Daniel W Moore

US Patent:

20130089528, Apr 11, 2013

Filed:

Oct 5, 2012

Appl. No.:

13/645754

Inventors:

Vanderbilt University - Nashville TN, US
Robert D. Collins - Nashville TN, US
Daniel J. Moore - Nashville TN, US
Jozef Zienkiewicz - , US
Ruth Ann Veach - Brentwood TN, US

Assignee:

VANDERBILT UNIVERSITY - Nashville TN

International Classification:

A61K 38/16
A61K 35/39
A61P 29/00
C12N 5/071
A61P 3/10
A61P 37/06

US Classification:

424 937, 514 213, 514 69, 435375, 514 73

Abstract:

Nuclear Transport Modifiers such as cSN50 and cSN50.1, afford in vivo islet protection following a 2-day course of intense treatment in autoimmune diabetes-prone, non-obese diabetic (NOD) mice, a widely used model of Type 1 diabetes (T1D), which resulted in a diabetes-free state for one year without apparent toxicity and the need to use insulin. cSN50 precipitously reduces the accumulation of islet-destructive autoreactive lymphocytes while enhancing activation-induced cell death of T and B lymphocytes derived from NOD mice. cSN50 attenuated pro-inflammatory cytokine and chemokine production in immune cells in this model of human T1D. cSN50 also provides cytoprotection of beta cells, therefore preserving residual insulin-producing capacity. Because intracellular delivery of a Nuclear Transport Modifier peptide such as cSN50 and cSN50.1 can result in lowering of blood glucose levels and may reducing insulin resistance, the compositions, methods and cells described herein can also be used for treating Type 2 diabetes (T2D).

US Patent:

20150191522, Jul 9, 2015

Filed:

Jan 9, 2015

Appl. No.:

14/593644

Inventors:

- Nashville TN, US
Daniel J. Moore - Nashville TN, US
Jozef Zienkiewicz - Nashville TN, US
Ruth Ann Veach - Brentwood TN, US

International Classification:

C07K 14/50
A61K 35/39
C12N 5/071

Abstract:

Nuclear Transport Modifiers such as cSN50 and cSN50.1, afford in vivo islet protection following a 2-day course of intense treatment in autoimmune diabetes-prone, non-obese diabetic (NOD) mice, a widely used model of Type 1 diabetes (T1D), which resulted in a diabetes-free state for one year without apparent toxicity and the need to use insulin. cSN50 precipitously reduces the accumulation of islet-destructive autoreactive lymphocytes while enhancing activation-induced cell death of T and B lymphocytes derived from NOD mice. cSN50 attenuated pro-inflammatory cytokine and chemokine production in immune cells in this model of human T1D. cSN50 also provides cytoprotection of beta cells, therefore preserving residual insulin-producing capacity. Because intracellular delivery of a Nuclear Transport Modifier peptide such as cSN50 and cSN50.1 can result in lowering of fasting blood glucose levels and may ameliorate (e.g., reduce, eliminate) insulin resistance, the compositions, methods and cells described herein can also be used for treating Type 2 diabetes (T2D).