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A Review of the Therapeutic Targeting of SCN9A and Nav1.7 for Pain Relief in Current Human Clinical Trials

INTRODUCTION: There is a great need to find alternative treatments for chronic pain which have become a healthcare problem. We discuss current therapeutic targeting Nav1.7. AREAS COVERED: Nav1.7 is a sodium ion channel protein that is associated with several human pain genetic syndromes. It has been...

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Autores principales: Dormer, Anton, Narayanan, Mahesh, Schentag, Jerome, Achinko, Daniel, Norman, Elton, Kerrigan, James, Jay, Gary, Heydorn, William
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Dove 2023
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10166096/
https://www.ncbi.nlm.nih.gov/pubmed/37168847
http://dx.doi.org/10.2147/JPR.S388896
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author Dormer, Anton
Narayanan, Mahesh
Schentag, Jerome
Achinko, Daniel
Norman, Elton
Kerrigan, James
Jay, Gary
Heydorn, William
author_facet Dormer, Anton
Narayanan, Mahesh
Schentag, Jerome
Achinko, Daniel
Norman, Elton
Kerrigan, James
Jay, Gary
Heydorn, William
author_sort Dormer, Anton
collection PubMed
description INTRODUCTION: There is a great need to find alternative treatments for chronic pain which have become a healthcare problem. We discuss current therapeutic targeting Nav1.7. AREAS COVERED: Nav1.7 is a sodium ion channel protein that is associated with several human pain genetic syndromes. It has been found that mutations associated with Nav1.7 lead to the loss of the ability to perceive pain in individuals that are otherwise normal. Several therapeutic interventions are presently undergoing preclinical and research using the methodology of damping Nav1.7 expressions as a methodology to decrease the sensation of pain leading to analgesia. EXPERT OPINION: It is our strong belief that there is a viable future in the targeting of protein of Nav1.7 for the relief of chronic pain in humans. The review will look at the genomics associated with SCN1A and proteomic of Nav1.7 as a foundation to explain the mechanism of the therapeutic interventions targeting Nav1.7, the human disease that are associated with Nav1.7, and the current development of treatment for chronic pain whether in preclinical or clinical trials targeting Nav1.7 expressions. The development of therapeutic antagonists targeting Nav1.7 could be a viable alternative to the current treatments which have led to the opioid crisis. Therefore, Nav1.7 targeted treatment has a major clinical significance that will have positive consequences as it relates to chronic pain interventions.
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spelling pubmed-101660962023-05-09 A Review of the Therapeutic Targeting of SCN9A and Nav1.7 for Pain Relief in Current Human Clinical Trials Dormer, Anton Narayanan, Mahesh Schentag, Jerome Achinko, Daniel Norman, Elton Kerrigan, James Jay, Gary Heydorn, William J Pain Res Review INTRODUCTION: There is a great need to find alternative treatments for chronic pain which have become a healthcare problem. We discuss current therapeutic targeting Nav1.7. AREAS COVERED: Nav1.7 is a sodium ion channel protein that is associated with several human pain genetic syndromes. It has been found that mutations associated with Nav1.7 lead to the loss of the ability to perceive pain in individuals that are otherwise normal. Several therapeutic interventions are presently undergoing preclinical and research using the methodology of damping Nav1.7 expressions as a methodology to decrease the sensation of pain leading to analgesia. EXPERT OPINION: It is our strong belief that there is a viable future in the targeting of protein of Nav1.7 for the relief of chronic pain in humans. The review will look at the genomics associated with SCN1A and proteomic of Nav1.7 as a foundation to explain the mechanism of the therapeutic interventions targeting Nav1.7, the human disease that are associated with Nav1.7, and the current development of treatment for chronic pain whether in preclinical or clinical trials targeting Nav1.7 expressions. The development of therapeutic antagonists targeting Nav1.7 could be a viable alternative to the current treatments which have led to the opioid crisis. Therefore, Nav1.7 targeted treatment has a major clinical significance that will have positive consequences as it relates to chronic pain interventions. Dove 2023-05-04 /pmc/articles/PMC10166096/ /pubmed/37168847 http://dx.doi.org/10.2147/JPR.S388896 Text en © 2023 Dormer et al. https://creativecommons.org/licenses/by-nc/3.0/This work is published and licensed by Dove Medical Press Limited. The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License (http://creativecommons.org/licenses/by-nc/3.0/ (https://creativecommons.org/licenses/by-nc/3.0/) ). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. For permission for commercial use of this work, please see paragraphs 4.2 and 5 of our Terms (https://www.dovepress.com/terms.php).
spellingShingle Review
Dormer, Anton
Narayanan, Mahesh
Schentag, Jerome
Achinko, Daniel
Norman, Elton
Kerrigan, James
Jay, Gary
Heydorn, William
A Review of the Therapeutic Targeting of SCN9A and Nav1.7 for Pain Relief in Current Human Clinical Trials
title A Review of the Therapeutic Targeting of SCN9A and Nav1.7 for Pain Relief in Current Human Clinical Trials
title_full A Review of the Therapeutic Targeting of SCN9A and Nav1.7 for Pain Relief in Current Human Clinical Trials
title_fullStr A Review of the Therapeutic Targeting of SCN9A and Nav1.7 for Pain Relief in Current Human Clinical Trials
title_full_unstemmed A Review of the Therapeutic Targeting of SCN9A and Nav1.7 for Pain Relief in Current Human Clinical Trials
title_short A Review of the Therapeutic Targeting of SCN9A and Nav1.7 for Pain Relief in Current Human Clinical Trials
title_sort review of the therapeutic targeting of scn9a and nav1.7 for pain relief in current human clinical trials
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10166096/
https://www.ncbi.nlm.nih.gov/pubmed/37168847
http://dx.doi.org/10.2147/JPR.S388896
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