|Source:||The seeds of Brassica oleracea L. var. botrytis L.|
|Biological Activity or Inhibitors:||1. Sulforaphene has herbicidal activity, the ED50 of it against velvetleaf seedlings was approximately 2×10(-4) M.
2. Sulforaphene may be a potential anti- triple negative breast cancer natural compound and its antiproliferation effects may be mediated by tumor suppressor Egr1.
3. Sulforaphene has chemotherapeutic potential, it promotes Bax/Bcl2, MAPK-dependent human gastric cancer AGS cells apoptosis and inhibits migration via EGFR, p-ERK1/2 down-regulation.
4. Sulforaphene enhances radiosensitivity of hepatocellular carcinoma through suppression of the NF-κB pathway.
5. Sulforaphene has anti-proliferative and antibacterial properties.
|Solvent:||Chloroform, Dichloromethane, Ethyl Acetate, DMSO, Acetone, etc.|
|Storage:||Providing storage is as stated on the product vial and the vial is kept tightly sealed, the product can be stored for up to 24 months(2-8C).
Wherever possible, you should prepare and use solutions on the same day. However, if you need to make up stock solutions in advance, we recommend that you store the solution as aliquots in tightly sealed vials at -20C. Generally, these will be useable for up to two weeks. Before use, and prior to opening the vial we recommend that you allow your product to equilibrate to room temperature for at least 1 hour.
Need more advice on solubility, usage and handling? Please email to: email@example.com
|After receiving:||The packaging of the product may have turned upside down during transportation, resulting in the natural compounds adhering to the neck or cap of the vial. take the vial out of its packaging and gently shake to let the compounds fall to the bottom of the vial. for liquid products, centrifuge at 200-500 RPM to gather the liquid at the bottom of the vial. try to avoid loss or contamination during handling.|
|1 mg||5 mg||10 mg||20 mg||25 mg|
|1 mM||5.7055 mL||28.5274 mL||57.0548 mL||114.1097 mL||142.6371 mL|
|5 mM||1.1411 mL||5.7055 mL||11.411 mL||22.8219 mL||28.5274 mL|
|10 mM||0.5705 mL||2.8527 mL||5.7055 mL||11.411 mL||14.2637 mL|
|50 mM||0.1141 mL||0.5705 mL||1.1411 mL||2.2822 mL||2.8527 mL|
|100 mM||0.0571 mL||0.2853 mL||0.5705 mL||1.1411 mL||1.4264 mL|
J Chem Ecol. 1993 Oct;19(10):2279-84.
|Herbicidal activity of sulforaphene from stock (Matthiola incana).[Pubmed: 24248575]|
|A herbicidal compound was isolated from extracts ofMatthiola incana and identified as Sulforaphene (4-methylsulfinyl-3-butenyl isothiocyanate). The ED50 of this compound against velvetleaf seedlings was approximately 2×10(-4) M. Glucoraphenin, the glucosinolate that is the natural precursor of Sulforaphene, was less phytotoxic, with an ED50 of near 6×10(-3)M.|
Breast Cancer Res Treat. 2016 Jul;158(2):277-86.
|Sulforaphene inhibits triple negative breast cancer through activating tumor suppressor Egr1.[Pubmed: 27377973 ]|
|Sulforaphene (SFE, 4-methylsufinyl-3-butenyl isothiocyanate) is a member of isothiocyanates, which is derived from radish seeds. It has shown that multiple isothiocyanates, such as sulforaphane, can effectively inhibit cancer cell proliferation in vitro and in vivo. However, it is still largely unknown if SFE could impact breast cancer. In this study, we investigated the anticancer effects of SFE on triple negative breast cancer (TNBC) via a series of in vitro and in vivo assays. We found that SFE can significantly inhibit cell proliferation in multiple TNBC cell lines through inducing G2/M phase arrest as well as cell apoptosis. Nude mice xenograft assays support the anti-TNBC role of SFE in vivo. Interestingly, SFE can repress expression of cyclinB1, Cdc2, and phosphorylated Cdc2, and, then, induced G2/M phase arrest of TNBC cells. To identify SFE target genes, we detected genome-wide gene expression changes through gene expression profiling and observed 27 upregulated and 18 downregulated genes in MDA-MB-453 cells treated with SFE. Among these genes, Egr1 was successfully validated as a consistently activated gene after SFE treatment in TNBC MDA-MB-453 and MDA-MB-436 cells. Egr1 overexpression inhibited proliferation of TNBC cells. However, Egr1 knockdown using siRNAs significantly promoted TNBC cell growth, indicating the tumor suppressor nature of Egr1. In sum, we for the first time found that SFE might be a potential anti-TNBC natural compound and its antiproliferation effects might be mediated by tumor suppressor Egr1.|
Gen Physiol Biophys. 2016 Jan;35(1):25-34.
|Sulforaphene promotes Bax/Bcl2, MAPK-dependent human gastric cancer AGS cells apoptosis and inhibits migration via EGFR, p-ERK1/2 down-regulation.[Pubmed: 26612919]|
|Gastric cancer migration and invasion considered as main causes of this cancer-related death around the world. Sulforaphene (4-isothiocyanato-4R-(methylsulfinyl)-1-butene), a structural analog of sulforaphane, has been found to exhibit anticancer potential against different cancers. Our aim was to investigate whether dietary isothiocyanate Sulforaphene (SFE) can promote human gastric cancer (AGS) cells apoptosis and inhibit migration. Cells were treated with various concentrations of SFE and cell viability, morphology, intracellular ROS, migration and different signaling protein expressions were investigated. The results indicate that SFE decreases AGS cell viability and induces apoptosis in a dose-dependent manner. Intracellular ROS generation, dose- and time-dependent Bax/Bcl2 alteration and signaling proteins like cytochrome c, Casp-3, Casp-8 and PARP-1 higher expression demonstrated the SFE-induced apoptotic pathway in AGS cells. Again, SFE induced apoptosis also accompanied by the phosphorylation of mitogen-activated protein kinases (MAPKs) like JNK and P-38. Moreover, dose-dependent EGFR, p-ERK1/2 down-regulation and cell migration inhibition at non-toxic concentration confirms SFE activity in AGS cell migration inhibition. Thus, this study demonstrated effective chemotherapeutic potential of SFE by inducing apoptisis as well as inhibiting migration and their preliminary mechanism for human gastric cancer management.|
J Biochem Mol Toxicol. 2017 Aug;31(8).
|Sulforaphene enhances radiosensitivity of hepatocellular carcinoma through suppression of the NF-κB pathway.[Pubmed: 28346727 ]|
|Sulforaphene (SFE), a naturally occurring isothiocyanate found in cruciferous vegetables, has attracted increasing attention for its anti-cancer effect in many cancers, including hepatocellular carcinoma (HCC). However, the precise role of SFE in the radiosensitivity of HCC is still unclear. Here, cell proliferation and apoptosis were detected by MTT and flow cytometry assay, respectively. The activity of NF-κB was further evaluated by ELISA. We also observed the effect of SFE and/or radiation on tumor growth. The results showed that SFE inhibited cell proliferation and induced apoptosis in HCC cells. Radiation increased NF-kB activity, while PDTC, a NF-kB inhibitor, enhanced radiation-induced cell death. SFE inhibited NF-kB activity and the downstream gene expressions of the NF-kB pathway in HCC cells. Moreover, SFE enhanced the inhibitory effect of radiation on tumor growth both in vitro and in vivo. This study indicated that SFE sensitized the radiosensitivity of HCC by blocking the NF-kB pathway.|
Ashs Conference. 2013.
|Characterization of Anti-proliferative and Antibacterial Properties of Sulforaphene Obtained from Radish Seeds,[Reference: WebLink]|
|Many isothiocyanates (ITCs), are a mainly hydrolysis product in glucosinolates (GSLs), have been demonstrated the noteworthy overcoming impact against the survival and proliferation of cancer cells and their modulation of apoptosis and cell cycle progression by numerous molecular basis studies (Zang et al., 2006) , such as sulforaphane (SFA) isolated from broccoli seed and sprouts. By the way, Sulforaphene (SFE), is a major ITCs in radish seed, have been reported the potency of biological activity, a little bit recently. On the other hands, while much researches were known that SFA in broccoli has the excellent anticancer effects such as induction of apoptosis and detoxification enzymes in vitro and in vivo (Fahey et al., 2002), SFE in radish was hardly the biological study in spite of their similar chemical structure in comparison with SFA. In the present study, I demonstrated the broadly biological activity of SFE against cancer cells, Helicobacter pylori (H. pylori) and multi-drug resistance pathogens. In 4 cancer cells isolated from each four organisms were notably inhibited the proliferation treated with purified SFE (IC50 = 10.0–23 μg/mL). I also characterized that SFE modulated an induction of apoptosis pathway against A549 cancer cell through the proteins expressions related with apoptosis pathway. In addition, the highly bacteriocidal potency (MIC90 = 0.6–5.0 μg/mL) of SFE was exhibited against H. pylori, particularly antibiotic resistant strain (212 strain, MIC90 = 0.6 μg/mL). MRSA (Methicillin-resistant staphylococcus aureus), is known as super bacteria, also were inhibited by SFE (MIC90 = 10–20 μg/mL), whereas the MIC 90 value of MSSA (Methicillin-susceptible staphylococcus aureus) by SFE had little significant. These results suggested that the antibiotic potency of SFE in radish seeds would be associated with the potency in a broad range of cancer cells and antibiotic resistant pathogens.|