alpha-Cypermethrin   中文名称: α-氯氰菊酯

Absorption, Distribution and Excretion
1. Dose excretion studies with cypermethrin (as a 1:1 cis/trans mixture) and alphacypermethrin (one of the two disasteroisomer pairs which constitute cis-cypermethrin) were out with, in each case, two volunteers per dose level. The studies included (a) single oral alphacypermethrin doses of 0.25 mg, 0.50 mg and 0.75 mg followed by repeated alphacypermethrin doses at the same levels, daily for five days, (b) repeated oral cypermethrin doses of 0.25 mg, 0.75 mg and 1.5 mg daily for five days, and (c) a single dermal application of 25 mg cypermethrin to the forearm. Urine was monitored for the free and conjugated 3-(2,2-dichlorovinyl)-2,2-dimethylcyclopropanecarboxylic acid before and after dosing. 2. Metabolism and rate of excretion of a single oral dose of alphacypermethrin was similar to that of cis cypermethrin, on average, 43% of the dose was excreted as the cyclopropanecarboxylic acid in the first 24 hr urine. There was no increase in urinary metabolite excretion when alphacypermethrin was administered as a repeated oral dose. Subjects excreted, on average, 49% of the dose as the cyclopropanecarboxylic acid in the subsequent 24 hr periods after dosing. 3. There was no increase in the urinary cyclopropanecarboxylic acid excretion when cypermethrin was administered as a repeated oral dose. Subjects excreted, on average, 72% of the trans isomer dose and 45% of the cis isomer dose respectively in the subsequent 24 hr periods after dosing. 4. Approximately 0.1% of the applied dermal dose of 25 mg cypermethrin was excreted within 72 hr as the urinary cyclopropanecarboxylic acid. No conclusions can be drawn from such urinary excretion data as to the concentration of cypermethrin and its metabolites in the skin or other organs, or the possibility of other routes of metabolism or excretion.
/PYRETHROIDS/ READILY PENETRATE INSECT CUTICLE AS SHOWN BY TOPICAL LD50 TO PERIPLANETA (COCKROACH) ... /PYRETHROIDS/
WHEN RADIOACTIVE PYRETHROID IS ADMIN ORALLY TO MAMMALS, IT IS ABSORBED FROM INTESTINAL TRACT OF THE ANIMALS & DISTRIBUTED IN EVERY TISSUE EXAMINED. EXCRETION OF RADIOACTIVITY IN RATS ADMIN TRANS-ISOMER: DOSAGE: 500 MG/KG; INTERVAL 20 DAYS; URINE 36%; FECES 64%; TOTAL 100%. /PYRETHROIDS/
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/
Although limited absorption may account for the low toxicity of some pyrethroids, rapid biodegradation by mammalian liver enzymes (ester hydrolysis and oxidation) is probably the major factor responsible. Most pyrethroid metabolites are promptly excreted, at least in part, by the kidney. /Pyrethroids/
On single oral administration of each of (14)C-(1RS)-trans- and (1RS)-cis-cypermethrin labeled in the benzyl ring, the cyclopropane ring, or the CN group to male and female rats at 1-5 mg/kg, carbon-14 from the acid and alcohol moieties was rapidly and almost completely excreted into the urine and feces. The carbon-14 from the CN group was relatively slowly excreted in the urine and feces, the total recovery being 50-67%. The tissue residues of rats treated with the acid- or alcohol-labeled preparations were generally very low except for the fat (ca. 1 ppm). In contrast, the CN-labeled preparation showed relatively high residue levels, especially in the stomach (contents), intestines, and skin.
Dermal exposure to cypermethrin during spray application at up to 46 mg/hr led to an estimation that approximately 3% was absorbed.
Exposure to cypermethrin & its absorption during aerial spraying of an ultra low volume formulation were studied. A contract pilot & mixer/loader at each of two commercial cotton farms in Mississippi were monitored for dermal exposure to cypermethrin during 12 aerial spray applications. Each operation consisted of 1 mixing/loading operation & 1 application of 50 gal of dilute spray soln for about 30 min. Three volunteer mixer/loaders collected their total urine output for 24 hr periods from 1 or 2 days before to 6 days after exposure. Absorption of cypermethrin was evaluated by determining cypermethrin urinary metabolites. All mixer/loaders wore protective equipment. Total potential & actual dermal exposures were estimated. Avg potential exposures (protected & exposed skin) were 1.07 & 10.5 mg/8 hr day (mg/day) for pilots & mixer/loaders, respectively. Actual skin exposures averaged 0.67 mg/day for pilots & 2.43 mg/day for mixer/loaders. 67% of the total potential exposures to pilots occurred on the hands. For the mixer/loaders, exposure involved primarily the arms, trunk, & hands, amounting to 37, 24, & 17% of total exposure, respectively. Absorption by mixer/loaders determined from analyses of urinary metabolites amounted to 46 to 78 ug cypermethrin equivalents per 3 mixed loads & per 12 simulated mixed loads. /It was/ concluded that exposure of pilots & mixer/loaders during aerial application of ultra low volumes is minimal. Only a small proportion of the cypermethrin that contacts the skin is absorbed.
1. Dose excretion studies with cypermethrin (as a 1:1 cis/trans mixture) & alphacypermethrin (1 of the 2 disastereoisomer pairs which constitute cis cypermethrin) were carried out with, in each case, 2 volunteers/dose level. The studies included (a) single oral alphacypermethrin doses of 0.25 mg, 0.50 mg & 0.75 mg followed by repeated alphacypermethrin doses at the same levels, daily for 5 days, (b) repeated oral cypermethrin doses of 0.25 mg, 0.75 mg & 1.5 mg daily for 5 days, & (c) a single dermal application of 25 mg cypermethrin to the forearm. Urine was monitored for the free & conjugated 3-(2,2-dichlorovinyl)-2,2-dimethylcyclopropanecarboxylic acid before & after dosing. 2. Metab & rate of excretion of a single oral dose of alphacypermethrin was similar to that of cis cypermethrin, on average, 43% of the dose was excreted as the cyclopropanecarboxylic acid in the first 24 hr urine. There was no incr in urinary metabolite excretion when alphacypermethrin was admin as a repeated oral dose. Subjects excreted, on average, 49% of the dose as the cyclopropanecarboxylic acid in the subsequent 24 hr periods after dosing. 3. There was no incr in the urinary cyclopropanecarboxylic acid excretion when cypermethrin was admin as a repeated oral dose. Subjects excreted, on average, 72% of the trans isomer dose & 45% of the cis isomer dose respectively in the subsequent 24 hr periods after dosing. 4. Approx 0.1% of the applied dermal dose of 25 mg cypermethrin was excreted within 72 hr as the urinary cyclopropanecarboxylic acid. No conclusions can be drawn from such urinary excretion data as to the concn of cypermethrin & its metabolites in the skin or other organs, or the possibility of other routes of metab or excretion.
For more Absorption, Distribution and Excretion (Complete) data for CYPERMETHRIN (9 total), please visit the HSDB record page.

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Metabolism / Metabolites
The metabolic pathways for the breakdown of the pyrethroids vary little between mammalian species but vary somewhat with structure. ... Essentially, pyrethrum and allethrin are broken down mainly by oxidation of the isobutenyl side chain of the acid moiety and of the unsaturated side chain of the alcohol moiety with ester hydrolysis playing and important part, whereas for the other pyrethroids ester hydrolysis predominates. /Pyrethrum and pyrethroids/
The relative resistance of mammals to the pyrethroids is almost wholly attributable to their ability to hydrolyze the pyrethroids rapidly to their inactive acid & alcohol components, since direct injection into the mammalian CNS leads to a susceptibility similar to that seen in insects. Some additional resistance of homeothermic organisms can also be attributed to the negative temperature coefficient of action of the pyrethroids, which are thus less toxic at mammalian body temperatures, but the major effect is metabolic. Metabolic disposal of the pyrethroids is very rapid, which means that toxicity is high by the iv route, moderate by slower oral absorption, & often unmeasureably low by dermal absorption. /Pyrethroids/
FASTEST BREAKDOWN IS SEEN WITH PRIMARY ALCOHOL ESTERS OF TRANS-SUBSTITUTED ACIDS SINCE THEY UNDERGO RAPID HYDROLYTIC & OXIDATIVE ATTACK. FOR ALL SECONDARY ALCOHOL ESTERS & FOR PRIMARY ALCOHOL CIS-SUBSTITUTED CYCLOPROPANECARBOXYLATES, OXIDATIVE ATTACK IS PREDOMINANT. /PYRETHROIDS/
Pyrethrins are reportedly inactivated in the GI tract following ingestion. In animals, pyrethrins are rapidly metabolized to water soluble, inactive compounds. /Pyrethrins/
Synthetic pyrethroids are generally metabolized in mammals through ester hydrolysis, oxidation, and conjugation, and there is no tendency to accumulate in tissues. In the environment, synthetic pyrethroids are fairly rapidly degraded in soil and in plants. Ester hydrolysis and oxidation at various sites on the molecule are the major degradation processes. /Synthetic pyrethroids/
In the case of cypermethrin, the relative importance of an esterase attack as opposed to an oxidative one is more important than for permethrin; for trans-cypermethrin the ratio is 93.2% to 17.3% and for cis-cypermethrin 41.5% to 37.6% in the mouse system. In case of deltamethrin (which has only a cis-isomer) the ratio is 28.3% to 41%. Since the mouse system shows a high oxidative ratio, the above figures seem to indicate that esterase metabolism in these pyrethroids is at least as important as the oxidative ones.
The major degradation pathway of cypermethrin is hydrolysis of the ester linkage to /yield ultimately/ 3-phenoxybenzoic acid and 3-(2,2-dichlorovinyl)-2,2- dimethylcyclopropanecarboxylic acid. (From the cis-isomer both cis- and trans- cyclopropanecarboxylic acids are found.) A minor degradative route is ring hydroxylation to give an alpha-cyano-3-(4-hydroxyphenyl)benzyl ester followed by hydrolysis to produce the corresponding hydroxycarboxylic acid.
When administered to rats and mice, a large part of trans-cypermethrin was eliminated in urine in 24 hr. Under similar conditions, 80% of administered 3-phenoxybenzoic acid was eliminated. When cis-cypermethrin was administered, more was excreted via feces. The major urinary metabolite in mice, from trans-cypermethrin and 3-phenoxybenzoic acid, was identified with the aid of MS and NMR as N-(3-phenoxybenzoyl)taurine. A minor metabolite was identified as the sulfate of 3-(4-hydroxyphenoxy)benzoic acid. The taurine conjugate was not found in the rat urine. In rats, the major metabolite was the sulfate conjugate of 3-(4-hydroxyphenoxy)-benzoic acid. Mouse liver microsomal + NADPH preparations hydroxylated trans- and cis-cypermethrin at the t- and c-methyl groups and the 4' and 5 positions. Hydroxylation at the 5 position of trans-cypermethrin was detected only with microsomes treated with tetraethyl pyrophosphate to inhibit esterase activity.
The major metabolic reactions of trans- and cis-cypermethrin were cleavage of ester linkage, oxidation at the trans- and cis-methyl cyclopropane ring and at 4'-position of the phenoxy group, and conversion of the CN group to SCN ion. The following minor species differences were observed: (1) oxidation at 5- and 6-positions of the alcohol moiety was observed in mice but not in rats; (2) ester metabolites such as 2'-OH, 5-OH, and trans-OH,4'-OH-cypermethrin were detected in feces of mice but not of rats. The remarkable species difference in metabolites was the PBacid-taurine conjugate, which was the predominant metabolite in mice, but it was not detected in rats.
For more Metabolism/Metabolites (Complete) data for CYPERMETHRIN (9 total), please visit the HSDB record page.
Cypermethrin has been shown to be well absorbed after oral administration, extensively metabolized, and eliminated as polar conjugates in urine. The main route of metabolism was, as anticipated, via hydrolysis of the ester linkage. The cyclopropane-carboxylic acid moiety is subsequently excreted via the urine as the glucuronide conjugate (L857).

Toxicity Summary
IDENTIFICATION: Alpha-cypermethrin is a highly active pyrethroid insecticide, effective against a wide range of pests encountered in agriculture and animal husbandry. It is supplied as emulsifiable concentrate, ultra-low-volume formulation, suspension concentrate and in mixtures with other insecticides. The technical product is a crystalline powder with good solubility in acetone, cyclohexanone and xylene, but its solubility in water is low. It is stable under acidic and neutral conditions. HUMAN EXPOSURE: Exposure of the general population to alpha-cypermethrin is negligible, provided its use follows good agricultural practice. With good work practices, hygiene measures, and safety precautions, the use of alpha-cypermethrin is unlikely to present a hazard to those occupationally exposed to it. The occurrence of "facial sensations" is an indication of exposure. Under these circumstances work practices should be reviewed. ANIMAL STUDIES: Alpha-cypermethrin has moderate to high acute oral toxicity to rodents. Acute oral exposure results in clinical signs associated with central nervous system activity. Technical alpha-cypermetrhrin has been reported to be minimally irritating to rabbit skin. Some formulations cause severe eye irritations. In guinea-pigs, alpha-cypermethrin caused stimulation of sensory nerve-endings in the skin. An oral study in rats demonstrated that alpha-cypermethrin induces neurotoxicity due to histopathological alterations of the tibial and sciatic nerves, axonal degeneration and increased beta-galactosidase activity. No data are available on long-term toxicity, reproductive toxicity, teratogenicity, immunotoxicity, or carcinogenicity. From the available data on alpha-cypermethrin, it can be concluded that this compound is non-mutagenic in tests with Salmonella typhimurium, Escherichia coli and Saccharomyces cerevisiae, and in vivo and in vitro tests with rat liver cells for the induction of chromosome aberration and production of DNA single-strand damage. Alpha-cypermethrin is highly toxic to aquatic invertebrates, fish, and bees.
Both type I and type II pyrethroids exert their effect by prolonging the open phase of the sodium channel gates when a nerve cell is excited. They appear to bind to the membrane lipid phase in the immediate vicinity of the sodium channel, thus modifying the channel kinetics. This blocks the closing of the sodium gates in the nerves, and thus prolongs the return of the membrane potential to its resting state. The repetitive (sensory, motor) neuronal discharge and a prolonged negative afterpotential produces effects quite similar to those produced by DDT, leading to hyperactivity of the nervous system which can result in paralysis and/or death. Other mechanisms of action of pyrethroids include antagonism of gamma-aminobutyric acid (GABA)-mediated inhibition, modulation of nicotinic cholinergic transmission, enhancement of noradrenaline release, and actions on calcium ions. They also inhibit calium channels and Ca2+, Mg2+-ATPase. (T10, T18, L857)

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Toxicity Data
LC50 (rat) > 400 mg/m3/4h
LD50: 250-300 mg/kg (Oral, Mouse) (L873)

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Interactions
/Pyrethroid/ detoxification ... important in flies, may be delayed by the addition of synergists ... organophosphates or carbamates ... to guarantee a lethal effect. ... /Pyrethroid/
Piperonyl butoxide potentiates /insecticidal activity/ of pyrethrins by inhibiting the hydrolytic enzymes responsible for pyrethrins' metab in arthropods. When piperonyl butoxide is combined with pyrethrins, the insecticidal activity of the latter drug is increased 2-12 times /Pyrethrins/
At dietary level of 1000 ppm pyrethrins & 10000 ppm piperonyl butoxide ... /enlargement, margination, & cytoplasmic inclusions in liver cells of rats/ were well developed in only 8 days, but ... were not maximal. Changes were proportional to dosage & similar to those produced by DDT. Effects of the 2 ... were additive. /Pyrethrins/
The effects of dissolved organic carbon in the form of Aldrich humic acid on the accumulation and acute toxicities of three synthetic pyrethroids - fenvalerate, deltamethrin, and cyhalothrin - to Daphnia magna in laboratory experiments were investigated. Concn of dissolved organic carbon as low as 2.6 mg/L, 3.2 mg/L, and 3.1 mg/L for deltamethrin fenvalerate, and cyhalothrin, respectively, resulted in a significant decrease in bioaccumulation. Acute toxicities of all three pyrethroids were found to decrease as dissolved organic carbon concn increased; eg, at a dissolved organic carbon concn of 15.5 mg/L, the acute toxicity of fenvalerate was reduced by a factor of 17. The percentages of deltamethrin and fenvalerate bound to dissolved organic carbon increased as dissolved organic carbon concn increased after 2 hr and 24 hr contact times. At low concn of dissolved organic carbon (eg, 1.7 mg/L), as much as 40% of fenvalerate and 20% of deltamethrin were found sorbed to the dissolved material. After 24 hr contact times, 76.4 and 80.8% of fenvalerate and deltamethrin, respectively, were bound to dissolved organic carbon. Reverse-phase partition coefficients for both fenvalerate and deltamethrin were found to vary with dissolved organic carbon concn and were in the range 1.0 to 4.8 to 5.6.
The acute administration of 1R,cis, alpha S-cypermethrin, deltamethrin fenvalerate and permethrin produced a dose-dependent lowering of the dose of pentylenetetrazol required to elicit a seizure in rats. The proconvulsant action of cypermethrin displayed stereospecificity in that the 1R, cis, alpha S isomer of cypermethrin was the most potent compound tested, while the non-insecticidal isomer, 1S,cis, alpha R-cypermethrin, was devoid of proconvulsant activity. Pretreatment of rats with PK 11195, an antagonist of the peripheral-type benzodiazepine binding site, elicited a complete reversal of the proconvulsant actions of both deltamethrin and permethrin. In contrast, pretreatment with phenytoin did not alter the pyrethroid-induced proconvulsant activity. These results suggest that the effects of pyrethroids on pentylenetetrazol seizure threshold are mediated via an interaction with peripheral-type benzodiazepine binding sites.
/Pyrethroid/ detoxification ... important in flies, may be delayed by the addition of synergists ... organophosphates or carbamates ... to guarantee a lethal effect. ... /Pyrethroid/
Piperonyl butoxide potentiates /insecticidal activity/ of pyrethrins by inhibiting the hydrolytic enzymes responsible for pyrethrins' metabolism in arthropods. When piperonyl butoxide is combined with pyrethrins, the insecticidal activity of the latter drug is increased 2-12 times /Pyrethrins/
For more Interactions (Complete) data for CYPERMETHRIN (9 total), please visit the HSDB record page.

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Non-Human Toxicity Values
LD50 Rat oral 79-400 mg/kg (in corn oil, value depending on concentration), 474 mg tech./kg
LD50 Rat percutaneous > 2000 mg tech./kg
LD50 Rabbit percutaneous >2000 mg tech./kg
LD50 Rat (8 day old) oral 14.9 mg/kg
LD50 Rat (adult male) oral 250.0 mg/kg
LD50 Rat oral 4123 mg/kg
LD50 Rabbit dermal >2460 mg/kg
For more Non-Human Toxicity Values (Complete) data for CYPERMETHRIN (10 total), please visit the HSDB record page.

Therapeutic Uses
Pyrethrins with piperonyl butoxide are used for topical treatment of pediculosis(lice infestations). Combinations of pyrethrins with piperonyl butoxide are not effective for treatment of scabies (mite infestations). Although there are no well-controlled comparative studies, many clinicians consider 1% lindane to be pediculicide of choice. However, some clinicians recommend use of pyrethrins with piperonyl butoxide, esp in infants, young children, & pregnant or lactating women ... . If used correctly, 1-3 treatments ... are usually 100% effective ... Oil based (eg, petroleum distillate) combinations ... produce the quickest results. ... For treatment of pediculosis, enough gel, shampoo, or solution ... should be applied to cover affected hairy & adjacent areas ... After 10 min, hair is ... washed thoroughly ... treatment should be repeated after 7-10 days to kill any newly hatched lice. /Pyrethrins/
Therapeutic Category (Veterinary): ectoparasiticide

415.074

67375-30-8

2912

Viscous yellowish brown semisolid mass.
Colorless crystals
Viscous semi-solid
Colorless crystals - pure isomers

1.3±0.1 g/cm3

511.3±50.0 °C at 760 mmHg

78-81ºC

263.0±30.1 °C

0.0±1.3 mmHg at 25°C

1.622

6.27

118.64

0

4

7

28

643

0

KAATUXNTWXVJKI-UHFFFAOYSA-N

InChI=1S/C22H19Cl2NO3/c1-22(2)17(12-19(23)24)20(22)21(26)28-18(13-25)14-7-6-10-16(11-14)27-15-8-4-3-5-9-15/h3-12,17-18,20H,1-2H3

[cyano-(3-phenoxyphenyl)methyl] 3-(2,2-dichloroethenyl)-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)

May dissolve in DMSO (in most cases), if not, try other solvents such as H2O, Ethanol, or DMF with a minute amount of products to avoid loss of samples

注意: 如下所列的是一些常用的体内动物实验溶解配方，主要用于溶解难溶或不溶于水的产品（水溶度<1 mg/mL）。 建议您先取少量样品进行尝试，如该配方可行，再根据实验需求增加样品量。

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注射用配方1: DMSO : Tween 80： Saline = 10 : 5 : 85 (如： 100 μL DMSO → 50 μL Tween 80 → 850 μL Saline)
*生理盐水/Saline的制备：将0.9g氯化钠/NaCl溶解在100 mL ddH ₂ O中，得到澄清溶液。
注射用配方 2: DMSO : PEG300 ：Tween 80 : Saline = 10 : 40 : 5 : 45 (如： 100 μL DMSO → 400 μL PEG300 → 50 μL Tween 80 → 450 μL Saline)
注射用配方 3: DMSO : Corn oil = 10 : 90 (如： 100 μL DMSO → 900 μL Corn oil)
示例: 以注射用配方 3 (DMSO : Corn oil = 10 : 90) 为例说明, 如果要配制 1 mL 2.5 mg/mL的工作液, 您可以取 100 μL 25 mg/mL 澄清的 DMSO 储备液，加到 900 μL Corn oil/玉米油中, 混合均匀。

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注射用配方 4: DMSO : 20% SBE-β-CD in Saline = 10 : 90 [如：100 μL DMSO → 900 μL (20% SBE-β-CD in Saline)]
*20% SBE-β-CD in Saline的制备（4°C，储存1周）：将2g SBE-β-CD (磺丁基-β-环糊精) 溶解于10mL生理盐水中，得到澄清溶液。
注射用配方 5: 2-Hydroxypropyl-β-cyclodextrin : Saline = 50 : 50 (如： 500 μL 2-Hydroxypropyl-β-cyclodextrin (羟丙基环胡精)→ 500 μL Saline)
注射用配方 6: DMSO : PEG300 : Castor oil : Saline = 5 : 10 : 20 : 65 (如： 50 μL DMSO → 100 μL PEG300 → 200 μL Castor oil → 650 μL Saline)
注射用配方 7: Ethanol : Cremophor : Saline = 10： 10 : 80 (如： 100 μL Ethanol → 100 μL Cremophor → 800 μL Saline)
注射用配方 8: 溶解于Cremophor/Ethanol (50 : 50), 然后用生理盐水稀释。
注射用配方 9: EtOH : Corn oil = 10 : 90 (如： 100 μL EtOH → 900 μL Corn oil)
注射用配方 10: EtOH : PEG300：Tween 80 : Saline = 10 : 40 : 5 : 45 (如： 100 μL EtOH → 400 μL PEG300 → 50 μL Tween 80 → 450 μL Saline)

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口服配方 1: 悬浮于0.5% CMC Na (羧甲基纤维素钠)
口服配方 2: 悬浮于0.5% Carboxymethyl cellulose (羧甲基纤维素)
示例: 以口服配方 1 (悬浮于 0.5% CMC Na)为例说明, 如果要配制 100 mL 2.5 mg/mL 的工作液, 您可以先取0.5g CMC Na并将其溶解于100mL ddH2O中，得到0.5%CMC-Na澄清溶液；然后将250 mg待测化合物加到100 mL前述 0.5%CMC Na溶液中，得到悬浮液。

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口服配方 3: 溶解于 PEG400 (聚乙二醇400)
口服配方 4: 悬浮于0.2% Carboxymethyl cellulose (羧甲基纤维素)
口服配方 5: 溶解于0.25% Tween 80 and 0.5% Carboxymethyl cellulose (羧甲基纤维素)
口服配方 6: 做成粉末与食物混合

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注意: 以上为较为常见方法，仅供参考， InvivoChem并未独立验证这些配方的准确性。具体溶剂的选择首先应参照文献已报道溶解方法、配方或剂型，对于某些尚未有文献报道溶解方法的化合物，需通过前期实验来确定（建议先取少量样品进行尝试），包括产品的溶解情况、梯度设置、动物的耐受性等。

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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。