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ProMIS Neurosciences Inc PMN

ProMIS Neurosciences Inc. is a clinical-stage biotechnology company. It is focused on generating and developing antibody therapeutics selectively targeting toxic misfolded proteins in neurodegenerative diseases such as Alzheimer’s disease (AD), amyotrophic lateral sclerosis (ALS) and multiple system atrophy (MSA). Its proprietary target discovery engine applies a thermodynamic, computational discovery platform-ProMIS and Collective Coordinates-to predict novel targets known as Disease Specific Epitopes on the molecular surface of misfolded proteins. Using this approach, the Company is developing novel antibody therapeutics for AD, ALS and MSA. Its product candidates are PMN310, PMN267, and PMN442. The PMN310 is a monoclonal antibody designed to treat AD by selectively targeting toxic, misfolded oligomers of amyloid-beta. PMN267 product candidate targeting ALS. PMN442 is a drug candidate being developed for MSA designed to selectively target and protect against pathogenic a-syn species.


NDAQ:PMN - Post by User

Post by goldtechon May 05, 2024 4:13pm
188 Views
Post# 36024043

The bottom line

The bottom line

Abstract

A large body of clinical and nonclinical evidence supports the role of neurotoxic soluble beta amyloid (amyloid, Aβ) oligomers as upstream pathogenic drivers of Alzheimer’s disease (AD). Recent late-stage trials in AD that have evaluated agents targeting distinct species of Aβ provide compelling evidence that inhibition of Aβ oligomer toxicity represents an effective approach to slow or stop disease progression: (1) only agents that target soluble Aβ oligomers show clinical efficacy in AD patients; (2) clearance of amyloid plaque does not correlate with clinical improvements; (3) agents that predominantly target amyloid monomers or plaque failed to show clinical effects; and (4) in positive trials, efficacy is greater in carriers of the ε4 allele of apolipoprotein E (APOE4), who are known to have higher brain concentrations of Aβ oligomers. These trials also show that inhibiting Aβ neurotoxicity leads to a reduction in tau pathology, suggesting a pathogenic sequence of events where amyloid toxicity drives an increase in tau formation and deposition. The late-stage agents with positive clinical or biomarker data include four antibodies that engage Aβ oligomers (aducanumab, lecanemab, gantenerumab, and donanemab) and ALZ-801, an oral agent that fully blocks the formation of Aβ oligomers at the clinical dose.


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