Highly potent, non-peptidic blocker of the apamin-sensitive Ca2+-activated K+ channel (KCa2.1) (IC50 = 3 nM in rat sympathetic neurons). Blocks hKCa2.1 and rKCa2.2 channels expressed in HEK 293 cells with IC50 values of 762 and 364 pM respectively.
Sold with the permission of University College, London
|Storage||Desiccate 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 654.44. 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||1.53 mL||7.64 mL||15.28 mL|
|5 mM||0.31 mL||1.53 mL||3.06 mL|
|10 mM||0.15 mL||0.76 mL||1.53 mL|
|50 mM||0.03 mL||0.15 mL||0.31 mL|
References are publications that support the products' biological activity.
Campos Rosa et al (2000) Synthesis, molecular modeling, and pharmacological testing of bis-quinolinium cyclophanes: potent, non-peptidic blockers of the apamin-sensitive Ca2+-activated K+ channel. J.Med.Chem. 43 420 PMID: 10669569
Malik-Hall et al (2000) Compounds that block intermediate-conductance (IKCa) and small-conductance (SKCa) calcium-activated potassium channels. Br.J.Pharmacol. 129 1431 PMID: 10742299
Strobaek et al (2000) Pharmacological characterization of small-conductance Ca2+-activated K+ channels stably expressed in HEK 293 cells. Br.J.Pharmacol. 129 991 PMID: 10696100
If you know of a relevant reference for UCL 1684, please let us know.
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Keywords: UCL 1684, supplier, potent, blockers, SKCa, Potassium, Channels, K+, ca2+-activated, ca2+-dependent, SK1, SK2, UCL1684, Ca2+-Activated, Potassium, Channels, Ca2+-Activated, Potassium, Channels, Tocris Bioscience
11 Citations for UCL 1684
Citations are publications that use Tocris products. Selected citations for UCL 1684 include:
Hilgers et al (2010) Twenty-four-hour exposure to altered blood flow modifies endothelial Ca2+-activated K+ channels in rat mesenteric arteries. J Pharmacol Exp Ther 333 210 PMID: 20040579
Lamy et al (2010) Allosteric block of KCa2 channels by apamin. PLoS One 285 27067 PMID: 20562108
Giachini et al (2009) Upregulation of intermediate calcium-activated potassium channels counterbalance the impaired endothelium-dependent vasodilation in stroke-prone spontaneously hypertensive rats. Transl Res 154 183 PMID: 19766962
Abdulkareem et al (2016) Knockdown of the small conductance Ca(2+) -activated K(+) channels is potently cytotoxic in breast cancer cell lines. Heart Rhythm 173 177 PMID: 26454020
Benton et al (2013) Iberiotoxin-sensitive and -insensitive BK currents in Purkinje neuron somata. J Neurophysiol 109 2528 PMID: 23446695
Alpert and Alford (2013) Synaptic NMDA receptor-dependent Ca2+ entry drives membrane potential and Ca2+ oscillations in spinal ventral horn neurons. PLoS One 8 e63154 PMID: 23646190
Chien and Su (2015) 5-hydroxytryptamine has an endothelium-derived hyperpolarizing factor-like effect on coronary flow in isolated rat hearts. J Biol Chem 22 42 PMID: 26076928
Geier et al (2011) Dynamic interplay of excitatory and inhibitory coupling modes of neuronal L-type calcium channels. Am J Physiol Cell Physiol 300 C937 PMID: 21228322
Hsueh et al (2013) Proarrhythmic effect of blocking the small conductance calcium activated potassium channel in isolated canine left atrium. J Biomed Sci 10 891 PMID: 23376397
Kurahashi et al (2014) Platelet-derived growth factor receptor-α-positive cells and not smooth muscle cells mediate purinergic hyperpolarization in murine colonic muscles. Am J Physiol Cell Physiol 307 C561 PMID: 25055825
Szollosi et al (2007) Glucose stimulates Ca2+ influx and insulin secretion in 2-week-old β-cells lacking ATP-sensitive K+ channels. Br J Pharmacol 282 1747 PMID: 17138557
Do you know of a great paper that uses UCL 1684 from Tocris? If so please let us know.
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