S-Bioallethrin
(Synonyms: 烯丙菊酯,D-Trans-Allethrin; Esbiol) 目录号 : GC63821
S-Bioallethrin 是一种拟除虫菊酯类杀虫剂。S-Bioallethrin 通过改变电压门控钠通道的导电和非导电状态之间转换的门控动力学来破坏神经功能。
Cas No.:28434-00-6
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
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- Purity: >99.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
S-Bioallethrin is a pyrethroid insecticide. S-Bioallethrin disrupts nerve function by modifying the gating kinetics of transitions between the conducting and nonconducting states of voltage-gated sodium channels[1].
[1]. McCavera SJ, et al. Differential state-dependent modification of inactivation-deficient Nav1.6 sodium channels by the pyrethroid insecticides S-bioallethrin, tefluthrin and deltamethrin. Neurotoxicology. 2012;33(3):384-390.
| Cas No. | 28434-00-6 | SDF | Download SDF |
| 别名 | 烯丙菊酯,D-Trans-Allethrin; Esbiol | ||
| 分子式 | C19H26O3 | 分子量 | 302.41 |
| 溶解度 | DMSO : 100 mg/mL (330.68 mM; Need ultrasonic) | 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 | 3.3068 mL | 16.5338 mL | 33.0677 mL |
| 5 mM | 0.6614 mL | 3.3068 mL | 6.6135 mL |
| 10 mM | 0.3307 mL | 1.6534 mL | 3.3068 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。
In vitro effects of the pyrethroid S-Bioallethrin on lymphocytes and basophils from atopic and nonatopic subjects
Allergy 1998 Nov;53(11):1052-9.PMID:9860237DOI:10.1111/j.1398-9995.1998.tb03814.x.
Synthetic pyrethroids are increasingly used as insecticides and marketed as having relatively low human toxicity. The aim of this study was to examine the in vitro effects of the synthetic pyrethroid S-Bioallethrin on human blood lymphocytes and basophils in atopic individuals and nonatopic control subjects. S-Bioallethrin caused inhibition of lymphocyte proliferation after a 72-h culture period in a concentration-dependent manner. The inhibition of the lymphocyte proliferation by S-Bioallethrin at the concentration 6.5 microM correlated well with the total serum IgE values (r = -0.89, P < 0.001). Samples from atopic subjects were more sensitive to this inhibition than those from nonatopic volunteers. The regulatory interleukin-4/interferon-gamma (JL-4/IFN-gamma) balance showed a significant difference between atopic and nonatopic subjects after a short-term culture period (24 h) in the presence of the same concentration range of S-Bioallethrin (P < 0.001). Additionally, IFN-gamma secretion was consistently lower in cells from the atopic donors. Furthermore, S-Bioallethrin induced histamine release from human basophils in a concentration-dependent manner. Although the effect was small compared to histamine liberators such as N-formyl-Met-Leu-Phe and anti-IgE, the response to S-Bioallethrin was significantly different in atopic donors from nonatopic (P = 0.0431). These findings are the first demonstration of the immunotoxicologic properties of the synthetic pyrethroid S-Bioallethrin by this combined in vitro approach with human lymphocytes and basophils. Further studies will investigate the responses of lymphocytes from patients who are sensitive to these agents.
Divergent actions of the pyrethroid insecticides S-Bioallethrin, tefluthrin, and deltamethrin on rat Na(v)1.6 sodium channels
Toxicol Appl Pharmacol 2010 Sep 15;247(3):229-37.PMID:20624410DOI:10.1016/j.taap.2010.07.001.
We expressed rat Na(v)1.6 sodium channels in combination with the rat beta(1) and beta(2) auxiliary subunits in Xenopus laevis oocytes and evaluated the effects of the pyrethroid insecticides S-Bioallethrin, deltamethrin, and tefluthrin on expressed sodium currents using the two-electrode voltage clamp technique. S-Bioallethrin, a type I structure, produced transient modification evident in the induction of rapidly decaying sodium tail currents, weak resting modification (5.7% modification at 100 microM), and no further enhancement of modification upon repetitive activation by high-frequency trains of depolarizing pulses. By contrast deltamethrin, a type II structure, produced sodium tail currents that were ~9-fold more persistent than those caused by S-Bioallethrin, barely detectable resting modification (2.5% modification at 100 microM), and 3.7-fold enhancement of modification upon repetitive activation. Tefluthrin, a type I structure with high mammalian toxicity, exhibited properties intermediate between S-Bioallethrin and deltamethrin: intermediate tail current decay kinetics, much greater resting modification (14.1% at 100 microM), and 2.8-fold enhancement of resting modification upon repetitive activation. Comparison of concentration-effect data showed that repetitive depolarization increased the potency of tefluthrin approximately 15-fold and that tefluthrin was approximately 10-fold more potent than deltamethrin as a use-dependent modifier of Na(v)1.6 sodium channels. Concentration-effect data from parallel experiments with the rat Na(v)1.2 sodium channel coexpressed with the rat beta(1) and beta(2) subunits in oocytes showed that the Na(v)1.6 isoform was at least 15-fold more sensitive to tefluthrin and deltamethrin than the Na(v)1.2 isoform. These results implicate sodium channels containing the Na(v)1.6 isoform as potential targets for the central neurotoxic effects of pyrethroids.
Stereoselectivity of a radioimmunoassay for the insecticide S-Bioallethrin
Experientia 1979 Dec 15;35(12):1619-20.PMID:520474DOI:10.1007/BF01953227.
The stereoselectivity of a radioimmunoassay (RIA) system using an S-Bioallethrin specific antiserum was studied by observing the abilities of the 8 allethrin isomers and other selected compounds to compete with a radiolabelled S-Bioallethrin tyramine derivative for antibody binding sites. The results demonstrate the feasibility of RIA as a rapid, sensitive and steroselective residue technique for compounds difficult to analyze by classical methods.
[Effect of S-Bioallethrin on human lymphocyte]
Nan Fang Yi Ke Da Xue Xue Bao 2006 Mar;26(3):321-4, 327.PMID:16546737doi
Objective: To study the effect of the S-Bioallethrin on human lymphocytes by microarray technique. Methods: The changes of normal human lymphocytes treated with S-Bioallethrin were examined with light microscope, flow cytometry, electron microscope, DNA ladder and microarray techniques. Results: Morphological study showed that the lymphocytes underwent apoptosis after S-Bioallethrin exposure, which as further confirmed by the expression changes of 346 genes. Conclusion: S-Bioallethrin can induce apoptosis of normal human lymphocytes and changes in their gene expression profiles.
Differential state-dependent modification of inactivation-deficient Nav1.6 sodium channels by the pyrethroid insecticides S-Bioallethrin, tefluthrin and deltamethrin
Neurotoxicology 2012 Jun;33(3):384-90.PMID:22465659DOI:10.1016/j.neuro.2012.03.007.
Pyrethroid insecticides disrupt nerve function by modifying the gating kinetics of transitions between the conducting and nonconducting states of voltage-gated sodium channels. Pyrethroids modify rat Na(v)1.6+β1+β2 channels expressed in Xenopus oocytes in both the resting state and in one or more states that require channel activation by repeated depolarization. The state dependence of modification depends on the pyrethroid examined: deltamethrin modification requires repeated channel activation, tefluthrin modification is significantly enhanced by repeated channel activation, and S-Bioallethrin modification is unaffected by repeated activation. Use-dependent modification by deltamethrin and tefluthrin implies that these compounds bind preferentially to open channels. We constructed the rat Na(v)1.6Q3 cDNA, which contained the IFM/QQQ mutation in the inactivation gate domain that prevents fast inactivation and results in a persistently open channel. We expressed Na(v)1.6Q3+β1+β2 sodium channels in Xenopus oocytes and assessed the modification of open channels by pyrethroids by determining the effect of depolarizing pulse length on the normalized conductance of the pyrethroid-induced sodium tail current. Deltamethrin caused little modification of Na(v)1.6Q3 following short (10ms) depolarizations, but prolonged depolarizations (up to 150ms) caused a progressive increase in channel modification measured as an increase in the conductance of the pyrethroid-induced sodium tail current. Modification by tefluthrin was clearly detectable following short depolarizations and was increased by long depolarizations. By contrast modification by S-Bioallethrin following short depolarizations was not altered by prolonged depolarization. These studies provide direct evidence for the preferential binding of deltamethrin and tefluthrin (but not S-Bioallethrin) to Na(v)1.6Q3 channels in the open state and imply that the pyrethroid receptor of resting and open channels occupies different conformations that exhibit distinct structure-activity relationships.