Blocker of IKur ultrarapid delayed rectifier potassium current and KV1.5 channels (IC50 = 0.31 μM for rKV1.5). Displays selectivity for inhibition of IKur over Ito (8-fold), IK1, IKr and IKs (20-fold) in native myocytes and selectivity for rat recombinant KV1.5 over KV3.1 (~ 15-fold). Increases action potential duration in atrial but not ventricular myocytes and prevents atrial arrhythmia.
|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 340.44. 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||2.94 mL||14.69 mL||29.37 mL|
|5 mM||0.59 mL||2.94 mL||5.87 mL|
|10 mM||0.29 mL||1.47 mL||2.94 mL|
|50 mM||0.06 mL||0.29 mL||0.59 mL|
References are publications that support the biological activity of the product.
Stump et al (2005) In vivo antiarrhythmic and cardiac electrophysiologic effects of a novel diphenylphosphine oxide IKur blocker (2-isopropyl-5-methylcyclohexyl) diphenylphosphine oxide. J.Pharmacol.Exp.Ther. 315 1362 PMID: 16157659
Regan et al (2006) In vivo cardiac electrophysiologic effects of a novel diphenylphosphine oxide IKur blocker, (2-isopropyl-5-methylcyclohexyl) diphenylphosphine oxide, in rat and nonhuman primate. J.Pharmacol.Exp.Ther. 316 727 PMID: 16243963
Lagrutta et al (2006) Novel, potent inhibitors of human Kv1.5 K+ channels and ultrarapid activating delayed rectifier potassium current. J.Pharmacol.Exp.Ther. 317 1054 PMID: 16522807
If you know of a relevant reference for DPO-1, please let us know.
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Keywords: DPO-1, DPO-1 supplier, blockers, KV15, channel, IKur, current, Potassium, KV, Channels, voltage-gated, voltage-dependent, K+, Diphenylphosphine, oxide1, Diphenyl, phosphine, oxide-1, Voltage-Gated, 2533, Tocris Bioscience
4 Citations for DPO-1
Citations are publications that use Tocris products. Selected citations for DPO-1 include:
Zhao et al (2013) Potent suppression of Kv1.3 potassium channel and IL-2 secretion by diphenyl phosphine oxide-1 in human T cells. PLoS One 8 e64629 PMID: 23717641
Haim et al (2010) Palmitate attenuates myocardial contractility through augmentation of repolarizing Kv currents. J Mol Cell Cardiol 48 395 PMID: 19857498
Ryland et al (2015) Polycomb-dependent repression of the potassium channel-encoding gene KCNA5 promotes cancer cell survival under conditions of stress. Oncogene 34 4591 PMID: 25435365
Tabarean (2014) Electrical remodeling of preoptic GABAergic neurons involves the Kv1.5 subunit. Pharmacol Res Perspect 9 e96643 PMID: 24797243
Do you know of a great paper that uses DPO-1 from Tocris? Please let us know.
Reviews for DPO-1
Average Rating: 5 (Based on 1 Review.)
Have you used DPO-1?
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DPO 1 was used to investigate its effect on Kv channels at different concentrations. Its shows increasing blocking effect on the channels with increasing concentrations. Worked ideally during the study and would recommend the product.
Literature in this Area
Tocris offers the following scientific literature in this area to showcase our products. We invite you to request* or download your copy today!
*Please note that Tocris will only send literature to established scientific business / institute addresses.
Epilepsy is a brain disease that affects 60 million people globally. More than 20 anti-seizure drugs are currently available, but these do not address the underlying causes of the condition. This poster summarizes current knowledge about the development of the condition and highlights some approaches that have disease-modifying effects in proof-of-concept studies.
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.