the binding was sensitive to pH and salt concentration. The binding of trazium was not saturable at a wide range of drug concentration. Trazium has both specific and non-specific binding sites on serum proteins.