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L-Sulforaphane

CAS# 142825-10-3

L-Sulforaphane

2D Structure

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L-Sulforaphane

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Chemical Properties of L-Sulforaphane

Cas No. 142825-10-3 SDF Download SDF
PubChem ID 9577379 Appearance Brown liquid
Formula C6H11NOs2 M.Wt 477.6
Type of Compound N/A Storage Desiccate at -20°C
Solubility Soluble in Chloroform,Dichloromethane,Ethyl Acetate,DMSO,Acetone,etc.
Chemical Name 1-isothiocyanato-4-[(R)-methylsulfinyl]butane
SMILES CS(=O)CCCCN=C=S
Standard InChIKey SUVMJBTUFCVSAD-SNVBAGLBSA-N
Standard InChI InChI=1S/C6H11NOS2/c1-10(8)5-3-2-4-7-6-9/h2-5H2,1H3/t10-/m1/s1
General tips For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.Stock solution can be stored below -20℃ for several months.
We recommend that you prepare and use the solution on the same day. However, if the test schedule requires, the stock solutions can be prepared in advance, and the stock solution must be sealed and stored below -20℃. In general, the stock solution can be kept for several months.
Before use, we recommend that you leave the vial at room temperature for at least an hour before opening it.
About Packaging 1. The packaging of the product may be reversed during transportation, cause the high purity compounds to adhere to the neck or cap of the vial.Take the vail out of its packaging and shake gently until the compounds fall to the bottom of the vial.
2. For liquid products, please centrifuge at 500xg to gather the liquid to the bottom of the vial.
3. Try to avoid loss or contamination during the experiment.
Shipping Condition Packaging according to customer requirements(5mg, 10mg, 20mg and more). Ship via FedEx, DHL, UPS, EMS or other couriers with RT, or blue ice upon request.

L-Sulforaphane Dilution Calculator

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Preparing Stock Solutions of L-Sulforaphane

1 mg 5 mg 10 mg 20 mg 25 mg
1 mM 2.0938 mL 10.469 mL 20.938 mL 41.876 mL 52.3451 mL
5 mM 0.4188 mL 2.0938 mL 4.1876 mL 8.3752 mL 10.469 mL
10 mM 0.2094 mL 1.0469 mL 2.0938 mL 4.1876 mL 5.2345 mL
50 mM 0.0419 mL 0.2094 mL 0.4188 mL 0.8375 mL 1.0469 mL
100 mM 0.0209 mL 0.1047 mL 0.2094 mL 0.4188 mL 0.5235 mL
* Note: If you are in the process of experiment, it's necessary to make the dilution ratios of the samples. The dilution data above is only for reference. Normally, it's can get a better solubility within lower of Concentrations.

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References on L-Sulforaphane

Identification of Non-Electrophilic Nrf2 Activators from Approved Drugs.[Pubmed:28587109]

Molecules. 2017 May 26;22(6). pii: molecules22060883.

Oxidative damage can lead to a wide range of diseases. Nrf2 is an important transcription factor that regulates many of the cytoprotective enzymes involved in the oxidative stress response. Therefore, targeting the regulation of Nrf2 activation is one logical and effective strategy to prevent or lower the risk of oxidative stress-related diseases. Until now, most research has focused on electrophilic indirect Nrf2 activators, but the risk of 'off-target' effects may be associated with these activators. To find novel small non-electrophilic modulators of Nrf2, we started from chemical agents derived from a connectivity map (cMap) and identified 22 non-electrophilic potential Nrf2-activating drugs through a drug repositioning tactic. By determining the expression changes of antioxidant genes in MCF7 cells that were treated with the potential Nrf2 activators using quantitative real-time polymerase chain reaction RT-PCR (real-time polymerase chain reaction) (qRT-PCR), astemizole was found to have a greater scale of upregulating antioxidant genes NQO1, HO-1, and GCLM than the positive control d,L-Sulforaphane, although the testing concentration was lower than that of the control. Astemizole is a good potential redox regulator and deserves more pharmacodynamic experimentation to test and verify its feasibility for use as an Nrf2 activator.

Sulforaphane delivery using mPEG-PCL co-polymer nanoparticles to breast cancer cells.[Pubmed:26916923]

Pharm Dev Technol. 2017 Aug;22(5):642-651.

PURPOSE: Among the potent anticancer agents, d,L-Sulforaphane (SF) is very effective against many different types of cancer cells. Its clinical application is restricted because of its hydrophobicity, low gastrointestinal absorption and poor bioavailability. In the present study, a reliable micellar delivery system using monomethoxypoly (ethylene glycol)-poly (varepsilon-caprolactone) (mPEG-PCL) was established. The encapsulation of SF inside mPEG-PCL as a nano-carrier was established and the cytotoxicity assay against human breast cancer cell line was evaluated. METHODS: In this study, SF was encapsulated within mPEG-PCL micelles through a single-step nano-precipitation method, leading to creation of SF-loaded mPEG-PCL (SF/mPEG-PCL) micelles. Di-block mPEG-PCL copolymers were synthesized and used to prepare micelles. MPEG-PCL copolymer was characterized by HNMR, FTIR, differential scanning calorimetry and gel permeation chromatography techniques. Characterization, stability of micelles, the particle size and morphology were determined. The release profile of the SF from the micelles which prepared by the drug-loaded copolymer, was evaluated. The cytotoxicity of free SF, mPEG-PCL and SF-loaded mPEG-PCL micelles was compared with each other by performing MTT assay of the treated MCF-7 cell line. Expression levels of BCL-2, MMP-9, BCL-XL, BAK, BAX and GAPDH (endogenous gene) as control were quantified by real time PCR. To evaluate the apoptotic effects of Free SF compared with SF-loaded mPEG-PCL micelles, flow cytometry analysis was done using the annexin V-FITC apoptosis detection kit. RESULTS: Our studies resulted in a successful establishment of uniformity and spherical SF-loaded mPEG-PCL micelles. The encapsulation efficiency of SF was 86 +/- 1.58%. The results of atomic force microscopy revealed that the micelles have spherical shapes with size of 107 nm. In vitro release of SF from SF-entrapped micelles was remarkably sustained. The mPEG-PCL micelle showed little cytotoxicity in the case of MCF-7 cell line with concentration up to 1.5 mg/ml, whereas the SF-loaded mPEG-PCL micelles at all concentrations significantly was cytotoxic in the case of MCF-7 cell line. Finally, real-time PCR and flow cytometry were used to demonstrate that the SF-loaded mPEG-PCL could be efficiently inducing apoptosis in MCF-7 cell line. CONCLUSION: We achieved to a successful formulation of SF-loaded m-PEG/PCL micelles in this study. Based on the cytotoxicity results of mPEG-PCL micelles against human breast cancer cell line (MCF-7) in this study, it suggested that SF/mPEG-PCL micelles can be an effective breast cancer treatment strategy in the future.

Chronic toxicity evaluation of Morinda citrifolia fruit and leaf in mice.[Pubmed:27871867]

Regul Toxicol Pharmacol. 2017 Feb;83:46-53.

Noni (Morinda citrifolia) leaf and fruit are used as food and medicine. This report compares the chronic toxicity of Noni fruit and edible leaf water extracts (two doses each) in female mice. The 6 months study showed the fruit extract produced chronic toxicity effects at the high dose of 2 mg/ml drinking water, evidenced through deteriorated liver histology (hepatocyte necrosis), reduced liver length, increased liver injury marker AST (aspartate aminotransferase) and albumin reduction, injury symptoms (hypoactivity, excessive grooming, sunken eyes and hunched posture) and 40% mortality within 3 months. This hepatotoxicity results support the six liver injury reports in humans which were linked to chronic noni fruit juice consumption. Both doses of the leaf extracts demonstrated no observable toxicity. The hepatotoxicity effects of the M. citrifolia fruit extract in this study is unknown and may probably be due to the anthraquinones in the seeds and skin, which had potent quinone reductase inducer activity that reportedly was 40 times more effective than L-Sulforaphane. This report will add to current data on the chronic toxicity cases of Morinda citrifolia fruit. No report on the chronic toxicity of Morinda citrifolia fruit in animal model is available for comparison.

L-Sulforaphane Confers Protection Against Oxidative Stress in an In Vitro Model of Age-Related Macular Degeneration.[Pubmed:29376497]

Curr Mol Pharmacol. 2018;11(3):237-253.

BACKGROUND: In age-related macular degeneration, oxidative damage and abnormal neovascularization in the retina are caused by the upregulation of vascular endothelium growth factor and reduced expression of Glutathione-S-transferase genes. Current treatments are only palliative. Compounds from cruciferous vegetables (e.g. L-Sulforaphane) have been found to restore normal gene expression levels in diseases including cancer via the activity of histone deacetylases and DNA methyltransferases, thus retarding disease progression. OBJECTIVE: To examine L-Sulforaphane as a potential treatment to ameliorate aberrant levels of gene expression and metabolites observed in age-related macular degeneration. METHOD: The in vitro oxidative stress model of AMD was based on the exposure of Adult Retinal Pigment Epithelium-19 cell line to 200muM hydrogen peroxide. The effects of L-Sulforaphane on cell proliferation were determined by MTS assay. The role of GSTM1, VEGFA, DNMT1 and HDAC6 genes in modulating these effects was investigated using quantitative real-time polymerase chain reaction. The metabolic profiling of L-Sulforaphane-treated cells via gas-chromatography massspectrometry was established. Significant differences between control and treatment groups were validated using one-way ANOVA, student t-test and post-hoc Bonferroni statistical tests (p<0.05). RESULTS: L-Sulforaphane induced a dose-dependent increase in cell proliferation in the presence of hydrogen peroxide by upregulating Glutathione-S-Transferase mu1 gene expression. Metabolic profiling revealed that L-Sulforaphane increased levels of 2-monopalmitoglycerol, 9, 12, 15,-(Z-Z-Z)- Octadecatrienoic acid, 2-[Bis(trimethylsilyl)amino]ethyl bis(trimethylsilyl)-phosphate and nonanoic acid but decreased beta-alanine levels in the absence or presence of hydrogen peroxide, respectively. CONCLUSION: This study supports the use of L-Sulforaphane to promote regeneration of retinal cells under oxidative stress conditions.

D, L-Sulforaphane Loaded Fe3O4@ Gold Core Shell Nanoparticles: A Potential Sulforaphane Delivery System.[Pubmed:26982588]

PLoS One. 2016 Mar 16;11(3):e0151344.

A novel design of gold-coated iron oxide nanoparticles was fabricated as a potential delivery system to improve the efficiency and stability of d, L-Sulforaphane as an anticancer drug. To this purpose, the surface of gold-coated iron oxide nanoparticles was modified for sulforaphane delivery via furnishing its surface with thiolated polyethylene glycol-folic acid and thiolated polyethylene glycol-FITC. The synthesized nanoparticles were characterized by different techniques such as FTIR, energy dispersive X-ray spectroscopy, UV-visible spectroscopy, scanning and transmission electron microscopy. The average diameters of the synthesized nanoparticles before and after sulforaphane loading were obtained approximately 33 nm and approximately 38 nm, respectively, when approximately 2.8 mmol/g of sulforaphane was loaded. The result of cell viability assay which was confirmed by apoptosis assay on the human breast cancer cells (MCF-7 line) as a model of in vitro-cancerous cells, proved that the bare nanoparticles showed little inherent cytotoxicity, whereas the sulforaphane-loaded nanoparticles were cytotoxic. The expression rate of the anti-apoptotic genes (bcl-2 and bcl-xL), and the pro-apoptotic genes (bax and bak) were quantified, and it was found that the expression rate of bcl-2 and bcl-xL genes significantly were decreased when MCF-7 cells were incubated by sulforaphane-loaded nanoparticles. The sulforaphane-loaded into the designed gold-coated iron oxide nanoparticles, acceptably induced apoptosis in MCF-7 cells.

d,l-Sulforaphane Induces ROS-Dependent Apoptosis in Human Gliomablastoma Cells by Inactivating STAT3 Signaling Pathway.[Pubmed:28054986]

Int J Mol Sci. 2017 Jan 4;18(1). pii: ijms18010072.

d,L-Sulforaphane (SFN), a synthetic analogue of broccoli-derived isomer l-SFN, exerts cytotoxic effects on multiple tumor cell types through different mechanisms and is more potent than the l-isomer at inhibiting cancer growth. However, the means by which SFN impairs glioblastoma (GBM) cells remains poorly understood. In this study, we investigated the anti-cancer effect of SFN in GBM cells and determined the underlying molecular mechanisms. Cell viability assays, flow cytometry, immunofluorescence, and Western blot results revealed that SFN could induced apoptosis of GBM cells in a dose- and time-dependent manner, via up-regulation of caspase-3 and Bax, and down-regulation of Bcl-2. Mechanistically, SFN treatment led to increase the intracellular reactive oxygen species (ROS) level in GBM cells. Meanwhile, SFN also suppressed both constitutive and IL-6-induced phosphorylation of STAT3, and the activation of upstream JAK2 and Src tyrosine kinases, dose- and time-dependently. Moreover, blockage of ROS production by using the ROS inhibitor N-acetyl-l-cysteine totally reversed SFN-mediated down-regulation of JAK2/Src-STAT3 signaling activation and the subsequent effects on apoptosis by blocking the induction of apoptosis-related genes in GBM cells. Taken together, our data suggests that SFN induces apoptosis in GBM cells via ROS-dependent inactivation of STAT3 phosphorylation. These findings motivate further evaluation of SFN as a cancer chemopreventive agent in GBM treatment.

Up-regulation of nuclear factor E2-related factor 2 (Nrf2) represses the replication of SVCV.[Pubmed:27693327]

Fish Shellfish Immunol. 2016 Nov;58:474-482.

Generation of reactive oxygen species (ROS) and failure to maintain an appropriate redox balance contribute to viral pathogenesis. Nuclear factor E2-related factor 2 (Nrf2) is an important transcription factor that plays a pivotal role in maintaining intracellular homoeostasis and coping with invasive pathogens by coordinately activating a series of cytoprotective genes. Previous studies indicated that the transcription and expression levels of Nrf2 were up-regulated in SVCV-infected EPC cells with the unknown mechanism(s). In this study, the interactions between the Nrf2-ARE signalling pathway and SVCV replication were investigated, which demonstrated that SVCV infection induced accumulation of ROS as well as protein carbonyl groups and 8-OHdG, accompanied by the up-regulation of Nrf2 and its downstream genes. At the same time, the activation of Nrf2 with D, L-Sulforaphane (SFN) and CDDO-Me could repress the replication of SVCV, and knockdown of Nrf2 by siRNA could promote the replication of SVCV. Taken together, these observations indicate that the Nrf2-ARE signal pathway activates a passive defensive response upon SVCV infection. The conclusions presented here suggest that targeting the Nrf2 pathway has potential for combating SVCV infection.

Description

(R)-Sulforaphane is a highly potent inducer of the Keap1/Nrf2/ARE pathway. (R)-Sulforaphane is a far more potent inducer of the carcinogen-detoxifying enzyme systems in rat liver and lung than the S-isomer.

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