D-Arabinose (D-Ara) is a reducing rare sugar. It is a substrate for by D-arabinose dehydrogenase (ARA) and participated in D-erythroascorbic acid synthesis in S. cerevisiae. D-Erythroascorbic acid (eAsA) is an important antioxidant molecule in yeast. It was found, that ARA 2p, not ARA 1p, mainly contributes to the production of eAsA. Recently was published the first report of biological of D-Ara. It was compared the growth inhibitory effects of aldohexose stereoisomers against the animal model Caenorhabditis elegans cultured in monoxenic conditions with Escherichia coli as food. The inhibitory effect of D-Ara was also observed in animals cultured in axenic conditions using a chemically defined medium; this excluded the possible influence of E. coli. Among these stereoisomers, the D-Ara showed particularly strong growth inhibition. The assumption was made pointing, that the inhibition could be induced by multiple mechanisms, for example, disturbance of D-ribose and D-fructose metabolism.

Carmoterol is a long-acting β2-adrenoceptor agonist with a rapid onset of action and potent bronchodilating activity. Carmoterol has a similar onset of action compared to salbutamol and formoterol, and a faster onset of action compared to salmeterol. Furthermore, the duration of tracheal smooth muscle relaxation is longer for carmoterol compared to both formoterol and salmeterol. In asthmatic patients, the PK of carmoterol is proportional to the dose, and nonlinear accumulation of the drug after repeated dosing treatments is negligible. In patients with persistent asthma carmoterol 2 µg administered once daily is as effective as formoterol 12 µg twice daily. Safety and tolerability results are similar between carmoterol and formoterol. There were no significant changes in ECG results, blood pressure or serum potassium or glucose levels

Abediterol, a fast and long-acting β2-adrenoceptor agonist (LABA), is being developed by AstraZeneca, for the treatment of asthma and chronic obstructive pulmonary disease. The investigational drug is a long-acting beta2-agonist (LABA) that has a bronchodilator effect, relaxing the muscles around the airways. It is currently under development and is in Phase II clinical trials.

Deltibant is the bradykinin receptor antagonist. It was found to be a potent and selective inhibitor of the depressor response to bradykinin in the anaesthetized rat and rabbit. Deltibant affords significant protection against traumatic shock where bradykinin plays an important role in tissue injury. Such protection may be achieved through inhibition of neutrophil-endothelial interaction and protection of vascular endothelial function. Deltibant may have some effect on survival in patients with systemic inflammatory response syndrome and gram-negative sepsis. Kinin-kallikrein system could be involved in cerebral edema - treatment with deltibant appeared to alter the natural history of traumatic brain contusions by preventing the 2 degrees brain swelling. In addition, deltibant obviated the need for surgery in the majority of treated patients. Deltibant could act on the cerebral vasculature to limit dys-autoregulation and brain swelling or on the blood brain barrier to reduce cerebral edema. Deltibant has been in phase II clinical trials for the treatment of pain, immune-inflammatory diseases and stroke. However, this research has been discontinued.

Elisidepsin (Irvalec®, PM02734) is a depsipeptide produced by chemical synthesis and chosen for development as an antineoplastic agent based on its in vitro activity against human solid tumor cell lines, in vivo activity in hollow fibers and xenografted human tumors, as well as its acceptable preclinical toxicology profile. Elisidepsin causes a typical necrotic cell death and induces profound alterations in tumor cell morphology. Elisidepsin inserts into the plasma membrane causing rapid loss of integrity and necrotic cell death in tumor cells. PharmaMar was developing elisidepsin for the treatment of cancer. However, development of the compound has been suspended.