Pyrethrin II   中文名称: 除虫菊素

Absorption, Distribution and Excretion
Pyrethrins are absorbed from the gastrointestinal tract following oral administration. Studies in male rats receiving 3 mg/kg orally resulted in almost complete absorption and metabolism within 100 hours. No pyrethrin was observed in urine, although substantial quantities of metabolites were present. In feces, small quantities of the parent pyrethrin were observed, again accompanied by metabolites.
Pyrethrins are absorbed through intact skin when applied topically. When animals were exposed to aerosols of pyrethrins with piperonyl butoxide being released into the air, little or none of the combination was systemically absorbed. /Pyrethrins/
The pyrethrins or their metabolites are not known to be stored in the body or to be excreted in the milk...
Following a single oral pyrethrin II dose to rats, 53% of the admin dose appeared as CO2 & 7% appeared in urine. After an equivalent dose of pyrethrin I, 0.3% could be accounted for as CO2 & 46% of the dose was eliminated in urine.

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Metabolism / Metabolites
Pyrethrins are extensively metabolized, the residues of the parent compound in feces and urine representing only 10%. Six metabolites were identified and two major metabolic pathways were suggested, the first involving oxidation of the double-bond and/or the methyl groups and the second involving hydrolysis of the ester bond. Pyrethrins I are metabolized mainly through oxidative processes, while pyrethrins II are metabolized through a combination of hydrolytic and oxidative processes.
... Within 48 hr of oral admin of (14)C-pyrethrin II to rats, 53% of the (14)C was recovered as exhaled carbon dioxide ... . The ... (14)C recovered from urine ... /was/ 7% ... some of the orally admin material is excreted in feces, at least partially in metabolized form. Three compounds have been isolated from urine & identified by NMR & mass spectra. All three are produced by ... pyrethrin I & II. All three are the result of oxidation of ... the acid & alcoholic moieties leaving the main structure of the molecule intact.
The oral administration of radio-labelled pyrethrin I, or pyrethrin II, to rats produced several urinary metabolites. Each contained a trans-2-carboxyprop-1-enyl side chain resulting from oxidation of the chrysanthemate isobutenyl group or hydrolysis of the pyrethrate methoxy-carbonyl group. Also, the cis-2',4'-pentadienyl side chain of pyrethrin I and pyrethrin II was oxidized at the penta-2,4-dienyl group to give a cis-4',5'-dihydroxypent-2'-enyl group, a 4' conjugate of this diol, or a trans-2',5'-dihydroxypent-3'-enyl group.
The 2-methylpropenyl group of (S)-bioallethrin (A) and the pentadienyl group of pyrethrin II are selectively oxidized by m-chloroperoxybenzoic acid in dichloromethane to yield the 7,8-epoxide (1) from A and a mixture of the 8',9'- and 10',11'-epoxides (7 and 8) from pyrethrin II. These epoxides are hydrated in aqueous acid to the corresponding diols and other hydroxy derivatives produced by opening of the cycloprophyl ring or migration of the adjacent double bond. The epoxy and hydroxy derivatives are identified by two dimensional NMR techniques. Mouse liver enzymes do not detectably hydrate epoxide 1 but quickly hydrate epoxides 7 and 8 without migration of the double bond. HPLC analyses of the microsomal metabolites of pyrethrins I and II identify the 10',11'-diols as major metabolites and the 8',9'-diols as minor products.
For more Metabolism/Metabolites (Complete) data for PYRETHRIN II (12 total), please visit the HSDB record page.

[1].Residual determination of pyrethrins in Lycium barbarum (goji) by GC-MS/MS and a dietary risk assessment of Chinese goji consumption. Food Addit Contam Part A Chem Anal Control Expo Risk Assess. 2020 Mar;37(3):478-487.

Pyrethrin II is a member of pyrethrins. It is functionally related to a pyrethrin I.

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Mechanism of Action
The symptoms of pyrethrin poisoning follow the typical pattern ... : (1) excitation, (2) convulsions, (3) paralysis, and (4) death. The effects of pyrethrins on the insect nervous system closely resemble those of DDT, but are apparently much less persistent. Regular, rhythmic, and spontaneous nerve discharges have been observed in insect and crustacean nerve-muscle preparations poisoned with pyrethrins. The primary target of pyrethrins seems to be the ganglia of the insect central nervous system although some pyrethrin-poisoning effect can be observed in isolated legs. /Pyrethrins/
Electrophysiologically, pyrethrins cause repetitive discharges and conduction block. /Pyrethrins/
The primary site of action for pyrethrins ... is the sodium channel of nerve cells. Using a variety of methods, including voltage clamp and patch clamp techniques, it has been shown that pyrethrins ... slow the closing of sodium channel gates following an initial influx of sodium during the depolarizing phase of an action potential, which results in a prolonged sodium tail current.
Following absorption through the chitinous exoskeleton of arthropods, pyrethrins stimulate the nervous system, apparently by competitively interfering with cationic conductances in the lipid layer of nerve cells, thereby blocking nerve impulse transmissions. Paralysis & death follow. /Pyrethrins/
The interactions of natural pyrethrins and 9 pyrethroids with the nicotinic acetylcholine (ACh) receptor/channel complex of Torpedo electronic organ membranes were studied. None reduced (3)H-ACh binding to the receptor sites, but all inhibited (3)H-labeled perhydrohistrionicotoxin binding to the channel sites in presence of carbamylcholine. Allethrin inhibited binding noncompetitively, but (3)H-labeled imipramine binding competitively, suggesting that allethrin binds to the receptor's channel sites that bind imipramine. The pyrethroids were divided into 2 types according to their action: type A, which included allethrin, was more potent in inhibiting (3)H-H12-HTX binding and acted more rapidly. Type B, which included permethrin, was less potent and their potency increased slowly with time. The high affinities that several pyrethroids have for this nicotinic ACh receptor suggest that pyrethroids may have a synaptic site of action in addition to their well known effects on the axonal channels. /Pyrethrins and Pyrethroids/

C22H28O5

372.45

372.193

121-29-9

5281555

Light yellow to yellow liquid

1.1±0.1 g/cm3

473.7±45.0 °C at 760 mmHg

203.8±28.8 °C

0.0±1.2 mmHg at 25°C

1.528

4.43

69.67

0

5

9

27

751

3

CC1=C(C(=O)C[C@@H]1OC(=O)[C@@H]2[C@H](C2(C)C)/C=C(\C)/C(=O)OC)C/C=C\C=C

VJFUPGQZSXIULQ-XIGJTORUSA-N

InChI=1S/C22H28O5/c1-7-8-9-10-15-14(3)18(12-17(15)23)27-21(25)19-16(22(19,4)5)11-13(2)20(24)26-6/h7-9,11,16,18-19H,1,10,12H2,2-6H3/b9-8-,13-11+/t16-,18+,19+/m1/s1

[(1S)-2-methyl-4-oxo-3-[(2Z)-penta-2,4-dienyl]cyclopent-2-en-1-yl] (1R,3R)-3-[(E)-3-methoxy-2-methyl-3-oxoprop-1-enyl]-2,2-dimethylcyclopropane-1-carboxylate

2934.99.9001

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)

DMSO :~100 mg/mL (~268.49 mM; with sonication)

配方 1 中的溶解度: ≥ 2.5 mg/mL (6.71 mM) (饱和度未知) in 10% DMSO + 40% PEG300 + 5% Tween-80 + 45% Saline (这些助溶剂从左到右依次添加，逐一添加),澄清溶液。
例如，若需制备1 mL的工作液，您可以添加 100 μL 25.0 mg/mL 透明 DMSO 储备液，并将其添加到 400 μL PEG300 中并充分混合。 然后向上述体系中加入50 μL Tween-80，混匀。 然后继续加入450 μL生理盐水至1 mL。
*生理盐水的制备：将 0.9 g 氯化钠溶解在 100 mL ddH₂O中，得到澄清溶液。

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请根据您的实验动物和给药方式选择适当的溶解配方/方案：
1、请先配制澄清的储备液(如：用DMSO配置50 或 100 mg/mL母液(储备液));
2、取适量母液，按从左到右的顺序依次添加助溶剂，澄清后再加入下一助溶剂。以 下列配方为例说明 (注意此配方只用于说明，并不一定代表此产品 的实际溶解配方):
10% DMSO → 40% PEG300 → 5% Tween-80 → 45% ddH2O (或 saline);
假设最终工作液的体积为 1 mL, 浓度为5 mg/mL: 取 100 μL 50 mg/mL 的澄清 DMSO 储备液加到 400 μL PEG300 中，混合均匀/澄清；向上述体系中加入50 μL Tween-80，混合均匀/澄清；然后继续加入450 μL ddH2O (或 saline)定容至 1 mL；
3、溶剂前显示的百分比是指该溶剂在最终溶液/工作液中的体积所占比例;
4、 如产品在配制过程中出现沉淀/析出，可通过加热(≤50℃)或超声的方式助溶;
5、为保证最佳实验结果，工作液请现配现用！
6、如不确定怎么将母液配置成体内动物实验的工作液，请查看说明书或联系我们;
7、 以上所有助溶剂都可在 Invivochem.cn网站购买。