UCL 1684 dibromide_product_DataBase

Bioactivity	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].
Target	Potassium Channel
Invitro	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].
Name	UCL 1684 dibromide
CAS	199934-16-2
Formula	C34H30Br2N4
Molar Mass	654.44
Transport	Room temperature in continental US; may vary elsewhere.
Storage	Please store the product under the recommended conditions in the Certificate of Analysis.
Reference	[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) [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.

PeptideDB

UCL 1684 dibromide

CAS: 199934-16-2 F: C34H30Br2N4 W: 654.44