DMSO is an organic solvent that is freely miscible with water, lipids and organic agents.Superior membrane penetration is made possible by these characteristics. It is believed that DMSO acts through a combination of nerve blockade, smooth muscle relaxation, collagen inhibition, and anti-inflammatory effects[2].

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Question: What is the stock concentration of a compound (e.g. in DMSO) do you recommend to use?
Answer: Usually 10 mM, 20 mM, or 50 mM. For preparing DMSO stock solutions, we suggest you to prepare a 10 mM or higher concentrations of a compound, as a more than 1000x dilution would be applied typically when making final concentrations of a compound in cell culture media, this is to minimize any solvent effects on your cells (typically less than 0.5% of DMSO might be used for most of cells).
Typically<0.5-1% DMSO is tolerable by most cancer cells in culture media. For more sensitive cells such as primary cells, try to use <0.1% DMSO in the cell culture media.

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1. Dimethyl sulfoxide exhibits anticholinesterase activity, free radical scavenging properties, and can enhance the penetration of other substances across biologic membranes in in vitro studies [1]
2. In an in vitro study using human blood cells, Dimethyl sulfoxide was found to repress the production of inflammatory cytokines; however, it did not show confirmed anticancer activity in the same research [3]

Dimethyl sulfoxide (DMSO) is a widely used solvent that is miscible with water and a wide range of organic solvents. It goes by several names, including methyl sulfoxide, sulfinylbismethane, and dozens of trade names.
DMSO was first discovered in the late 19th century as a byproduct of the kraft process for making paper from wood pulp. About the same time, Russian chemist Alexander Zaytsev synthesized it by oxidizing dimethyl sulfide, another kraft process byproduct. Zaytsev’s synthesis is the basis for the manufacturing process still used today.
DMSO is a laboratory and industrial solvent for many gases, synthetic fibers, paint, hydrocarbons, salts, and natural products. Because it is aprotic, relatively inert, nontoxic, and stable at high temperatures, it is a frequently used solvent for chemical reactions. Its deuterated form is an ideal solvent for NMR spectroscopy.
In the 1960s, scientists observed that DMSO penetrates human skin with little effect on tissues; and the solvent was tested as a way for medicines to be carried into the body as an alternative to oral formulations or injectables. Since then, DMSO has been used in some transdermal drug delivery systems (i.e., patches). In 1978 the US Food and Drug Administration approved it for use for the symptomatic relief of chronic interstitial cystitis (bladder pain syndrome)—the only FDA approval for DMSO as an actual medication.
As one might expect for the 1960s, DMSO was tried as an alternative drug for inflammation relief and as a solvent for introducing illicit drugs such as cocaine into the body. It was also wrongly touted as a cancer cure. In 1965, FDA put the kibosh on much of this activity by banning clinical trials with DMSO because the compound altered the refractive index of eye lenses of laboratory animals. The ban was lifted in 1980 after the intense interest in the substance abated.
Researchers continue to look at DMSO as a possible medical treatment. In 2016, Gerald Krystal and colleagues at the British Columbia Cancer Agency (Vancouver), the University of British Columbia (Vancouver), and Vancouver General Hospital reported that DMSO represses inflammatory cytokine production from human blood cells and thus reduces autoimmune arthritis. The authors also examined whether DMSO has any anticancer activity; they concluded that they could not confirm that it does.[3]

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1. For the treatment of interstitial cystitis/bladder pain syndrome (IC/BPS) via intravesical administration, response rates of Dimethyl sulfoxide based on subjective measurement scores range from 61% to 95% in clinical studies [2]
2. Dimethyl sulfoxide was shown to reduce autoimmune arthritis in relevant studies by repressing inflammatory cytokine production, as reported in a 2016 research [3]
3. In veterinary applications, Dimethyl sulfoxide has been used for the treatment of inflammation, ischemia, and wounds/injuries, though its approved veterinary uses are limited [1]

1. In a 2016 cell assay, human blood cells were treated with Dimethyl sulfoxide, and the production of inflammatory cytokines from these cells was measured and analyzed; the results indicated that Dimethyl sulfoxide could repress cytokine production, while the assay also evaluated its potential anticancer activity and found no confirmed evidence of such activity [3]
2. In vitro assays demonstrated that Dimethyl sulfoxide has anticholinesterase activity, with the experimental process involving the assessment of cholinesterase activity in the presence of Dimethyl sulfoxide to determine its inhibitory effect on the enzyme [1]

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.

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1. In veterinary research and applications, Dimethyl sulfoxide is administered via topical routes for conditions such as inflammation and wounds in animals like horses and rabbits; the specific dosage and frequency vary depending on the animal species and the treated condition [1]

Absorption, Distribution and Excretion
All routes of administration result in rapid absorption and systemic distribution. Dimethyl sulfoxide (DMSO) and dimethyl sulfone are excreted in urine and feces. Following topical application, DMSO is absorbed and widely distributed in tissues and body fluids. DMSO and dimethyl sulfone are excreted in urine and feces. DMSO can be excreted through respiration and skin, emitting a characteristic garlic odor. …After a single intravesical instillation, dimethyl sulfone can persist in serum for more than 2 weeks. No residual accumulation of DMSO was observed after long-term treatment. DMSO and one of its metabolites, dimethyl sulfone, are excreted in urine and feces. Dimethyl sulfide (another metabolite) is excreted through respiration and skin… This study used Fourier transform infrared spectroscopy (FTIR) imaging to detect the dynamic optical transparency process that occurs during the in vitro penetration of hypertonic biocompatible reagents into skin tissue. By continuously acquiring time-series images, the permeation kinetics of dimethyl sulfoxide (DMSO) and glycerol under the skin tissue surface over time can be evaluated. Two-dimensional infrared spectroscopy and three-dimensional pseudo-color images show that glycerol requires at least 30 minutes to finally penetrate into the epidermis, while DMSO is detectable in the epidermis 4 minutes after application to the stratum corneum of porcine skin. These results indicate that Fourier transform infrared spectroscopy can serve as an analytical tool for studying dynamic optical transparency effects when biological tissues are impregnated with hypertonic biocompatible agents such as glycerol and dimethyl sulfoxide. In humans, the radioactivity of 35S DMSO is detectable in the blood 5 minutes after skin application. Radioactivity is detectable in bones one hour later. For more complete data on the absorption, distribution, and excretion of dimethyl sulfoxide (9 types), please visit the HSDB record page. Metabolism/Metabolites: Dimethyl sulfoxide is metabolized in humans by oxidation to dimethyl sulfone or by reduction to dimethyl sulfide. Dimethyl sulfoxide (DMSO) and dimethyl sulfone (DMSO) are excreted in urine and feces. DMSO is metabolized in the human body via oxidation to DMSO or via reduction to dimethyl sulfide. Autoimmune strains MRL/Ipr, C3H/lpr, and male BXSB mice were given continuous treatment starting at 1-2 months of age, with 3% DMSO or 3% DMSO2 added to their drinking water, which was ingested freely. At this time, no spontaneous autoimmune lymphoproliferative disease was detected. The dosage of DMSO was 8-10 g/kg/day, and the dosage of DMSO2 was 6-8 g/kg/day. Both compounds extended the average lifespan of MRL/Ipr mice from 5.5 months to over 10 months. All strains of mice showed reduced antinuclear antibody responses, and the incidence of lymphadenopathy, splenomegaly, and anemia was also significantly reduced. However, serum IgG levels and splenic IgM antibody plaque formation were not different from the control group. No signs of systemic immunosuppression or antiproliferative effects were observed, and the treated animals remained healthy and vigorous without any toxic symptoms. These results indicate that high doses of DMSO and its major in vivo metabolite DMSO2 can significantly prevent the occurrence of autoimmune lymphoproliferative disease in mice. In humans, DMSO is oxidized to dimethyl sulfone DMSO2, a metabolite that is excreted in urine (17-22%). DMSO is reduced to dimethyl sulfide DMS, a volatile metabolite and a source of garlic odor in exhaled breath (1%). Approximately 85% is excreted unchanged, with 50% excreted in urine and 50% in feces. Dimethyl sulfoxide is metabolized in humans to dimethyl sulfone or dimethyl sulfide. Both dimethyl sulfoxide and dimethyl sulfone are excreted in urine and feces. Excretion routes: Both dimethyl sulfoxide and dimethyl sulfone are excreted in urine and feces.

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Biological half-life
The half-life of the original dimethyl sulfoxide is 12 to 15 hours.
/In rhesus monkeys/The half-life of dimethyl sulfoxide/is calculated to be about 38 hours, and its elimination rate constant is 0.018, that is, about 2% per hour.

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1. Dimethyl sulfoxide is an aprotic solvent with a very strong affinity for water; pure dimethyl sulfoxide is rapidly diluted when exposed to air[1].

Toxicity Summary
Identification and Uses: Dimethyl sulfoxide (DMSO) is a colorless, highly hygroscopic liquid. It has a long history in the pharmaceutical industry and is currently widely used as a penetration enhancer in topical drug formulations. Currently, DMSO is used in medications such as diclofenac sodium topical solution (approved in the US for the treatment of signs and symptoms of osteoarthritis) and idoxuridine topical solution (approved in Europe for the treatment of shingles). DMSO is also used to relieve symptoms of interstitial cystitis. DMSO is not a nutritional supplement; it is metabolized into methanesulfonylmethane (MSM), which can be used as a nutritional supplement. DMSO is used for the cryopreservation of cell populations, including stem cells, embryos, and various cell cultures. Additionally, DMSO is used as an industrial solvent and, when mixed with water, can be used as an antifreeze or hydraulic fluid. Human Exposure and Toxicity: Skin contact with dimethyl sulfoxide (DMSO) causes skin reactions, including erythema and pruritus, which usually appear immediately after exposure to undiluted DMSO; 70% DMSO solution is generally tolerated asymptomatically. However, in highly sensitive individuals, reactions can occur even after exposure to 10% DMSO solution. In humans, topical and intradermal application of DMSO can cause garlic-smelling breath, mast cell degranulation, polymorphonuclear leukocytosis and perivascular eosinophilia, pruritus, and histamine-mediated and non-histamine-dependent wheals and erythema. Two drops of >50% DMSO instilled into the eyes cause transient burning sensation and vasodilation; <50% DMSO has no such effect. There have been case reports of sulfohmoglobinemia following DMSO skin exposure. Animal Experiments: To investigate the effects of acute DMSO exposure, undressed rats were immersed in DMSO solution. No immediate reaction was observed in the rats, but within 24 hours, 13 out of 14 rats immersed in 100% DMSO solution died. Five male and five female rats were given a single intravenous injection of undiluted DMSO at doses of 2.5, 5.0, and 10 g/kg, respectively, with a 1-minute interval between injections. The animals were observed for 14 days after DMSO administration; all but one rat died within 24 hours. Before death, rats exhibited tremors, myasthenia gravis, dyspnea, and occasionally convulsions. Non-lethal doses of DMSO caused decreased motor activity and myasthenia gravis. Thirty-two male rats were exposed to 200 mg/m³ of DMSO in the air for 7 hours daily, 5 days a week, for 6 weeks, for a total of 30 exposures. During the 6-week experiment, none of the exposed animals showed any external signs of poisoning. A distinctive garlic odor characteristic of DMSO was detected in the breath of each rat after the first day of exposure. Four groups of rhesus monkeys were administered 90% pharmaceutical-grade DMSO solution via gastric tube for 7 days a week for up to 87 weeks. The administered doses were equivalent to 990, 2970, and 8910 mg/kg/day, respectively. The main signs in animals in the oral DMSO group included occasional salivation and vomiting. Anorexia occurred only in the high-dose oral group. Physical examination revealed no DMSO-related changes. Gross examination at necropsy revealed no obvious lesions caused by DMSO. No histological changes were observed in the lens of the treated animals. In developmental studies, 5–6 pregnant golden hamsters were divided into groups and administered DMSO intravenously on day 8 of gestation at doses ranging from 50 to 5500 mg/kg, or intraperitoneally at doses ranging from 5500 to 8250 mg/kg. Examination of the embryos 3 days later revealed no embryonic lethality or teratogenicity up to DMSO doses reaching 2500 mg/kg. At higher doses, malformations occurred, including encephalocele, rib fusion, microphthalmia, limb abnormalities, and cleft lip. DMSO had no significant effect on maternal weight gain or health. DMSO at concentrations up to 5000 μg/mL was tested in Chinese hamster ovary cells with or without metabolic activation. DMSO did not induce cytotoxicity or cell cycle delay, nor did it increase the incidence of sister chromatid exchange (SCE). Intraperitoneal injection of DMSO did not induce sex-linked recessive lethality, nor did it increase the frequency of sex chromosome loss in Drosophila melanogaster to above spontaneous levels. DMSO was tested in five Salmonella typhimurium test strains (TA 98, 100, 1535, 1537, and 1538). Results for DMSO were negative regardless of the presence or absence of metabolic activation. Ecotoxicity studies: Acute toxicity (g/kg body weight) of intraperitoneal injection of dimethyl sulfoxide (DMSO) to Chinook salmon (Oncorhynchus tshawytscha): LD50 = 12.0, sockeye salmon (Oncorhynchus nerka): LD50 = 13.0, coho salmon (Oncorhynchus kisutch): LD50 = 16.0, rainbow trout (Salmo gardneri): LD50 = 17.0. Fish typically die within 24 hours; however, a minority die within 24 to 48 hours. The mechanism of action of DMSO is not fully understood. DMSO exhibits antioxidant activity under certain biological conditions. For example, the cardiovascular protective effect of DMSO in copper-deficient rats is thought to be mediated through an antioxidant mechanism. The potential anti-inflammatory activity of DMSO is also believed to be attributable to its antioxidant properties.

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

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Interactions
Previous studies in our lab have shown that even low concentrations of peroxynitrite can cause rapid necrosis in U937 cells, but this necrosis can be prevented by a survival signaling pathway driven by arachidonic acid released from cytoplasmic phospholipase A2. The toxicity is mediated by peroxynitrite concentration, leading to H2O2-dependent inhibition of arachidonic acid release. This study demonstrates that U937 cells differentiated into monocytes after long-term treatment with dimethyl sulfoxide are resistant to peroxynitrite because they respond to it by enhancing arachidonic acid release. Another important finding is that these cells require more arachidonic acid than undifferentiated cells to maintain their survival signaling. The enhanced arachidonic acid release was not related to changes in cytoplasmic phospholipase A2 expression, but rather depended on increased sensitivity of this enzyme to calcium-dependent stimuli and decreased mitochondrial H₂O₂ production. The latter is considered a key factor because differentiated and undifferentiated cells showed similar sensitivity to peroxynitrite when H₂O₂ accumulation was enhanced by depletion of catalase or the addition of a complex III inhibitor. Therefore, the chosen strategy for responding to peroxynitrite during monocyte differentiation appears to involve a specific mechanism that prevents mitochondrial H₂O₂ production.
Rats were intraperitoneally injected with thioacetamide (400 mg/kg body weight). After 12 hours, plasma aspartate aminotransferase (AST) and alanine aminotransferase (GPT) activities were significantly higher than in the control group; after 24 hours, plasma GOT and GPT activities were significantly increased. These results indicate that the necrosis process initiates approximately 12 hours later and subsequently progresses. Administration of dimethyl sulfoxide (DMSO, 2.5 mL/kg body weight, orally) 18 hours, 1 hour, and 8 hours before administration of thioacetamide significantly reduced plasma aspartate aminotransferase (AST) and alanine aminotransferase (GPT) levels, even to levels comparable to the control group, indicating that DMSO completely inhibited the necrotizing effect of thioacetamide. At 12 and 24 hours after thioacetamide administration, liver vitamin C levels (the most sensitive chemical indicator of oxidative stress) significantly decreased, indicating that oxidative stress was significantly enhanced 12 hours after thioacetamide poisoning. DMSO completely restored liver vitamin C levels, indicating that DMSO effectively alleviated oxidative stress induced by thioacetamide, thereby preventing liver necrosis. At 12 hours after thioacetamide treatment, phosphorylated c-Jun N-terminal kinase (JNK) levels transiently and significantly increased. These results indicate that oxidative stress and JNK activation occur almost simultaneously. At 6–12 hours after thioacetamide injection, phosphorylated extracellular signal-regulated kinase (ERK) 2 levels significantly increased. Twenty-four hours after administration of thioacetamide, phosphorylated p38 MAPK (mitogen-activated protein kinase) levels were significantly reduced. DMSO treatment inhibited these MAPK changes induced by thioacetamide, consistent with the prevention of liver necrosis and reduction of oxidative stress. Increasing evidence suggests that irradiated cells produce signals that interact with unirradiated cells in the same population via the bystander effect. This study investigated whether DMSO could effectively inhibit radiation-induced bystander effects in CHO cells and repair-deficient xrs5 cells. When CHO cells irradiated with 1 Gy were treated with 0.5% DMSO for 1 hour before irradiation, the induction rate of micronuclei in irradiated cells was suppressed to 80% of that in untreated irradiated cells. The study also examined the inhibitory effect of DMSO on bystander signaling, showing that 0.5% DMSO treatment of irradiated cells completely inhibited bystander effect-induced micronucleus formation in unirradiated cells. This suggests that DMSO can prevent irradiated cells from producing bystander effect signals. To determine the role of reactive oxygen species (ROS) in bystander signaling, this study used 2,7-dichlorofluorescein (DCFH) staining to detect oxidative stress levels in irradiated cell populations. The results showed that treatment with 0.5% DMSO did not suppress oxidative stress levels. These results suggest that prevention of oxidative stress is not related to the inhibitory effect of DMSO on bystander signaling in irradiated cells. Therefore, it is speculated that the increase of ROS in irradiated cells is not a major trigger for bystander signaling.
Ultrasoft X-rays have been shown to induce chromosomal aberrations in mammalian cells very effectively. This study aimed to evaluate the effect of DMSO (a potent free radical scavenger) on the frequency of soft X-ray-induced chromosomal aberrations. Confluent G1-phase Chinese hamster cells (V79) were irradiated with or without 1M DMSO using carbon K ultrasoft X-rays, and the frequency of chromosomal aberrations in first-dividing cells was measured. DMSO reduced the frequency of exchangeable aberrations (dicentric chromosomes and centromere loops) by 2.1–3.5-fold. The results showed that free radicals induced by ultrasoft X-rays largely promoted the occurrence of chromosomal aberrations. This paper discusses the potential implications of these results in explaining the mechanism of ultrasoft X-rays' efficient induction of chromosomal aberrations.
For more complete data on interactions of dimethyl sulfoxide (33 in total), please visit the HSDB record page.

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Non-human toxicity values
Oral LD50 in rats: 17.9 mL/kg
Oral LD50 in rats: 14500 mg/kg
Intraperitoneal LD50 in rats: 8200 mg/kg
Subcutaneous LD50 in rats: 12000 mg/kg
For more complete data on non-human toxicity values of dimethyl sulfoxide (9 in total), please visit the HSDB record page.

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1. The systemic toxicity of dimethyl sulfoxide is considered to be low, but its toxicity is significantly increased when used in combination with other toxic substances[1].
2. Dimethyl sulfoxide can induce the release of histamine from mast cells, which may lead to some adverse reactions[1]. 3. In laboratory animals, dimethyl sulfoxide was found to alter the refractive index of the lens of the eye, which led the U.S. Food and Drug Administration (FDA) to temporarily ban its clinical trials in 1965[3]. 4. Under the Globally Harmonized Classification and Labelling System (GHS), dimethyl sulfoxide is classified as a Group 4 flammable liquid (flammable liquid) with a hazard statement of H227[3]. 5. Related toxicological studies have shown that dimethyl sulfoxide may cause chemical-induced liver and kidney disease[1].

[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
Cryoprotectant; Free radical scavenger; Solvent. Dimethyl sulfoxide (DMSO) may have anti-inflammatory, antioxidant, and analgesic effects. DMSO also readily penetrates cell membranes. Exploratory Therapeutic Objective: To evaluate the discomfort and long-term efficacy of DMSO instillation therapy. Materials and Methods: A total of 28 patients were included, including 13 patients (11 females, 2 males) with classic interstitial cystitis (IC) and 15 patients (13 females, 2 males) with non-ulcerative interstitial cystitis. All patients had received at least one course (6 sessions) of DMSO instillation therapy. In addition to studying voiding diaries before and after treatment, assessments included pain intensity and side effects after each instillation in each course using the visual analog scale (VAS). Data were obtained by reviewing clinical records. Patients who received DMSO treatment and were considered to have received successful treatment were followed up with telephone interviews. DMSO instillation therapy was considered successful if the patient reported symptom relief and chose to continue treatment. Results: The incidence and severity of side effects were not higher in patients with classic IC compared to patients with non-ulcerative interstitial cystitis (IC). For classic IC, significant differences were found in the side effects observed between the first three instillations and the subsequent three instillations. Residual therapeutic effects were observed for 16–72 months after DMSO instillation. Conclusion: Intravesical instillation of DMSO appears to be a viable treatment option for both subtypes of IC with relatively low discomfort. Dimethyl sulfoxide is indicated for symptom relief in patients with interstitial cystitis. /Included in US product label/
For more complete data on the therapeutic uses of dimethyl sulfoxide (of 12), please visit the HSDB record page.

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Drug Warning
Onyx injection is a new technology for embolization of cerebral aneurysms, but the "toxicity" of its solvent, dimethyl sulfoxide (DMSO), has been controversial. /This study/ Retrospectively analyzed 38 patients treated with the liquid polymer Onyx for aneurysms. Anesthesia was induced with propofol, fentanyl, and vecuronium bromide, and maintained with isoflurane, oxygen, and nitrous oxide. Following induction, the patient received 500 ml of fluids and bradycardia was prevented to maintain a hyperdynamic state. Throughout the procedure, electrocardiogram (ECG), noninvasive blood pressure (NIBP), pulse oximetry, core temperature, invasive blood pressure (BP), end-tidal carbon dioxide partial pressure (etCO2), and urine output were monitored. Changes in heart rate and blood pressure were recorded during balloon inflation, dimethyl sulfoxide (DMSO) injection, Onyx injection, and balloon deflation. Postoperatively, the patient underwent a series of neurological examinations, computed tomography (CT), and/or magnetic resonance imaging (MRI) to assess for neurological damage. The cumulative dose of DMSO was consistently well below previously reported systemic toxicity levels. No changes indicative of toxicity were observed during DMSO and Onyx injections. Balloon-induced changes returned to baseline levels within one minute of deflation. Two patients experienced permanent surgery-related complications (one suffered worsening cranial nerve palsy, and the other lost sight in one eye), and one patient developed intracranial hemorrhage and ultimately died. All patients exhibited a tendency towards decreased oxygen saturation, but this finding did not result in any clinical consequences. Anesthesiologists need to closely monitor patients receiving treatments using novel or developing technologies. This study found no evidence of any toxicity or anesthetic complications in our patient group; our only clinical concern was the tendency towards decreased oxygen saturation, which may have been due to clearance from inhaled DMSO. This study describes the trigeminal cardiac reflex (TCR) that occurred during DMSO pre-flushing of the microcatheter prior to Onyx embolization via the internal maxillary artery. Previously, TCR had not been associated with embolization of epidural lesions. Familiarity with this clinical reflex and its proper management may aid in planning neurointerventional procedures involving DMSO injection into the trigeminal nerve innervation region. Stem cell transplantation is a well-established therapy for hematologic malignancies and solid tumors. Known neurological complications of stem cell transplantation include central nervous system infections, seizures, stroke, metabolic encephalopathy, and hemorrhage. This article reports two cases of cerebral infarction and myocardial injury following autologous stem cell transplantation. The cryopreservative dimethyl sulfoxide (DMSO) is suspected to be the culprit. It is currently unclear whether this drug is excreted into human breast milk… Caution should be exercised when using DMSO in breastfeeding women. For more complete data on DMSO (20 total), please visit the HSDB records page. Pharmacodynamics: DMSO may have anti-inflammatory, antioxidant, and analgesic effects. DMSO also readily penetrates cell membranes. The membrane-penetrating ability of DMSO may enhance the diffusion of other substances through the skin. Therefore, in the UK, mixtures of idoxuridine and DMSO have been used for the topical treatment of herpes zoster.

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1. Dimethyl sulfoxide (DMSO) is a simple aprotic solvent that was first discovered in the late 19th century as a byproduct of the kraft papermaking process; it was also synthesized by Russian chemist Alexander Zaitsev through the oxidation of dimethyl sulfide, a method that remains the basis for its modern production.[3]
2. In 1978, the U.S. Food and Drug Administration (FDA) approved DMSO for the relief of symptoms of chronic interstitial cystitis (bladder pain syndrome), the only indication for which the FDA approved DMSO as a drug.[3]
3. Dimethyl sulfoxide (DMSO) has been wrongly touted as a cancer treatment drug and has also been misused as a solvent for injecting illicit drugs into the body.[3]
4. Dimethyl sulfoxide is a widely used solvent in laboratories and industries, and can be used for gases, synthetic fibers, paints, hydrocarbons, salts and natural products; its deuterated form is an ideal solvent for nuclear magnetic resonance spectroscopy.[3]
5. Dimethyl sulfoxide (DMSO) is a useful C1 source in organic synthesis, participating in iodine-catalyzed [2+2+1] cascade reactions to generate pyrazole derivatives, and it is also a solvent for this reaction [3]. 6. In clinical studies of intravesical instillation of DMSO for the treatment of interstitial cystitis/bladder pain syndrome (IC/BPS), there are significant differences in diagnostic criteria, instillation protocols, and response measurement methods; there is no consensus on optimal dose, residence time, patient subtype, and number of treatments [2]. 7. Dimethyl sulfoxide (DMSO) has been used in some transdermal drug delivery systems (e.g., patches) due to its ability to penetrate human skin and minimal impact on tissues [3]. 8. In 1980, after a period of intense interest in DMSO, the FDA lifted its ban on clinical trials of it [3].

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

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

Note: Please store DMSO in a sealed and protected environment, avoid exposure to moisture.

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.

Note: Listed below are some common formulations that may be used to formulate products with low water solubility (e.g. < 1 mg/mL), you may test these formulations using a minute amount of products to avoid loss of samples.

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Injection Formulation 1: DMSO : Tween 80： Saline = 10 : 5 : 85 (i.e. 100 μL DMSO stock solution → 50 μL Tween 80 → 850 μL Saline)
*Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH ₂ O to obtain a clear solution.
Injection Formulation 2: DMSO : PEG300 ：Tween 80 : Saline = 10 : 40 : 5 : 45 (i.e. 100 μL DMSO → 400 μLPEG300 → 50 μL Tween 80 → 450 μL Saline)
Injection Formulation 3: DMSO : Corn oil = 10 : 90 (i.e. 100 μL DMSO → 900 μL Corn oil)
Example: Take the Injection Formulation 3 (DMSO : Corn oil = 10 : 90) as an example, if 1 mL of 2.5 mg/mL working solution is to be prepared, you can take 100 μL 25 mg/mL DMSO stock solution and add to 900 μL corn oil, mix well to obtain a clear or suspension solution (2.5 mg/mL, ready for use in animals).

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Injection Formulation 4: DMSO : 20% SBE-β-CD in saline = 10 : 90 [i.e. 100 μL DMSO → 900 μL (20% SBE-β-CD in saline)]
*Preparation of 20% SBE-β-CD in Saline (4°C，1 week): Dissolve 2 g SBE-β-CD in 10 mL saline to obtain a clear solution.
Injection Formulation 5: 2-Hydroxypropyl-β-cyclodextrin : Saline = 50 : 50 (i.e. 500 μL 2-Hydroxypropyl-β-cyclodextrin → 500 μL Saline)
Injection Formulation 6: DMSO : PEG300 : castor oil : Saline = 5 : 10 : 20 : 65 (i.e. 50 μL DMSO → 100 μLPEG300 → 200 μL castor oil → 650 μL Saline)
Injection Formulation 7: Ethanol : Cremophor : Saline = 10： 10 : 80 (i.e. 100 μL Ethanol → 100 μL Cremophor → 800 μL Saline)
Injection Formulation 8: Dissolve in Cremophor/Ethanol (50 : 50), then diluted by Saline
Injection Formulation 9: EtOH : Corn oil = 10 : 90 (i.e. 100 μL EtOH → 900 μL Corn oil)
Injection Formulation 10: EtOH : PEG300：Tween 80 : Saline = 10 : 40 : 5 : 45 (i.e. 100 μL EtOH → 400 μLPEG300 → 50 μL Tween 80 → 450 μL Saline)

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Oral Formulation 1: Suspend in 0.5% CMC Na (carboxymethylcellulose sodium)
Oral Formulation 2: Suspend in 0.5% Carboxymethyl cellulose
Example: Take the Oral Formulation 1 (Suspend in 0.5% CMC Na) as an example, if 100 mL of 2.5 mg/mL working solution is to be prepared, you can first prepare 0.5% CMC Na solution by measuring 0.5 g CMC Na and dissolve it in 100 mL ddH2O to obtain a clear solution; then add 250 mg of the product to 100 mL 0.5% CMC Na solution, to make the suspension solution (2.5 mg/mL, ready for use in animals).

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Oral Formulation 3: Dissolved in PEG400
Oral Formulation 4: Suspend in 0.2% Carboxymethyl cellulose
Oral Formulation 5: Dissolve in 0.25% Tween 80 and 0.5% Carboxymethyl cellulose
Oral Formulation 6: Mixing with food powders

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Note: Please be aware that the above formulations are for reference only. InvivoChem strongly recommends customers to read literature methods/protocols carefully before determining which formulation you should use for in vivo studies, as different compounds have different solubility properties and have to be formulated differently.

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 (Please use freshly prepared in vivo formulations for optimal results.)