Comparative Study of the Influence of Iem-1556 and Glatiramer Acetate (Copaxon) on the Severity of Neurologic Disorders and the Duration of Experimental Allergic Encephalomielitis in the Rats

Abstract

The effect of N-decyltropine chloride (IEM-1556) and the reference drug glatiramer acetate (GA) on the severity of neurological disorders and the duration of the experimental allergic encephalomyelitis (EAE), modeling the processes of neural inflammation, demyelination and neurodegeneration characteristic for multiple sclerosis were studied. EAE in female Wistar rats was induced by a single subcutaneous (SC) inoculation of the homologous spinal cord homogenate in complete Freund’s adjuvant. The test preparations were administered from 2 to 16 days after induction of EAE. The severity of the disease was assessed in scores (from 0 to 6) by the presence in animals of persistent paresis and paralysis. The course systemic administration of IEM-1556 in a dose of 3 mg/kg reduced the severity and duration of EAE in rats, comparable to GA. Advantage of IEM-1556 before GA is the possibility of non-invasive application, as well as the presence of analgesic, antiparkinsonian and antidepressant action. It is assumed that the therapeutic effect of IEM-1556 is related to its ability to release endogenous adenosine, which causes neuroprotective, analgesic, antiparkinsonian and antidepressant effects of the drug.