{"id":27732,"date":"2024-04-24T15:31:08","date_gmt":"2024-04-24T10:01:08","guid":{"rendered":"https:\/\/www.delveinsight.com\/blog\/?p=27732"},"modified":"2024-04-24T15:31:10","modified_gmt":"2024-04-24T10:01:10","slug":"prx012-and-prx123-for-alzheimers-disease","status":"publish","type":"post","link":"https:\/\/www.delveinsight.com\/blog\/prx012-and-prx123-for-alzheimers-disease","title":{"rendered":"Prothena&#8217;s Promise: Revolutionizing Alzheimer&#8217;s Treatment with a Breakthrough Therapy"},"content":{"rendered":"\n<ul class=\"wp-block-list\">\n<li>PRX012, a next-generation subcutaneous antibody, has the potential to eliminate treatment obstacles due to its unique pharmacological properties and improved binding profile compared to conventional amyloid-beta targeting medicines.<\/li>\n\n\n\n<li>PRX123, targeting the hallmarks of Alzheimer\u2019s, A\u03b2 plaque, and tau tangles, has the potential to revolutionize the treatment regime, and offers a beacon of hope for Alzheimer\u2019s prevention.<\/li>\n<\/ul>\n\n\n\n<p>The Alzheimer&#8217;s drugs market has made significant progress, especially in the last half-decade, with more amyloid beta-protein-targeted monoclonal antibodies entering the market space. With the evolving paradigm&nbsp; of \u201camyloid hypothesis\u201d, there are many hopes and dreams for finding disease-modifying therapies for Alzheimer\u2019s.&nbsp;<\/p>\n\n\n\n<p>At the recently concluded American Academy of Neurology Annual Meeting (2024), in Denver, Prothena presented results from its two transformative assets, PRX012, which targets amyloid beta (A\u03b2), and PRX123, a novel dual amyloid beta-tau (A\u03b2-Tau) vaccine.&nbsp;<\/p>\n\n\n\n<p>In the abstract titled \u201c<strong>Binding Characteristics of PRX012 Surrogate Demonstrate Potent Engagement of Toxic Amyloid Beta Protofibrils and Robust Clearance of Pyroglutamate-modified Amyloid Beta\u201d, <\/strong>Prothena<strong> <\/strong>described evaluations that compared the binding of a PRX012 surrogate and lecanemab to A\u03b2 protofibrils, characterized by surface plasmon resonance. It also compared the ability of PRX012 and donanemab to induce microglial clearance of pyroglutamate-A\u03b2 from Alzheimer\u2019s disease plaques<strong>.<\/strong><\/p>\n\n\n\n<p>PRX012, a next-generation subcutaneous antibody targeting epitope at the N-terminus of A\u03b2, outperformed LEQEMBI, by having a 20 times higher affinity to A\u03b2 soluble protofibrils. It also removed pyroglutamate-modified A\u03b2, a component of senile plaques and vascular amyloid, at lower quantities than Eli Lilly&#8217;s donanemab.&nbsp; A\u03b2 plaque reduction, neutralization of toxic A\u03b2 protofibrils, and clearance of pyroglutamate-modified A\u03b2 in plaques, all correlate with slowing clinical decline in Alzheimer\u2019s.<\/p>\n\n\n\n<p>Prothenas\u2019s PRX012, a US FDA-designated drug, neutralizes and clears aggregated forms of amyloid beta, such as protofibrils and plaques, at low doses due to its high binding avidity. Its unique pharmacological attribute along with a superior binding profile, is an almost perfect recipe to reduce barriers to treatment and establish it as a potential best-in-class anti-A\u03b2 immunotherapy at a low volume, with infrequent subcutaneous dose.&nbsp;<\/p>\n\n\n\n<p>Prothena also presented results from the preclinical studies evaluating the in vivo efficacy of PRX123, in a transgenic mouse model expressing human amyloid precursor protein and with aggressively high A\u03b2 pathology in an abstract titled \u201c <strong>Dual Amyloid Beta\/Tau Vaccine PRX123 Surrogate Results in Robust Clearance of Amyloid Plaques in Brains of Aggressive APP\/PS1 Mouse Model.\u201d<\/strong><\/p>\n\n\n\n<p>Accumulation of A\u03b2 plaque and tau tangles throughout the brain are hallmarks of Alzheimer\u2019s disease. &nbsp;Clinical evidence demonstrates that N-terminal anti-A\u03b2 antibodies capable of robustly reducing A\u03b2 plaques in the brain, mostly slow cognitive decline in Alzheimer\u2019s, while anti-MTBR-tau antibodies suppress the pathogenic spatiotemporal spread of tau. It is therefore hypothesized that simultaneously disrupting these pathologic processes has the potential to address the major unmet of Alzheimer\u2019s treatment and provide the much-needed preventive treatment.<\/p>\n\n\n\n<p>Vaccines that target A\u03b2 and tau may prevent or delay the clinical manifestation of Alzheimer\u2019s by generating responses capable of intercepting both pathologic processes simultaneously. Attempts were made earlier as well to develop vaccines but were shelved after enrolled participants developed a brain inflammation known as meningoencephalitis.&nbsp;<\/p>\n\n\n\n<p>PRX123 generated robust immunogenic responses, producing antibodies that help remove A\u03b2 plaques and neutralize MTBR-tau. It generated robust antibody titers strong enough to bind structural elements of A\u03b2 plaques and tau tangles in post-mortem Alzheimer\u2019s brain tissue, reaching concentrations comparable to those found in plasma (0.3%). Immunohistochemical analysis of brain tissue from vaccinated APP\/PS1 mice established a significant reduction in cortical A\u03b2 plaques compared with a nonsense peptide control group. The degree of plaque clearance achieved with PRX123s immunization was comparable to a plaque-clearing N-terminal monoclonal antibody, used as positive control.<\/p>\n\n\n\n<p>A dual A\u03b2-Tau vaccine, PRX123, targets epitopes within A\u03b2 and tau proteins, promoting amyloid clearance while blocking pathogenic tau interaction. This combination has the potential to not only treat but also prevent Alzheimer\u2019s, offering a unique advantage not that only enhances its commercial viability but also underscores its potential to reach patients in need. The US FDA has cleared its IND application, with Phase I scheduled for 2024.<\/p>\n\n\n\n<p>Despite all the positives, experimental vaccines still have a long and challenging path ahead, but breakthroughs in this space will be instrumental in driving growth and changing the Alzheimer\u2019s treatment landscape, answering the unmet.<\/p>\n","protected":false},"excerpt":{"rendered":"<p>The Alzheimer&#8217;s drugs market has made significant progress, especially in the last half-decade, with more amyloid beta-protein-targeted monoclonal antibodies entering the market space. With the evolving paradigm&nbsp; of \u201camyloid hypothesis\u201d, there are many hopes and dreams for finding disease-modifying therapies for Alzheimer\u2019s.&nbsp; At the recently concluded American Academy of Neurology Annual Meeting (2024), in Denver, [&hellip;]<\/p>\n","protected":false},"author":14,"featured_media":27734,"comment_status":"closed","ping_status":"closed","sticky":false,"template":"","format":"standard","meta":{"_acf_changed":false,"_editorskit_title_hidden":false,"_editorskit_reading_time":0,"_editorskit_is_block_options_detached":false,"_editorskit_block_options_position":"{}","advgb_blocks_editor_width":"","advgb_blocks_columns_visual_guide":"","footnotes":""},"categories":[17126],"tags":[22059,22060,22061],"industry":[17225],"therapeutic_areas":[17245],"class_list":["post-27732","post","type-post","status-publish","format-standard","has-post-thumbnail","hentry","category-others","tag-aan","tag-aan-2024","tag-aan-2024-conference","industry-pharmaceutical","therapeutic_areas-neurology"],"acf":[],"yoast_head":"<!-- This site is optimized with the Yoast SEO Premium plugin v25.8 (Yoast SEO v25.8) - https:\/\/yoast.com\/wordpress\/plugins\/seo\/ -->\n<title>PRX012 and PRX123 for Alzheimer&#039;s Disease | AAN 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