PeptideDB

NAQ

CAS: F: C30H31N3O4 W: 497.58

NAQ is a potent and selective μ opioid receptor partial agonist, with a Ki of 0.55 nM. NAQ shows selectivity for Mu opi
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Bioactivity NAQ is a potent and selective μ opioid receptor partial agonist, with a Ki of 0.55 nM. NAQ shows selectivity for Mu opioid receptor over the δ receptor (Ki=132.50 nM) and the κ receptor (Ki=26.45 nM). NAQ can be used for the research of opioid withdrawal or dependence[1].
Invitro NAQ is a μ opioid receptor (MOR) partial agonist, with an EC50 of 4.36 nM in MOR-expressing CHO cell line[1].NAQ (45 min) inhibits hERG with an IC50 of 220 nM in CHO-K1 cells stably transfected with human hERG cDNA[3].
In Vivo NAQ (a single s.c.) antagonizes the antinociceptive effects of Morphine in the mouse tail immersion test, with an AD50 of 0.45 mg/kg[1].NAQ (0.32-10 mg/kg; s.c.) produces weak intracranial self-stimulation (ICSS) facilitation in rats but more robust ICSS facilitation during and after Morphine treatment and also reverses Morphine withdrawal-associated depression of ICSS[2].Pharmacokinetics of NAQ in rats[3]
Name NAQ
Formula C30H31N3O4
Molar Mass 497.58
Transport Room temperature in continental US; may vary elsewhere.
Storage

Please store the product under the recommended conditions in the Certificate of Analysis.

Reference [1]. Li G, et, al. Design, synthesis, and biological evaluation of 6alpha- and 6beta-N-heterocyclic substituted naltrexamine derivatives as mu opioid receptor selective antagonists. J Med Chem. 2009 Mar 12;52(5):1416-27. [2]. Altarifi AA, et, al. Effects of the novel, selective and low-efficacy mu opioid receptor ligand NAQ on intracranial self-stimulation in rats. Psychopharmacology (Berl). 2015 Feb;232(4):815-24. [3]. P. Pagare P, et, al. Preclinical Characterization and Development on NAQ as a Mu Opioid Receptor Partial Agonist for Opioid Use Disorder Treatment. ACS Pharmacol. Transl. Sci. 2022, 5, 11, 1197-1209.