| Size | Price | Stock | Qty |
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| 10mg |
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| 25mg |
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| 50mg |
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| 100mg |
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| 500mg | |||
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| Other Sizes |
| Targets |
- Kelch-like ECH-associated protein 1 (Keap1), activating nuclear factor erythroid 2-related factor 2 (Nrf2) [7]
- Aryl hydrocarbon receptor (AhR) [5] - Estrogen receptor α (ERα) [5] - AMP-activated protein kinase (AMPK) [7] |
|---|---|
| ln Vitro |
- In HT29 human colon cancer cells, R-sulforaphane induced cell cycle arrest at G2/M phase and apoptosis in a dose-dependent manner. It reduced cyclin B1 and cdc2 expression, increased p21 levels, triggered cytochrome c release from mitochondria, activated caspases-3 and -9, and cleaved poly(ADP-ribose) polymerase (PARP) [3]
- In rat H9c2 cells, R-sulforaphane prevented doxorubicin-induced oxidative stress and cell death. It elevated activities of superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx), reduced reactive oxygen species (ROS) and malondialdehyde (MDA) levels, upregulated Bcl-2, and downregulated Bax and cleaved caspase-3 [4] - In human breast cell lines (MCF-7, MDA-MB-231, and MCF-10A), R-sulforaphane modulated the expression profile of AhR, ERα, Nrf2, NQO1, and GSTP. It increased Nrf2, NQO1, and GSTP levels, and altered AhR and ERα expression in a cell type-specific manner [5] - In pancreatic cancer cells under high glucose conditions, R-sulforaphane activated Nrf2 via AMPK-dependent signaling, inhibiting cell proliferation, migration, invasion, and promoting apoptosis. This effect was reversed by AMPK inhibition [7] - R-sulforaphane inhibited phase I enzymes (e.g., cytochrome P450 1A1) and induced phase II detoxifying enzymes (e.g., quinone reductase) in various cancer cell lines, contributing to anticarcinogenic activity [6] |
| ln Vivo |
- In rats, R-sulforaphane was a more potent inducer of carcinogen-detoxifying enzyme systems (e.g., quinone reductase, glutathione S-transferase) in liver and lung compared to the S-isomer. It increased enzyme activities and mRNA levels in these tissues [2]
- In mice, R-sulforaphane exhibited anticarcinogenic activity by reducing carcinogen-induced preneoplastic lesions in the colon and inducing phase II detoxifying enzymes in liver, colon, and small intestine [6] |
| Enzyme Assay |
- For phase II enzyme activity: Tissue or cell homogenates were prepared and incubated with specific substrates. The activity of quinone reductase was measured by monitoring the reduction of a substrate at a specific wavelength. Glutathione S-transferase activity was assessed by measuring the conjugation of glutathione with a substrate, with absorbance changes recorded over time [2,6]
- For antioxidant enzyme activity: Cell lysates were reacted with substrates for SOD, CAT, and GPx. SOD activity was determined by inhibiting the reduction of a tetrazolium salt, CAT by measuring H2O2 decomposition, and GPx by monitoring glutathione oxidation [4] |
| Cell Assay |
- For HT29 colon cancer cells: Cells were treated with R-sulforaphane (0-40 μM) for varying durations. Cell cycle was analyzed by propidium iodide staining and flow cytometry. Apoptosis was assessed via annexin V-FITC/PI staining, TUNEL assay, and caspase activity kits. Western blot measured cyclin B1, cdc2, p21, cytochrome c, caspases, and PARP [3]
- For H9c2 cells: Cells were pretreated with R-sulforaphane (0-5 μM) before doxorubicin exposure. ROS and MDA levels were measured using fluorescent probes and colorimetric kits, respectively. Cell viability was determined by MTT assay, and protein expression (Bcl-2, Bax, cleaved caspase-3) was analyzed by western blot [4] - For breast cell lines: Cells were treated with R-sulforaphane, and mRNA and protein levels of AhR, ERα, Nrf2, NQO1, and GSTP were measured by RT-PCR and western blot, respectively [5] - For pancreatic cancer cells: High glucose-cultured cells were treated with R-sulforaphane. Proliferation was assessed by CCK-8 assay, migration/invasion by transwell assays, and apoptosis by flow cytometry. Western blot detected Nrf2, HO-1, NQO1, and p-AMPK, while immunofluorescence analyzed Nrf2 nuclear translocation [7] |
| Animal Protocol |
- In rat studies: Rats were administered R-sulforaphane via oral gavage at specific doses. After treatment, liver and lung tissues were collected. Enzyme activities (quinone reductase, glutathione S-transferase) were measured in tissue homogenates, and mRNA levels were analyzed by RT-PCR [2]
- In mouse studies: Mice received R-sulforaphane (200 μmol/kg) via oral gavage. Tissues (liver, colon, small intestine) were harvested to assess phase II enzyme activities. For carcinogenesis models, mice were co-treated with carcinogens and R-sulforaphane, and preneoplastic lesions were counted histologically [6] |
| References |
|
| Additional Infomation |
R-sulforaphane is the enantiomer of sulforaphane, a naturally occurring isothiocyanate found in cruciferous vegetables. It is obtained by enzymatic hydrolysis of sulforaphane from Tuscan black cabbage seeds [1]. Its anticancer effects include inducing phase II detoxification enzymes, inhibiting phase I enzymes, and regulating cell cycle and apoptosis pathways [3,6]. Compared with the S-isomer, R-sulforaphane has higher potency in inducing detoxification enzymes, indicating a stereoselective interaction with the molecular target [2]. R-sulforaphane is a sulforaphane with an R configuration of sulfinyl group. It is a naturally occurring compound in broccoli and can act as a potent inducer of phase II detoxification enzymes. It is the enantiomer of (S)-sulforaphane. Sulforaphane is a naturally occurring phytochemical belonging to the isothiocyanate class. As an aglycone metabolite of glucoraphane glucoside (sulforaphane glucoside), sulforaphane has antioxidant activity and can effectively activate endogenous detoxification enzymes. Because it can induce the activity of phase II detoxification enzymes (such as glutathione S-transferase and quinone reductase), it possesses anti-cancer properties, thus enabling it to resist certain carcinogens and toxic reactive oxygen species. Broccoli sprouts contain large amounts of sulforaphane, which is also found in other cruciferous vegetables (such as cabbage and kale). (NCI04)
|
| Molecular Formula |
C6H11NOS2
|
|---|---|
| Molecular Weight |
177.28
|
| Exact Mass |
177.028
|
| Elemental Analysis |
C, 40.65; H, 6.25; N, 7.90; O, 9.02; S, 36.17
|
| CAS # |
142825-10-3
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| Related CAS # |
4478-93-7 (racemic); 142825-10-3 (R-isomer); 155320-20-0 (S-isomer);
|
| PubChem CID |
9577379
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| Appearance |
Colorless to light yellow liquid
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| Density |
1.2±0.1 g/cm3
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| Boiling Point |
368.2±25.0 °C at 760 mmHg
|
| Flash Point |
176.5±23.2 °C
|
| Vapour Pressure |
0.0±0.8 mmHg at 25°C
|
| Index of Refraction |
1.567
|
| LogP |
0.23
|
| Hydrogen Bond Donor Count |
0
|
| Hydrogen Bond Acceptor Count |
4
|
| Rotatable Bond Count |
5
|
| Heavy Atom Count |
10
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| Complexity |
152
|
| Defined Atom Stereocenter Count |
1
|
| SMILES |
[S@@](C([H])([H])[H])(C([H])([H])C([H])([H])C([H])([H])C([H])([H])N=C=S)=O
|
| InChi Key |
SUVMJBTUFCVSAD-SNVBAGLBSA-N
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| InChi Code |
InChI=1S/C6H11NOS2/c1-10(8)5-3-2-4-7-6-9/h2-5H2,1H3/t10-/m1/s1
|
| Chemical Name |
1-isothiocyanato-4-[(R)-methylsulfinyl]butane
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| Synonyms |
(R)-Sulforaphane; L-Sulforaphane; L-Sulforaphane; (R)-sulforaphane; 142825-10-3; (-)-Sulforaphane; (R)-1-Isothiocyanato-4-(methylsulfinyl)butane; 1-isothiocyanato-4-[(R)-methylsulfinyl]butane; 4-Methylsulfinylbutyl isothiocyanate; CHEBI:47808; (-)-Sulforaphane
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| HS Tariff Code |
2934.99.9001
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| Storage |
Powder -20°C 3 years 4°C 2 years In solvent -80°C 6 months -20°C 1 month Note: This product requires protection from light (avoid light exposure) during transportation and storage. |
| Shipping Condition |
Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)
|
| Solubility (In Vitro) |
DMSO : ~100 mg/mL (~564.05 mM)
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|---|---|
| Solubility (In Vivo) |
Solubility in Formulation 1: ≥ 2.5 mg/mL (14.10 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. Solubility in Formulation 2: ≥ 2.5 mg/mL (14.10 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. View More
Solubility in Formulation 3: ≥ 2.5 mg/mL (14.10 mM) (saturation unknown) in 10% DMSO + 90% Corn Oil (add these co-solvents sequentially from left to right, and one by one), clear solution. |
| Preparing Stock Solutions | 1 mg | 5 mg | 10 mg | |
| 1 mM | 5.6408 mL | 28.2040 mL | 56.4079 mL | |
| 5 mM | 1.1282 mL | 5.6408 mL | 11.2816 mL | |
| 10 mM | 0.5641 mL | 2.8204 mL | 5.6408 mL |
*Note: Please select an appropriate solvent for the preparation of stock solution based on your experiment needs. For most products, DMSO can be used for preparing stock solutions (e.g. 5 mM, 10 mM, or 20 mM concentration); some products with high aqueous solubility may be dissolved in water directly. Solubility information is available at the above Solubility Data section. Once the stock solution is prepared, aliquot it to routine usage volumes and store at -20°C or -80°C. Avoid repeated freeze and thaw cycles.
Calculation results
Working concentration： mg/mL；
Method for preparing DMSO stock solution： mg drug pre-dissolved in μL DMSO (stock solution concentration mg/mL). Please contact us first if the concentration exceeds the DMSO solubility of the batch of drug.
Method for preparing in vivo formulation:：Take μL DMSO stock solution, next add μL PEG300, mix and clarify, next addμL Tween 80, mix and clarify, next add μL ddH2O，mix and clarify.
(1) Please be sure that the solution is clear before the addition of next solvent. Dissolution methods like vortex, ultrasound or warming and heat may be used to aid dissolving.
(2) Be sure to add the solvent(s) in order.
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