World Library  
Flag as Inappropriate
Email this Article


Article Id: WHEBN0045179243
Reproduction Date:

Title: Hioc  
Author: World Heritage Encyclopedia
Language: English
Subject: Tryptamines, 7,8-Dihydroxyflavone, TrkB receptor agonists, Carboxamides, Indoles
Publisher: World Heritage Encyclopedia


Systematic (IUPAC) name
ATC code None
PubChem CID:
Chemical data
Formula C16H19N3O3
Molecular mass 301.340

HIOC is a small-molecule agent which acts as a selective TrkB receptor agonist (active at at least 100 nM; prominent activation at 500 nM).[1][2][3] It was derived from N-acetylserotonin (NAS).[2][3][4] Relative to NAS, HIOC possesses greater potency and a longer half-life (~30 min or less for NAS in rats, while HIOC is still detectable up to 24 hours after administration to mice; ~4 hour half-life for HIOC in mouse brain tissues).[2][3] It is described as producing long-lasting activation of the TrkB receptor and downstream signaling kinases associated with the receptor.[2] HIOC is systemically-active and is able to penetrate the blood-brain-barrier.[2] In animal studies, HIOC was found to robustly protect against glutamate-induced excitotoxicity, an action which was TrkB-dependent.[3]

See also


  1. ^ Longo, Frank M.; Massa, Stephen M. (2013). "Small-molecule modulation of neurotrophin receptors: a strategy for the treatment of neurological disease". Nature Reviews Drug Discovery 12 (7): 507–525.  
  2. ^ a b c d e Iuvone, P. Michael; Boatright, Jeffrey H.; Tosini, Gianluca; Ye, Keqiang (2014). "N-Acetylserotonin: Circadian Activation of the BDNF Receptor and Neuroprotection in the Retina and Brain" 801. pp. 765–771.  
  3. ^ a b c d Shen, J.; Ghai, K.; Sompol, P.; Liu, X.; Cao, X.; Iuvone, P. M.; Ye, K. (2012). "N-acetyl serotonin derivatives as potent neuroprotectants for retinas". Proceedings of the National Academy of Sciences 109 (9): 3540–3545.  
  4. ^ Tosini, G.; Ye, K.; Iuvone, P. M. (2012). "N-Acetylserotonin: Neuroprotection, Neurogenesis, and the Sleepy Brain". The Neuroscientist 18 (6): 645–653.  

This article was sourced from Creative Commons Attribution-ShareAlike License; additional terms may apply. World Heritage Encyclopedia content is assembled from numerous content providers, Open Access Publishing, and in compliance with The Fair Access to Science and Technology Research Act (FASTR), Wikimedia Foundation, Inc., Public Library of Science, The Encyclopedia of Life, Open Book Publishers (OBP), PubMed, U.S. National Library of Medicine, National Center for Biotechnology Information, U.S. National Library of Medicine, National Institutes of Health (NIH), U.S. Department of Health & Human Services, and, which sources content from all federal, state, local, tribal, and territorial government publication portals (.gov, .mil, .edu). Funding for and content contributors is made possible from the U.S. Congress, E-Government Act of 2002.
Crowd sourced content that is contributed to World Heritage Encyclopedia is peer reviewed and edited by our editorial staff to ensure quality scholarly research articles.
By using this site, you agree to the Terms of Use and Privacy Policy. World Heritage Encyclopedia™ is a registered trademark of the World Public Library Association, a non-profit organization.

Copyright © World Library Foundation. All rights reserved. eBooks from Project Gutenberg are sponsored by the World Library Foundation,
a 501c(4) Member's Support Non-Profit Organization, and is NOT affiliated with any governmental agency or department.