IUPAC name
3D model (JSmol)
  • 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
  • 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
  • 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
Molar mass 571.667 g/mol
Except where otherwise noted, data are given for materials in their standard state (at 25 °C [77 °F], 100 kPa).

Endomorphin-2 (EM-2) is an endogenous opioid peptide and one of the two endomorphins.[1] It has the amino acid sequence Tyr-Pro-Phe-Phe-NH2. It is a high affinity, highly selective agonist of the μ-opioid receptor, and along with endomorphin-1 (EM-1), has been proposed to be the actual endogenous ligand of this receptor (that is, rather than the endorphins).[1][2][3][4] Like EM-1, EM-2 produces analgesia in animals, but whereas EM-1 is more prevalent in the brain, EM-2 is more prevalent in the spinal cord.[1] In addition, the action of EM-2 differs from that of EM-1 somewhat, because EM-2 additionally induces the release of dynorphin A and [Met]enkephalin in the spinal cord and brain by an unknown mechanism, which in turn go on to activate the κ- and δ-opioid receptors, respectively, and a portion of the analgesic effects of EM-2 is dependent on this action.[5][6] Moreover, while EM-1 produces conditioned place preference, a measure of drug reward, EM-2 produces conditioned place aversion, an effect which is dynorphin A-dependent.[6] Similarly to the case of EM-1, the gene encoding for EM-2 has not yet been identified.[4][7]

See also


  1. ^ a b c Richard 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. ^ a b Stefan 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. ^ a b Austin (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.