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product name Nilvadipine


Description: Nilvadipine (also known as ARC029, FR34235) is a potent calcium channel blocker with an IC50 of 0.03 NM. Nilvadipine strongly inhibits the chemotaxis of interleukin-1 (IL-1), leukotriene B4 (LTB4), platelet-derived growth factor (PDGF) with IC50 of 0.1 nM in rat aortic smooth muscle cells (SMC). Nilvadipine is reported to increase renal blood flow and reduce filtration fraction in the isolated perfused hydronephrotic kidney, suggesting indirectly afferent and efferent arteriolar vasodilation.

References: Atherosclerosis. 1988 Aug;72(2-3):213-9; Invest Ophthalmol Vis Sci. 2002 Apr;43(4):919-26.



Molecular Weight (MW)

385.37 
Formula

C19H19N3O6 
CAS No.

75530-68-6 
Storage

-20℃ for 3 years in powder form
-80℃ for 2 years in solvent
Solubility (In vitro)

DMSO: 77 mg/mL (199.8 mM) 
Water: <1 mg/mL
Ethanol: 33 mg/mL (85.6 mM) 
Solubility (In vivo)

 
Synonyms

ARC029, FR34235 

other peoduct :References PubMed ID::http://www.ncbi.nlm.nih.gov/pubmed/19403902

In Vitro

In vitro activity: Nilvadipine strongly inhibits the chemotaxis of interleukin-1 (IL-1), leukotriene B4 (LTB4), platelet-derived growth factor (PDGF) with IC50 of 0.1 nM in rat aortic smooth muscle cells (SMC). Nilvadipine is reported to increase renal blood flow and reduce filtration fraction in the isolated perfused hydronephrotic kidney, suggesting indirectly afferent and efferent arteriolar vasodilation.


Kinase Assay:


Cell Assay

In Vivo Nilvadipine preserves retinal morphology and electroretinogram responses in RCS rats during the initial stage of retinal degeneration. Nilvadipine significantly enhances rhodopsin kinase and alphaA-crystallin expression and suppression of caspase 1 and 2 expression in the retina of RCS rats. Nilvadipine completely inhibits the vasoactivity elicited by Abeta in rat aortae and in human middle cerebral arteries. Nilvadipine restores cortical perfusion levels in Tg APPsw to values similar to those observed in control littermates without notably affecting the CBF of control mice. Nilvadipine suppresses ischemia (20 min)-reflow (20 min)-induced paw edema of mice (ED30:0.4 mg/kg i.v. and 2 mg/kg p.o.). Nilvadipine suppresses carrageenan-induced paw edema (ED30:15 mg/kg in rats and 20 mg/kg in mice) at a potency corresponding to that of an anti-inflammatory drug, ibuprofen. Nifedipine, nicardipine and nimodipine results in a suppression of 30% only with 100 mg/kg oral dosing in rats. Nilvadipine inhibits superoxide radical (O-2production from xanthine oxidase (XOD) both with lactate dehydrogenase + NADH method and cytochrome c method (IC50:90 and 100 mg/mL, respectively).  
Animal model  
Formulation & Dosage  
References Atherosclerosis. 1988 Aug;72(2-3):213-9; Invest Ophthalmol Vis Sci. 2002 Apr;43(4):919-26. 

Succinyl phosphonate

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Author: Sodium channel

Share this post on:

product name Nilvadipine


Description: Nilvadipine (also known as ARC029, FR34235) is a potent calcium channel blocker with an IC50 of 0.03 NM. Nilvadipine strongly inhibits the chemotaxis of interleukin-1 (IL-1), leukotriene B4 (LTB4), platelet-derived growth factor (PDGF) with IC50 of 0.1 nM in rat aortic smooth muscle cells (SMC). Nilvadipine is reported to increase renal blood flow and reduce filtration fraction in the isolated perfused hydronephrotic kidney, suggesting indirectly afferent and efferent arteriolar vasodilation.

References: Atherosclerosis. 1988 Aug;72(2-3):213-9; Invest Ophthalmol Vis Sci. 2002 Apr;43(4):919-26.



Molecular Weight (MW)

385.37 
Formula

C19H19N3O6 
CAS No.

75530-68-6 
Storage

-20℃ for 3 years in powder form
-80℃ for 2 years in solvent
Solubility (In vitro)

DMSO: 77 mg/mL (199.8 mM) 
Water: <1 mg/mL
Ethanol: 33 mg/mL (85.6 mM) 
Solubility (In vivo)

 
Synonyms

ARC029, FR34235 

other peoduct :References PubMed ID::http://www.ncbi.nlm.nih.gov/pubmed/19403902

In Vitro

In vitro activity: Nilvadipine strongly inhibits the chemotaxis of interleukin-1 (IL-1), leukotriene B4 (LTB4), platelet-derived growth factor (PDGF) with IC50 of 0.1 nM in rat aortic smooth muscle cells (SMC). Nilvadipine is reported to increase renal blood flow and reduce filtration fraction in the isolated perfused hydronephrotic kidney, suggesting indirectly afferent and efferent arteriolar vasodilation.


Kinase Assay:


Cell Assay

In Vivo Nilvadipine preserves retinal morphology and electroretinogram responses in RCS rats during the initial stage of retinal degeneration. Nilvadipine significantly enhances rhodopsin kinase and alphaA-crystallin expression and suppression of caspase 1 and 2 expression in the retina of RCS rats. Nilvadipine completely inhibits the vasoactivity elicited by Abeta in rat aortae and in human middle cerebral arteries. Nilvadipine restores cortical perfusion levels in Tg APPsw to values similar to those observed in control littermates without notably affecting the CBF of control mice. Nilvadipine suppresses ischemia (20 min)-reflow (20 min)-induced paw edema of mice (ED30:0.4 mg/kg i.v. and 2 mg/kg p.o.). Nilvadipine suppresses carrageenan-induced paw edema (ED30:15 mg/kg in rats and 20 mg/kg in mice) at a potency corresponding to that of an anti-inflammatory drug, ibuprofen. Nifedipine, nicardipine and nimodipine results in a suppression of 30% only with 100 mg/kg oral dosing in rats. Nilvadipine inhibits superoxide radical (O-2production from xanthine oxidase (XOD) both with lactate dehydrogenase + NADH method and cytochrome c method (IC50:90 and 100 mg/mL, respectively).  
Animal model  
Formulation & Dosage  
References Atherosclerosis. 1988 Aug;72(2-3):213-9; Invest Ophthalmol Vis Sci. 2002 Apr;43(4):919-26. 

Succinyl phosphonate

Share this post on:

Author: Sodium channel