α-glucosidase (IC50 = 35.01 μg/mL); Rebaudioside A (Reb A) interacts with multiple targets. It stimulates GLP-1 (glucagon-like peptide-1) release from enteroendocrine cells via activation of bitter taste signaling pathways. Functional screening identified that Reb A activates the murine bitter taste receptors Tas2r108, Tas2r123, and Tas2r134. In human HuTu-80 cells, evidence indicates that TAS2R4 and TRPM5 (transient receptor potential cation channel subfamily M member 5) are involved in Reb A-induced GLP-1 secretion . Additionally, Reb A has been shown to enhance LDL cholesterol uptake in HepG2 cells via suppression of HMGCR expression .
Rebaudioside A (Reb A) does not have a defined biological or pharmacological target. It functions as a non-nutritive sweetener interacting with sweet taste receptors, but no specific receptor binding data (IC50, Ki, EC50) are reported in this article. [1]

Rebaudioside A (Reb A) stimulates GLP-1 release from enteroendocrine cells in a concentration-dependent manner, as demonstrated in mouse STC-1 and human HuTu-80 cell lines. This effect occurs independently of the sweet taste receptor, as shown by experiments with selective inhibitors of sweet signaling . In HepG2 cells, Reb A treatment (1 and 5 μM) enhances hepatocellular cholesterol internalization and ameliorates the expression of cholesterol-regulating genes including HMGCR, LDLR, and ACAT2. The cytotoxicity of Reb A in HepG2 cells was determined at 27.72 μM . Reb A at concentrations ranging from 0.001% to 0.5% showed no obvious changes in cellular viability, inflammatory cytokine yield, or protein yield in human HT-29 and T84 cells, as well as mouse liver and spleen cells, indicating non-cytotoxicity in vitro .

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In vitro activity: Rebaudioside A is a steviol glycoside, α-glucosidase inhibitor with IC50 of 35.01 μg/ml. In vitro: rebaudioside A stimulat the insulin secretion from MIN6 cells in a dose- and glucose-dependent manner. In conclusion, the insulinotropic effect of rebaudioside A is mediated via inhibition of ATP-sensitive K+-channels and requires the presence of high glucose.

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Kinase Assay: Rebaudioside A is a steviol glycoside, α-glucosidase inhibitor with IC50 of 35.01 μg/ml.

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Cell Assay: In vitro: rebaudioside A stimulat the insulin secretion from MIN6 cells in a dose- and glucose-dependent manner. In conclusion, the insulinotropic effect of rebaudioside A is mediated via inhibition of ATP-sensitive K+-channels and requires the presence of high glucose.

Rebaudioside A (Reb A) has been evaluated in patients with type 2 diabetes mellitus (T2DM). In a randomized, placebo-controlled, open-label, two-way crossover trial involving 30 subjects, oral administration of Reb A (3 g) did not lower glucose excursion during an oral glucose tolerance test (OGTT) performed at the time of maximal metabolite concentrations (19 h post-dose). The difference in AUCGlucose(0-2h) between Reb A and placebo was -0.7 (95% CI -22.3; 20.9) h•mg/dL, P = 0.95. Insulin and C-peptide concentrations were also comparable between both conditions (P > 0.05), indicating that no antidiabetic properties could be observed in patients with T2DM after single oral use . In animal studies, glucose-lowering properties have been observed in mice, attributed to the metabolites steviol and steviol glucuronide .

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In vivo mouse micronucleus test at doses up to 750 mg/kg bw and an unscheduled DNA synthesis test in rats at doses up to 2000 mg/kg bw, rebaudioside A do not cause any genotoxic effects at any of the doses tested

Functional screening of 34 murine bitter taste receptors (Tas2rs) was performed to identify activation responses, revealing Tas2r108, Tas2r123, and Tas2r134 as responsive receptors .

Rebaudioside A (Reb A) was evaluated in several cell-based assays. For GLP-1 secretion studies, mouse STC-1 and human HuTu-80 enteroendocrine cells were treated with Reb A at various concentrations, and GLP-1 release was measured. Selective inhibitors of sweet signaling were used to confirm that the effect occurs independently of the sweet taste receptor . For cytotoxicity evaluation, human HT-29 and T84 cells, as well as mouse liver and spleen cells, were treated with Reb A at concentrations ranging from 0.001% to 0.5%. Cellular viability was assessed using MTT and LDH assays, inflammatory cytokines were measured by ELISA, and protein expression was analyzed by 2-DE and qPCR . For cholesterol regulation studies, HepG2 cells were incubated with Reb A at concentrations of 1 and 5 μM. MTT assay was used to determine cytotoxicity (IC50 at 27.72 μM), total cellular lipid was extracted and quantified by colorimetric assay, LDL receptor expression was visualized by immunofluorescence microscopy, and expression of HMGCR, LDLR, and ACAT2 genes was analyzed .

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Rebaudioside A (Reb A) was evaluated for genotoxicity in three in vitro cell-based assays. [1]
Bacterial reverse mutation test (Ames test): Salmonella typhimurium tester strains TA98, TA100, TA1535, TA1537 and Escherichia coli strain WP2uvrA were incubated with Reb A at concentrations of 31.6, 100, 316, 1000, 2500 and 5000 μg/plate, both in the presence and absence of metabolic activation (S9 fraction from rat liver). Both plate incorporation and preincubation methods were used. Toxicity was evaluated based on decreased revertant colonies and/or thinning of the bacterial lawn. Reb A was non-mutagenic in all strains at all concentrations tested. [1]
In vitro mammalian chromosome aberration test: Chinese hamster V79 cells were exposed to Reb A at concentrations of 1000, 2500 and 5000 μg/mL for short-term (4 h) and long-term (20 h) exposure periods, with and without S9 metabolic activation. The incidence of chromosomal aberrations and polyploidy was evaluated. Reb A did not induce a statistically significant increase in chromosomal aberrations or polyploidy at any dose tested. [1]
Mouse lymphoma assay: Mouse lymphoma L5178Y tk+/- cells were exposed to Reb A for 4 h (concentrations: 10, 39, 156, 313, 625, 1250, 2500, 5000 μg/mL with and without S9) and 24 h (concentrations: 100, 200, 400, 800, 1500, 2500, 3750, 5000 μg/mL with S9; 20, 39, 156, 625, 1250, 4000, 4500, 5000 μg/mL without S9). Forward mutations at the thymidine kinase locus were evaluated. Reb A did not induce any treatment-related increases in mutation incidence or clastogenic effects. [1]

Rebaudioside A (Reb A) subchronic toxicity studies were conducted in Wistar rats. In a 4-week study, Reb A was administered at dietary concentrations of 0, 25,000, 50,000, 75,000, and 100,000 ppm. In a 13-week study, dietary concentrations of 0, 12,500, 25,000, and 50,000 ppm were used. The test material was incorporated into the basal diet, and animals were fed ad libitum. The NOAEL in the 13-week study was determined to be 50,000 ppm (approximately 4,161 and 4,645 mg/kg body weight/day in male and female rats, respectively) . In the human clinical trial, patients with T2DM received a single oral dose of Reb A (3 g) in a randomized, placebo-controlled, crossover design. Blood samples were collected at multiple time points to measure plasma concentrations of Reb A, steviol, and steviol glucuronide. An oral glucose tolerance test (OGTT) was performed 19 h post-dose to assess effects on glucose homeostasis .

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Rebaudioside A (Reb A) was evaluated in two in vivo genotoxicity assays. [1]
Mouse bone marrow micronucleus test: Adult NMRI mice (5 males and 5 females per group) were administered Reb A via intraperitoneal injection at doses of 150, 375, or 750 mg/kg body weight. Negative control received 0.9% NaCl; positive control received cyclophosphamide at 40 mg/kg. Animals were observed for 44 h (all dose groups) and 68 h (vehicle and high dose groups). Peripheral blood samples were collected from the tail vein. The number of micronucleated polychromatic erythrocytes was counted in 1000 polychromatic erythrocytes per animal. The ratio of polychromatic to normochromatic erythrocytes was determined after scoring 1000 total erythrocytes. Reb A did not induce statistically significant increases in polychromatic immature erythrocytes or micronucleated immature erythrocytes. Signs of toxicity (reduced spontaneous activity, rough fur, prone position, cramps) were observed in the highest dose group (750 mg/kg). [1]
Unscheduled DNA synthesis (UDS) test: Male Wistar rats (4 per group) were fasted for 6-18 h then treated via gavage with a single dose of Reb A at 2000 mg/kg body weight. Vehicle control received distilled water; positive controls received 2-acetylaminofluorene (100 mg/kg) and dimethylnitrosamine (5 mg/kg). At 2 h and 16 h post-dose, rats were anesthetized and hepatocytes were isolated by liver perfusion with collagenase type IV solution. The number of silver grains above the nucleus and over one nucleus-equivalent area of cytoplasm was counted. At least two slides per animal and 50 cells per slide were evaluated. Reb A did not cause any signs of toxicity and did not induce UDS in hepatocytes. [1]

Absorption, Distribution and Excretion
This study aimed to compare the absorption, plasma concentrations, metabolism, and excretion of 14C-rebaudioside A, 14C-stevioside, and 14C-stevioside. Male and female Sprague-Dawley rats, both intact and cannulated, were administered the drugs via single gavage. In the absorption, metabolism, and excretion portion of the study, the doses of 14C-rebaudioside A, 14C-stevioside, and 14C-stevioside were 5 mg/kg body weight, 4.2 mg/kg body weight, and 1.6 mg/kg body weight, respectively; these doses were equivalent when converted to stevioside. To determine plasma concentrations, three rats of each sex were used for each substance, and blood samples were collected at 0.5, 1, 4, 8, 12, and 24 hours post-administration. Peak plasma concentrations (C_max) of the three test compounds (¹⁴C-rebaudioside A, ¹⁴C-stevioside, and ¹⁴C-stevioside) were recorded at 8, 4, and 0.5 hours post-administration. In the primary study, 27 male and female animals were used for each compound, and blood samples were collected at 0.25, 0.5, 1, 2, 4, 8, 24, 28, and 72 hours post-administration. Results showed that the radioactive concentrations of ¹⁴C-rebaudioside A and ¹⁴C-stevioside decreased within 15 minutes to 1 hour post-administration, then increased within 1 to 2–8 hours, before decreasing again. The peak plasma concentration (Cmax) and area under the plasma concentration-time curve (AUC) of steviol were both lower in rebaudioside A than in steviol, indicating that the amount of steviol converted to steviol was slightly higher in rebaudioside A than in rebaudioside A. Following oral administration of 14C-stevioside, Cmax appeared within 15 minutes and decreased rapidly within 15 minutes to 1 hour. Cmax slightly increased at 2 hours, followed by a further decrease. Single-dose administration was performed on five intact rats and five cannulated rats of each sex. For intact rats, urine and feces were collected periodically within 96 hours post-administration. For cannulated rats, bile, urine, and feces were collected periodically within 48 hours post-administration. In intact rats, 97-98% of the total dose of 14C-rebaudioside A and 14C-stevioside, and 90% of 14C-stevioside, were excreted in feces. Most of the fecal radioactivity of all compounds was eliminated within 24 hours of administration (64-89%), with an additional 10-22% eliminated within 24 to 48 hours. 96 hours after administration, no radioactivity was detected in the carcasses of any of the test compounds. In cannulated rats, 70-80% of the dose of 14C-rebaudioside A and 14C-stevioside was eliminated in bile within 24 hours. The remaining dose was eliminated in feces (21-30%), urine, and cage flushing fluid (1-2%). Stevioside was excreted more rapidly in bile, with 50-70% of the dose eliminated within 3 hours of administration. Only 1-2% of the dose was eliminated in feces, and approximately 1% in urine and cage flushing fluid. /Steviol Glycosides/ Five male Sprague-Dawley rats were intravenously injected with 8 mg/kg body weight of isosteviside. Blood samples were collected before and within 48 hours after administration. Urine samples were collected up to 24 hours after administration. The content of isostevirol in plasma and urine samples was analyzed by liquid chromatography-tandem mass spectrometry (LC-MS/MS). Plasma concentration decreased rapidly within 150 minutes, followed by a significant decrease in clearance. Renal excretion was low, with a calculated terminal half-life of 406 ± 31.7 minutes. This relatively long terminal half-life is attributed to its large volume of distribution (suggesting widespread distribution outside plasma) and relatively low clearance. /Isostevirol/

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Metabolism/Metabolites
Five male and five female healthy volunteers (aged 21–29 years) took capsules containing 250 mg of steviol glycosides (97% steviol glycosides, 2.8% steviol glycosides, 0.2% rebaudioside A) three times daily for 3 consecutive days. The dosage, calculated as steviol, was 299 mg/day or 4.60 mg/kg body weight/day for women and 4.04 mg/kg body weight/day for men. Urine samples were collected at enrollment and 24 hours after administration. The levels of bound steviol and steviol glucuronide in the urine samples were analyzed. Blood samples were collected before and after administration, and the levels of alkaline phosphatase, alanine aminotransferase (ALT), alanine aminotransferase (GPT), creatine kinase, and lactate dehydrogenase were analyzed. No significant differences in electrolytes or tissue damage markers were observed. The only metabolite detected in urine was steviol glycosides. The study concludes that due to the molecular size of steviol glycosides, their absorption rate in the intestine is likely low, and they are not degraded by enzymes in the gastrointestinal tract. However, bacteria in the gut microbiota can metabolize steviol glycosides into easily absorbed free steviol glycosides. It is speculated that after degradation by the gut microbiota, steviol glycosides are partially absorbed by the colon and transported to the liver via the portal vein, where they bind with glucuronic acid and are ultimately excreted in the urine. (14)C-rebaudioside A, (14)C-stevioside, and (14)C-stevioside were administered to intact and cannulated male and female Sprague-Dawley rats via gavage. The fecal metabolite profiles of the three test substances were similar, with steviol being the dominant metabolite in all cases. Small amounts of steviol glucoside and trace amounts of unidentified metabolites were also detected. Steviol glucoside was the main radioactive component in bile, indicating that the debinding reaction occurred in the lower intestine. /Steviol Glycosides/
This study investigated the metabolism of steviol glycosides (purity not specified) in human saliva, gastric juice, and fecal bacteria, as well as in the intestinal brush border membrane and gut microbiota of rats, mice, and hamsters. Steviosides showed no changes after incubation with human saliva and gastric juice or intestinal brush border membrane vesicles from rats, mice, and hamsters. The gut microbiota of rats, mice, hamsters, and humans were found to metabolize steviol glycosides to steviol. Human fecal bacteria can produce steviol-16,17α-epoxide, but this substance can be converted back to steviol by further action of fecal bacteria. /Steviol Glycoside/

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Biological Half-Life
Five male Sprague-Dawley rats received an intravenous injection of isosteviol at 8 mg/kg body weight. Blood samples were collected immediately before administration and continued to be collected for up to 48 hours after administration. …The calculated terminal half-life was 406 ± 31.7 minutes. Such a long terminal half-life is due to a large volume of distribution (suggesting widespread distribution outside plasma) and a relatively low clearance rate. /Isoflavones/

Interactions
This study aimed to elucidate the anti-inflammatory and immunomodulatory activities of steviol and its metabolite. 1 mM steviol significantly inhibited lipopolysaccharide (LPS)-induced release of TNF-α and IL-1β in THP-1 cells and slightly inhibited nitric oxide release without exhibiting any direct toxic effects; 100 μM steviol, however, showed no such effects. Western blotting results indicated that steviol inhibited the activation of IKKβ and the transcription factor NF-κB. Furthermore, only steviol could induce the release of TNF-α, IL-1β, and nitric oxide from unstimulated THP-1 cells. Anti-TLR4 antibody partially neutralized TNF-α release. This study demonstrates that steviol attenuates the synthesis of inflammatory mediators in LPS-stimulated THP-1 cells by interfering with the IKKβ and NF-κB signaling pathways, and that steviol-induced TNF-α secretion is partially mediated by TLR4. In a study on chemoprevention, researchers investigated the effects of rebaudioside A (purity >99.5%) on azomethine-induced abnormal crypt foci in male F344 rats. One group of 16 rats received subcutaneous injections of azomethine three times weekly for 1 week before and 2 weeks after azomethine administration, and were fed a diet containing 200 mg/kg rebaudioside A for 5 weeks before sacrifice. The dose, calculated as steviol, was 6.6 μg/kg body weight/day. Other groups received either a diet containing rebaudioside A but without azomethine injection (6 rats), a basal diet without azomethine (6 rats), or a basal diet containing only azomethine injection (16 rats). At the end of the study, colons were removed from 8 animals in the experimental groups and 1 animal in each control group to examine for the presence of abnormal crypt foci. The colonic mucosa of the remaining animals from each group was mixed, and ornithine decarboxylase activity was measured. Simultaneously, silver-stained nucleolar tissue region (AgNOR) protein counts were measured in each group. Ornithine decarboxylase and AgNOR protein counts are both biomarkers of cell proliferation. The mean body weight and mean liver weight of animals receiving both the test compound and azomethane were significantly lower than those receiving only azomethane. No toxic reactions were observed, and treatment had no effect on food intake. Rebaudioside A showed a trend towards reducing the number of azomethane-induced abnormal crypt foci, mucosal ornithine decarboxylase activity, and the number of AgNORs, but this did not reach statistical significance. /Rebaudioside A/
Steviol inhibits the effects of atrazine on energy metabolism in isolated perfused rat liver. Stevioside reduces the effects of atrazine on glycolysis, glycogenolysis, gluconeogenesis, and oxygen uptake. The half-maximal effective concentration (MCD) is 0.5 mM. The site of action is extracellular. Stevioside may affect the transmembrane transport of atrazine.

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Rebaudioside A (Reb A) was evaluated for genotoxicity (not general toxicity) in this study. [1]
In vitro genotoxicity: Reb A was non-mutagenic in the Ames test (S. typhimurium TA98, TA100, TA1535, TA1537 and E. coli WP2uvrA) at concentrations up to 5000 μg/plate with and without metabolic activation. Reb A was non-genotoxic in the in vitro chromosome aberration test (Chinese hamster V79 cells) at concentrations up to 5000 μg/mL with and without S9. Reb A was non-mutagenic in the mouse lymphoma assay (L5178Y tk+/- cells) at concentrations up to 5000 μg/mL with and without S9. [1]
In vivo genotoxicity: Reb A did not induce genotoxicity in the mouse bone marrow micronucleus test at doses up to 750 mg/kg body weight (i.p.). Signs of toxicity (reduced spontaneous activity, rough fur, prone position, cramps) were observed at the highest dose of 750 mg/kg. Reb A did not induce genotoxicity in the rat unscheduled DNA synthesis test at a dose of 2000 mg/kg body weight (oral gavage) and caused no signs of toxicity. [1]

[1]. Food Chem Toxicol.2009 Aug;47(8):1831-6;
[2]. Curr Pharm Des.2017;23(11):1616-1622.

Rebaudioside A is a rebaudioside, a derivative of rubugin, in which the 3- and 4-hydroxyl groups at the 13α-β-D-glucopyranoside are converted to the corresponding β-D-glucopyranoside. It is a sweetener. It is both a β-D-glucoside and a rebaudioside. Functionally, it is associated with a rhodioloside and β-D-glucoside-(1->2)-[β-D-glucoside-(1->3)]-β-D-glucoside. Rebaudioside A is being investigated in the clinical trial NCT03510624 (Acute effects of rebaudioside A on glycemic fluctuations in oral glucose tolerance tests in patients with type 2 diabetes). Rebaudioside A has been reported in bovine (Bos taurus) and stevia (Stevia rebaudiana), with relevant data available. See also: Stevia leaf (partial); Stevia rebaudiana extract. (Notes moved to)

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Therapeutic Uses
Traditional Medicine: Multiple studies have shown that, in addition to their sweetness, steviol and related compounds, including rebaudioside A (the second most abundant component in stevia leaves), steviol, and isosteviol (metabolites of steviol), may also have therapeutic effects due to their hypoglycemic, hypotensive, anti-inflammatory, antitumor, antidiarrheal, diuretic, and immunomodulatory effects. It is noteworthy that their effects on blood glucose and blood pressure are only observed when these parameters are above normal. Because steviol can interact with drug transporters, it has been proposed that it may act as a drug modulator…
/EXPL THER/… This study aimed to evaluate the effects of steviol on hypertension in humans. This was a multicenter, randomized, double-blind, placebo-controlled study. The study included 106 Chinese patients with hypertension, diastolic blood pressure between 95 and 110 mmHg, and ages 28 to 75 years. Sixty participants (34 males, 26 females; mean age ± standard deviation: 54.1 ± 3.8 years) were assigned to the active treatment group, and 46 participants (19 males, 27 females; mean age ± standard deviation: 53.7 ± 4.1 years) were assigned to the placebo group. Each participant took capsules containing steviol glycosides (250 mg) or placebo three times daily and was followed up monthly for one year. After 3 months, both systolic and diastolic blood pressure in the steviol glycoside group decreased significantly (systolic blood pressure: from 166.0 ± 9.4 mmHg to 152.6 ± 6.8 mmHg; diastolic blood pressure: from 104.7 ± 5.2 mmHg to 90.3 ± 3.6 mmHg, P < 0.05), and this effect lasted for one year. No significant changes were observed in blood biochemical indicators such as blood lipids and blood glucose. No significant adverse reactions were observed, and the quality of life assessment results did not deteriorate. This study shows that oral stevioside is well tolerated and has significant therapeutic effects, and can be used as an alternative or adjunctive treatment option for patients with hypertension.

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Rebaudioside A (Reb A) is a steviol glycoside isolated from the leaves of Stevia rebaudiana. It is a non-nutritive, natural sweetener reported to be 250-450 times sweeter than sucrose. Extracts of S. rebaudiana (mainly stevioside) have been used extensively as sweeteners in Japan and Korea. In the United States, steviol glycosides including Reb A have been used as dietary supplements since the Dietary Supplement Health and Education Act of 1994. Reb A is generally recognized as safe (GRAS) for use as a food ingredient in the United States. [1]
The objective of this study was to supplement the safety database on Reb A by describing genotoxicity results conducted according to OECD guidelines. Previous in vitro genotoxicity studies with steviol glycosides had reported positive effects, but those studies used crude or poorly characterized extracts or non-standard test systems. The current study used high-purity Reb A (95.6%) and standard OECD guideline assays. [1]
Based on the totality of evidence including these empirical observations, the authors concluded that rebaudioside A is non-genotoxic, supporting its GRAS determination. This conclusion is consistent with the Joint FAO/WHO Expert Committee on Food Additives (JECFA) review, which found no conclusive evidence of genotoxicity for steviol glycosides. [1]

C₄₄H₇₀O₂₃

967.01

966.43

C, 54.65; H, 7.30; O, 38.05

58543-16-1

6918840

White to off-white solid powder

1.6±0.1 g/cm3

1102.8±65.0 °C at 760 mmHg

242-244ºC

319.9±27.8 °C

0.0±0.6 mmHg at 25°C

1.659

-1.13

14

23

13

67

1760

26

C[C@@]12CCC[C@@]([C@H]1CC[C@]34[C@H]2CC[C@](C3)(C(=C)C4)O[C@H]5[C@@H]([C@H]([C@@H]([C@H](O5)CO)O)O[C@H]6[C@@H]([C@H]([C@@H]([C@H](O6)CO)O)O)O)O[C@H]7[C@@H]([C@H]([C@@H]([C@H](O7)CO)O)O)O)(C)C(=O)O[C@H]8[C@@H]([C@H]([C@@H]([C@H](O8)CO)O)O)O

HELXLJCILKEWJH-NCGAPWICSA-N

InChI=1S/C44H70O23/c1-17-11-43-9-5-22-41(2,7-4-8-42(22,3)40(59)66-38-33(58)30(55)26(51)20(14-47)62-38)23(43)6-10-44(17,16-43)67-39-35(65-37-32(57)29(54)25(50)19(13-46)61-37)34(27(52)21(15-48)63-39)64-36-31(56)28(53)24(49)18(12-45)60-36/h18-39,45-58H,1,4-16H2,2-3H3/t18-,19-,20-,21-,22+,23+,24-,25-,26-,27-,28+,29+,30+,31-,32-,33-,34+,35-,36+,37+,38+,39+,41-,42-,43-,44+/m1/s1

[(2S,3R,4S,5S,6R)-3,4,5-trihydroxy-6-(hydroxymethyl)oxan-2-yl] (1R,4S,5R,9S,10R,13S)-13-[(2S,3R,4S,5R,6R)-5-hydroxy-6-(hydroxymethyl)-3,4-bis[[(2S,3R,4S,5S,6R)-3,4,5-trihydroxy-6-(hydroxymethyl)oxan-2-yl]oxy]oxan-2-yl]oxy-5,9-dimethyl-14-methylidenetetracyclo[11.2.1.01,10.04,9]hexadecane-5-carboxylate

Rebaudioside A; 58543-16-1; Stevioside A3; Rebaudioside-A; Truvia; Reb A

2934.99.9001

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

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

Solubility in Formulation 1: ≥ 2.5 mg/mL (2.59 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 25.0 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.

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Solubility in Formulation 2: ≥ 2.5 mg/mL (2.59 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 25.0 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.

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Solubility in Formulation 3: ≥ 2.5 mg/mL (2.59 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 25.0 mg/mL clear DMSO stock solution to 900 μL of corn oil and mix evenly.

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