Abstract: This disclosure provides a method of stabilizing the interaction of a Retinoic Acid Receptor-alpha (RAR?) and a corepressor, Nuclear Receptor Corepressor 1 (NCoR1) by contacting the RARa with an amount of a Chaperone Mediated Autophagy (CMA) Activator sufficient to stabilize the RAR?-NCoR1 interaction. Stabilizing the RAR?/corepressor interaction can prevent a neurodegenerative disorder in a subject at risk for developing the neurodegenerative disorder or slow the advancement of a neurodegenerative disorder in a subject having an early symptom or biomarker of the neurodegenerative disorder. The disclosure also provides a method of maintaining preventing or slowing the advancement of a retinal degenerative disorder in a subject having an early symptom or biomarker of the retinal degenerative disorder.

Abstract: The disclosure provides method of enhancing neuronal, vascular cell, and macrophage proteostasis, in a subject by administering a CMA activator to the subject. Enhancing proteostasis is a method of preventing or slowing advancement of an age-related neurodegenerative disease, atherosclerosis, or an inflammatory disease in a subject. The age related neurodegenerative disease can be Alzheimer A disease (AD), Lewy body dementia, Parkinson's disease (PD), Huntington's disease, Amyotrophic lateral sclerosis (ALS), Frontotemporal dementia (FTD). Spinocerebellar ataxias (SC As), or Progressive subcortical gliosis. The disclosure further provides a method of reducing the progression of beta-amyloid and/or tau pathology in the subject, and/or reduces pre-existing beta-amyloid and/or tau pathology in the subject.

Abstract: The present disclosure provides methods of treating disease and disorders of the hematological system. The disclosure provides a method of expanding a population of hematopoietic stem cells (HSCs) while maintaining the population in an undifferentiated state comprising contacting the population of HSCs in the presence of a CMA activator for a period of time until a sufficient number of HSCs is obtained thereby producing an expanded HSC population.

Abstract: Compounds and pharmaceutically acceptable salts thereof of Formula I are disclosed. Certain compounds and salts of Formula I are active as CMA modulators. The disclosure provides pharmaceutical compositions containing a compound of Formula I.

Abstract: Compounds, compositions and methods are provided for selectively activating chaperone-mediated autophagy (CMA), protecting cells from oxidative stress, proteotoxicity and lipotoxicity, and/or antagonizing activity of retinoic acid receptor alpha (RAR?) in subjects in need thereof.

Abstract: Compounds and pharmaceutically acceptable salts thereof of Formula I are disclosed. The variables, e.g. R1-R9, X, and Y are defined herein. Certain compounds and salts of Formula I are active as CMA modulators. The disclosure provides pharmaceutical compositions containing a compound of Formula I and methods of treating disorders responsive to CMA modulation.

Abstract: Compounds and pharmaceutically acceptable salts thereof of Formula I are disclosed. Certain compounds and salts of Formula I are active as CMA modulators. The disclosure provides pharmaceutical compositions containing a compound of Formula I.

Abstract: Compounds, compositions and methods are provided for selectively activating chaperone-mediated autophagy (CMA), protecting cells from oxidative stress, proteotoxicity and lipotoxicity, and/or antagonizing activity of retinoic acid receptor alpha (RAR?) in subjects in need thereof.

Abstract: Compounds, compositions and methods are provided for selectively activating chaperone-mediated autophagy (CMA), protecting cells from oxidative stress, proteotoxicity and lipotoxicity, and/or antagonizing activity of retinoic acid receptor alpha (RAR?) in subjects in need thereof.

Abstract: Compounds, compositions and methods are provided for selectively activating chaperone-mediated autophagy (CMA), protecting cells from oxidative stress, proteotoxicity and lipotoxicity, and/or antagonizing activity of retinoic acid receptor alpha (RAR?) in subjects in need thereof.

Abstract: Compounds, compositions and methods are provided for selectively activating chaperone-mediated autophagy (CMA), protecting cells from oxidative stress, proteotoxicity and lipotoxicity, and/or antagonizing activity of retinoic acid receptor alpha (RAR?) in subjects in need thereof.

Abstract: Compounds, compositions and methods are provided for selectively activating chaperone-mediated autophagy (CMA), protecting cells from oxidative stress, proteotoxicity and lipotoxicity, and/or antagonizing activity of retinoic acid receptor alpha (RAR?) in subjects in need thereof.

Abstract: Compounds, compositions and methods are provided for selectively activating chaperone-mediated autophagy (CMA), protecting cells from oxidative stress, proteotoxicity and lipotoxicity, and/or antagonizing activity of retinoic acid receptor alpha (RAR?) in subjects in need thereof.

Abstract: Compounds, compositions and methods are provided for selectively activating chaperone-mediated autophagy (CMA), protecting cells from oxidative stress, proteotoxicity and lipotoxicity, and/or antagonizing activity of retinoic acid receptor alpha (RAR?) in subjects in need thereof.

Abstract: Compounds, compositions and methods are provided for selectively activating chaperone-mediated autophagy (CMA), protecting cells from oxidative stress, proteotoxicity and lipotoxicity, and/or antagonizing activity of retinoic acid receptor alpha (RAR?) in subjects in need thereof.

Abstract: Compounds, compositions and methods are provided for selectively activating chaperone-mediated autophagy (CMA), protecting cells from oxidative stress, proteotoxicity and lipotoxicity, and/or antagonizing activity of retinoic acid receptor alpha (RAR?) in subjects in need thereof.