Somatostatin as an Anti-Inflammatory Neuropeptide. From Physiological Basis to Drug Development

Research output: Contribution to journalArticle

6 Citations (Scopus)

Abstract

This chapter demonstrates a promising opportunity for anti-inflammatory drug therapy. The theoretical background of the development of these novel-type compounds is an original observation derived from our laboratory. According to our experimental data, somatostatin is released from the capsaicin-sensitive sensory nerve endings by different stimuli. It reaches distant parts of the body by the circulation and exerts systemic anti-inflammatory effects via binding to G-protein-coupled membrane receptors. This receptor family consists of five subtypes (sst1-sst5). Presumably, sst1 and sst4 are responsible for the mediation of anti-inflammatory actions. Somatostatin influences neurogenic inflammation by presynaptic and postsynaptic actions. It inhibits the release of proinflammatory neuropeptides from the sensory nerve endings and also acts on receptors of vascular endothelial, inflammatory, and immune cells. As somatostatin itself is not a suitable lead molecule for drug development because of its wide spectrum of actions and very short elimination half-life, stable, selective, well-tolerated somatostatin agonists with anti-inflammatory activity have been synthesized and investigated. TT-232, a heptapeptide anti-inflammatory analog, is under clinical investigation and several nonpeptide analogs have been preclinically tested. Somatostatin analog anti-inflammatory agents would mean a novel chance in the pharmacotherapy of chronic inflammatory and immune diseases.

Original languageEnglish
JournalNeuroImmune Biology
Volume8
Issue numberC
DOIs
Publication statusPublished - 2009

Fingerprint

Somatostatin
Neuropeptides
Anti-Inflammatory Agents
Pharmaceutical Preparations
Sensory Receptor Cells
Neurogenic Inflammation
Drug Therapy
Capsaicin
Immune System Diseases
G-Protein-Coupled Receptors
Human Body
Blood Vessels
Half-Life
Chronic Disease
Observation
Membranes

ASJC Scopus subject areas

  • Immunology
  • Clinical Neurology
  • Neurology

Cite this

@article{6f6d537f42ed44638d79f03ffce87f7a,
title = "Somatostatin as an Anti-Inflammatory Neuropeptide. From Physiological Basis to Drug Development",
abstract = "This chapter demonstrates a promising opportunity for anti-inflammatory drug therapy. The theoretical background of the development of these novel-type compounds is an original observation derived from our laboratory. According to our experimental data, somatostatin is released from the capsaicin-sensitive sensory nerve endings by different stimuli. It reaches distant parts of the body by the circulation and exerts systemic anti-inflammatory effects via binding to G-protein-coupled membrane receptors. This receptor family consists of five subtypes (sst1-sst5). Presumably, sst1 and sst4 are responsible for the mediation of anti-inflammatory actions. Somatostatin influences neurogenic inflammation by presynaptic and postsynaptic actions. It inhibits the release of proinflammatory neuropeptides from the sensory nerve endings and also acts on receptors of vascular endothelial, inflammatory, and immune cells. As somatostatin itself is not a suitable lead molecule for drug development because of its wide spectrum of actions and very short elimination half-life, stable, selective, well-tolerated somatostatin agonists with anti-inflammatory activity have been synthesized and investigated. TT-232, a heptapeptide anti-inflammatory analog, is under clinical investigation and several nonpeptide analogs have been preclinically tested. Somatostatin analog anti-inflammatory agents would mean a novel chance in the pharmacotherapy of chronic inflammatory and immune diseases.",
author = "E. Pint{\'e}r and Z. Helyes and J. N{\'e}meth and J. Szolcs{\'a}nyi",
year = "2009",
doi = "10.1016/S1567-7443(08)10406-9",
language = "English",
volume = "8",
journal = "NeuroImmune Biology",
issn = "1567-7443",
publisher = "Elsevier",
number = "C",

}

TY - JOUR

T1 - Somatostatin as an Anti-Inflammatory Neuropeptide. From Physiological Basis to Drug Development

AU - Pintér, E.

AU - Helyes, Z.

AU - Németh, J.

AU - Szolcsányi, J.

PY - 2009

Y1 - 2009

N2 - This chapter demonstrates a promising opportunity for anti-inflammatory drug therapy. The theoretical background of the development of these novel-type compounds is an original observation derived from our laboratory. According to our experimental data, somatostatin is released from the capsaicin-sensitive sensory nerve endings by different stimuli. It reaches distant parts of the body by the circulation and exerts systemic anti-inflammatory effects via binding to G-protein-coupled membrane receptors. This receptor family consists of five subtypes (sst1-sst5). Presumably, sst1 and sst4 are responsible for the mediation of anti-inflammatory actions. Somatostatin influences neurogenic inflammation by presynaptic and postsynaptic actions. It inhibits the release of proinflammatory neuropeptides from the sensory nerve endings and also acts on receptors of vascular endothelial, inflammatory, and immune cells. As somatostatin itself is not a suitable lead molecule for drug development because of its wide spectrum of actions and very short elimination half-life, stable, selective, well-tolerated somatostatin agonists with anti-inflammatory activity have been synthesized and investigated. TT-232, a heptapeptide anti-inflammatory analog, is under clinical investigation and several nonpeptide analogs have been preclinically tested. Somatostatin analog anti-inflammatory agents would mean a novel chance in the pharmacotherapy of chronic inflammatory and immune diseases.

AB - This chapter demonstrates a promising opportunity for anti-inflammatory drug therapy. The theoretical background of the development of these novel-type compounds is an original observation derived from our laboratory. According to our experimental data, somatostatin is released from the capsaicin-sensitive sensory nerve endings by different stimuli. It reaches distant parts of the body by the circulation and exerts systemic anti-inflammatory effects via binding to G-protein-coupled membrane receptors. This receptor family consists of five subtypes (sst1-sst5). Presumably, sst1 and sst4 are responsible for the mediation of anti-inflammatory actions. Somatostatin influences neurogenic inflammation by presynaptic and postsynaptic actions. It inhibits the release of proinflammatory neuropeptides from the sensory nerve endings and also acts on receptors of vascular endothelial, inflammatory, and immune cells. As somatostatin itself is not a suitable lead molecule for drug development because of its wide spectrum of actions and very short elimination half-life, stable, selective, well-tolerated somatostatin agonists with anti-inflammatory activity have been synthesized and investigated. TT-232, a heptapeptide anti-inflammatory analog, is under clinical investigation and several nonpeptide analogs have been preclinically tested. Somatostatin analog anti-inflammatory agents would mean a novel chance in the pharmacotherapy of chronic inflammatory and immune diseases.

UR - http://www.scopus.com/inward/record.url?scp=77957037445&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=77957037445&partnerID=8YFLogxK

U2 - 10.1016/S1567-7443(08)10406-9

DO - 10.1016/S1567-7443(08)10406-9

M3 - Article

AN - SCOPUS:77957037445

VL - 8

JO - NeuroImmune Biology

JF - NeuroImmune Biology

SN - 1567-7443

IS - C

ER -