Pharmacodynamics In animals,<unk>  rapidly elevates the levels and expression of brain-derived neurotrophic factor (BDNF) and its signaling receptor TrkB in the hippocampus, and rapidly activates serotonergic and dopaminergic brain systems. Accordingly, it has been found to produce antidepressant-like and anxiolytic-like effects, attenuate the behavioral effects of exposure to chronic stress, and potentiate the locomotor activity produced by D-amphetamine. As such, it has been suggested that<unk>  may be effective in the treatment of depression. Though the exact mechanism of action of<unk>  is unclear, there is evidence that it may act through melanocortin receptors. Specifically, there is a report of<unk>  competitively antagonizing the action of the melanocortin receptor full agonist α-melanocyte-stimulating hormone (α-MSH) at the MC4 and MC5 receptors in both in vitro and in vivo experimental conditions, indicating that it may act as an antagonist or partial agonist of these receptors.<unk>  did not antagonize α-MSH at the MC3 receptor, though this receptor could still be a target of the drug. As for the MC1 and MC2 receptors, they were not assayed. In addition to actions at receptors,<unk> , as well as a related peptide drug, Selank, have been found to inhibit enzymes involved in the degradation of enkephalins and other endogenous regulatory peptides (IC50 = 10 μM), though the clinical significance of this property is uncertain. Pharmacokinetics As a peptide,<unk>  has poor oral bioavailability and hence is administered parenterally as a nasal spray or subcutaneous injection.
Semax
Cimex
Paro 
Chalazion
Limen
Tenapanor
Ices
Glabella