NBI 27914 hydrochloride
Selective, non-peptide corticotropin-releasing factor1 (CRF1) receptor antagonist (Ki = 1.7 nM); has no activity at CRF2 receptors. Blocks behavioral seizures in vivo.
|Storage||Store at RT|
The technical data provided above is for guidance only. For batch specific data refer to the Certificate of Analysis.
All Tocris products are intended for laboratory research use only.
|Solvent||Max Conc. mg/mL||Max Conc. mM|
Preparing Stock Solutions
The following data is based on the product molecular weight 470.66. Batch specific molecular weights may vary from batch to batch due to solvent of hydration, which will affect the solvent volumes required to prepare stock solutions.
|Concentration / Solvent Volume / Mass||1 mg||5 mg||10 mg|
|1 mM||2.12 mL||10.62 mL||21.25 mL|
|5 mM||0.42 mL||2.12 mL||4.25 mL|
|10 mM||0.21 mL||1.06 mL||2.12 mL|
|50 mM||0.04 mL||0.21 mL||0.42 mL|
References are publications that support the biological activity of the product.
Baram et al (1997) The CRF1 receptor mediates the excitatory actions of corticotropin releasing factor (CRF) in the developing rat brain: in vivo evidence using a novel, selective, non-peptide CRF receptor antagonist. Brain Res. 770 89 PMID: 9372207
Chen et al (1996) Design and synthesis of a series of non-peptide high-affinity human corticotropin-releasing factor1 receptor antagonists. J.Med.Chem. 39 4358 PMID: 8893829
McCarthy et al (1999) Recent advances with the CRF1 receptor: design of small molecule inhibitors, receptor subtypes and clinical indications. Curr.Pharm.Des. 5 289 PMID: 10213797
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Keywords: NBI 27914 hydrochloride, NBI 27914 hydrochloride supplier, Selective, non-peptide, CRF1, antagonists, Corticotropin-Releasing, Factor1, Receptors, NBI27914, hydrochloride, 1591, Tocris Bioscience
12 Citations for NBI 27914 hydrochloride
Citations are publications that use Tocris products. Selected citations for NBI 27914 hydrochloride include:
Jia et al (2013) Role of nesfatin-1 in a rat model of visceral hypersensitivity. Cereb Cortex 19 3487 PMID: 23801843
Wang et al (2011) CRF receptor antagonist astressin-B reverses and prevents alopecia in CRF over-expressing mice. PLoS One 6 e16377 PMID: 21359208
Gutknecht et al (2008) Expression, binding, and signaling properties of CRF2(a) receptors endogenously expressed in human retinoblastoma Y79 cells: passage-dependent regulation of functional receptors. J Neurochem 104 926 PMID: 17976162
Navarro et al (2015) Orexin-corticotropin-releasing factor receptor heteromers in the ventral tegmental area as targets for cocaine. Stroke 35 6639 PMID: 25926444
Gallopin et al (2006) Cortical sources of CRF, NKB, and CCK and their effects on pyramidal cells in the neocortex. J Neurosci 16 1440 PMID: 16339088
Lowery-Gionta et al (2012) Corticotropin releasing factor signaling in the central amygdala is recruited during binge-like ethanol consumption in C57BL/6J mice. J Neurosci 32 3405 PMID: 22399763
Silberman and Winder (2013) Corticotropin releasing factor and catecholamines enhance glutamatergic neurotransmission in the lateral subdivision of the central amygdala. Neuropharmacology 70 316 PMID: 23470280
Liu et al (2010) Differential actions of urocortins on neurons of the myenteric division of the enteric nervous system in guinea pig distal colon. Br J Pharmacol 159 222 PMID: 20002096
Delawary et al (2010) NMDAR2B tyrosine phosphorylation regulates anxiety-like behavior and CRF expression in the amygdala. Mol Brain 3 37 PMID: 21118530
Nakamura and Sapru (2009) Cardiovascular responses to microinjections of urocortins into the NTS: role of inotropic glutamate receptors. Am J Physiol Heart Circ Physiol 296 H2022 PMID: 19395554
Rajbhandari et al (2015) Predator Stress-Induced CRF Release Causes Enduring Sensitization of Basolateral Amygdala Norepinephrine Systems that Promote PTSD-Like Startle Abnormalities. J Neurosci 35 14270 PMID: 26490866
Ji et al (2013) Non-pain-related CRF1 activation in the amygdala facilitates synaptic transmission and pain responses. Mol Pain 9 2 PMID: 23410057
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Literature in this Area
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Major depressive disorder is characterized by depressed mood and a loss of interest and/or pleasure. Updated in 2015 this poster highlights presynaptic and postsynaptic targets for the potential treatment of major depressive disorder, as well as outlining the pharmacology of currently approved antidepressant drugs.