UCL 1684

Names

[ CAS No. ]:
199934-16-2

[ Name ]:
UCL 1684

[Synonym ]:
ucl 1684

Biological Activity

[Description]:

UCL 1684 (dibromide) is a first nanomolar, non-peptidic small conductance calcium-activated potassium (SK) channel blocker. UCL 1684 (dibromide) is effective in preventing the development of atrial fibrillation due to potent atrial-selective inhibition of INa. UCL 1684 (dibromide) causes atrial-selective prolongation of ERP secondary to induction of postrepolarization refractoriness[1][2][3].

[Related Catalog]:

Research Areas >> Cardiovascular Disease

Signaling Pathways >> Membrane Transporter/Ion Channel >> Potassium Channel

[Target]

Potassium Channel[1]

[In Vitro]

UCL 1684 (dibromide) (0.5 μM; HEK cells) produces direct atrial-selective inhibition of sodium channel current (INa) and shifts SS inactivation of the cardiac sodium channels. UCL 1684 (dibromide) (0.5 μM) induces PRR, decreases V max, increases DTE, and extends the shortest S1-S1 interval[1].

[In Vivo]

UCL 1684 (dibromide) (3 mg/kg; i.v.) increases wenckebach cycle length to 115.0±5.1 % of baseline value[3].

[References]

[1]. Burashnikov A, et al. The Small Conductance Calcium-Activated Potassium Channel Inhibitors NS8593 and UCL1684 Prevent the Development of Atrial Fibrillation Through Atrial-Selective Inhibition of Sodium Channel Activity. J Cardiovasc Pharmacol. 2020;76(2):164-172.

[2]. Rosa JC, et al. Bis-quinolinium cyclophanes: 6,10-diaza-3(1,3),8(1,4)-dibenzena-1,5(1,4)- diquinolinacyclodecaphane (UCL 1684), the first nanomolar, non-peptidic blocker of the apamin-sensitive Ca(2+)-activated K+ channel. J Med Chem. 1998;41(1):2-5.

[3]. Diness JG, et al. Effects on atrial fibrillation in aged hypertensive rats by Ca(2+)-activated K(+) channel inhibition. Hypertension. 2011;57(6):1129-1135.

Chemical & Physical Properties

[ Molecular Formula ]:
C₃₈H₃₀F₆N₄O₄

[ Molecular Weight ]:
720.66000

[ Exact Mass ]:
720.21700

[ PSA ]:
112.08000

[ LogP ]:
5.07540

Related Compounds

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