It has also been demonstrated that sesamol is a well-known inhibitor of lipid peroxidation [1]. Human liver cancer (HepG2) cells can be successfully induced to undergo apoptosis by sesamol (0–1 mM) [2]. Sesamol causes both endogenous and extrinsic apoptosis and suppresses the growth of HepG2 cells [2]. Treatment with sesamol results in loss of mitochondrial membrane potential, which leads to mitochondrial malfunction. PI3K Class III/Belin-1 pathway blockade by sesamol results in the inhibition of mitophagy and autophagy. Sesamol had no effect on the expression of the apoptosis signal Bax, but it did decrease the expression of the anti-apoptotic protein Bcl-2. Sesamol can activate tBid and caspase-8, which are implicated in the extrinsic apoptosis pathway, and raise the expression of the Fas/FasL protein [2].

---

- In the Epstein-Barr virus (EBV) early antigen (EA) activation assay using Raji cells, Sesamol exhibited chemopreventive activity by inhibiting EBV EA activation induced by 12-O-tetradecanoylphorbol-13-acetate (TPA). The inhibitory effect was concentration-dependent [1]
- In human hepatocellular carcinoma (HCC) cell lines (HepG2 and Hep3B), Sesamol induced apoptosis. It reduced cell viability in a time- and concentration-dependent manner: treatment with Sesamol (25-100 μM) for 24-48 hours significantly decreased cell viability compared to the control group. Sesamol also disrupted mitochondrial function, as shown by reduced mitochondrial membrane potential (ΔΨm), increased release of cytochrome c from mitochondria to cytoplasm, and altered expression of apoptotic proteins (upregulated Bax, downregulated Bcl-2). Additionally, Sesamol suppressed autophagy, evidenced by decreased LC3-I to LC3-II conversion and increased p62 protein accumulation. [2]

Treatment with sesamol for 35 days did not significantly affect body weight, but tumor volume was significantly inhibited (the volume inhibition rate of 200 mg/kg sesamol was 40.56% compared with the control group). However, the lower dose (100 mg/kg sesamol) only had a significant anti-tumor growth effect within 27 days after the first treatment [2]. The Bcl-2/Bax ratio in tumor tissue was also reduced. In addition, in the Sesamol treatment group, compared with the control group, the level of cell proliferation marker Ki76 was down-regulated and the level of apoptotic marker cleaved-caspase 3 was elevated. Sesamol can drastically suppress the expression of LC3 protein in a dose-dependent manner [2].

---

- In the mouse skin two-stage carcinogenesis model, Sesamol showed chemopreventive effects. Female ICR mice were first initiated with 7,12-dimethylbenz[a]anthracene (DMBA) (100 μg/mouse) via intradermal injection. After 1 week, mice were promoted with TPA (1 μg/mouse) twice weekly for 20 weeks. Topical application of Sesamol (0.5, 1, or 2 mg/mouse) 30 minutes before each TPA treatment reduced skin tumor incidence, the average number of tumors per mouse, and tumor size compared to the TPA-only control group. [1]

- EBV EA activation assay (Raji cells): Raji cells (EBV-carrying human B lymphoblastoid cells) were cultured in RPMI 1640 medium supplemented with fetal bovine serum and antibiotics. Cells were seeded in 24-well plates, then treated with TPA (40 ng/mL) to induce EBV EA activation. Sesamol was added to the culture medium at different concentrations simultaneously with TPA. After 48 hours of incubation at 37°C with 5% CO₂, cells were fixed with acetone-methanol (1:1, v/v) and stained with anti-EBV EA monoclonal antibody. The number of EA-positive cells was counted under a fluorescence microscope, and the inhibition rate of Sesamol on EBV EA activation was calculated. [1]
- HCC cell viability and apoptosis assay (HepG2/Hep3B cells): HepG2 and Hep3B cells were cultured in DMEM medium supplemented with fetal bovine serum and antibiotics. For cell viability assay, cells were seeded in 96-well plates, incubated overnight, then treated with Sesamol (0-100 μM) for 24 or 48 hours. A cell counting kit was used to measure absorbance at 450 nm, and cell viability was calculated relative to the control group. For apoptosis detection, cells were treated with Sesamol (50 μM) for 24 hours, stained with Annexin V-FITC and propidium iodide, and analyzed by flow cytometry to determine the apoptotic rate. For mitochondrial membrane potential detection, cells were treated with Sesamol (50 μM) for 24 hours, stained with JC-1 dye, and analyzed by flow cytometry to measure ΔΨm changes. For western blot analysis, cells treated with Sesamol (25-100 μM) for 24 hours were lysed, and proteins (Bax, Bcl-2, cytochrome c, LC3, p62) were separated by SDS-PAGE, transferred to membranes, and probed with specific primary antibodies and secondary antibodies; band intensity was quantified by densitometry. [2]

- Mouse skin two-stage carcinogenesis experiment: Female ICR mice (6-8 weeks old) were acclimated for 1 week before the experiment. On day 0, all mice received an intradermal injection of DMBA (100 μg/mouse) in 0.1 mL acetone on the dorsal skin to initiate carcinogenesis. One week later, mice were randomly divided into groups: TPA control group (topical application of 1 μg TPA in 0.1 mL acetone twice weekly) and Sesamol treatment groups (topical application of Sesamol at 0.5, 1, or 2 mg/mouse in 0.1 mL acetone 30 minutes before each TPA application). The treatment lasted for 20 weeks. During the experiment, mice were monitored weekly for skin tumor formation (tumors ≥1 mm in diameter were counted), and tumor size was measured with calipers. At the end of the experiment, mice were euthanized, and skin tissues were collected for further analysis (if any). [1]

Absorption, Distribution and Excretion
Sesamol is generally considered the main antioxidant component of sesame oil, generated from sesamin through roasting sesame seeds or bleaching sesame oil. This article reports the bioavailability of sesamol in Sprague-Dawley (SD) rats. Biological fluid samples were collected from SD rats after administration of 50 mg/kg sesamol via gastric perfusion (po) or intravenous injection. Pharmacokinetic data of sesamol were calculated using a non-compartmental model. The tissue distribution of 100 mg/kg sesamol in SD rats was also investigated. Concentration changes of sesamol in various tissues and plasma were measured within 24 hours after oral administration. The results showed that the oral bioavailability of sesamol was 35.5 ± 8.5%. Sesamol was found to cross the blood-brain barrier and be excreted via the hepatobiliary system. Sesamol-bound metabolites were widely distributed in SD rat tissues, with the highest concentrations in the liver and kidneys and the lowest in the brain. It is speculated that sesamol is first absorbed by the liver and then transported to other tissues (lung, kidney, and brain). The main sesamol metabolites distributed in the lungs and kidneys are glucuronide and sulfate. Sesamol (3,4-methylenedioxyphenol) is a phenolic component of roasted sesame seeds and has been reported to possess various beneficial activities. To understand the metabolic transformation of sesamol in vivo, this study administered sesamol to rats via intravenous injection and oral administration, and collected blood samples via cardiac puncture at specific time points. High-performance liquid chromatography (HPLC) was used to analyze serum samples before and after hydrolysis by sulfatase and β-glucuronidase. The results showed that sesamol decreased rapidly after intravenous or oral administration, while its sulfate/glucuronide content appeared immediately. The peak serum concentration and systemic exposure of sesamol were significantly lower than those of its sulfate/glucuronide content. In vitro experiments showed that sesamol significantly induced hemolysis with 2,2'-azobis(2-amidinylpropane) dihydrochloride than its serum metabolites. In summary, sesamol sulfate and glucuronide are the main metabolites of sesamol in rat blood. Further research is warranted on the conjugated metabolites of sesamol to understand its in vivo effects. This article reports the bioavailability of sesamol in Sprague-Dawley (SD) rats… Sesamol conjugated metabolites are widely distributed in SD rat tissues, with the highest concentrations in the liver and kidneys, and the lowest concentrations in the brain. It is speculated that sesamol is first absorbed by the liver and then transported to other tissues (lung, kidney, and brain). The main sesamol metabolites distributed in the lungs and kidneys are glucuronide and sulfate.

Toxicity Summary
Identification and Uses: Sesamol is generally considered the main antioxidant component of sesame oil, generated through roasting sesame seeds or bleaching sesamin in sesame oil. The sesamol content increases after heating sesame oil at frying temperatures for 1 to 2 hours. Sesamol possesses antioxidant, lipid-lowering, and antidepressant activities. It has been used in experimental therapies. Human Studies: In patients allergic to sesame oil, patch tests showed a positive reaction to sesamol in 8 out of 13 patients. In tests on human breast cancer cells, sesamol exhibited weak estrogenic/anti-estrogenic activity. Sesamol effectively induced apoptosis in HepG2 cells. The oxidation product of sesamol—tetramer—inhibited the growth of human leukemia K562 cells. Animal Studies: In mice, acute toxicity was observed at a dose of 2000 mg/kg, while no adverse reactions were observed at a dose of 300 mg/kg. A dose of 2000 mg/kg resulted in severe histopathological changes in all organs (femur, spleen, gastrointestinal tract, lung, heart, kidney, liver, stomach, and brain), with excessive DNA strand breaks in femoral bone marrow cells and spleen cells. Dietary supplementation with 2% sesamol induced squamous cell carcinoma of the forestomach in rats and mice, with males being more susceptible than females. However, after 20 weeks of treatment with 12-O-tetradecanoylphorbol-13-acetate (TPA), sesamol treatment reduced cutaneous papillomas in mice by 50%. Sesamol exhibits protective effects against ionizing and ultraviolet radiation both in vivo and in vitro. Sesamol demonstrated strong antimutagenic activity in the Ames test lines TA100 and TA102. Mutagenicity was induced by oxygen free radicals generated from tert-butyl hydrogen peroxide or hydrogen peroxide. Sesamol also protects the body from carbon tetrachloride poisoning and acute liver injury caused by acetaminophen overdose. Sesamol also exhibits protective effects in animal models of streptozotocin-induced diabetes and isoproterenol-induced myocardial infarction. Sesamol is a nutrient found in sesame seeds and possesses antioxidant, lipid-lowering, and antidepressant activities. However, few studies have reported its effects on cognitive decline induced by high-energy-density diets. This study aimed to elucidate the role of sesamol in central nervous system insulin resistance and learning and memory impairment induced by a high-fat, high-fructose (HFFD) “Western” diet, and to further explore its potential mechanisms. Three-month-old C57BL/6J mice were randomly divided into three groups, with or without sesamol (0.05%, w/v) added to their drinking water, and fed a standard diet, a high-fat, high-sugar (HFFD) diet, and a high-fat, high-sugar diet supplemented with sesamol, respectively. Morris water maze tests showed that sesamol could improve learning and memory decline induced by a high-fat, high-sugar diet in mice. Furthermore, sesamol could also alleviate neuronal damage in mice fed a high-fat, high-sugar diet. Importantly, sesamol treatment upregulated brain insulin signaling by activating the IRS-1/AKT and ERK/CREB/BDNF pathways; simultaneously, it downregulated the neuronal death signaling pathways GSK3β and JNK. Furthermore, sesamol restored normal mRNA expression of neurotrophic factors, including BDNF and NT-3, as well as genes related to mitochondrial metabolism and biosynthesis, Sirt1 and PGC1α. Sesamol persistently reversed high glucose-induced oxidative state, mitochondrial membrane potential loss, insulin signaling inhibition, and cell death in SH-SY5Y neurons. In summary, this study demonstrates that sesamol alleviates high-fat diet-induced cognitive deficits in mice by inhibiting insulin resistance, normalizing mitochondrial function and cellular redox state, and improving IRS/AKT cell survival and energy metabolism regulatory signaling pathways. This compelling evidence suggests that sesamol is a potential nutritional supplement for preventing learning and memory loss caused by unhealthy diets.
Ionizing radiation exposure is harmful; high doses can lead to acute hematopoietic radiation syndrome. Therefore, drugs that can protect the hematopoietic system are crucial for the development of radioprotective agents. Sesamol possesses potent free radical scavenging and antioxidant properties, making it a potential molecule for radioprotective agent development. This study evaluated the effects of sesamol on DNA damage and repair in the hematopoietic system of CB57BL/6 mice irradiated with gamma rays, comparing it with amifostine. Male CB57BL/6 mice were intraperitoneally injected with 20 mg/kg sesamol and then subjected to whole-brain irradiation (WBI) at 2 Gy 30 minutes later. Mice were sacrificed at 0.5, 3, and 24 hours post-irradiation; bone marrow, spleen cells, and peripheral blood lymphocytes were isolated, and DNA damage and repair were assessed using the basic comet test, γ-H2AX test, and micronucleus test. The results showed that the percentage of tail DNA was increased in all organs of mice in the WBI group. Pre-injection of sesamol reduced the percentage of tail DNA (P=0.05). Sesamol also reduced the formation of radiation-induced γ-H2AX foci in these organs (after 0.5 hours) and further reduced them to the corresponding control levels 24 hours after whole-brain irradiation (WBI). Similar reductions in tail DNA percentage and γ-H2AX foci were observed with amifostine (P=0.05). Analysis of mnPCE frequency after 24 hours showed that sesamol and amifostine had similar protective effects. Notably, both sesamol and amifostine, alone or in combination with radiation, significantly increased granulocyte counts (P=0.05). These results suggest that sesamol has significant potential to protect the hematopoietic system by reducing radiation-induced DNA damage and to prevent acute hematopoietic syndrome in mice.
Background: Sesamol is a component of sesame oil and has shown significant antioxidant activity in a range of in vitro and in vitro studies, including lipid peroxidation induced in rat liver homogenate. The latter confirms its hepatoprotective potential. However, its limited oral bioavailability, rapid clearance (in conjugate form), and tendency to cause gastric irritation/toxicity (especially in the rodent forestomach) may limit its application. Currently, we encapsulate sesamol in solid lipid nanoparticles (S-SLNs) to enhance its biopharmaceutical properties and compare its efficacy with that of free sesamol and silymarin (a known hepatoprotective agent) in a carbon tetrachloride-induced rat model of liver injury. This study established a self-healing group that received no treatment to observe the liver's self-healing capacity. Methods: S-SLNs were prepared using a microemulsion method and administered to rats treated with CCl4 (1 mL/kg body weight, twice weekly for 2 weeks; followed by 1.5 mL/kg body weight, twice weekly for 2 weeks). Liver injury and post-treatment recovery were assessed by histopathology, serum injury markers (alanine aminotransferase, aspartate aminotransferase), oxidative stress markers (lipid peroxidation, superoxide dismutase, and reduced glutathione), and pro-inflammatory markers (tumor necrosis factor-α). Results: S-SLNs (120.30 nm) at a dose of 8 mg/kg body weight showed significantly better hepatoprotective effects than the corresponding dose of free sesamol (FS) (p < 0.001). The effect achieved using S-SLNs was comparable to that of silymarin (SILY) administered at a dose of 25 mg/kg body weight. The self-healing group demonstrated a lack of regenerative capacity of liver tissue after injury. Conclusion: Delivery of sesamol using a lipid nanocarrier system can improve its efficiency in controlling liver injury. The enhanced effect may be attributed to: a) improved oral bioavailability; b) the controllable and longer-lasting effects of encapsulated sesamol; and c) reduced irritation and toxicity (if any) after oral administration. S-SLNs have been shown to be effective after inducing liver injury and can therefore be considered a treatment option for liver diseases. /Solid lipid nanoparticles loaded with sesamol/
Ionizing radiation causes free radical-mediated damage to cellular DNA. This damage manifests as chromosomal aberrations and micronuclei (MNs) in proliferating cells. Sesamol, found in sesame seeds, has the potential to scavenge free radicals; therefore, it can reduce radiation-induced cellular genetic damage. This study aimed to investigate the radioprotective effect of sesamol on mouse bone marrow cells and related hematopoietic systems against radiation-induced genotoxicity. A comparative experiment with melatonin was designed to evaluate the radioprotective effect of sesamol. C57BL/6 mice were intraperitoneally injected with either sesamol or melatonin (10 and 20 mg/kg body weight) 30 minutes before receiving 2 Gy whole-body irradiation (WBI) and sacrificed 24 hours later. Total chromosomal aberrations (TCA), micronuclei (MN), and cell cycle analysis were performed on bone marrow cells. Comet assays were performed on bone marrow cells, spleen cells, and lymphocytes. Blood samples were collected to detect hematological parameters. In irradiated mice, prophylactic administration of sesamol (10 and 20 mg/kg) reduced the frequency of trichloroacetic acid (TCA) and micronucleated polychromatic erythrocytes in bone marrow cells by 57% and 50%, respectively, compared to the irradiation-only group. Sesamol reduced radiation-induced apoptosis and promoted cell proliferation. In the comet assay, sesamol (20 mg/kg) treatment significantly reduced radiation-induced comet formation (percentage of DNA in the comet tail) compared to the radiation-only group (P < 0.05). Sesamol also increased the number of granulocytes in peripheral blood, with effects similar to melatonin. Overall, the radioprotective effect of sesamol was similar to that of melatonin. Sesamol treatment also showed some recovery of spleen relative weight 24 hours after whole-brain irradiation (WBI). The results strongly suggest that sesamol has a radioprotective effect on the hematopoietic system in mice.
For more complete data on interactions of sesamol (39 records in total), please visit the HSDB record page.

[1]. Chemopreventive effect of resveratrol, sesamol, sesame oil and sunflower oil in the Epstein-Barrvirus early antigen activation assay and the mouse skin two-stage carcinogenesis. Pharmacol Res. 2002 Jun;45(6):499-505.

[2]. Sesamol Induces Human Hepatocellular Carcinoma Cells Apoptosis by Impairing MitochondrialFunction and Suppressing Autophagy. Sci Rep. 2017 Apr 4;7:45728.

Sesamol belongs to the benzodioxane class of compounds. It has been reported that sesamol is present in sesame (Sesamum indicum), and relevant data exist. See also: Sesame oil (partial).
Therapeutic Uses
/EXPL THER/ Chronic Exposure or Carcinogenicity/ Excessive production of prostaglandins by cyclooxygenase-2 in stromal and epithelial cells is a pathogenic factor in the development of colorectal cancer. Therefore, compounds that inhibit the transcriptional activity of cyclooxygenase-2 in colonic epithelial cells may be candidate drugs for anticancer treatment. Cyclooxygenase-2 transcriptional activity in the human colon cancer cell line DLD-1 has been determined using a β-galactosidase reporter gene system. Using this system, we demonstrated that a basal cyclooxygenase-2 transcriptional activity was reduced by 50% at a sesamol (a lignan in sesame seeds) concentration of 100 μM. Other compounds in sesame seeds, such as sesamin, sesamol, ferulic acid, and syringic acid, did not show significant inhibitory effects on cyclooxygenase-2 transcriptional activity at concentrations up to 100 μM. In subsequent experiments, we divided 6-week-old male Min mice (Apc gene-deficient mice) into an untreated group and a 500 ppm sesamol-treated group. At 15 weeks of age, we found that sesamol treatment reduced the number of polyps in the mid-small intestine to 66.1% of the untreated group. In addition, sesamol also inhibited the mRNA expression of cyclooxygenase-2 and cytosolic prostaglandin E2 synthase in polyp sites. The results of this study may reveal novel anticancer properties of sesamol and suggest that drugs that can inhibit cyclooxygenase-2 expression may have the potential as cancer chemopreventive agents.
/EXPL THER/ Increased oxidative stress and inflammation caused by obesity are core pathogenic factors in the pathogenesis and progression of cardiovascular metabolic syndrome (CMetS). This study aimed to investigate the potential role of sesamol (a natural, potent antioxidant and anti-inflammatory agent derived from sesame oil) in chronically high-cholesterol/high-fat diet (HFD)-induced CMetS in rats and to explore its molecular mechanism of action. Rats were fed an HFD diet (55% energy from fat, 2% cholesterol) for 60 days to induce obesity, dyslipidemia, insulin resistance (IR), hepatic steatosis, and hypertension. On day 30, rats with total cholesterol >150 mg/dL were defined as having hypercholesterolemia and were given sesamol at 2, 4, and 8 mg/kg daily for the next 30 days, respectively. Sesamol treatment reduced insulin resistance, hyperinsulinemia, hyperglycemia, dyslipidemia, TNF-α, IL-6, leptin, resistin, high-sensitivity C-reactive protein (hs-CRP), liver transaminases, and alkaline phosphatase levels in a dose-dependent manner, while normalizing adiponectin, nitric oxide, and arterial blood pressure. Increased levels of TBARS and nitrotyrosine and decreased antioxidant enzyme activity were also improved in the high-fat diet group rats. Similarly, sesamol restored hepatic steatosis and hepatocyte ultrastructural pathological changes to normal, although the effect was more significant in the 8 mg/kg dose group. Furthermore, sesamol treatment increased the expression of hepatic PPARγ, PPARα, and eNOS proteins, while decreasing the expression of LXRa, SERBP-1c, P-JNK, and NF-κB. These results indicate that sesamol reduces oxidative stress, inflammation, insulin resistance, hepatic steatosis, and hypertension in high-fat diet-fed rats by regulating the expression of PPARγ, NF-κB, P-JNK, PPARα, LXRa, SERBP-1c, and eNOS proteins, thereby preventing chronic metabolic syndrome (CMetS). Therefore, this study confirms the therapeutic potential of sesamol in alleviating CMetS.
/EXPL THER/ Objective: Postmenopausal estrogen deficiency is associated with increased oxidative stress. This study aimed to investigate the role of sesamol (3,4-methylenedioxyphenol), a phenolic antioxidant and anti-inflammatory molecule, in oxidative stress-induced changes in the central nervous, cardiovascular, and skeletal systems of ovariectomized rats (a widely used postmenopausal animal model). Design: Animals were divided into eight distinct groups (n = 6–8). Five groups underwent ovariectomy; starting on day 2 post-opvariectomy, three of these groups received oral sesamol (2, 4, and 8 mg/kg), respectively, while the fourth group received oral α-tocopherol (100 mg/kg), for 7 weeks. The fifth ovariectomized group received no drug treatment. Rats in the unoperated and sham-operated groups received no drug treatment, while the eighth group received no treatment but oral sesamol 8 mg/kg daily for 7 weeks. After 7 weeks, 24 hours after the last administration, behavioral tests were performed (elevated cruciate maze and Morris water maze were used to assess anxiety and memory, respectively). After the behavioral studies, the animals were sacrificed for various biochemical assays. Results: Compared with the ovariectomized control group, oral administration of sesamol (2, 4, 8 mg/kg) for 7 weeks significantly and dose-dependently improved memory, reduced anxiety, decreased cerebral oxidative stress, improved lipid profile, and reduced serum tumor necrosis factor-α levels in ovariectomized rats. Similar protective effects were observed in skeletal studies. Sesamol increased bone ash content and mechanical stress parameters in the treatment group. Conclusion: The results highlight the role of oxidative stress and inflammation in the pathophysiological changes induced by ovariectomy and point to the potential application value of sesamol in the treatment of menopausal diseases. The physicochemical properties of sesamol (logP 1.29; solubility 38.8 mg/mL) significantly enhanced its tissue distribution and minimized its delivery to the brain. We prepared sesamol-loaded solid lipid nanoparticles (S-SLN) with an average particle size of 122 nm and an encapsulation efficiency of 75.9 ± 2.91%. Biochemical and behavioral results clearly demonstrate the significant advantages of oral administration of S-SLN. The results were clearly confirmed by scintillation imaging of rabbits injected with radiolabeled SLN and by confocal microscopy of brain slices of rats injected with similarly prepared fluorescently labeled SLN. This study shows that the use of phosphatidylcholine (as a cosurfactant) is of particular importance in the preparation of SLN to improve memory deficits. This study aims to develop sesamol as a drug for the treatment of central nervous system disorders. For more complete data on the therapeutic uses of sesamol (7 types), please visit the HSDB record page. Sesamol is a natural phenolic compound derived from sesame, and its chemopreventive effects in EBV EA assays and mouse skin carcinogenesis models suggest its potential application value in cancer prevention. [1] Sesamol induces apoptosis in hepatocellular carcinoma cells through mitochondrial dysfunction and autophagy inhibition, suggesting its potential as a therapeutic drug for human hepatocellular carcinoma, but further in vivo studies are needed to confirm its efficacy. [2]

C7H6O3

138.1207

138.031

533-31-3

68289

White to light brown solid powder

1.4±0.1 g/cm3

274.0±29.0 °C at 760 mmHg

62-65 °C(lit.)

119.5±24.3 °C

0.0±0.6 mmHg at 25°C

1.609

1.52

1

3

0

10

126

0

LUSZGTFNYDARNI-UHFFFAOYSA-N

InChI=1S/C7H6O3/c8-5-1-2-6-7(3-5)10-4-9-6/h1-3,8H,4H2

1,3-benzodioxol-5-ol

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 this product in a sealed and protected environment (e.g. under nitrogen), 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)

DMSO : ≥ 100 mg/mL (~724.01 mM)
Ethanol :≥ 100 mg/mL (~724.01 mM)
H2O : ≥ 50 mg/mL (~362.00 mM)

Solubility in Formulation 1: ≥ 10 mg/mL (72.40 mM) (saturation unknown) in 10% DMSO + 40% PEG300 + 5% Tween80 + 45% Saline (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 100.0 mg/mL clear DMSO stock solution to 400 μL PEG300 and mix evenly; then add 50 μL Tween-80 to the above solution and mix evenly; then add 450 μL normal saline to adjust the volume to 1 mL.
Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH₂ O to obtain a clear solution.

---

Solubility in Formulation 2: ≥ 10 mg/mL (72.40 mM) (saturation unknown) in 10% DMSO + 90% (20% SBE-β-CD in Saline) (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 100.0 mg/mL clear DMSO stock solution to 900 μL of 20% SBE-β-CD physiological saline solution and mix evenly.
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.

---

View More

Solubility in Formulation 3: ≥ 10 mg/mL (72.40 mM) (saturation unknown) in 10% DMSO + 90% Corn Oil (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 100.0 mg/mL clear DMSO stock solution to 900 μL of corn oil and mix evenly.

---

Solubility in Formulation 4: ≥ 2.5 mg/mL (18.10 mM) (saturation unknown) in 10% EtOH + 40% PEG300 + 5% Tween80 + 45% Saline (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear EtOH stock solution to 400 μL of PEG300 and mix evenly; then add 50 μL of Tween-80 to the above solution and mix evenly; then add 450 μL of normal saline to adjust the volume to 1 mL.
Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH₂ O to obtain a clear solution.

---

Solubility in Formulation 5: ≥ 2.5 mg/mL (18.10 mM) (saturation unknown) in 10% EtOH + 90% (20% SBE-β-CD in Saline) (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear EtOH stock solution to 900 μL of 20% SBE-β-CD physiological saline solution and mix evenly.
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.

---

Solubility in Formulation 6: ≥ 2.5 mg/mL (18.10 mM) (saturation unknown) in 10% EtOH + 90% Corn Oil (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear EtOH stock solution to 900 μL of corn oil and mix evenly.

---

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