Dimethyl sulfoxide   中文名称: 二甲基亚砜

DMSO 是一种可与水、脂质和有机试剂自由混溶的有机溶剂。这些特性使得优异的膜渗透性成为可能。人们认为 DMSO 通过神经阻滞、平滑肌松弛、胶原蛋白抑制和抗炎作用的组合发挥作用[2]。

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问题： 将化合物配置成DMSO母液（储备液）时常用的浓度是多少？
回答：通常为10 mM, 20 mM, 或 50 mM.。配置DMSO储备液时，我们建议您配置的浓度为10mM 或 更高，为了尽量减少溶剂（如DMSO）对细胞的影响，一般会用细胞培养基将母液稀释1000倍（对于大多数细胞，通常最终DMSO浓度应<0.5%）。
*在细胞培养基中，大多数细胞通常可耐受的DMSO含量为：＜0.5-1%。对于更敏感的细胞，如原代细胞，建议最终工作液中DMSO的含量<0.1%。

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注意: DMSO的吸湿性非常强，吸湿后的DMSO对化合物（产品）的溶解度有较大影响。为确保试验结果的准确性，请尽量使用新开封的DMSO。 为了尽量减少溶剂（如DMSO）对细胞的影响，一般会用细胞培养基将母液稀释1000倍（对于大多数细胞，通常最终DMSO浓度应<0.5%）。

注意: 在动物实验中，DMSO的浓度应保持在一定的限制范围内以确保动物的健康和实验的准确性。对于正常的成年健康小鼠，DMSO的终浓度建议不超过10%。然而，对于体弱多病或裸鼠等，建议的DMSO终浓度应尽量控制在2%以下。
1）对于正常鼠：DMSO的终浓度建议不大于10%。
2）对于裸鼠或体弱鼠：DMSO的终浓度建议尽量不要超过2%。
3）如果给药频率超过一天三次，对于正常小鼠或大鼠，建议DMSO的终浓度不要大于5%。

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二甲基亚砜（DMSO）是一种广泛使用的溶剂，可与水和多种有机溶剂混溶。它有几个名字，包括甲基亚砜、亚磺酰基双乙烷和几十个商品名
二甲基亚砜最早发现于19世纪末，是用木浆造纸的硫酸盐法的副产品。大约在同一时间，俄罗斯化学家Alexander Zaytsev通过氧化另一种硫酸盐法副产品二甲基硫来合成它。Zaytsev的合成是至今仍在使用的制造工艺的基础
二甲基亚砜是许多气体、合成纤维、油漆、碳氢化合物、盐和天然产物的实验室和工业溶剂。因为它是非质子的、相对惰性的、无毒的、在高温下稳定的，所以它是化学反应中常用的溶剂。它的氘化形式是核磁共振波谱的理想溶剂
在20世纪60年代，科学家们观察到二甲基亚砜渗透人体皮肤，对组织几乎没有影响；并测试了溶剂作为药物携带到体内的一种方式，作为口服制剂或注射剂的替代品。从那时起，二甲基亚砜已被用于一些透皮给药系统（即贴片）。1978年，美国食品药品监督管理局批准其用于慢性间质性膀胱炎（膀胱疼痛综合征）的症状缓解，这是美国食品药品管理局唯一批准二甲基亚砜作为实际药物
正如人们在20世纪60年代所预期的那样，二甲基亚砜被尝试作为一种缓解炎症的替代药物和将可卡因等非法药物引入体内的溶剂。它也被错误地宣传为癌症的治疗方法。1965年，美国食品药品监督管理局禁止二甲基亚砜的临床试验，因为该化合物改变了实验动物晶状体的折射率，从而终止了大部分这种活动。在人们对该物质的强烈兴趣减弱后，该禁令于1980年解除
研究人员继续将二甲基亚砜视为一种可能的医疗方法。2016年，不列颠哥伦比亚癌症机构（温哥华）、不列颠哥伦比亚大学（温哥华）和温哥华综合医院的Gerald Krystal及其同事报告称，二甲基亚砜抑制人体血细胞产生炎症细胞因子，从而减少自身免疫性关节炎。作者还研究了二甲基亚砜是否具有任何抗癌活性；他们得出的结论是，他们无法证实这一点。[3]

Note: In animal experiments, the percentage of DMSO should be maintained within a certain range to avoid toxicity to animals and to obtain accurate experiment results. For normal/healthy adult mice, it is recommended that the final concentration/percentage of DMSO should not exceed 10%. However, for weak and sickly individuals or nude mice, it is recommended to keep the final concentration/percentage of DMSO below 2% (<2%).
1) For normal mice, it is recommended that the final concentration of DMSO should not exceed 10%.
2) For nude or weak mice, it is recommended that the final concentration of DMSO should not exceed 2%.
3) If the frequency of administration exceeds three times a day, it is recommended that the final concentration of DMSO should not exceed 5% for normal mice or rats.

Absorption, Distribution and Excretion
Readily and rapidly absorbed following administration by all routes and distributed throughout the body.
Dimethyl sulfoxide and dimethyl sulfone are excreted in the urine and feces.
Following topical application, DMSO is absorbed and widely distributed in tissue and body fluids. DMSO and dimethyl sulfone are excreted in the urine and feces. DMSO is eliminated through the breath and skin and is responsible for the characteristic garlic odor. ... Dimethyl sulfone can persist in serum > 2 weeks after a single intravesical instillation. No residual accumulation of DMSO has occurred after treatment from protracted periods of time.
Dimethyl sulfoxide and /one of its metabolites/ dimethyl sulfone, are excreted in the urine and feces. Dimethyl sulfide /another metabolite/ is eliminated through the breath and skin...
By use of a Fourier transform infrared (FTIR) spectroscopic imaging technique, /this study examined/ the dynamic optical clearing processes occurring in hyperosmotically biocompatible agents penetrating into skin tissue in vitro. The sequential collection of images in a time series provides an opportunity to assess penetration kinetics of dimethyl sulphoxide (DMSO) and glycerol beneath the surface of skin tissue over time. From 2-D IR spectroscopic images and 3-D false color diagrams, ...show/s/ that glycerol takes at least 30 min to finally penetrate the layer of epidermis, while DMSO can be detected in epidermis after only 4 min of being topically applied over stratum corneum sides of porcine skin. The results demonstrate the potential of a FTIR spectroscopic imaging technique as an analytical tool for the study of dynamic optical clearing effects when the bio-tissue is impregnated by hyperosmotically biocompatible agents such as glycerol and DMSO.
In man radioactivity of 35S DMSO appeared in blood 5 min after cutaneous application. One hour later, radioactivity could detected in bones.
For more Absorption, Distribution and Excretion (Complete) data for DIMETHYL SULFOXIDE (9 total), please visit the HSDB record page.

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Metabolism / Metabolites
Dimethyl sulfoxide is metabolized in man by oxidation to dimethyl sulfone or by reduction in dimethyl sulfide. Dimethyl sulfoxide and dimethyl sulfone are excreted in the urine and feces.
Dimethyl sulfoxide is metabolized in man by oxidation to dimethyl sulfone or by reduction to dimethyl sulfide.
Autoimmune strain MRL/Ipr, C3H/lpr, and male BXSB mice were placed on a continuous treatment regimen with 3% DMSO or 3% DMS02 in the drinking water, ad libitum, commencing at 1 to 2 months of age, before spontaneous autoimmune lymphoproliferative disease development could be detected. This represented doses of 8-10 g/kg/day of DMSO and 6-8 g/kg/day of DMS02. Both compounds were observed to extend the mean life span of MRL/Ipr mice from 5.5 months to over 10 months of age. All strains showed decreased antinuclear antibody responses and significant diminution of lymphadenopathy, splenomegaly, and anemia development. Serum IgG levels and spleen IgM antibody plaque formation, however, did not differ from control values. There was no indication of involvement of systemic immunosuppressive or antiproliferative effects, and treated animals were observed to remain healthy and vigorous with no signs of toxicity. These results demonstrate that high doses of both DMSO and its major in vivo metabolite, DMSO2, provide significant protection against the development of murine autoimmune lymphoproliferative disease.
In man, DMSO is oxidized into dimethylsulfone DMSO2, metabolite excreted by urine (17-22 %). DMSO is reduced into dimethylsulfide, DMS, a volatile metabolite, responsible for garlic odour of exhaled air (1 %). About 85 % is excreted unchanged, both by urine (50 %) and feces (50 %).
Dimethyl sulfoxide is metabolized in man by oxidation to dimethyl sulfone or by reduction in dimethyl sulfide. Dimethyl sulfoxide and dimethyl sulfone are excreted in the urine and feces.
Route of Elimination: Dimethyl sulfoxide and dimethyl sulfone are excreted in the urine and feces.

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Biological Half-Life
Unchanged DMSO has a half-life of 12 to 15 hours.
/The/ half-life /of DMSO in the rhesus monkey/ was calculated to be about 38 hrs and its elimination rate constant equaled 0.018, or about 2% per hr.

Toxicity Summary
IDENTIFICATION AND USE: Dimethyl sulfoxide (DMSO) is a colorless, very hygroscopic, liquid. It is a molecule with a long history in pharmaceutics and is now well established as a penetration enhancer in topical pharmaceutical formulations. It is currently prescribed as medication for this purpose in diclofenac sodium topical solution (approved in the United States to treat signs and symptoms of osteoarthritis) and idoxuridine topical solution (approved in Europe for the treatment of herpes zoster). DMSO is used as a medication for symptomatic relief of interstitial cystitis. DMSO is not a nutritional supplement, it is metabolized to methylsulfonylmethane (MSM), which is available as a nutritional supplement. DMSO is used in the cryopreservation of cell populations including stem cells, embryos, and various cell cultures. It is also used as an Industrial solvent and as antifreeze or hydraulic fluid when mixed with water. HUMAN EXPOSURE AND TOXICITY: Dermal exposure to DMSO causes skin reactions, erythema and pruritis, which appear immediately after contact with the undiluted substance; 70% solutions are usually tolerated without symptoms. In very sensitive individuals, however, reactions have been seen after contact with 10% solutions. In humans, topical and intradermal application of DMSO produced garlic breath, mast cell degranulation, an increase in polymorphonuclear leukocytes and perivascular eosinophils, itching, and histamine mediated and non-histamine dependent whealing and erythematous flare. Two drops of >50% DMSO in the eye caused a temporary burning sensation and vasodilatation; concentrations of <50% exhibited no effects. A case of sulhemoglobinemia after dermal exposure to DMSO has been described. ANIMAL STUDIES: To study the effects of acute DMSO exposure unshaven rats were immersed in a DMSO solution. There was no immediate response, but within 24 hours 13/14 rats dipped into 100% DMSO were dead. Single i.v. injections of undiluted DMSO were administered to groups of 5 male and 5 female rats. Dose levels were 2.5, 5.0, and 10 g/kg. Each dose was administered over a 1-minute interval. Animals were observed for 14 days following DMSO administration and with one exception, deaths occurred within the first 24 hours. Death was preceded by tremors, myasthenia, dyspnea, and occasionally, convulsions. Non-lethal doses of DMSO produced decreased motoractivity and myasthenia. A total of 32 male rats were exposed to 200 mg DMSO per cubic meter of air for 7 hr/day, 5 days a week, for 6 weeks for 30 exposures. There were no outward toxic signs noted in any of the exposed animals throughout the experimental period of 6 weeks. A garlic-like odor, characteristic of DMSO exposure, was detected in the breath of each of the rats after the first day of exposure. Pharmaceutical-grade DMSO was administered as a 90% solution to 4 groups of rhesus monkeys by gastric intubation, 7 days a week for up to 87 weeks. Dosages administered were equivalent to 990, 2970, and 8910 mg/kg/day. The principal physical signs seen in the animals given DMSO orally included sporadic excess salivation and emesis. Anorexia only occurred at high oral doses. No DMSO-related changes were found in the treated monkeys during physical examinations. No significant lesions attributable to DMSO were found upon gross examination at necropsy. No histologic changes were visible in the lenses of treated animals. In developmental studies groups of 5 -6 pregnant golden hamsters were injected with dilutions of DMSO ranging from 50 to 5500 mg/kg iv or 5500 and 8250 mg/kg ip on the eighth day of gestation. Examination of the embryos 3 days later revealed that no embryocidal or teratogenic effects were noted until levels of 2500 mg/kg were reached. At higher levels, malformations, including exencephaly, rib fusions, microphthalmia, limb abnormalities and cleft lip were found. There was no appreciable effect of DMSO on maternal weight gain or health. DMSO was tested in Chinese hamster ovary cells to a maximum concentration of 5000 ug/mL with and without metabolic activation. DMSO did not induce cell toxicity or cell cycle delay, and did not induce an increase in the incidence of SCEs. Intraabdominal injection of DMSO did not induce sex-linked recessive lethals and did not raise the frequency of sex chromosome loss above the spontaneous level in Drosophila melanogaster. DMSO was tested in five S. typhimurium tester strains (TA 98, 100, 1535, 1537, 1538). DMSO was negative, in the presence and absence of metabolic activation. ECOTOXICITY STUDIES: The acute toxicity (g/kg bw) of i.p. DMSO injection to chinook salmon (Oncorhynchus tshawytscha): LD50 = 12.0, sockeye salmon (Oncorhynchus nerka): LD50 = 13.0, coho salmon (Oncorhynchus kisutch): LD50 = 16.0 and rainbow trout (Salmo gardneri): LD50 = 17.0. Fish usually died within 24 hr; however, a few died between 24 and 48 hours.
The mechanism of dimethyl sulfoxide's actions is not well understood. Dimethyl sulfoxide has demonstrated antioxidant activity in certain biological settings. For example, the cardiovascular protective effect of dimethyl sulfoxide in copper-deficient rats is thought to occur by an antioxidant mechanism. It is also thought that dimethyl sulfoxide's possible anti-inflammatory activity is due to antioxidant action.

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Toxicity Data
LC50 (rat) >1600 mg/m3 (aerosol)/4 hr; [CHEMINFO]
LD50: >10 gm/kg (Oral, Dog) (A308)

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Interactions
Previous studies performed in our laboratory indicated that non-toxic concentrations of peroxynitrite nevertheless commit U937 cells to a rapid necrosis that is however prevented by a survival signaling driven by cytosolic phospholipase A(2)-released arachidonic acid. Toxicity was mediated by concentrations of peroxynitrite resulting in H(2)O(2)-dependent inhibition of arachidonic acid release. The present study shows that U937 cells differentiated to monocytes by prolonged exposure to dimethyl sulfoxide are resistant to peroxynitrite because able to respond with enhanced release of arachidonic acid. An additional important observation was that these cells require more arachidonate than the undifferentiated cells to support the survival signaling. The enhanced arachidonic acid release was not associated with changes in cytosolic phospholipase A(2) expression but was rather dependent on the increased responsiveness of the enzyme to calcium-dependent stimulation as well as on reduced mitochondrial formation of H(2)O(2). The latter event was found to be critical, since differentiated and undifferentiated cells were equally sensitive to peroxynitrite when the accumulation of H(2)O(2) was enhanced via depletion of catalase, or addition of a complex III inhibitor. Thus, the strategy selected by the differentiation process to allow monocytes to cope with peroxynitrite appears to involve some specific mechanism preventing the mitochondrial formation of H(2)O(2).
Thioacetamide (400 mg/kg body weight, i.p.) was administered to rats. After 12 hr the activity of plasma glutamate-oxaloacetate transaminase (GOT) and glutamate-pyruvate transaminase (GPT) was significantly higher than that of the control group, and after 24 hr plasma GOT and GPT activities strongly increased. These results indicated that the necrotic process was initiated at about 12 hr and developed thereafter. By co-administration of dimethyl sulphoxide (DMSO, 18 and 1 hr before, and 8 hr after administration of thioacetamide: each time, 2.5 mL/kg body weight, p.o.), plasma GOT and GPT were significantly decreased and were even comparable to the control group, showing that DMSO totally prevented the necrotic action of thioacetamide. After 12 and 24 hr of thioacetamide administration, the hepatic level of vitamin C, the most sensitive chemical indicator of oxidative stress, decreased significantly, indicating that oxidative stress was significantly enhanced 12 hr after thioacetamide intoxication and thereafter. DMSO totally restored the liver vitamin C level, demonstrating that DMSO effectively ameliorated the oxidative stress caused by thioacetamide, resulting in the prevention of necrosis of the liver. Phosphorylated c-Jun NH(2)-terminal kinase (JNK) significantly increased transiently 12 hr after treatment with thioacetamide. These results indicated that oxidative stress and the activation of JNK took place almost simultaneously. Phosphorylated extracellular signal-related kinase (ERK) 2 was significantly increased 6-12 hr after thioacetamide injection. Phosphorylated p38 MAPK (mitogen activated protein kinase) was significantly decreased 24 hr after administration of thioacetamide. DMSO treatment inhibited the change of these MAPKs by thioacetamide, corresponding with the prevention of the liver necrosis as well as the attenuation of oxidative stress.
Evidence is accumulating that irradiated cells produce some signals which interact with non-exposed cells in the same population via a bystander effect. Here, /research/ examined whether DMSO is effective in suppressing radiation induced bystander effects in CHO and repair deficient xrs5 cells. When 1 Gy-irradiated CHO cells were treated with 0.5% DMSO for 1 hr before irradiation, the induction of micronuclei in irradiated cells was suppressed to 80% of that in non-treated irradiated cells. The suppressive effect of DMSO on the formation of bystander signals was examined and the results demonstrated that 0.5% DMSO treatment of irradiated cells completely suppressed the induction of micronuclei by the bystander effect in non-irradiated cells. It is suggested that irradiated cells ceased signal formation for bystander effects by the action of DMSO. To determine the involvement of reactive oxygen species on the formation of bystander signals, /research/ examined oxidative stress levels using the /2,7-dichlorofluorescin/ DCFH staining method in irradiated populations. The results showed that the treatment of irradiated cells with 0.5% DMSO did not suppress oxidative stress levels. These results suggest that the prevention of oxidative stress is independent of the suppressive effect of DMSO on the formation of the bystander signal in irradiated cells. It is suggested that increased ROS in irradiated cells is not a substantial trigger of a bystander signal.
Ultrasoft X-rays have been shown to be very efficient in inducing chromosomal aberrations in mammalian cells. The present study was aimed to evaluate the modifying effects of DMSO (a potent scavenger of free radicals) on the frequencies of chromosome aberrations induced by soft X-rays. Confluent held G1 Chinese hamster cells (V79) were irradiated with Carbon K ultrasoft X-rays in the presence and absence of 1M DMSO and frequencies of chromosome aberrations in the first division cells were determined. DMSO reduced the frequencies of exchange types of aberrations (dicentrics and centric rings) by a factor of 2.1-3.5. The results indicate that free radicals induced by ultrasoft X-rays contribute to a great extent to the induction of chromosome aberrations. The possible implications of these results in interpreting the mechanisms involved in the high efficiency of ultrasoft X-rays in the induction of chromosome aberrations are discussed.
For more Interactions (Complete) data for DIMETHYL SULFOXIDE (33 total), please visit the HSDB record page.

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Non-Human Toxicity Values
LD50 Rat oral 17.9 mL/kg
LD50 Rat oral 14500 mg/kg
LD50 Rat ip 8200 mg/kg
LD50 Rat sc 12000 mg/kg
For more Non-Human Toxicity Values (Complete) data for DIMETHYL SULFOXIDE (9 total), please visit the HSDB record page.

[1]. C F Brayton. Dimethyl sulfoxide (DMSO): a review. Cornell Vet. 1986 Jan;76(1):61-90.

[2]. Dimethyl sulfoxide (DMSO) as intravesical therapy for interstitial cystitis/bladder pain syndrome: A review. Neurourol Urodyn. 2017 Sep;36(7):1677-1684.

[3]. https://www.acs.org/molecule-of-the-week/archive/d/dimethyl-sulfoxide.html

Therapeutic Uses
Cryoprotective Agents; Free Radical Scavengers; Solvents
DMSO may have anti-inflammatory, antioxidant and analgesic activities. DMSO also readily penetrates cellular membranes.
EXPL THER OBJECTIVE: To evaluate the discomfort and long-term efficacy associated with instillation of dimethyl sulfoxide (DMSO). MATERIAL AND METHODS: A total of 28 patients, 13 (11 females, 2 males) with classic interstitial cystitis (IC) and 15 (13 females, two males) with non-ulcer disease, who had received at least one series of six instillations of DMSO were studied. In addition to studying micturition diaries before and after the treatment, the evaluation included assessments of pain using a visual analog scale and of side-effects after each instillation in every series. Data were obtained by surveying the clinical records. A follow-up telephone interview was conducted for those patients who were treated with DMSO and in whom the treatment was considered successful. DMSO instillations were considered successful if the patient reported symptom amelioration and chose to continue with the treatment. RESULTS: Side-effects were not more common or pronounced in patients with classic compared to non-ulcer IC. For classic IC a significant difference could be seen when comparing side-effects experienced during the first three instillations and the three subsequent instillations. After DMSO instillations, a residual treatment effect lasting 16-72 months could be seen. CONCLUSIONS: Intravesical instillation therapy with DMSO appears to be a feasible treatment option for both subtypes of IC and is associated with a reasonably low degree of discomfort.
/Dimethyl sulfoxide is indicated/ for the symptomatic relief of patients with interstitial cystitis. /Included in US product labeling/
For more Therapeutic Uses (Complete) data for DIMETHYL SULFOXIDE (12 total), please visit the HSDB record page.

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Drug Warnings
Onyx injection is a new technique for embolization of cerebral aneurysms that is involved in a controversy about the 'toxicity' of its solvent, dimethyl sulfoxide (DMSO). /The study/ retrospectively studied 38 patients treated for aneurysms with the liquid polymer, Onyx. Induction was with propofol, fentanyl and vecuronium, and anesthesia was maintained with isoflurane in O2 and N2O. The patients were given 500 mL of fluid after induction, and bradycardia was prevented in order to keep patients hyperdynamic. Electrocardiography (ECG), non-invasive blood pressure (NIBP), pulse oximetry, core temperatures, invasive blood pressure (BP), etCO2, and urine output were monitored throughout the intervention. Heart rate and BP changes in response to balloon inflation, DMSO injection, Onyx injection and balloon deflation were recorded. The patients were followed with serial neurological examinations, computerized tomography and/or magnetic resonance imaging postoperatively for evidence of any neurological injury. Cumulative DMSO doses were always well under previously implicated doses for systemic toxicity. No changes implicating toxic reactions were observed during DMSO and Onyx injections. Balloon-induced changes returned to baseline within 1 min of balloon deflation. Technique-related permanent morbidity occurred in two patients (worsening of cranial nerve palsies in one and monocular blindness in another) and intracranial hemorrhage with resulting death in one patient. All patients showed a tendency to oxygen desaturation, but this finding did not cause any clinical consequence. Anesthesiologists need to be vigilant in monitoring patients treated with techniques that are new or are being developed. /The study/ have seen no evidence of toxicity or any anesthetic complications in our group of patients, our only clinical concern being a tendency to oxygen desaturation, which may be explained by the inhalational elimination of DMSO.
/This study/ describe/s/ the occurrence of the trigeminocardiac reflex (TCR) during DMSO pre-flushing of the microcatheter in preparation for Onyx embolization via the internal maxillary artery. TCR has not been previously associated with embolization of extradural entities. Familiarity with this clinical reflex and its proper management may help in planning neurointerventional procedures involving DMSO injection in the trigeminal territory.
Stem cell transplants are established therapy for hematologic and solid tumor malignancies. Known neurological complications of stem cell transplantation include CNS infection, seizures, strokes, metabolic encephalopathy, and hemorrhage. /This paper/ report/s/ two cases of autologous stem cell transplantation complicated by cerebral infarction and myocardial injury. /It is postulated/ that the cryopreservative dimethyl sulfoxide may be responsible.
It is not known whether this drug is excreted in human milk ... caution should be exercised when dimethyl sulfoxide is administered to a nursing woman.
For more Drug Warnings (Complete) data for DIMETHYL SULFOXIDE (20 total), please visit the HSDB record page.

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Pharmacodynamics
Dimethyl Sulfoxide may have anti-inflammatory, antioxidant and analgesic activities. Dimethyl Sulfoxide also readily penetrates cellular membranes. The membrane-penetrating ability of dimethyl sulfoxide may enhance diffusion of other substances through the skin. For this reason, mixtures of idoxuridine and dimethyl sulfoxide have been used for topical treatment of herpes zoster in the United Kingdom.

C2H6OS

78.13

78.013

67-68-5

679

Colorless to off-white liquid (>18.4°C) or solid (<18.4°C);
Melting Point: 18.4 °C

1.1±0.1 g/cm3

189.0±9.0 °C at 760 mmHg

18.4 °C

85.0±0.0 °C

0.8±0.3 mmHg at 25°C

1.480

-1.35

36.28

0

2

0

4

29

0

S(C([H])([H])[H])(C([H])([H])[H])=O

IAZDPXIOMUYVGZ-UHFFFAOYSA-N

InChI=1S/C2H6OS/c1-4(2)3/h1-2H3

methylsulfinylmethane

dimethyl sulfoxide;Methyl sulfoxide; Methylsulfinylmethane; Dimethylsulfoxide; Dimethyl sulphoxide

2934.99.9001

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

注意： 请将 DMSO 存放在密封、受保护的环境中，避免暴露在潮湿环境中。

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

Note: It is recommended to use freshly opened DMSO, as DMSO is highly hydroscopic and moisture absorption has a significant impact on the solubility of the products.

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。