Detail of "66085-59-4"

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CAS Number:
66085-59-4
Name:
Nimodipine
Molecular Structure:
Formula:
C₂₁H₂₆N₂O₇
Molecular Weight:
418.45
Synonyms:
3,5-Pyridinedicarboxylicacid, 1,4-dihydro-2,6-dimethyl-4-(3-nitrophenyl)-, 2-methoxyethyl 1-methylethylester (9CI);Admon;3,5-Pyridinedicarboxylicacid, 1,4-dihydro-2,6-dimethyl-4-(3-nitrophenyl)-, 3-(2-methoxyethyl)5-(1-methylethyl) ester;Nimodipine AP;Nimotop;Periplum;
EINECS:
266-127-0
Density:
1.212 g/cm³
Melting Point:
125 °C
Boiling Point:
534.8 °C at 760 mmHg
Flash Point:
277.3 °C
Solubility:
methanol: 62.5 mg/mL
Appearance:
Crystalline solid
Hazard Symbols:
Xn
Risk Codes:
20/21/22
Safety:
36 Details

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Reference

Inhibition by dihydropyridine class calcium channel blockers of tumor cell-platelet-endothelial cell interactions in vitro and metastasis in vivo: Inhibition by dihydropyridine class calcium channel blockers of tumor cell-platelet-endothelial cell interactions in vitro and metastasis in vivo. Honn, Kenneth V.; Onoda, James M.; Pampalona, Kim; Battaglia, Marjorie; Neagos, Gregory; Taylor, John D.; Diglio, Clement A.; Sloane, Bonnie F. (Dep. Radiat. Oncol., Wayne State Univ., Detroit, MI 48202, USA). Biochem. Pharmacol., 34(2), 235-41 (English) 1985. CODEN: BCPCA6. ISSN: 0006-2952. DOCUMENT TYPE: Journal CA Section: 1 (Pharmacology) Three Ca channel blockers of the dihydropyridine class were tested in vitro for their effects on tumor cell-platelet-endothelial cell interactions and in vivo for antimetastatic properties. Felodipine [72509-76-3], nimodipine [66085-59-4] and nifedipine [21829-25-4] inhibited tumor cell-induced platelet aggregation in vitro in a dose-dependent manner. These compds. also inhibited platelet-enhanced tumor cell adhesion to endothelial cells in vitro. Lung colony formation ("exptl." metastasis) and spontaneous pulmonary metastasis were inhibited by felodipine, nimodipine and nifedipine. Thus, Ca channel blockers may represent a new generic class of antimetastatic agents.

Effects of dihydropyridine calcium channel blocking drugs on rat brain muscarinic and a-adrenergic receptors: Effects of dihydropyridine calcium channel blocking drugs on rat brain muscarinic and a-adrenergic receptors. Thayer, Stanley A.; Welcome, Michael; Chhabra, Ajinder; Fairhurst, Alan S. (Coll. Med., Univ. California, Irvine, CA 92717, USA). Biochem. Pharmacol., 34(2), 175-80 (English) 1985. CODEN: BCPCA6. ISSN: 0006-2952. DOCUMENT TYPE: Journal CA Section: 1 (Pharmacology) The dihydropyridine (DHP) Ca2+ channel blocking drugs nicardipine, nitrendipine [39562-70-4], nimodipine [66085-59-4], felodipine [72509-76-3], nifedipine [21829-25-4] and nisoldipine [63675-72-9] were examd. for activity in inhibiting specific (-)-[3H]quinuclidinyl benzilate (QNB) and [3H]WB4101 binding to the muscarinic and a-adrenergic receptors, resp., of rat brain. Muscarinic receptor binding was affected most by nicardipine, with felodipine having less activity; the other DHP were essentially inactive at 3 ′ 10-5 M. The (+)-stereoisomer of nicardipine [76093-35-1] (K1 = 4.07 ′ 10-7M) was 27 times more potent than the (-)-isoimer [76093-36-2] in inhibiting [3H]QNB binding, and this inhibition was competitive. This inhibitory effect of nicardipine was not mediated via interaction with the high-affinity DHP binding site assumed to be assocd. with a Ca2+ channel. (+)-Nicardipine inhibited the binding of [3H]nitrendipine to this DHP binding site of brain, with a K1 of 9.01 ′ 10-11 M, and was 10 times more potent than the (-)-isomer. Thus, the muscarinic receptor was 4200 times less sensitive to (+)-nicardipine than was this DHP binding site. Nicardipine was also the most potent DHP drug inhibiting [3H]WB4104 binding to the a-adrenergic receptor, although the other drugs were also somewhat active, in the rank order sequence listed above. This effect of nicardipine on the adrenergic receptor was also stereoselective, with (+)-nicardipine (K1 = 3.46 ′ 10-7 M) being about 3 times more potent than the (-)-isomer, in producing competitive inhibition of radioligand binding. Apparently, the effects on brain receptors occur as a result of direct, stereospecific effects of DHP drugs on these receptors and are not due to Ca2+ channel blocking activity of these drugs. Structure-activity relations are briefly discussed.

Detail of "66085-59-4"

Nimodipine

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