PHA 543613 hydrochloride
Potent α7 nAChR agonist that displays selectivity over α3β4, α1β1γδ, α4β2 and 5-HT3 receptors. Positively influences sensory gating and memory in in vivo models of schizophrenia. Orally active and brain penetrant.
Sold for research purposes under agreement from Pfizer Inc.
|Storage||Store at +4°C|
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 307.78. 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||3.25 mL||16.25 mL||32.49 mL|
|5 mM||0.65 mL||3.25 mL||6.5 mL|
|10 mM||0.32 mL||1.62 mL||3.25 mL|
|50 mM||0.06 mL||0.32 mL||0.65 mL|
References are publications that support the products' biological activity.
Wishka et al (2006) Discovery of N-[(3R)-1-azabicyclo[2.2.2]oct-3-yl]furo[2,3-c]pyridine-5-carboxamide, an agonist of the α7 nicotinic acetylcholine receptor, for the potential treatment of cognitive deficits in schizophrenia; synthesis and st J.Med.Chem. 49 4425 PMID: 16821801
Faghih et al (2008) Allosteric modulators of the α7 nicotinic acetylcholine receptor. J.Med.Chem. 51 701 PMID: 18198823
Acker et al (2008) Discovery of N-[3R,5R)-1-azabicyclo[3.2.1]ocy-3-yl]furo-[2,3-c]pyridine-5-carboxamide as an agonist of the α7 nicotinic acetylcholine receptor: in vitro and in vivo activity. Bioorg.Med.Chem.Letts. 18 3611 PMID:
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Keywords: PHA 543613 hydrochloride, supplier, Potent, selective, α7, alpha7, a7, nAChR, agonists, Nicotinic, Receptors, Acetylcholine, PHA543613, hydrochloride, Pfizer, Nicotinic, (a7), Receptors, Nicotinic, (a7), Receptors, Tocris Bioscience
4 Citations for PHA 543613 hydrochloride
Citations are publications that use Tocris products. Selected citations for PHA 543613 hydrochloride include:
Sérriàre et al (2015) Assessment of the Protection of Dopaminergic Neurons by an α7 Nicotinic Receptor Agonist, PHA 543613 Using [(18)F]LBT-999 in a Parkinson's Disease Rat Model. Cell Death Differ 2 61 PMID: 26389120
Foucault-Fruchard (2017) Neuroprotective effect of the alpha 7 nicotinic receptor agonist PHA 543613 in an in vivo excitotoxic adult rat model. Neuroscience 356 52 PMID: 28527955
Bali et al (2015) Differential effects of α7 nicotinic receptor agonist PHA-543613 on spatial memory performance of rats in two distinct pharmacological dementia models. Behav Brain Res 278 404 PMID: 25447295
Macpherson et al (2014) The α7 nicotinic receptor agonist PHA-543613 hydrochloride inhibits Porphyromonas gingivalis-induced expression of interleukin-8 by oral keratinocytes. Front Med (Lausanne) 63 557 PMID: 24609617
Do you know of a great paper that uses PHA 543613 hydrochloride from Tocris? If so please let us know.
Reviews for PHA 543613 hydrochloride
Average Rating: 5 (Based on 1 Review)
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We used PHA 543613 in behavioral pharmacology experiments and tested its cognitive enhancer effect. PHA 543613 was found effective in different behavioral paradigms, and in different models of cognitive impairment. For instance, PHA 543613 dose-dependently reversed scopolamine induced transient amnesia in the spontaneous alternation (t-maze) task of rats.
Sometimes we experienced poor solubility in physiological saline. Slight warming and ultrasonics might help.
Literature in this Area
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Alzheimer's disease (AD) is a degenerative brain disease and the most common cause of dementia, affecting approximately 47 million people worldwide. Updated in 2015, this poster summarizes the structural and functional changes observed in the progression of this neurodegenerative disease, as well as classic AD drug targets.
Learning & Memory Poster
Recognition memory enables us to make judgements about whether or not we have encountered a particular stimulus before. This poster outlines the cellular mechanisms underlying recognition memory and its links to long-term depression, as well as the use of pharmacological intervention to assess the role of neurotransmitters in recognition memory.
Peripheral sensitization is the reduction in the threshold of excitability of sensory neurons that results in an augmented response to a given external stimulus. This poster outlines the excitatory and inhibitory signaling pathways involved in modulation of peripheral sensitization. The role of ion channels, GPCRs, neurotrophins, and cytokines in sensory neurons are also described.