Benzcyclane (Bencyclane)
(Synonyms: 苄环庚烷; Bencyclane; Benzcyclan) 目录号 : GC32506
苯环烷(Bencyclane) (Bencyclane; Benzcyclan) 是一种血小板聚集抑制剂和血管扩张剂，对多种外周循环障碍有效。
Cas No.:2179-37-5
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
Benzcyclane (Bencyclane; Benzcyclan) is a platelet aggregation inhibitor and a vasodilator effective in a variety of peripheral circulation disorders.
Benzcyclane, although capable of aggregating platelets by itself at very high concentrations, shows a striking inhibitory effect, over a wide range of concentrations, both on platelet aggregation induced by ADP, epinephrine or collagen and on platelet adhesiveness to glass or collagen. Clot retraction is also clearly inhibited[1]. Benzcyclane induces use-dependent inhibition of Na channels in muscle, similarly as do class 1 antiarrhytnmic drugs. Inhibition was observed with both normal and cevadine-modified Na channels[2].
[1]. Ponari O, et al. In vitro effects of bencyclan on coagulation, fibrinolysis and platelet function. Arzneimittelforschung. 1976;26(8):1532-8. [2]. Nánási PP, et al. Effects of bencyclane on normal and cevadine-modified Na channels in frog skeletal muscle. Gen Physiol Biophys. 1989 Oct;8(5):447-58.
| Cas No. | 2179-37-5 | SDF | |
| 别名 | 苄环庚烷; Bencyclane; Benzcyclan | ||
| Canonical SMILES | CN(C)CCCOC1(CC2=CC=CC=C2)CCCCCC1 | ||
| 分子式 | C19H31NO | 分子量 | 289.46 |
| 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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| Shipping Condition | 评估样品解决方案：配备蓝冰进行发货。所有其他可用尺寸：配备RT，或根据请求配备蓝冰。 | ||
| 制备储备液 | |||
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1 mg | 5 mg | 10 mg |
| 1 mM | 3.4547 mL | 17.2735 mL | 34.5471 mL |
| 5 mM | 0.6909 mL | 3.4547 mL | 6.9094 mL |
| 10 mM | 0.3455 mL | 1.7274 mL | 3.4547 mL |
| 第一步：请输入基本实验信息（考虑到实验过程中的损耗，建议多配一只动物的药量） | ||||||||||
| 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 |
| 第二步：请输入动物体内配方组成（配方适用于不溶于水的药物；不同批次药物配方比例不同，请联系GLPBIO为您提供正确的澄清溶液配方） | ||||||||||
| % DMSO % % Tween 80 % saline | ||||||||||
| 计算重置 | ||||||||||
计算结果:
工作液浓度： mg/ml；
DMSO母液配制方法： mg 药物溶于 μL DMSO溶液（母液浓度 mg/mL，
体内配方配制方法：取 μL DMSO母液，加入 μL PEG300，混匀澄清后加入μL Tween 80，混匀澄清后加入 μL saline，混匀澄清。
1. 首先保证母液是澄清的；
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。
3. 以上所有助溶剂都可在 GlpBio 网站选购。
Treatment for calcium channel blocker poisoning: a systematic review
Clin Toxicol (Phila) 2014 Nov;52(9):926-44.PMID:25283255DOI:10.3109/15563650.2014.965827.
Context: Calcium channel blocker poisoning is a common and sometimes life-threatening ingestion. Objective: To evaluate the reported effects of treatments for calcium channel blocker poisoning. The primary outcomes of interest were mortality and hemodynamic parameters. The secondary outcomes included length of stay in hospital, length of stay in intensive care unit, duration of vasopressor use, functional outcomes, and serum calcium channel blocker concentrations. Methods: Medline/Ovid, PubMed, EMBASE, Cochrane Library, TOXLINE, International pharmaceutical abstracts, Google Scholar, and the gray literature up to December 31, 2013 were searched without time restriction to identify all types of studies that examined effects of various treatments for calcium channel blocker poisoning for the outcomes of interest. The search strategy included the following Keywords: [calcium channel blockers OR calcium channel antagonist OR calcium channel blocking agent OR (amlodipine or Bencyclane or bepridil or cinnarizine or felodipine or fendiline or flunarizine or gallopamil or isradipine or lidoflazine or mibefradil or nicardipine or nifedipine or nimodipine or nisoldipine or nitrendipine or prenylamine or verapamil or diltiazem)] AND [overdose OR medication errors OR poisoning OR intoxication OR toxicity OR adverse effect]. Two reviewers independently selected studies and a group of reviewers abstracted all relevant data using a pilot-tested form. A second group analyzed the risk of bias and overall quality using the STROBE (STrengthening the Reporting of OBservational studies in Epidemiology) checklist and the Thomas tool for observational studies, the Institute of Health Economics tool for Quality of Case Series, the ARRIVE (Animal Research: Reporting In Vivo Experiments) guidelines, and the modified NRCNA (National Research Council for the National Academies) list for animal studies. Qualitative synthesis was used to summarize the evidence. Of 15,577 citations identified in the initial search, 216 were selected for analysis, including 117 case reports. The kappa on the quality analysis tools was greater than 0.80 for all study types. Results: The only observational study in humans examined high-dose insulin and extracorporeal life support. The risk of bias across studies was high for all interventions and moderate to high for extracorporeal life support. High-dose insulin. High-dose insulin (bolus of 1 unit/kg followed by an infusion of 0.5-2.0 units/kg/h) was associated with improved hemodynamic parameters and lower mortality, at the risks of hypoglycemia and hypokalemia (low quality of evidence). Extracorporeal life support. Extracorporeal life support was associated with improved survival in patients with severe shock or cardiac arrest at the cost of limb ischemia, thrombosis, and bleeding (low quality of evidence). Calcium, dopamine, and norepinephrine. These agents improved hemodynamic parameters and survival without documented severe side effects (very low quality of evidence). 4-Aminopyridine. Use of 4-aminopyridine was associated with improved hemodynamic parameters and survival in animal studies, at the risk of seizures. Lipid emulsion therapy. Lipid emulsion was associated with improved hemodynamic parameters and survival in animal models of intravenous verapamil poisoning, but not in models of oral verapamil poisoning. Other studies. Studies on decontamination, atropine, glucagon, pacemakers, levosimendan, and plasma exchange reported variable results, and the methodologies used limit their interpretation. No trial was documented in humans poisoned with calcium channel blockers for Bay K8644, CGP 28932, digoxin, cyclodextrin, liposomes, bicarbonate, carnitine, fructose 1,6-diphosphate, PK 11195, or triiodothyronine. Case reports were only found for charcoal hemoperfusion, dialysis, intra-aortic balloon pump, Impella device and methylene blue. Conclusions: The treatment for calcium channel blocker poisoning is supported by low-quality evidence drawn from a heterogeneous and heavily biased literature. High-dose insulin and extracorporeal life support were the interventions supported by the strongest evidence, although the evidence is of low quality.
Bencyclane as an anti-sickling agent
Br J Haematol 1996 Feb;92(2):329-31.PMID:8602994DOI:10.1046/j.1365-2141.1996.d01-1466.x.
A vasodilating Ca2+ channel blocker, Bencyclane, was used in 18 patients with homozygous sickle cell anaemia (SCD) to test the possible anti-sickling effect. With Bencyclane intervention the Na(+)-K+ ATPase activity increased from 256 +/- 29 to 331 +/- 37 nmol Pi/mg protein/h (P < 0.0001) and the Ca(2+)-Mg2+ ATPase level increased from 172 +/- 12 to 222 +/- 44 nmol Pi/mg protein/h (P < 0.0001). The intracytoplasmic Ca2+ concentration reduced from 3.5 +/- 0.6 to 2.7 +/- 0.25 mumol/l (P < 0.0001). The patient's blood contained fewer irreversibly sickled cells (ISCs) (a reduction from 21.4% to 14.4%) (P < 0.05). At the same time MCHC of the erythrocytes decreased from 34.5 to 33.0 g/dl (P < 0.05). Bencyclane appears to be a promising anti-sickling agent that can be used orally in SCD.
A contribution to the pharmacokinetics of Bencyclane (Fludilat) in man
Int J Clin Pharmacol Biopharm 1976 Jun;13(4):246-52.PMID:965131doi
The quantitative determination of Bencyclane from the biological material was carried out with the aid of a combined microchemical method (thin-layer chromatography and measurement of fluorescence) using NBD chloride. The original method [J. Reisch, Z. Analyt. Chemie, 247 (1969) 56; J. Monforte, Clinical Chemistry 18 (1972) 1329; R.S. Fager, Anal. Biochemistry, 53 (1973) 290, etc.] was so modified as to enable attainment of optimal results in respect of sensitivity and accuracy in the determination of Bencyclane. The sensitivity of this modified method is 0.1 mug/ml plasma. Volunteer subjects and patients received under standard conditions 2 coated tablets Fludilat (i.e. 200 mg Bencyclane hydrogen fumarate) orally as a single dose or repeated 3 times daily over 5 days, or 4 ampoules (= 200 mg) in a single intravenous injection. After a single oral administration, maximum plasma concentrations of approximately 2 mug/ml were attained in about 2 hours. The elimination half-life was about 360-480 min. The appearance of a second peak after about 6-7 hours indicates involvement of several compartments. On intravenous administration, maximum plasma concentrations of above 2 mug/ml were attained. A second peak in the late phase of the elimination was also detected here. The repeated oral administration led to maximum plasma concentrations of above 3 mug/ml without there being any indication of accumulation. Protein binding of about 30% was determined with the aid of the equilibrium dialysis method. A parallel "in vitro" study with 14C-bencyclane (U.R. Kleeberg, 1973, unpublished) showed an approx. 40% protein binding, an approx. 30% erythrocyte binding, and an approx. 10% thrombocyte binding. About 20% Bencyclane remain free.
Effects of Bencyclane on normal and cevadine-modified Na channels in frog skeletal muscle
Gen Physiol Biophys 1989 Oct;8(5):447-58.PMID:2556322doi
The effect of 10(-5) mol/l Bencyclane on the repetitive electrical activity of muscle membrane was studied with the conventional microelectrode technique. Electrical activity was induced by repetitive stimulation in normal Ringer solution (train) or by a single depolarizing current pulse in the presence of 10(-6) mol/l cevadine (volley). Bencyclane decreased, in a use-dependent manner, the maximum rates of depolarization and repolarization (Vmax+ and Vmax-, resp.) of the action potentials both of the train and the volley. The inhibition of Vmax+ and Vmax- was proportional; however, it was stronger for the volleys than for the trains. The cycle length (mean interspike interval) of the volley was increased by Bencyclane; the prolongation was progressive during consecutive cycles. The dissociation of Bencyclane from the Na channel was studied by applying trains of different durations with equal pulse numbers. Bencyclane at a higher concentration (5 x 10(-5) mol/l) caused a reversible tonic block: the overshoot potentials, Vmax+ and Vmax- were markedly reduced. The reduction of Vmax- was slightly stronger than that of Vmax+. Slow membrane potential oscillation (SMPO) was evoked by treating the muscle with 10(-4) mol/l of cevadine. The administration of 5 x 10(-6) mol/l Bencyclane decreased the frequency of SMPO, while 10(-5) mol/l Bencyclane terminated the slow oscillation activity without changing its baseline potential. The present results indicate that Bencyclane induces use-dependent inhibition of Na channels in muscle, similarly as do class 1 antiarrhytnmic drugs. Inhibition was observed with both normal and cevadine-modified Na channels.
Effect of Bencyclane fumarate on intestinal ischaemia reperfusion injury
ANZ J Surg 2008 Jun;78(6):476-81.PMID:18522569DOI:10.1111/j.1445-2197.2008.04358.x.
Background: Post-ischaemic intestinal tissue damage appears to be due to the formation of oxygen radicals. Free radical-initiated lipid peroxidation following intestinal ischaemia/reperfusion (I/R) may disrupt mucosal integrity. Indirectly, the radicals trigger the accumulation of neutrophils within the affected tissue, initiating inflammatory processes that lead to severe mucosal lesions. We have investigated the protective effect of Bencyclane fumarate, a vasodilating Ca(2+) channel blocker, which has been used for the treatment of peripheral arterial occlusive diseases, on intestinal ischaemia reperfusion (IR) injury in rats. Methods: Forty-eight Wistar albino rats were divided into three groups: a sham-operated group (no IR injury, n = 16), an ischaemic control group (IR, n = 16), and BF-treated group (pretreatment 5 mg/kg Bencyclane fumarate + IR, n = 16). A marker for lipid peroxidation, namely malondialdehyde; free radical scavengers, glutathione peroxidase, catalase and superoxide dismutase levels; an index of polymorphonuclear neutrophils, myeloperoxidase activity and mucosal damage were investigated. Results: Malondialdehyde levels, myeloperoxidase activity and the severity of mucosal damage were decreased in the BF group. In addition, in the BF group, glutathione peroxidase, catalase and superoxide dismutase levels were higher compared with the IR group. Conclusion: The pretreatment of rats with Bencyclane fumarate before intestinal ischaemia attenuates the mucosal damage in intestinal IR injury, probably by altering lipid peroxidation, neutrophil accumulation and antioxidant activity.