Bunaftide (Bunaftine)
(Synonyms: 丁萘夫汀; Bunaftine; Bunaphtide; Meregon) 目录号 : GC32661
布那非肽（Bunaftine）（Bunaftine；Bunaphtide；Meregon）是一种抗心律失常药。
Cas No.:32421-46-8
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
- View current batch:
- Purity: >98.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
Cell experiment: | Human embryonic fibroblasts and HeLa cells are seeded into 35-mm plastic Petri dishes at a density of 1x105 cells/cm2. Bunaftide is used in final concentrations of 0.1-2.0 mM. The cells are exposed to the drug for periods ranging from 15 min to 24 h. To allow the cells to recover, the Bunaftide medium is removed and the cultures are left in standard medium for 4-24 h[1]. |
References: [1]. Moskalewski S, et al. Effects of bunaftine on morphology, microfilament integrity, and mitotic activity in cultured human fibroblasts and HeLa cells. Cell Tissue Res. 1984;236(1):107-15. | |
Bunaftide (Bunaftine; Bunaphtide; Meregon) is an antiarrhythmic agent.
At concentrations of 0.5-2.0 mM, Bunaftide causes contraction and rounding of the cells with loss of microvilli-like processes. Aggregates of dense, partly granular, partly fibrillar material form in the cytoplasm and the rough endoplasmic reticulum became vesiculated. Bundles of actin filaments are disrupted, forming rings, coils, and granules. 0.4 mM Bunaftide increases and 0.8-1.0 mM markedly decreases the percentage of mitotic cells, without accumulation of cells in any particular stage of mitosis. The drug may arrest the cell cycle at some point before mitosis; it may have a critical concentration above which the arrest becomes permanent[1]. Bunaftide at 1, 5 and 10 mg/L produces a concentration-dependent depression of the maximum rate of rise of the action potential in guinea pig papillary muscle preparations without affecting the resting membrane potential and the action potential amplitude. The action potential duration (APD50, APD90) is significantly prolonged by the treatment with 1 and 5 mg/L Bunaftide, while it is not changed by the treatment with 10 mg/L[2].
[1]. Moskalewski S, et al. Effects of bunaftine on morphology, microfilament integrity, and mitotic activity in cultured human fibroblasts and HeLa cells. Cell Tissue Res. 1984;236(1):107-15. [2]. Kimura T, et al. Electrophysiological effects of bunaftine, an antiarrhythmic drug, on action potential characteristics in ventricular muscle preparations. Nihon Yakurigaku Zasshi. 1986 Jul;88(1):1-7.
| Cas No. | 32421-46-8 | SDF | |
| 别名 | 丁萘夫汀; Bunaftine; Bunaphtide; Meregon | ||
| Canonical SMILES | O=C(C1=C2C=CC=CC2=CC=C1)N(CCCC)CCN(CC)CC | ||
| 分子式 | C21H30N2O | 分子量 | 326.48 |
| 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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| 制备储备液 | |||
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1 mg | 5 mg | 10 mg |
| 1 mM | 3.063 mL | 15.3149 mL | 30.6297 mL |
| 5 mM | 0.6126 mL | 3.063 mL | 6.1259 mL |
| 10 mM | 0.3063 mL | 1.5315 mL | 3.063 mL |
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| 给药剂量 | mg/kg |  |
动物平均体重 | g | |
每只动物给药体积 | ul | |
动物数量 | 只 |
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| % DMSO % % Tween 80 % saline | ||||||||||
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DMSO母液配制方法： mg 药物溶于 μL DMSO溶液（母液浓度 mg/mL，
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2.
一定要按照顺序依次将溶剂加入，进行下一步操作之前必须保证上一步操作得到的是澄清的溶液，可采用涡旋、超声或水浴加热等物理方法助溶。
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Effects of Bunaftine on morphology, microfilament integrity, and mitotic activity in cultured human fibroblasts and HeLa cells
Cell Tissue Res 1984;236(1):107-15.PMID:6201280DOI:10.1007/BF00216519.
Human fibroblasts and HeLa cells were treated with Bunaftine (N-butyl-N-/2-(diethylamino)ethyl/-1-naphthalenecarboxamide ) in vitro. At concentrations of 0.5-2.0 mM, the drug caused contraction and rounding of the cells with loss of microvilli-like processes. Aggregates of dense, partly granular, partly fibrillar material formed in the cytoplasm and the rough endoplasmic reticulum became vesiculated. Immunofluorescence microscopy with DNase I and anti-DNase I demonstrated that bundles of actin filaments were disrupted, forming rings, coils, and granules. Filaments stained with antibodies to vimentin (fibroblasts) and prekeratin (HeLa cells) showed less characteristic rearrangements, probably related to the rounding up of the cells. 0.4 mM Bunaftine increased and 0.8-1.0 mM markedly decreased the percentage of mitotic cells, without accumulation of cells in any particular stage of mitosis. The drug may arrest the cell cycle at some point before mitosis; it may have a critical concentration above which the arrest becomes permanent. These results suggest that Bunaftine interferes with the integrity of microfilament bundles in a different manner from that of cytochalasins. It does not cause any depletion of cellular ATP, indicating that its effect is not a result of inhibition of cell metabolism. It is proposed that Bunaftine may be used a complement to cytochalasins in studies of the microfilament system of the cell. The possible binding of Bunaftine to actin or myosin and further details of its mechanism of action remain to be elucidated.
[Electrophysiological effects of Bunaftine, an antiarrhythmic drug, on action potential characteristics in ventricular muscle preparations]
Nihon Yakurigaku Zasshi 1986 Jul;88(1):1-7.PMID:3093338DOI:10.1254/fpj.88.1.
The electrophysiological effects of Bunaftine were studied using the glass microelectrode technique. Bunaftine at 1, 5 and 10 mg/l produced a concentration-dependent depression of the maximum rate of rise of the action potential in guinea pig papillary muscle preparations without affecting the resting membrane potential and the action potential amplitude. The action potential duration (APD50, APD90) was significantly prolonged by the treatment with 1 and 5 mg/l Bunaftine, while it was not changed by the treatment with 10 mg/l. The absolute refractory period (ARP) was also prolonged dose-dependently by the treatment of Bunaftine; It was excessively prolonged (177% of control) at the concentration of 10 mg/l. Disopyramide produced similar electrophysiological changes to those of Bunaftine except for the prolongation of ARP. ARP/APD90 ratio was significantly increased by Bunaftine, but not by disopyramide. These electrophysiological effects of Bunaftine and disopyramide observed in guinea pig ventricular preparations were similarly found in canine ventricular muscle preparations. These results indicate that the electrophysiological characteristics of Bunaftine are similar to those of disopyramide in that the most prominent effect was the prolongation of ARP.
[Effect of Bunaftine on the aconitine-induced atrial arrhythmias in the dog]
Arch Sci Med (Torino) 1976 Oct-Dec;133(4):371-80.PMID:1023843doi
Bunaftine has a quinidine-like vagolytic effect and does not act as a beta-blocking agent. Its effect on aconitine-induced atrial fibrillation in the dog was examined. It led to suproventricular tachycardia in all cases, but re-established the sinus rhythm in only 5/15. It is felt that this lack of success is attributable to the slowing of the frequency of the primary pacemaker on the part of the drug. Slowing down of atrioventricular and intraventricular conduction by Bunaftine was revealed by lengthening of the P-R interval and widening of the Q-RS complex. Decreased blood pressure following administration of the drug appears to be due to reduction of heart rate rather than altered myocardial inotropism or peripheral resistance.
[Effect of Bunaftine on the ventricular tachycardia due to aconitine in the dog]
Arch Sci Med (Torino) 1976 Oct-Dec;133(4):363-70.PMID:1023842doi
Suppression of aconitine-induced ventricular tachycardia in the dog with various doses of Bunaftine was attempted. Stable re-establishment of the sinus rhythm was achieved in only 3/15 cases, whereas in 3 tachicardia was unchanged, and in 9 fibrillation appeared, due, it is thought, to the effect of the drug on myocardial conductivity, since fibrillation was the most frequent outcome when high doses were used.
Metabolic effects of Bunaftine, a new antiarrhythmic agent: comparison with quinidine, ajmaline, procainamide, xylocaine and propranolol
Arzneimittelforschung 1976 Feb;26(2):241-4.PMID:947206doi
The effects of Bunaftine (Meregon), quinidine, ajmaline, procainamide, xylocaine and propranolol have been investigated on glycolysis and oxygen consumption of rabbit heart and on the metabolic rate of trained rats. Quinidine, Bunaftine and ajmaline stimulated glycolysis, procainamide was inactive while xylocaine and propranolol inhibited it. Myocardial oxygen consumption was reduced by quinidine and Bunaftine only at high concentrations. However quinidine at 1-10(5) g/ml showed stimulating effect. Ajmaline and procainamide were inactive; xylocaine had a weak stimulating effect at 1-10(-6), propranolol had a stimulating effect at 3-10(-5) and 1-10(6) while it had an inhibiting effect at 1-10(-4) and 5-10(-3). With the exception of xylocaine and propranolol, which inhibited metabolic rate of trained animals, all the other drugs were inactive. In view of these findings, the mechanism of action of anti-arrhythmic drugs is discussed and it is suggested that the metabolic changes they induce are to be considered as secondary or toxic effects, the main site of action being the myocardial cell membrane.