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Biotech Identifies Antibody Drug Candidates to Target Toxic Protein Implicated in Parkinson's Disease
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The Canadian company continues seeking partners to leverage its discovery and development platform.

ProMIS Neurosciences Inc. (PMN:TSX; ARFXF:OTCQB) announced in a news release it identified several monoclonal antibody drug candidates for Parkinson's disease. The candidates precisely target only the toxic forms of the protein alpha-synuclein, considered to be a root cause of Parkinson's disease.

"We used our proprietary discovery platform to generate several antibody drug candidates for Parkinson's disease that precisely target only the toxic forms of alpha-synuclein," stated Dr. James Kupiec, ProMIS' chief medical officer. "Selectivity represents the essential feature of a successful antibody therapy, for it is critical that treatment not hinder normal forms of alpha-synuclein that play an important functional role in the brain. In preclinical studies, ProMIS antibody candidates showed a high degree of selectivity for only the toxic forms of alpha-synuclein in a side-by-side comparison with other alpha-synuclein targeting antibodies that are currently in development."

Preclinical in vitro studies demonstrated these candidates block neurotoxicity and the spreading of toxic alpha-synuclein while binding only to the toxic forms of the protein, the company noted.

ProMIS stated it has "created a novel, proprietary method for discovering and developing antibodies that can uniquely and precisely target these specific toxic forms."

"Competitive differentiation of ProMIS antibodies is key to ongoing partnering discussions with large pharmaceutical companies," the company stated.


1) Doresa Banning compiled this article for Streetwise Reports LLC and provides services to Streetwise Reports as an independent contractor. She or members of her household own securities of the following companies mentioned in the article: None. She or members of her household are paid by the following companies mentioned in this article: None.
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