Abstract: The present disclosure provides GLP-1R agonists, and compositions, methods, and kits thereof. Such compounds are generally useful for treating a GLP-1R mediated disease or condition in a human.

Abstract: The present disclosure provides GLP-1R agonists, and compositions, methods, and kits thereof. Such compounds are generally useful for treating a GLP-1R mediated disease or condition in a human.

Abstract: The present disclosure provides GLP-1R agonists, and compositions, methods, and kits thereof. Such compounds are generally useful for treating a GLP-1R mediated disease or condition in a human.

Abstract: A compound of Formula (I): pharmaceutically acceptable salts thereof, deuterated analogs thereof, compositions thereof, and methods of treating disease using a compound thereof, wherein the variable substituents are disclosed herein.

Abstract: The present disclosure provides GLP-1R agonists, and compositions, methods, and kits thereof. Such compounds are generally useful for treating a GLP-1R mediated disease or condition in a human.

Abstract: Background: HIV capsid (CA) is an emerging target for antiretroviral treatment PF-3450074 (P74) is a small-molecule CA binder that has been proposed to inhibit reverse transcription (RT) by accelerating HIV core uncoating. PF74 antiviral potency can depend on cyclophilin A (CypA) binding to CA in some cells and it shares a CA binding site with the host nuclear transport factor CPSF6, which restrict HIV infection when mislocalized to the cell cytoplasm. Here we further interrogate the mechanism of action (MOA) for PF74 in human T cells and clarify its potential dependence on CypA and CPSF6. Methodology: HIV reporter viruses were produced in HEK293T cells and used to infect MT2 cells and primary CD4+ T cells to determine the antiviral effect of PF74. Compound exposure was controlled by staggered addition and cell washing at various times post-infection. DNA products of infection were analyzed by qPCR. CypA and CPSF6 levels were varied in MT2 cells by overexpression and shRNA knockdown.

Abstract: The present disclosure provides GLP-1R agonists, and compositions, methods, and kits thereof. Such compounds are generally useful for treating a GLP-1R mediated disease or condition in a human.

Abstract: The present disclosure provides GLP-1R agonists, and compositions, methods, and kits thereof. Such compounds are generally useful for treating a GLP-1R mediated disease or condition in a human.

Abstract: The present disclosure provides GLP-1R agonists, and compositions, methods, and kits thereof. Such compounds are generally useful for treating a GLP-1R mediated disease or condition in a human.

Abstract: The present disclosure provides GLP-1R agonists, and compositions, methods, and kits thereof. Such compounds are generally useful for treating a GLP-1R mediated disease or condition.

Abstract: The present disclosure provides GLP-1R agonists, and compositions, methods, and kits thereof. Such compounds are generally useful for treating a GLP-1R mediated disease or condition in a human.

Abstract: The present disclosure provides GLP-1R agonists, and compositions, methods, and kits thereof. Such compounds are generally useful for treating a GLP-1R mediated disease or condition in a human.