| Size | Price | Stock | Qty |
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| 5mg |
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| 10mg |
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| 25mg |
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| Targets |
L‑type calcium channel (LCC) and T‑type calcium channel (TCC). The R(–)-enantiomer of Efonidipine selectively blocks T‑type but not L‑type calcium channels. [1][3]
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| ln Vitro |
In NCI‑H295R human adrenocortical carcinoma cells, Efonidipine (10⁻⁶ mol/L) alone did not significantly affect StAR mRNA expression, but it dose‑dependently enhanced dbcAMP (10⁻³ mol/L)‑induced StAR mRNA (P < 0.01 vs. dbcAMP alone) and StAR protein (approx. 16.4‑fold of DMSO) as measured by real‑time PCR and Western blot. [1]
In the same cells, Efonidipine (10⁻⁶ mol/L) enhanced angiotensin II (10⁻⁷ mol/L)‑induced StAR mRNA expression (P < 0.01 vs. angiotensin II alone). [1] In NCI‑H295R cells, Efonidipine (10⁻⁶ mol/L) and R(–)-efonidipine (10⁻⁶ mol/L) significantly increased dbcAMP‑induced DHEA‑S production (P < 0.01 vs. dbcAMP alone), whereas other CCBs did not. Angiotensin II alone decreased DHEA‑S production, and Efonidipine further decreased it. [1] In HepG2 human hepatoma cells, Efonidipine (10⁻⁶ mol/L) and nifedipine (10⁻⁶ mol/L) significantly increased StAR mRNA expression (P < 0.01 vs. DMSO) as assessed by real‑time PCR and Western blot. [1] In ventricular myocytes isolated from UM‑X7.1 cardiomyopathic hamsters (20 weeks old), Efonidipine inhibited the T‑type calcium current (Icat) in a dose‑dependent manner (tested at 0.33 μmol/L and 0.66 μmol/L). The average current density of Icat in UM‑X7.1 myocytes was –4.2 ± 0.5 pA/pF. [3] Efonidipine did not affect the expression of TCC α1G mRNA in either golden or UM‑X7.1 hamster hearts as determined by quantitative RT‑PCR. [3] |
| ln Vivo |
In a randomized crossover clinical study of 20 hypertensive patients on maintenance hemodialysis, Efonidipine (20–60 mg twice daily for 12 weeks) significantly lowered plasma aldosterone concentration compared to amlodipine (123 ± 118 pg/mL vs. 146 ± 150 pg/mL, P = 0.027), while plasma renin activity and angiotensin II levels were not significantly different between the two treatments. Blood pressure reductions were comparable between Efonidipine and amlodipine periods (151±15/77±8 vs. 153±15/76±8 mmHg). [2]
In UM‑X7.1 cardiomyopathic hamsters, administration of Efonidipine (0.1% in diet from 20 weeks of age for 4 weeks) significantly attenuated the decrease in left ventricular ejection fraction (LVEF) compared to vehicle‑treated UM‑X7.1 hamsters (50±5% vs. 43±7%, P < 0.05). Efonidipine did not affect blood pressure but decreased heart rate by approximately 10% in both UM‑X7.1 and golden hamsters. Serum BNP levels were significantly decreased in Efonidipine‑treated UM‑X7.1 hamsters (30.5±3.3 pg/mL) compared to untreated UM‑X7.1 hamsters (40.5±11.5 pg/mL, P < 0.05). [3] |
| Cell Assay |
NCI‑H295R human adrenocortical carcinoma cells were cultured in DMEM/F12 with 5% FBS, transferrin, insulin, BSA, and antibiotics, then seeded into 6‑well plates at 2.0×10⁶ cells/well for 48 hours. For experiments, cells were cultured in stimulation medium (DMEM/F12 containing 0.1% BSA) with or without dbcAMP (10⁻³ mol/L) or angiotensin II (10⁻⁷ mol/L), and with or without CCBs (including Efonidipine at 10⁻⁶ mol/L) for 6 or 24 hours. Total RNA was extracted using the isothiocyanate‑acid‑phenol‑chloroform method, cDNA synthesized, and real‑time PCR performed for StAR mRNA with normalization to GAPDH. For Western blot, proteins were extracted, separated by SDS‑PAGE, transferred to PVDF membranes, and probed with anti‑StAR, anti‑CYP11A1, anti‑HSD3B2, or anti‑CYP21A2 antibodies, then visualized by chemiluminescence. DHEA‑S and cortisol in culture medium were measured by specific enzyme immunoassay kits and normalized to protein content. [1]
HepG2 human hepatoma cells were cultured in DMEM with 10% FBS, seeded into 6‑well plates at 4.0×10⁶ cells/well for 48 hours, then cultured in FBS‑free DMEM with or without Efonidipine (10⁻⁶ mol/L) for 24 hours. StAR mRNA and protein expression were analyzed as above. [1] Ventricular myocytes from UM‑X7.1 and golden hamsters (20 weeks old) were enzymatically isolated. Calcium currents were recorded using whole‑cell patch‑clamp with an EPC‑9 amplifier. Bath solution (Na⁺‑free) contained TEA‑Cl, CaCl₂ (1.8 mmol/L), MgCl₂, glucose, HEPES, and TTX (0.05 mmol/L). Pipette solution contained CsCl, MgATP, creatine phosphate, Na₂GTP, HEPES, and EGTA (10 mmol/L). Icat was isolated by subtracting currents from a holding potential of –40 mV (L‑type) from those from –100 mV (total). Efonidipine (0.33 and 0.66 μmol/L) was applied to assess inhibition of Icat. [3] |
| Animal Protocol |
In UM‑X7.1 cardiomyopathic hamsters and age‑matched golden hamsters, Efonidipine was administered via diet at 0.1% (w/w) starting at 20 weeks of age for 4 weeks. The dose was chosen based on a pilot study showing this regimen significantly increased serum levels of Efonidipine without producing a significant decrease in blood pressure. [3]
In a human clinical study (randomized crossover design), hypertensive patients on maintenance hemodialysis received Efonidipine at 20–60 mg twice daily (after breakfast and supper) for 12 weeks, titrated to achieve blood pressure <140/90 mmHg. [2] |
| References |
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| Additional Infomation |
Efonidipine hydrochloride is a dihydropyridine compound.
Efonidipine is a dihydropyridine CCB that blocks both L‑type and T‑type calcium channels, whereas most other dihydropyridines block only L‑type. Its R(–)-enantiomer selectively blocks T‑type but not L‑type channels. [1][3] The enhancement of StAR expression and DHEA‑S production by Efonidipine appears independent of extracellular Ca²⁺, as chelation with EGTA or blockade with non‑dihydropyridine CCBs (diltiazem, verapamil) did not mimic the effect. [1] Efonidipine’s reduction of plasma aldosterone in hemodialysis patients suggests an additional cardiovascular protection benefit beyond blood pressure lowering, possibly via direct inhibition of adrenal aldosterone synthesis. [2] In cardiomyopathic hamsters, re‑expression of T‑type calcium channels during heart failure is associated with abnormal Ca²⁺ homeostasis, and Efonidipine improves cardiac function without affecting blood pressure, suggesting a role for T‑type blockade in heart failure therapy. [3] |
| Molecular Formula |
C36H45CLN3O8P
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|---|---|
| Molecular Weight |
714.1846
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| Exact Mass |
631.244
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| CAS # |
111011-76-8
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| Related CAS # |
Efonidipine;111011-63-3;Efonidipine hydrochloride;111011-53-1
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| PubChem CID |
163838
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| Appearance |
Light yellow to yellow solid powder
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| Density |
1.3±0.1 g/cm3
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| Boiling Point |
746.9±60.0 °C at 760 mmHg
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| Melting Point |
151° (dec)
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| Flash Point |
405.5±32.9 °C
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| Vapour Pressure |
0.0±2.5 mmHg at 25°C
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| Index of Refraction |
1.625
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| LogP |
6.99
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| Hydrogen Bond Donor Count |
3
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| Hydrogen Bond Acceptor Count |
10
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| Rotatable Bond Count |
10
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| Heavy Atom Count |
49
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| Complexity |
1170
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| Defined Atom Stereocenter Count |
0
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| InChi Key |
IKBJGZQVVVXCEQ-UHFFFAOYSA-N
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| InChi Code |
InChI=1S/C34H38N3O7P.C2H6O.ClH/c1-24-30(33(38)42-19-18-36(28-15-9-6-10-16-28)21-26-12-7-5-8-13-26)31(27-14-11-17-29(20-27)37(39)40)32(25(2)35-24)45(41)43-22-34(3,4)23-44-45;1-2-3;/h5-17,20,31,35H,18-19,21-23H2,1-4H3;3H,2H2,1H3;1H
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| Chemical Name |
2-(N-benzylanilino)ethyl 5-(5,5-dimethyl-2-oxo-1,3,2λ5-dioxaphosphinan-2-yl)-2,6-dimethyl-4-(3-nitrophenyl)-1,4-dihydropyridine-3-carboxylate;ethanol;hydrochloride
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| HS Tariff Code |
2934.99.9001
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| Storage |
Powder -20°C 3 years 4°C 2 years In solvent -80°C 6 months -20°C 1 month Note: Please store this product in a sealed and protected environment, avoid exposure to moisture. |
| Shipping Condition |
Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)
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| Solubility (In Vitro) |
DMSO : ~125 mg/mL (~175.03 mM)
H2O : < 0.1 mg/mL |
|---|---|
| Solubility (In Vivo) |
Solubility in Formulation 1: ≥ 2.5 mg/mL (3.50 mM) (saturation unknown) in 10% DMSO + 40% PEG300 +5% Tween-80 + 45% Saline (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear DMSO stock solution to 400 μL PEG300 and mix evenly; then add 50 μL Tween-80 + to the above solution and mix evenly; then add 450 μL normal saline to adjust the volume to 1 mL. Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH₂ O to obtain a clear solution. (Please use freshly prepared in vivo formulations for optimal results.) |
| Preparing Stock Solutions | 1 mg | 5 mg | 10 mg | |
| 1 mM | 1.4002 mL | 7.0010 mL | 14.0021 mL | |
| 5 mM | 0.2800 mL | 1.4002 mL | 2.8004 mL | |
| 10 mM | 0.1400 mL | 0.7001 mL | 1.4002 mL |
*Note: Please select an appropriate solvent for the preparation of stock solution based on your experiment needs. For most products, DMSO can be used for preparing stock solutions (e.g. 5 mM, 10 mM, or 20 mM concentration); some products with high aqueous solubility may be dissolved in water directly. Solubility information is available at the above Solubility Data section. Once the stock solution is prepared, aliquot it to routine usage volumes and store at -20°C or -80°C. Avoid repeated freeze and thaw cycles.
Calculation results
Working concentration： mg/mL；
Method for preparing DMSO stock solution： mg drug pre-dissolved in μL DMSO (stock solution concentration mg/mL). Please contact us first if the concentration exceeds the DMSO solubility of the batch of drug.
Method for preparing in vivo formulation:：Take μL DMSO stock solution, next add μL PEG300, mix and clarify, next addμL Tween 80, mix and clarify, next add μL ddH2O，mix and clarify.
(1) Please be sure that the solution is clear before the addition of next solvent. Dissolution methods like vortex, ultrasound or warming and heat may be used to aid dissolving.
(2) Be sure to add the solvent(s) in order.
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