Chronic inflammation in the body is deeply related to all diseases that can be induced throughout the body (especially aging-related diseases). METImedi Pharmaceutical is conducting a sequential efficacy assessment for diseases that are highly severe and do not have therapeutic agents, considering the severity of diseases or the absence of therapeutic drugs among the candidates for various systemic diseases that can be induced by chronic inflammation. To date, the therapeutic efficacy of METI-101 has been confirmed in central nervous system, cardiovascular, digestive, ophthalmic and musculoskeletal disorders (Figure 5-15; Table 1).
(Figure 5) Inhibition of brain tissue damage and nerve cell death by METI-101 administration in the process of brain tissue break-down and neuronal cell damage in animal model induced by Alzheimer’s disease and stroke.
(Figure 6) Re-activation of dopaminergic neurons by METI-101 administration after inhibition of activation of dopaminergic neurons in animal models induced by Parkinson’s disease.
(Figure 7) Inhibition of demyelination and inflammatory immune cell infiltration by METI-101 administration after induction of demyelination and inflammatory immune cell infiltration in an animal model induced by multiple sclerosis.
(Figure 8) Reduction of arteriosclerosis lesions, infiltration foam cell number and fat accumulation sites by METI-101 administration in arteriosclerosis-induced animal model.
(Table 1) Histopathological examination shows that the aortic thickness, atherosclerosis lesions, infiltration foam cells and fat accumulation sites are significantly inhibited by METI-101 administration in the atherosclerosis-induced animal model.
(Figure 9) Inhibition of degeneration across retinal epithelium, choroid and sclera and choroidal neovascularization by METI-101 administration in macular degeneration-induced animal model.
(Figure 10) Reduction of inflammation and recovery of periodontal tissues by METI-101 administration after inducing the inflammation and periodontal tissue damage in periodontitis and pulpitis-induced animal model.
(Figure 11) Reduction of inflammation and tissue normalization of toe and joint by METI-101 administration in rheumatoid arthritis-induced animal model.
(Figure 12) Reduction of liver fat accumulation by METI-101 administration in non-alcoholic fat liver disease animal model.
(Figure 13) Inhibition of hepatic fibrosis by METI-101 administration in non-alcoholic fat liver disease animal model.
(Figure 14) Tissue normalization due to inhibition of ulcer and inflammation by METI-101 administration after induction of ulcer and intestinal wall permeable inflammation in Crohn’s disease-induced animal model
(Figure 15) Tissue normalization duet to inhibition of ulceration, polyp formation and inflammation by METI-101 administration after induction of intestinal epithelial ulcer, polyp and inflammation in ulcerative enteritis animal model.