Cambridge, MA, United States

Proteostasis Therapeutics

www.proteostasis.com
Cambridge, MA, United States

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Patent
Proteostasis Therapeutics | Date: 2017-01-18

The invention encompasses compounds such as compounds having the Formula (I) or (II), compositions thereof, and methods of modulating CFTR activity. The invention also encompasses methods of treating a condition associated with CFTR activity or condition associated with a dysfunction of proteostasis comprising administering to a subject an effective amount of a disclosed compound.


Patent
Proteostasis Therapeutics | Date: 2017-04-26

The present disclosure features disclosed compounds which can increase cystic fibrosis transmembrane conductance regulator (CFTR) activity as measured in human bronchial epithelial (hBE) cells. The present disclosure also features methods of treating a condition associated with decreased CFTR activity or a condition associated with a dysfunction of proteostasis comprising administering to a subject an effective amount of a disclosed compound.


Patent
Proteostasis Therapeutics | Date: 2017-01-18

The disclosure encompasses compounds having e.g., Formula (la) or (lb), compositions thereof, and methods of modulating CFTR activity. The diclosure also encompasses methods of treating a condition associated with CFTR activity or condition associated with a dysfunction of proteostasis comprising administering to a subject an effective amount of a compound of Formula (I) or (lb).


Kaufman R.J.,Sanford Burnham Institute for Medical Research | Malhotra J.D.,Proteostasis Therapeutics
Biochimica et Biophysica Acta - Molecular Cell Research | Year: 2014

Calcium homeostasis is central to all cellular functions and has been studied for decades. Calcium acts as a critical second messenger for both extracellular and intracellular signaling and is fundamental in cell life and death decisions (Berridge et al., 2000) [1]. The calcium gradient in the cell is coupled with an inherent ability of the divalent cation to reversibly bind multiple target biological molecules to generate an extremely versatile signaling system [2]. Calcium signals are used by the cell to control diverse processes such as development, neurotransmitter release, muscle contraction, metabolism, autophagy and cell death. "Cellular calcium overload" is detrimental to cellular health, resulting in massive activation of proteases and phospholipases leading to cell death (Pinton et al., 2008) [3]. Historically, cell death associated with calcium ion perturbations has been primarily recognized as necrosis. Recent evidence clearly associates changes in calcium ion concentrations with more sophisticated forms of cellular demise, including apoptosis (Kruman et al., 1998; Tombal et al., 1999; Lynch et al., 2000; Orrenius et al., 2003) [4-7]. Although the endoplasmic reticulum (ER) serves as the primary calcium store in the metazoan cell, dynamic calcium release to the cytosol, mitochondria, nuclei and other organelles orchestrate diverse coordinated responses. Most evidence supports that calcium transport from the ER to mitochondria plays a significant role in regulating cellular bioenergetics, production of reactive oxygen species, induction of autophagy and apoptosis. Recently, molecular identities that mediate calcium traffic between the ER and mitochondria have been discovered (Mallilankaraman et al., 2012a; Mallilankaraman et al., 2012b; Sancak et al., 2013)[8-10]. The next questions are how they are regulated for exquisite tight control of ER-mitochondrial calcium dynamics. This review attempts to summarize recent advances in the role of calcium in regulation of ER and mitochondrial function. This article is part of a Special Issue entitled: Calcium signaling in health and disease. Guest Editors: Geert Bultynck, Jacques Haiech, Claus W. Heizmann, Joachim Krebs, and Marc Moreau. © 2014.


Patent
Proteostasis Therapeutics | Date: 2014-07-17

The present invention is directed to compounds having the Formula (I), (Ia) or (Ib), compositions thereof and methods for the treatment of a condition associated with a dysfunction in proteostasis.


Patent
Proteostasis Therapeutics | Date: 2014-07-17

The present invention is directed to compounds having the Formula (I), (Ia) or (Ib), compositions thereof and methods for the treatment of a condition associated with a dysfunction in proteostasis.


Patent
Proteostasis Therapeutics | Date: 2016-05-12

The present invention is directed to compounds having the Formula (I), (II), (III), (IV), and (V), compositions thereof, and methods for the treatment of a condition associated with a dysfunction in proteostasis.


Patent
Proteostasis Therapeutics | Date: 2014-06-25

The invention encompasses methods of modulating CFTR activity in a subject in need thereof comprising administering an effective amount of a compound of Formula (I). The invention also encompasses methods of treating a condition associated with CFTR activity or condition associated with a dysfunction of proteostasis comprising administering to a subject an effective amount of a compound of Formula (I).


Patent
Proteostasis Therapeutics | Date: 2015-03-13

The disclosure encompasses compounds having e.g., Formula (Ia) or (Ib), compositions thereof, and methods of modulating CFTR activity. The disclosure also encompasses methods of treating a condition associated with CFTR activity or condition associated with a dysfunction of proteostasis comprising administering to a subject an effective amount of a compound of Formula (I) or (Ib).


Patent
Proteostasis Therapeutics | Date: 2015-03-13

The invention encompasses compounds such as compounds having the Formula (I) or (II), compositions thereof, and methods of modulating CFTR activity. The invention also encompasses methods of treating a condition associated with CFTR activity or condition associated with a dysfunction of proteostasis comprising administering to a subject an effective amount of a disclosed compound.

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