Abstract: This document provides methods and materials for increasing TFEB polypeptide levels. For example, compounds (e.g., organic compounds) having the ability to increase TFEB polypeptide levels within cells and/or within a nucleus of cells, formulations containing compounds having the ability to increase TFEB polypeptide levels within cells and/or within a nucleus of cells, methods for making compounds having the ability to increase TFEB polypeptide levels within cells and/or within a nucleus of cells, methods for making formulations containing compounds having the ability to increase TFEB polypeptide levels within cells and/or within a nucleus of cells, methods for increasing TFEB polypeptide levels within cells and/or within a nucleus of cells, and methods for treating mammals (e.g., humans) having a condition responsive to an increase in TFEB polypeptide levels are provided.

Abstract: Small molecule inhibitors that block the interaction between B-cell lymphoma 10 protein (BCL10) and mucosa- associated lymphoid tissue lymphoma translocation protein 1 (MALT1), thereby inhibiting both the protease and scaffolding activities of MALT1, and MALT1- dependent downstream signaling, including IL-6 and IL-10 secretion by B-cell lymphoma cells and IL-2 transcription and secretion by Jurkat T cells.

Abstract: This document provides compounds that can inhibit CB1 activity within a mammal (e.g., a human), as well as the methods of using such compounds for treating diseases, disorders, and conditions such as obesity, fear, metabolic-related disorders, diabetes, dyslipidaemia, and atherosclerosis.

Abstract: A compound, or a pharmaceutically acceptable salt or ester thereof, having a structure of: wherein X is a divalent linking moiety; and R1-R10 are each individually H, optionally-substituted alkyl, optionally-substituted alkoxy, optionally-substituted aryl, optionally-substituted cycloalkyl, optionally-substituted heterocyclic, halogen, amino, or hydroxy, provided that at least one of R3 or R8 is an optionally-substituted alkyl, a substituted alkoxy, optionally-substituted aryl, optionally-substituted cycloalkyl, optionally-substituted heterocyclic, or halogen.

Abstract: This document provides compounds that are inhibitors of NAMPT activity, as well as the methods of using such compounds for treating diseases and conditions such as cancer, inflammatory conditions, autoimmune conditions, and conditions characterized by acute or sub-acute neuronal injury.

Abstract: This document provides compounds that can increase NAMPT activity, as well as the methods of using such compounds to treat diseases, disorders, and conditions such as traumatic nerve and/or brain injuries, chemotherapeutic-induced or diabetic neuropathies, and neurodegenerative diseases.

Abstract: Various salt forms of Compound I and Compound II represented by the following structural formulae, and their corresponding pharmaceutical compositions, are disclosed. (I), (II) Particular single crystalline forms of 1:1 Compound I tris salt, 1:1 Compound II tris salt, and 1:1 Compound II citrate salt are characterized by a variety of properties and physical measurements. Methods of preparing specific crystalline forms are also disclosed. The present disclosure also provides methods of treating type 2 diabetes mellitus, pre-diabetes, obesity, non-alcoholic fatty liver disease, non-alcoholic steatohepatitis, and cardiovascular disease in a subject.

Abstract: Described herein are compounds that disrupt the interaction between Fbxo48 and phosphorylated-AMPK.

Abstract: This document provides compounds that are inhibitors of NF-?B activity, as well as the methods of using such compounds for treating diseases and conditions such as cancer, inflammatory conditions, or autoimmune diseases.

Abstract: This document provides methods and materials for increasing the level of phosphorylated AMPK. For example, compounds (e.g., organic compounds) having the ability to increase the level of phosphorylated AMPK within cells, formulations containing compounds having the ability to increase the level of phosphorylated AMPK within cells, methods for making compounds having the ability to increase the level of phosphorylated AMPK within cells, methods for making formulations containing compounds having the ability to increase the level of phosphorylated AMPK within cells, methods for increasing the level of phosphorylated AMPK within cells, and methods for treating mammals (e.g., humans) having a condition responsive to an increase in the level of phosphorylated AMPK are provided.

Abstract: A method for treating a neurodegenerative disease or an inflammatory disorder in a subject, comprising administering to the subject in need thereof, a compound, or a pharmaceutically acceptable salt thereof, of formula II: wherein each of R3-R7 is independently H, halogen, optionally-substituted alkyl, amino, alkoxy or hydroxy; R8 is an optionally-substituted heterocycloalkyl; and a is 0 to 3.

Abstract: This document provides methods and materials for increasing or maintaining NMNAT2 polypeptide levels within cells. For example, compounds (e.g., organic compounds) having the ability to increase or maintain NMNAT2 polypeptide levels within cells, formulations containing compounds having the ability to increase or maintain NMNAT2 polypeptide levels within cells, methods for making compounds having the ability to increase or maintain NMNAT2 polypeptide levels within cells, methods for making formulations containing compounds having the ability to increase or maintain NMNAT2 polypeptide levels within cells, methods for increasing or maintain NMNAT2 polypeptide levels within cells, and methods for treating mammals (e.g., humans) having a condition responsive to an increase in NMNAT2 polypeptide levels are provided (or for preventing said condition).

Abstract: Described herein are compounds that disrupt the interaction between Fbxo48 and phosphorylated-AMPK.

Abstract: This document provides methods and materials for increasing TFEB polypeptide levels. For example, compounds (e.g., organic compounds) having the ability to increase TFEB polypeptide levels within cells and/or within a nucleus of cells, formulations containing compounds having the ability to increase TFEB polypeptide levels within cells and/or within a nucleus of cells, methods for making compounds having the ability to increase TFEB polypeptide levels within cells and/or within a nucleus of cells, methods for making formulations containing compounds having the ability to increase TFEB polypeptide levels within cells and/or within a nucleus of cells, methods for increasing TFEB polypeptide levels within cells and/or within a nucleus of cells, and methods for treating mammals (e.g., humans) having a condition responsive to an increase in TFEB polypeptide levels are provided.

Abstract: A method for treating a neurodegenerative disease or an inflammatory disorder in a subject, comprising administering to the subject in need thereof, a compound, or a pharmaceutically acceptable salt thereof, of formula II: wherein each of R3-R7 is independently H, halogen, optionally-substituted alkyl, amino, alkoxy or hydroxy; R8 is an optionally-substituted heterocycloalkyl; and a is 0 to 3.

Abstract: A compound, or a pharmaceutically acceptable salt or ester thereof, having a structure of: wherein X is a divalent linking moiety; and R1-R10 are each individually H, optionally-substituted alkyl, optionally-substituted alkoxy, optionally-substituted aryl, optionally-substituted cycloalkyl, optionally-substituted heterocyclic, halogen, amino, or hydroxy, provided that at least one of R3 or R8 is an optionally-substituted alkyl, a substituted alkoxy, optionally-substituted aryl, optionally-substituted cycloalkyl, optionally-substituted heterocyclic, or halogen.

Abstract: A compound of Formula II, or a salt, ester, solvate, hydrate or prodrug thereof: where: X1 is a branched or unbranched C1-10 alkyl, (CH2)s—NH—(CH2)t, (CH2)s—O—(CH2)t, or (CH2)s—C(NH2)—(CH2)v—NH—(CH2)t, where s, t and v are each, independently an integer from 1 to 5; A and B are each, independently, C6-10aryl, C6-10aryl-C1-6alkyl, C3-9 heteroaryl, or C3-9heteroaryl-C1-6alkyl, each optionally substituted with 1, 2 or 3 independently selected Rg groups; C and D are each, independently, C3-7 cycloalkyl, C3-7 cycloalkyl-C1-6alkyl, C3-7 heterocycloalkyl, C3-7 heterocycloalkyl-C1-6 alkyl, C6-10aryl, C6-10aryl-C1-6alkyl, C3-9 heteroaryl, or C3-9heteroaryl-C1-6alkyl, each optionally substituted with 1, 2 or 3 independently selected Rg groups; each Rg is, independently, halogen, C1-6 alkyl, C1-6 haloalkyl, hydroxyl, C1-6 alkoxy, C1-6 haloalkoxy, amino, C1-6alkylamino, or di-C1-6alkylamino; and n1 and p1 are each, independently, integers from 1 to 10.

Abstract: Described herein are compounds that disrupt the interaction between Fbxo48 and phosphorylated-AMPK.

Abstract: Novel compounds are disclosed along with methods of inhibiting the TGF? pathway and methods of treating Idiopathic Pulmonary Fibrosis (IPF) using such compounds.