EFONIDIPINE - CAS 111011-63-3
Catalog number:
Not Intended for Therapeutic Use. For research use only.
Molecular Formula:
Molecular Weight:
Calcium Channel
Efonidipine could be effective in the treatment of cardiovascular disease as a blocker of T-type and L-type calcium channels. It could also present as the hydrochloride salt form.
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10 mM in DMSO
-20ºC Freeze
Efonidipine could be effective in the treatment of cardiovascular disease as a blocker of T-type and L-type calcium channels.
Shelf Life:
As supplied, 2 years from the QC date provided on the Certificate of Analysis, when stored properly
Boiling Point:
746.9ºC at 760mmHg
1.3 g/cm3
Canonical SMILES:
1.A molecular signature of tissues with pacemaker activity in the heart and upper urinary tract involves coexpressed hyperpolarization-activated cation and T-type Ca2+ channels.
Hurtado R1, Bub G, Herzlinger D. FASEB J. 2014 Feb;28(2):730-9. doi: 10.1096/fj.13-237289. Epub 2013 Nov 4.
Renal pacemakers set the origin and frequency of the smooth muscle contractions that propel wastes from the kidney to the bladder. Although congenital defects impairing this peristalsis are a leading cause of pediatric renal failure, the mechanisms underlying renal pacemaker activity remain unknown. Using ratiometric optical mapping and video microscopy, we discovered that hyperpolarization-activated cation (HCN) channel block with the specific anatagonist ZD7288 (30 μm; IC50) abolished the pacemaker depolarizations that initiate murine upper urinary tract peristalsis. Optical mapping and immunohistochemistry indicate that pacemaker potentials are generated by cells expressing HCN isoform-3, and that HCN3(+) cells are coupled to definitive smooth muscle via gap junctions. Furthermore, we demonstrate that HCN3(+) cells coexpress T-type Ca(2+) (TTC) channels and that TTC channel inhibition with R(-)efonidipine or NNC55-0396 decreased contractile frequency in a dose-dependent manner.
2.Dual T-type and L-type calcium channel blocker exerts beneficial effects in attenuating cardiovascular dysfunction in iron-overloaded thalassaemic mice.
Kumfu S1,2,3, Chattipakorn SC1,3,4, Fucharoen S5, Chattipakorn N1,2,3. Exp Physiol. 2016 Apr 1;101(4):521-39. doi: 10.1113/EP085517. Epub 2016 Feb 29.
NEW FINDINGS: What is the central question of this study? Head-to-head comparison of the therapeutic efficacy among commercial iron chelators and a dual T- (TTCC) and L-type calcium channel (LTCC) blocker on cardiac function, mitochondrial function and the protein expression of cardiac iron transporters in thalassaemic mice in iron-overloaded conditions has not been assessed. What is the main finding and its importance? The dual TTCC and LTCC blocker efonidipine could provide broad beneficial effects in the heart, liver, plasma and mitochondria in both wild-type and thalassaemic mice in iron-overloaded conditions. Its beneficial effects are of the same degree as the three commercial iron chelators currently used clinically. It is possible that efonidipine could be an alternative choice in patients unable to take iron chelators for the treatment of iron-overload conditions. Iron chelation therapy is a standard treatment in thalassaemia patients; however, its poor cardioprotective efficacy and serious side-effects are a cause for concern.
3.L/T-type and L/N-type calcium-channel blockers attenuate cardiac sympathetic nerve activity in patients with hypertension.
Ogura C1, Ono K, Miyamoto S, Ikai A, Mitani S, Sugimoto N, Tanaka S, Fujita M. Blood Press. 2012 Dec;21(6):367-71. doi: 10.3109/08037051.2012.694200. Epub 2012 Jul 3.
Sympathetic nerve activity is augmented by calcium-channel blocker treatment as a result of decreased blood pressure. Dihydropyridine calcium-channel blockers are divided into three different types. The purpose of the present study was to investigate whether treatment effects on hemodynamics, cardiac autonomic nerve activity and plasma norepinephrine levels differ among amlodipine (L type), efonidipine (L + T type) and cilnidipine (L + N type). We enrolled 14 hypertensive patients (seven males, seven females, 70 ± 6 years old) undergoing a monotherapy of amlodipine, efonidipine or cilnidipine into this prospective, open-labeled, randomized, crossover study. At baseline and every 6 months of the treatment period, we repeated the evaluation of hemodynamics, spectral analysis of heart rate variability and plasma norepinephrine levels. Blood pressure and pulse rate were comparable among the three treatments. The low-frequency (LF)/high-frequency (HF) power ratio, an index of cardiac sympathovagal balance, was significantly lower with efonidipine and cilnidipine than with amlodipine, while the HF/total power ratio, an index of cardiac vagal activity, revealed the opposite results.
4.The Ca(2+) channel inhibitor efonidipine decreases voltage-dependent K(+) channel activity in rabbit coronary arterial smooth muscle cells.
Park MH1, Son YK, Hong da H, Choi IW, Kim DJ, Lee H, Bang H, Na SH, Li H, Jo SH, Park WS. Vascul Pharmacol. 2013 Sep-Oct;59(3-4):90-5. doi: 10.1016/j.vph.2013.07.005. Epub 2013 Jul 19.
The effect of efonidipine, a commercially available antihypertensive drug and Ca(2+) channel inhibitor, on voltage-dependent K(+) (Kv) channels was studied in freshly isolated rabbit coronary arterial smooth muscle cells using the whole-cell patch clamp technique. The amplitude of Kv current was decreased by application of efonidipine in a dose-dependent manner, with IC50 of 0.26μM and a Hill coefficient of 0.91, which suggests 1:1 binding stoichiometry. Efonidipine did not affect voltage-dependent activation of the Kv channel, but shifted the inactivation curve by -8.87mV. The inhibitory effect of efonidipine was not significantly changed by depletion of extracellular Ca(2+) or intracellular ATP, which indicated no involvement of the Ca(2+) channel or intracellular protein kinase-dependent cascades. We conclude that efonidipine dose-dependently inhibits Kv current in a phosphorylation- and Ca(2+) channel-independent manner.
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