Researchers from Eli Lilly & Co. reported preclinical data on LY-3954068, a MAPT small-interference RNA (siRNA) strategy in AD models. The therapy is designed to reduce tau protein synthesis by inhibiting the translation of MAPT mRNA, with the goal of effectively lowering all forms of tau.
Biohaven Pharmaceuticals Inc. has presented preclinical data on their novel bispecific degrader BHV-1310 for the potential treatment of autoimmune disorders. To date, about 10% of the global population is affected by autoimmune diseases. IgG-lowering agents have suboptimal pharmacology and pharmacodynamic effects and have safety and tolerability challenges.
Researchers from Tridem Bioscience GmbH & Co. KG provided details on the development of TRB-001, an anti-α-synuclein construct consisting of a B-cell epitope derived from human α-synuclein (SNCA), conjugated to CRM197 and C-type lectin (CLEC) β-glucan.
The etiology of epilepsy, as well as its pathology, still remains evasive. The role that FK506-binding protein 51 (FKBP51) might play in this disease was investigated in a murine model of kainic acid-induced excitotoxic brain injury.
Researchers from AC Immune SA recently presented the discovery of ACI-21018, a novel α-synuclein aggregation inhibitor developed using AC Immune’s proprietary Morphomer platform.
Praetego Inc. and University of California San Diego scientists reported preclinical results for the new small-molecule amadorin PTG-630, a brain-penetrant drug candidate that inhibits the formation of advanced glycation end-products (AGEs).
The specific tau isoforms, such as 3-repeat (3R) and 4-repeat (4R) isoforms, and the distinct conformational strains that misfolded tau can adopt are determinants of the molecular and clinical heterogeneity observed across tauopathies.
Neddylation is a post-translational modification that conjugates the NEDD8 protein to protein substrates, such as the cullins, which once neddylated join complex to form cullin-RING ubiquitin E3 ligases (CRLs), which in turn play a crucial role in regulating proteasomal degradation. The University of Kentucky has presented preclinical data on their neddylation inhibitor TK-59 as a cancer therapeutic.
Nitrated α-synuclein is upregulated in the CSF of patients with Parkinson’s Disease (PD), Lewy body dementia (DLB), multiple system atrophy (MSA), and other synucleinopathies.