product name Cilnidipine
Description: Cilnidipine (also known as FRC-8653) is a unique dual L-type and N-type calcium channel blocker used for high blood pressure treatment. Cilnidipine lowers mean blood pressure and reduces the size of cerebral infarction in the rat model of focal brain ischemia. Cilnidipine has displayed renal and vascular protective effects and improved baroreflex sensitivity in patients with hypertension. It has also demonstrated neuroprotective effects in a rat focal brain ischemia model by removing free radicals and activating the phosphatidylinositol 3-kinase pathway.
References: Hypertens Res. 2003 Sep;26(9):743-7; J Hypertens. 2010 May;28(5):1034-43.
492.52
Formula
C27H28N2O7
CAS No.
132203-70-4
Storage
-20℃ for 3 years in powder form
-80℃ for 2 years in solvent
Solubility (In vitro)
DMSO: 99 mg/mL (201.0 mM)
Water: <1 mg/mL
Ethanol: 15 mg/mL (30.5 mM)
Solubility (In vivo)
5% DMSO+Corn oil: 7 mg/mL
Synonyms
FRC-8653
other peoduct :References PubMed ID：:http://www.ncbi.nlm.nih.gov/pubmed/19403473
| In Vitro |
In vitro activity: Cilnidipine (10 mM) suppresses the elevation of the ratio induced by 40 mM KCl, and this suppression is effectively inhibited after the treatment with omega-conotoxin GVIA. Kinase Assay: Cell Assay: |
|---|---|
| In Vivo | Cilnidipine reduces Ca(2+) influx via N-type Ca(2+) channels after NMDA receptors activation and then protects neurons against ischemia-reperfusion injury in the rat retina in vivo. Cilnidipine significantly prevents the increase in desmin staining and restores the glomerular podocin and nephrin expression compared with amlodipine in spontaneously hypertensive rat/ND mcr-cp (SHR/ND). Cilnidipine also prevents the increase in renal angiotensin II content, the expression and membrane translocation of NADPH oxidase subunits and dihydroethidium staining in SHR/ND. Cilnidipine (30 mg/kg/d as food admix) treatment suppresses the increase in systolic blood pressure in Dahl salt-sensitive rats. Cilnidipine inhibits the increase in blood urea nitrogen and decrease in creatinine clearance as well as progression of glomerular sclerosis. Cilnidipine reduces plasma norepinephrine level and plasma rennin activity compared with vehicle-treated Dahl S rats. Cilnidipine suppresses the pressor response induced by sympathetic nerve stimulation and angiotensin II in pithed rats. Cilnidipine or omega-conotoxin MVIIA decreases mean blood pressure, but slightly increases heart rate in anesthetized rats. Cilnidipine can affect sympathetic N-type Ca(2+) channels in addition to vascular L-type Ca(2+) channels in antihypertensive doses in the rat in vivo. |
| Animal model | |
| Formulation & Dosage | |
| References | Hypertens Res. 2003 Sep;26(9):743-7; J Hypertens. 2010 May;28(5):1034-43. |
Related Posts
product name Cilnidipine
Description: Cilnidipine (also known as FRC-8653) is a unique dual L-type and N-type calcium channel blocker used for high blood pressure treatment. Cilnidipine lowers mean blood pressure and reduces the size of cerebral infarction in the rat model of focal brain ischemia. Cilnidipine has displayed renal and vascular protective effects and improved baroreflex sensitivity in patients with hypertension. It has also demonstrated neuroprotective effects in a rat focal brain ischemia model by removing free radicals and activating the phosphatidylinositol 3-kinase pathway.
References: Hypertens Res. 2003 Sep;26(9):743-7; J Hypertens. 2010 May;28(5):1034-43.
492.52
Formula
C27H28N2O7
CAS No.
132203-70-4
Storage
-20℃ for 3 years in powder form
-80℃ for 2 years in solvent
Solubility (In vitro)
DMSO: 99 mg/mL (201.0 mM)
Water: <1 mg/mL
Ethanol: 15 mg/mL (30.5 mM)
Solubility (In vivo)
5% DMSO+Corn oil: 7 mg/mL
Synonyms
FRC-8653
other peoduct :References PubMed ID：:http://www.ncbi.nlm.nih.gov/pubmed/19403473
| In Vitro |
In vitro activity: Cilnidipine (10 mM) suppresses the elevation of the ratio induced by 40 mM KCl, and this suppression is effectively inhibited after the treatment with omega-conotoxin GVIA. Kinase Assay: Cell Assay: |
|---|---|
| In Vivo | Cilnidipine reduces Ca(2+) influx via N-type Ca(2+) channels after NMDA receptors activation and then protects neurons against ischemia-reperfusion injury in the rat retina in vivo. Cilnidipine significantly prevents the increase in desmin staining and restores the glomerular podocin and nephrin expression compared with amlodipine in spontaneously hypertensive rat/ND mcr-cp (SHR/ND). Cilnidipine also prevents the increase in renal angiotensin II content, the expression and membrane translocation of NADPH oxidase subunits and dihydroethidium staining in SHR/ND. Cilnidipine (30 mg/kg/d as food admix) treatment suppresses the increase in systolic blood pressure in Dahl salt-sensitive rats. Cilnidipine inhibits the increase in blood urea nitrogen and decrease in creatinine clearance as well as progression of glomerular sclerosis. Cilnidipine reduces plasma norepinephrine level and plasma rennin activity compared with vehicle-treated Dahl S rats. Cilnidipine suppresses the pressor response induced by sympathetic nerve stimulation and angiotensin II in pithed rats. Cilnidipine or omega-conotoxin MVIIA decreases mean blood pressure, but slightly increases heart rate in anesthetized rats. Cilnidipine can affect sympathetic N-type Ca(2+) channels in addition to vascular L-type Ca(2+) channels in antihypertensive doses in the rat in vivo. |
| Animal model | |
| Formulation & Dosage | |
| References | Hypertens Res. 2003 Sep;26(9):743-7; J Hypertens. 2010 May;28(5):1034-43. |