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Endomorphin-2

From Wikipedia, the free encyclopedia
Endomorphin-2
Names
IUPAC name
L-Tyrosyl-L-prolyl-L-phenylalanyl-L-phenylalaninamide
Identifiers
3D model (JSmol)
ChemSpider
UNII
  • InChI=1S/C32H37N5O5/c33-25(18-23-13-15-24(38)16-14-23)32(42)37-17-7-12-28(37)31(41)36-27(20-22-10-5-2-6-11-22)30(40)35-26(29(34)39)19-21-8-3-1-4-9-21/h1-6,8-11,13-16,25-28,38H,7,12,17-20,33H2,(H2,34,39)(H,35,40)(H,36,41)/t25-,26-,27-,28-/m0/s1
    Key: XIJHWXXXIMEHKW-LJWNLINESA-N
  • InChI=1/C32H37N5O5/c33-25(18-23-13-15-24(38)16-14-23)32(42)37-17-7-12-28(37)31(41)36-27(20-22-10-5-2-6-11-22)30(40)35-26(29(34)39)19-21-8-3-1-4-9-21/h1-6,8-11,13-16,25-28,38H,7,12,17-20,33H2,(H2,34,39)(H,35,40)(H,36,41)/t25-,26-,27-,28-/m0/s1
    Key: XIJHWXXXIMEHKW-LJWNLINEBE
  • c1ccc(cc1)C[C@@H](C(=O)N)NC(=O)[C@H](Cc2ccccc2)NC(=O)[C@@H]3CCCN3C(=O)[C@H](Cc4ccc(cc4)O)N
Properties
C32H37N5O5
Molar mass571.667 g/mol
Except where otherwise noted, data are given for materials in theirstandard state (at 25 °C [77 °F], 100 kPa).
Chemical compound

Endomorphin-2 (EM-2) is anendogenousopioid peptide and one of the twoendomorphins.[1] It has theamino acid sequence Tyr-Pro-Phe-Phe-NH2. It is a highaffinity, highly selectiveagonist of theμ-opioid receptor, and along with endomorphin-1 (EM-1), has been proposed to be the actual endogenousligand of this receptor (that is, rather than theendorphins).[1][2][3][4] Like EM-1, EM-2 producesanalgesia in animals, but whereas EM-1 is more prevalent in thebrain, EM-2 is more prevalent in thespinal cord.[1] In addition, the action of EM-2 differs from that of EM-1 somewhat, because EM-2 additionally induces the release ofdynorphin A and[Met]enkephalin in the spinal cord and brain by an unknownmechanism, which in turn activate theκ- andδ-opioid receptors, respectively, and a portion of the analgesic effects of EM-2 is dependent on this action.[5][6] Moreover, while EM-1 producesconditioned place preference, a measure ofdrug reward, EM-2 producesconditioned placeaversion, an effect which is dynorphin A-dependent.[6] Similarly to the case of EM-1, thegene encoding for EM-2 has not yet been identified.[4][7]

See also

[edit]

References

[edit]
  1. ^abcRichard J. Bodnar; Kathryn Grace Commons; Donald W. Pfaff (3 April 2002).Central Neural States Relating Sex and Pain. JHU Press. pp. 67–.ISBN 978-0-8018-6827-6.
  2. ^H.-J. Krammer; M.V. Singer (31 May 2000).Neurogastroenterology - From the Basics to the Clinics. Springer Science & Business Media. pp. 76–.ISBN 978-0-7923-8757-2.
  3. ^Susan Brain; P.K. Moore (1999).Pain and Neurogenic Inflammation. Springer Science & Business Media. pp. 28–.ISBN 978-3-7643-5875-4.
  4. ^abStefan Offermanns; Walter Rosenthal (14 August 2008).Encyclopedia of Molecular Pharmacology. Springer Science & Business Media. pp. 904–.ISBN 978-3-540-38916-3.
  5. ^William D. Willis Jr.; Richard E. Coggeshall (31 January 2004).Sensory Mechanisms of the Spinal Cord: Volume 1 Primary Afferent Neurons and the Spinal Dorsal Horn. Springer Science & Business Media. pp. 343–.ISBN 978-0-306-48033-1.
  6. ^abAustin (24 September 2010).Zen-Brain Reflections. MIT Press. pp. 125–.ISBN 978-0-262-26037-4.
  7. ^Brian E. Cairns (1 September 2009).Peripheral Receptor Targets for Analgesia: Novel Approaches to Pain Management. John Wiley & Sons. pp. 520–.ISBN 978-0-470-52221-9.
Hormones
Opioid peptides
Dynorphins
Endomorphins
Endorphins
Enkephalins
Others
Other
neuropeptides
Kinins
Neuromedins
Orexins
Other
μ-opioid
(MOR)
Agonists
(abridged;
full list)
Antagonists
δ-opioid
(DOR)
Agonists
Antagonists
κ-opioid
(KOR)
Agonists
Antagonists
Nociceptin
(NOP)
Agonists
Antagonists
Others

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