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Selective TRPM4 blocker (IC50 = 20 μM in HEK293 cells). Exhibits no effect on CFTR or TRPM5 (at 0.25 and 1 mM respectively). Abolishes arrhythmias induced by hypoxia in a mouse heart model.
|Storage||Store at +4°C|
The technical data provided above is for guidance only. For batch specific data refer to the Certificate of Analysis.
Tocris products are intended for laboratory research use only, unless stated otherwise.
|Solvent||Max Conc. mg/mL||Max Conc. mM|
Preparing Stock Solutions
The following data is based on the product molecular weight 194.23. Batch specific molecular weights may vary from batch to batch due to the degree 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||5.15 mL||25.74 mL||51.49 mL|
|5 mM||1.03 mL||5.15 mL||10.3 mL|
|10 mM||0.51 mL||2.57 mL||5.15 mL|
|50 mM||0.1 mL||0.51 mL||1.03 mL|
References are publications that support the biological activity of the product.
Simard et al (2012) Transient receptor potential melastatin 4 inhibitor 9-phenanthrol abolishes arrhythmias induced by hypoxia and re-oxygenation in mouse ventricle. Br.J.Pharmacol. 165 2354 PMID: 22014185
Grand et al (2008) 9-phenanthrol inhibits human TRPM4 but not TRPM5 cationic channels. Br.J.Pharmacol. 153 1697 PMID: 18297105
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Keywords: 9-Phenanthrol, 9-Phenanthrol supplier, Transient, receptor, potential, TRPM4, blockers, TRP, channels, arrhythmias, cardiac, heart, anti-arrhythmic, depolarisations, TRPM, 4999, Tocris Bioscience
2 Citations for 9-Phenanthrol
Citations are publications that use Tocris products. Selected citations for 9-Phenanthrol include:
O'Malley et al (2020) TRPM4 Conductances in Thalamic Reticular Nucleus Neurons Generate Persistent Firing during Slow Oscillations. J Neurosci 40 4813 PMID: 32414784
Lin et al (2017) Differential Contribution of Ca2+-Dependent Mechanisms to Hyperexcitability in Layer V Neurons of the Medial Entorhinal Cortex. Front Cell Neurosci 11 182 PMID: 28713246
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Literature in this Area
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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.