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Sulforaphane

MCE China：Sulforaphane

Brand：MedChemExpress (MCE)

Cat. No.HY-13755

CAS：4478-93-7

Purity：98.87%

Storage：-20°C, sealed storage, away from moisture and light *The compound is unstable in solutions, freshly prepared is recommended.

Shipping：Room temperature in continental US; may vary elsewhere.

Description：Sulforaphane is an orally active inducer of the Keap1/Nrf2/ARE pathway. Sulforaphane promotes the transcription of tumor-suppressing proteins and effectively inhibits the activity of HDACs. Through the activation of the Keap1/Nrf2/ARE pathway and further induction of HO-1 expression, Sulforaphane protects the heart. Sulforaphane suppresses high glucose-induced pancreatic cancer through AMPK-dependent signal transmission. Sulforaphane exhibits both anticancer and anti-inflammatory properties.

In Vitro：Sulforaphane (0-30 μM) induces cell cycle arrest and apoptosis in a dose-dependent manner. Sulforaphane-induced cell cycle arrest is associated with an increase in the expression of cyclin A and B1[1]. Sulforaphane (0-30 μM) inhibits the re-initiation of growth and decreases cell viability in HT29 cells, exhibiting lower toxicity towards differentiated cells[1]. Sulforaphane (10 μM, 24 hours) pre-treatment reduces the number of apoptotic cells, decreases the expression of pro-apoptotic proteins (Bax, caspase-3, cytochrome c), and counteracts the increase in mitochondrial membrane potential induced by Doxorubicin (HY-15142A) (1 μM, 2 hours) in H9c2 cells[2]. Sulforaphane (10 μM, 2 or 24 hours) effectively reduces ROS production and cell apoptosis in H9c2 cells induced by Doxorubicin (1 μM, 2 or 24 hours) through the activation of the Keap1/Nrf2/ARE pathway and further induction of HO-1 expression[2].

In Vivo：Sulforaphane (13.3, 17.7, 26.6 mg/kg; Oral gavage; 5 days) is capable of inhibiting the formation of mammary tumors in female Sprague-Dawley rats following a single-dose treatment with DMBA (HY-W011845) (8 mg/mL)[3]. Sulforaphane (13.3, 17.7, 26.6 mg/kg; Oral gavage; 5 days) can reduce the incidence, multiplicity, and weight of mammary tumors induced by DMBA (8 mg/mL) in female Sprague-Dawley rats, and delay their development[3].

IC50 & Target：HDAC Bax Caspase-3

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References：

[1]. Gamet-Payrastre L, et al. Sulforaphane, a naturally occurring isothiocyanate, induces cell cycle arrest and apoptosis in HT29 human colon cancer cells. Cancer Res. 2000 Mar 1;60(5):1426-33.  [Content Brief]

[2]. Li B, et al. Sulforaphane prevents doxorubicin-induced oxidative stress and cell death in rat H9c2 cells. Int J Mol Med. 2015 Jul;36(1):53-64.  [Content Brief]

[3]. Zhang Y, et al. Anticarcinogenic activities of sulforaphane and structurally related synthetic norbornylisothiocyanates. Proc Natl Acad Sci U S A. 1994 Apr 12;91(8):3147-50.  [Content Brief]

[4]. Chen X, et al. Activation of Nrf2 by Sulforaphane Inhibits High Glucose-Induced Progression of PancreaticCancer via AMPK Dependent Signaling. ell Physiol Biochem. 2018;50(3):1201-1215.  [Content Brief]

[5]. De Nicola GR, et al. Novel gram-scale production of enantiopure R-sulforaphane from Tuscan black kale seeds. Molecules. 2014 May 27;19(6):6975-86.  [Content Brief]

[6]. Abdull Razis AF, et al. The natural chemopreventive phytochemical R-sulforaphane is a far more potent inducer of the carcinogen-detoxifying enzyme systems in rat liver and lung than the S-isomer. Int J Cancer. 2011 Jun 15;128(12):2775-82.  [Content Brief]