X11α Inhibitors

X11α inhibitors primarily function by modulating the processing of Amyloid Precursor Protein (APP), a key player in Alzheimer's disease pathology. The inhibitors listed target various enzymes and pathways involved in APP metabolism, such as BACE1 (Beta-site APP cleaving enzyme 1) and gamma-secretase. LY2811376, for example, is a non-peptidic BACE1 inhibitor, reducing amyloid beta production, a process closely linked to X11α's role in APP interactions. By inhibiting BACE1, the production of amyloid beta is reduced, thereby potentially lessening the pathological interaction between APP and X11α.

Gamma-secretase inhibitors like Semagacestat, DAPT, Avagacestat, and several others, function by altering the cleavage of APP. Gamma-secretase is responsible for the final step in the production of amyloid beta. Inhibiting this enzyme alters the production of amyloid beta peptides, which are central to the development of Alzheimer's plaques. These inhibitors, therefore, indirectly impact the X11α-APP interaction by modulating the availability and form of APP. Additionally, some inhibitors, like TAPI-1, target ADAM17, a protease that influences APP processing outside of the amyloidogenic pathway. This can indirectly impact the role of X11α in APP metabolism. The chemical class of X11α inhibitors is diverse, as it includes compounds targeting different enzymes and pathways involved in APP processing. This diversity reflects the complex nature of APP metabolism and the various points at which it can be modulated to potentially influence X11α activity. The development and study of these inhibitors are crucial for understanding molecular mechanisms.