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Our science

Our goal is to progress the clinical development of our discoveries,

substantially increase their values, and to ultimately market or out-license.

CID

The human body always has the characteristic of maintain the balance of the body, that is, homeostasis. However, the homeostasis is collapsed by aging or other causes. These symptoms lead to chronic inflammation, which disturbs the body’s immune system and induces chronic inflammatory diseases throughout the body. METI-101 acts on the site where chronic inflammation is induced and shows the therapeutic effect for chronic inflammatory diseases by correcting the metabolism of various cells induced by chronic inflammation to the same metabolism as normal cells and minimizing the expression of inflammatory response factors.

METI-101 metabolic regulation mechanism

The tissues of specific areas where inflammatory disease is induced begin to break down and low-oxygen environment (hypoxia) is formed around the broken tissues. The hypoxic environment causes normal cells to have the same metabolism as the Warburg effect, the cancer-specific metabolism, and to suffer a vicious cycle that maintains chronic inflammation. When METI-101 is treated to inflammation-activated cells, the target protein is expressed by the unique mechanism of METI-101 (Figure 1) and the expression of various inflammatory-inducing factors is reduced by normalizing the broken metabolism (Figure 2-4).
(Figure 1) Activation of target protein by METI-101 in inflammatory response-induced cells.
(Figure 2) Suppression of TLR4 expression, an inflammatory factor, by METI-101 in inflammatory response-induced cells.
(Figure 3) Suppression of NF-κB expression, an inflammatory factor, by METI-101 in inflammatory response-induced cells.
(Figure 4) Suppression of HIF-1α expression, an inflammatory factor, by METI-101 in inflammatory response-induced cells.

Effect of METI-101 on chronic inflammatory diseases

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.
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