SM-6586
目录号 : GC32552
SM-6586是一种calciumchannel的拮抗剂，同时能够抑制Na+/H+和Na+/Ca2+exchangetransport，主要用于研究脑血管疾病和高血压等疾病。
Cas No.:103898-38-0
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
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- Purity: >98.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
SM-6586 is a calcium channel antagonist and inhibitor of Na+/H+ and Na+/Ca2+ exchange transport, potentially for the treatment of cerebrovasular diseases and hypertension.
In SM-6586-treated spontaneously hypertensive rats, the survival rate after bilateral common carotid artery ligation is higher, the brain water content is lower, and the ATP level is higher and lactate level. In focal ischemia models, the SM-treated group shows a reduction of T1 relaxation time. The brain water content is significantly decreased in the SM-treated group[1].
[1]. Kashiwagi F, et al. Effect of a new calcium antagonist (SM-6586) on experimental cerebral ischemia. Acta Neurochir Suppl (Wien). 1994;60:289-92.
| Cas No. | 103898-38-0 | SDF | |
| Canonical SMILES | O=C(C1=C(C)NC(C)=C(C2=NC(CN(C)CC3=CC=CC=C3)=NO2)C1C4=CC=CC([N+]([O-])=O)=C4)OC | ||
| 分子式 | C26H27N5O5 | 分子量 | 489.52 |
| 溶解度 | Soluble in DMSO | 储存条件 | Store at -20°C |
| General tips | 请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液；一旦配成溶液，请分装保存，避免反复冻融造成的产品失效。 储备液的保存方式和期限：-80°C 储存时，请在 6 个月内使用，-20°C 储存时，请在 1 个月内使用。 为了提高溶解度，请将管子加热至37℃，然后在超声波浴中震荡一段时间。 |
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1 mg | 5 mg | 10 mg |
| 1 mM | 2.0428 mL | 10.2141 mL | 20.4282 mL |
| 5 mM | 0.4086 mL | 2.0428 mL | 4.0856 mL |
| 10 mM | 0.2043 mL | 1.0214 mL | 2.0428 mL |
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动物平均体重 | g | |
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2.
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Effect of a new calcium antagonist (SM-6586) on experimental cerebral ischemia
Acta Neurochir Suppl (Wien) 1994;60:289-92.PMID:7976569DOI:10.1007/978-3-7091-9334-1_77.
SM-6586 (SM) is a new derivative of dihydropyridine with potent calcium blocking activity and inhibitory activity of the Na+/H+ and Na+/Ca++ exchange transport. The effect of SM on survival rate, brain edema and metabolites was evaluated using two different models in spontaneously hypertensive rat (SHR). Global ischemia was induced by bilateral common carotid artery ligation (BLCL) and focal ischemia was induced by middle cerebral artery occlusion. The survival rate after BLCL was higher in the SM-treated group. The brain water content was lower, the ATP level was higher and lactate level was lower in the SM-treated group compared to the control group. In focal ischemia models, the SM-treated group showed a reduction of T1 relaxation time. The brain water content was significantly decreased in the SM-treated group. These results indicate that SM was effective in ameliorating the ischemic insult in global and focal cerebral ischemia models.
Calcium channel blocking properties of SM-6586 in rat heart and brain as assessed by radioligand binding assay
Jpn J Pharmacol 1993 Oct;63(2):165-9.PMID:8283826DOI:10.1254/jjp.63.165.
The interaction of SM-6586 (methyl 1,4-dihydro-2,6-dimethyl-3-[3-(N-benzyl-N-methyl-aminomethyl)-1,2,4- oxadiazolyl-5-yl]-4-(3-nitrophenyl)pyridine-5-carboxylate) with the specific binding of 3H-PN200-110 to rat heart and brain membranes was characterized and compared with those of other Ca2+ antagonists. The blockade of 3H-PN200-110 binding sites induced by nifedipine, nitrendipine and nimodipine was reversed by washing, whereas the blockade by SM-6586 was not readily reversed under these conditions. No significant difference was found in irreversibility between SM-6586 enantiomers. When rat aortic strips were pretreated with SM-6586, the contractions induced by 50 mM KCl were inhibits even though SM-6586 was not present in the extracellular medium. This residual inhibitory effect was much stronger than that of nicardipine. The inhibition of KCl-induced contractions by nifedipine and nitrendipine was easily reversed by washing. Thus, we suggest that (+)SM-6586 is a novel 1,4-dihydropyridine derivative having a very slow rate of dissociation from the binding site. This property may explain its long-lasting antihypertensive effect.
Assessment of Ca(2+)-antagonistic effect of SM-6586 and its isomers, novel 1,4-dihydropyridine derivatives, by radioligand binding assay
Jpn J Pharmacol 1992 Jan;58(1):75-8.PMID:1640663DOI:10.1254/jjp.58.75.
The Ca(2+)-antagonistic effects of the 1,4-dihydropyridine derivative (+/-)SM-6586 and its optical isomers were compared with those of its two derivatives ((+/-)SM-7297 and (+/-)SM-7548) and other Ca(2+)-antagonists using a radioligand binding assay. The Ca(2+)-antagonistic effects of the optical isomers of SM-6586 were in the order of (+) greater than (+/-) greater than (-)SM-6586 in both rat brain and heart. The pKi value of (+)SM-6586 was comparable to those of nimodipine, nicardipine, nifedipine and nitrendipine. The pA2 value for (+)SM-6586 was the highest among the SM-6586 isomers, thus suggesting that (+)SM-6586 has a potent Ca(2+)-antagonistic effect.
Residual inhibition in density of [3H]isradipine binding sites in rat brain membrane pretreated with amlodipine
Zhongguo Yao Li Xue Bao 1995 Jul;16(4):289-93.PMID:7668092doi
Aim: To test changes in the density of [3H] isradipine binding sites in rat brain membrane pretreated with amlodipine and to compare with those of nifedipine and (+) SM-6586 (methyl 1, 4-dihydro-2, 6-dimethyl-3-(3-(N-benzyl-N-methylaminomethyl)-1,2,4- oxadiazolyl-5-yl)-4-(3-nitrophenyl) pyridine-5-carboxylate). Methods: The membrane-enriched fractions were prepared from rat brain. The brain membranes were preincubated with nifedipine (10 nmol L-1), amlodipine (1 mumol L-1) and SM-6586 (1 nmol L-1) or with no antagonists added for 45 min, and washing and centrifugation were performed 3 times. They were assayed with [3H]isradipine in incubation media. The Kd and Bmax values of the membrane fractions pretreated with the drugs were determined by Scatchard analysis. Results: The blockage of the [3H]isradipine binding sites induced by nifedipine was reversed by washing, enabling the low values of the specific binding sites to be observed. The blockages by amlodipine and SM-6586, on the other hand, were not readily reversed. No significant difference was found, however, between in the Kd walues of these drugs. Conclusion: Amlodipine and SM-6586 are Ca2+ antagonists which dissociate slowly from the Ca2+ channel in membranes.
Slow association of positively charged Ca2+ channel antagonist amlodipine to dihydropyridine receptor sites in rat brain membranes
Gen Pharmacol 1996 Jan;27(1):137-40.PMID:8742511DOI:10.1016/0306-3623(95)00085-2.
1. No significant differences were observed in Kd and Bmax values between pH 7.2 (0.16 +/- 0.01 nM and 155.36 +/- 16.07 fmol/mg protein) and pH 10.0 (0.15 +/- 0.01 nM and 158.63 +/- 13.80 fmol/mg protein) in rat brain membranes. 2. The IC50 ratios at 0- and 270-min preincubations of amlodipine and manidipine at pH 7.2 were 23.09 and 10.25, respectively, whereas these ratios for these two drugs at pH 10.0 were 2.63 and 1.34, respectively. 3. In contrast, on treatment with nisoldipine, benidipine, SM-6586 and nifedipine, no significant differences were observed in the IC50 ratios between 0- and 270-min preincubations at pH 7.2 and 10.0.