[Asia Economy Reporter Hyunseok Yoo] Mediphron, a biopharmaceutical company specializing in new drug development, announced on the 17th that it has obtained a domestic patent for a new drug candidate that inhibits the production of pyroGlu-Aβ, a beta-amyloid modified by the glutaminyl cyclase enzyme, thereby blocking the formation of beta-amyloid plaques and neurotoxicity, which are the main causes of Alzheimer's dementia.
Beta-amyloid modified by the glutaminyl cyclase (QC) enzyme is known as a protein that forms amyloid plaques due to its strong adhesiveness and acts as a seed for plaque formation. It exhibits neurotoxicity and has been identified as a major cause of Alzheimer's disease. According to the company, inhibiting the QC enzyme to prevent the modification of typical beta-amyloid (Aβ) can block the formation of amyloid plaques and the occurrence of neurotoxicity, thereby opening a path to suppress or treat Alzheimer's disease.
Recently, Eli Lilly announced results from a Phase 2 clinical trial of Donanemab, a new antibody drug that reacts only to modified beta-amyloid, conducted on patients with early Alzheimer's disease, showing a reduction in amyloid plaques and prevention of cognitive decline.
By obtaining a domestic patent for the glutaminyl cyclase enzyme inhibitor (QC-inhibitor) mechanism of its new drug candidate, Mediphron has secured diversity in candidates targeting beta-amyloid alongside existing beta-amyloid aggregation inhibitors and RAGE inhibitors.
Nogiseon, CEO of Mediphron, stated, "The beta-amyloid hypothesis remains a valid approach for developing treatments, and if Biogen's Aducanumab receives approval from the U.S. FDA, the beta-amyloid-targeting candidates held by Mediphron will be re-evaluated."
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