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Prothena Announces Achievement of $40 Million Clinical Milestone Payment from Novo Nordisk for PRX004/NNC6019 Under Investigation for the Treatment of ATTR Cardiomyopathy
Prothena is eligible to receive development and sales milestone payments from Novo Nordisk totaling up to $1.2 billion, including $100 million announced to
About this update from Prothena Corporation Plc
[{"type":"text","content":"\n\nProthena is eligible to receive development and sales milestone payments from Novo Nordisk totaling up to $1.2 billion, including $100 million announced to date\n\n\nPRX004/NNC6019 continues to advance in a Phase 2 study in patients with ATTR cardiomyopathy being conducted by Novo Nordisk\n\n\n DUBLIN--(BUSINESS WIRE)--\nProthena Corporation plc (NASDAQ:PRTA), a late-stage clinical biotechnology company with a robust pipeline of investigational therapeutics built on protein dysregulation expertise, today announced that the Company has earned a $40 million milestone payment from Novo Nordisk related to the continued advancement of NNC6019 (formerly PRX004) in a Phase 2 clinical study for the treatment of ATTR cardiomyopathy. There remains a high unmet medical need in moderate to advanced ATTR amyloidosis patients at high risk for early mortality due to amyloid deposition in vital organs.\n\nUnder the terms of the agreement, Prothena is eligible to receive up to $1.2 billion dollars upon achievement of several clinical development and sales milestones, including the $100 million earned to date. Novo Nordisk gained full worldwide rights to the intellectual property and related rights of the ATTR amyloidosis business and pipeline it acquired from Prothena in July 2021.\n\nAbout NNC6019 (formerly PRX004)\n\nNNC6019 (formerly PRX004) is an investigational antibody designed to deplete amyloid associated with disease pathology in hereditary and wild type ATTR amyloidosis, without affecting the native, normal tetrameric form of the protein. NNC6019’s proposed mechanism of action is to deplete both the deposited amyloid to improve organ function and circulating non-native TTR to prevent further organ deposition. In preclinical studies, PRX004 demonstrated ability to inhibit amyloid fibril formation, bind soluble aggregate forms of non-native TTR and promote clearance of insoluble amyloid fibrils through antibody-mediated phagocytosis. This differentiated depleter mechanism of action could be developed as a monotherapy approach to ATTR amyloidosis and might also complement existing therapeutic approaches which either stabilize or reduce production of the native TTR tetramer.\n\nAbout Phase 2 Clinical Study for NNC6019 (formerly PRX004)\n\nPrior to Novo Nordisk’s acquisition in 2021 of Prothena’s ATTR amyloidosis program, Prothena compl...