THOUSAND OAKS, Calif., July 11, 2019/PRNewswire/ -- Amgen (NASDAQ:AMGN), Novartis and Banner Alzheimer's Institute today announced the collective decision to discontinue investigation of the
BACE1 inhibitor CNP520 (umibecestat) in two pivotal Phase 2/3 studies in the Alzheimer's Prevention Initiative Generation Program.
THOUSAND OAKS, Calif., July 11, 2019/PRNewswire/--Amgen (NASDAQ:AMGN), Novartis and Banner Alzheimer's Institute today announced the collective decision to discontinue investigation of the
BACE1 inhibitor CNP520 (umibecestat) in two pivotal Phase 2/3 studies in the Alzheimer's Prevention Initiative Generation Program.
Switzerland-based Novartis, United States-based Amgen and Banner Alzheimer's Institute have decided to stop the clinical programme with
BACE1 inhibitor, CNP520 (umibecestat), for the prevention of Alzheimer's disease, it was reported on Friday.
(Alliance News) - Swiss pharma firm Novartis AG, American biotechnology company Amgen Inc and Banner Alzheimer's Institute on Thursday announced the partners will discontinue investigation of the
BACE1 inhibitor CNP520 in two pivotal second and third phase studies.
Amgen (AMGN), Novartis (NVS) and Banner Alzheimer's Institute announced the collective decision to discontinue investigation of the
BACE1 inhibitor CNP520 in two pivotal Phase 2/3 studies in the Alzheimer's Prevention Initiative Generation Program.
Indeed, the glycan is carried by several brain-derived proteins such as prostaglandin D synthetase (16) and [beta]- secretase (or
BACE1).
The beta-site APP-cleaving enzyme 1 (
BACE1) has been identified as an important [beta]-secretase in that process (9).
Zlokovic and colleagues found that 3K3A-APC protects the brain by preventing nerve cells from producing an enzyme called
BACE1 that is required to produce amyloid-EaA-.
BACE1 activity regulates cell surface contactin-2 levels.
Moreover, leptin also decreases the
BACE1 ([beta]-site APP cleaving enzyme 1) activity in SH-SY5Y cell line (10).
Regulatory relationships were seen linking viral abundance and modulators of APP metabolism; HHV-6A induced APBB2, APPBP2, BIN1,
BACE1, CLU, PICALM, and PSEN1.