Cilnidipine - CAS 132203-70-4
Catalog number:
132203-70-4
Category:
Inhibitor
Not Intended for Therapeutic Use. For research use only.
Molecular Formula:
C27H28N2O7
Molecular Weight:
492.52
COA:
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Targets:
Calcium Channel
Description:
Cilnidipine is a unique L-type and N-type calcium channel blocker, used for high blood pressure treatment.
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Purity:
>98%
Synonyms:
FRC-8653
MSDS:
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1.Long-term effects of L- and N-type calcium channel blocker on uric acid levels and left atrial volume in hypertensive patients.
Masaki M1,2,3, Mano T4, Eguchi A1,2,3, Fujiwara S1, Sugahara M1, Hirotani S1, Tsujino T5, Komamura K1,6, Koshiba M2,3, Masuyama T1. Heart Vessels. 2016 Jan 29. [Epub ahead of print]
Left ventricular (LV) diastolic dysfunction is associated with hypertension and hyperuricemia. However, it is not clear whether the L- and N-type calcium channel blocker will improve LV diastolic dysfunction through the reduction of uric acid. The aim of this study was to investigate the effects of anti-hypertensive therapy, the L- and N-type calcium channel blocker, cilnidipine or the L-type calcium channel blocker, amlodipine, on left atrial reverse remodeling and uric acid in hypertensive patients. We studied 62 patients with untreated hypertension, randomly assigned to cilnidipine or amlodipine for 48 weeks. LV diastolic function was assessed with the left atrial volume index (LAVI), mitral early diastolic wave (E), tissue Doppler early diastolic velocity (E') and the ratio (E/E'). Serum uric acid levels were measured before and after treatment. After treatment, systolic and diastolic blood pressures equally dropped in both groups. LAVI, E/E', heart rate and uric acid levels decreased at 48 weeks in the cilnidipine group but not in the amlodipine group.
2.Activation of Phosphatidylinositol-Linked Dopamine Receptors Induces a Facilitation of Glutamate-Mediated Synaptic Transmission in the Lateral Entorhinal Cortex.
Glovaci I1, Chapman CA1. PLoS One. 2015 Jul 2;10(7):e0131948. doi: 10.1371/journal.pone.0131948. eCollection 2015.
The lateral entorhinal cortex receives strong inputs from midbrain dopamine neurons that can modulate its sensory and mnemonic function. We have previously demonstrated that 1 µM dopamine facilitates synaptic transmission in layer II entorhinal cortex cells via activation of D1-like receptors, increased cAMP-PKA activity, and a resulting enhancement of AMPA-receptor mediated currents. The present study assessed the contribution of phosphatidylinositol (PI)-linked D1 receptors to the dopaminergic facilitation of transmission in layer II of the rat entorhinal cortex, and the involvement of phospholipase C activity and release of calcium from internal stores. Whole-cell patch-clamp recordings of glutamate-mediated evoked excitatory postsynaptic currents were obtained from pyramidal and fan cells. Activation of D1-like receptors using SKF38393, SKF83959, or 1 µM dopamine induced a reversible facilitation of EPSCs which was abolished by loading cells with either the phospholipase C inhibitor U-73122 or the Ca2+ chelator BAPTA.
3.Comparison of direct effects of clinically available vasodilators; nitroglycerin, nifedipine, cilnidipine and diltiazem, on human skeletonized internal mammary harvested with ultrasonic scalpel.
Fukuda S1, Nakamura Y2, Egi K3, Fujioka S1, Nagasaka S1, Minh PN4, Toguchi K1, Wada T2, Izumi-Nakaseko H2, Ando K2, Mizoue T4, Takazawa K3, Hosaka S1, Sugiyama A5. Heart Vessels. 2016 Jan 28. [Epub ahead of print]
Direct vasodilator effects of nitroglycerin, nifedipine, cilnidipine and diltiazem on human skeletonized internal mammary artery graft harvested with ultrasonic scalpel were assessed in the presence of 0.1 or 0.2 µM of noradrenaline. Ring preparations were made of distal end section of the bypass grafts, and those dilated by acetylcholine were used for assessment. Each drug dilated the artery in a concentration-related manner (0.01-10 µM, n = 6 for each drug) with a potency of nitroglycerin > nifedipine = cilnidipine > diltiazem. These results indicate that nitroglycerin can be useful for treating internal mammary artery spasm, that clinical utility of diltiazem may not depend on its vasodilator effect on the bypass graft, and that cilnidipine as well as nifedipine will have anti-spastic action which is in the middle between those of nitroglycerine and diltiazem.
4.Development and Characterization of Solid Self-emulsifying Drug Delivery System of Cilnidipine.
Bakhle SS1, Avari JG. Chem Pharm Bull (Tokyo). 2015;63(6):408-17. doi: 10.1248/cpb.c14-00326.
The present investigations highlight the development of solid self-emulsifying drug delivery system (solid-SEDDS) for improved oral delivery of the poorly water-soluble drug; cilnidipine. Liquid SEDDS of the drug were formulated using Capryol 90 as the oil phase, Tween 80 as the surfactant, and Transcutol HP as the co-surfactant after screening various vehicles. The prepared systems were characterized for self-emulsification time, robustness to dilution, % transmittance, globule size, drug release, and thermodynamic stability. Ternary phase diagrams were plotted to identify the area of microemulsification. The optimized liquid SEDDS was transformed into a free-flowing powder using Neusilin US2 as the adsorbent. Solid self-emulsifying powder retained the self-emulsifying property of the liquid SEDDS. Differential scanning calorimetric, X-ray powder diffraction studies revealed the possibility of transformation of the crystalline form of the drug to the amorphous form in the SEDDS prepared with the carrier.
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CAS 132203-70-4 Cilnidipine

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