The patent badge is an abbreviated version of the USPTO patent document. The patent badge does contain a link to the full patent document.

The patent badge is an abbreviated version of the USPTO patent document. The patent badge covers the following: Patent number, Date patent was issued, Date patent was filed, Title of the patent, Applicant, Inventor, Assignee, Attorney firm, Primary examiner, Assistant examiner, CPCs, and Abstract. The patent badge does contain a link to the full patent document (in Adobe Acrobat format, aka pdf). To download or print any patent click here.

Date of Patent:
Apr. 28, 2015

Filed:

Jun. 10, 2011
Applicant:

Rajesh Khanna, Indianapolis, IN (US);

Inventor:

Rajesh Khanna, Indianapolis, IN (US);

Assignee:
Attorney:
Primary Examiner:
Assistant Examiner:
Int. Cl.
CPC ...
A61K 38/16 (2006.01); A61K 38/10 (2006.01); A61K 38/00 (2006.01); A61K 47/00 (2006.01); A61P 25/02 (2006.01); A61P 23/00 (2006.01); C07K 5/00 (2006.01); C07K 7/00 (2006.01); C07K 16/00 (2006.01); C07K 17/00 (2006.01); A61K 38/04 (2006.01); C07K 14/005 (2006.01); C07K 14/47 (2006.01);
U.S. Cl.
CPC ...
C07K 14/005 (2013.01); C07K 14/4702 (2013.01); A61K 38/00 (2013.01); C07K 2319/00 (2013.01);
Abstract

N-type voltage-gated calcium channels (CaV2.2) are critical mediators of neurotransmitter release and are thought to be involved with transmission of nociception. The use of conventional CaV2.2 blockers in pain therapeutics is limited by side effects. Reported herein is a means to suppress both inflammatory and neuropathic pain without directly blocking CaV2.2, but rather by inhibiting the binding of the axonal collapsin response mediator protein 2 (CRMP-2), a protein known to enhance CaV2.2 function. A 15 amino acid peptide of CRMP-2 fused to the protein transduction domain of the HIV tat protein (TAT CBD3) reduced meningeal blood flow induced by activation of the trigeminovascular system, prevented inflammation-induced tactile hypernociception induced by intraplantar formalin and nocifensive behavior following corneal capsaicin application, and reversed neuropathic hypernociception produced by the antiretroviral drug 2',3′-dideoxycytidine. Preventing CRMP-2—mediated enhancement of CaV2.2 function suppressed inflammatory and neuropathic nociception, providing a method for treating pain and inflammation.


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