Sulforaphane

Research use only, not for human use.

Sulforaphane (SFN) is an antioxidant agent that exerts protective effects against cell damage by activating Nrf2.

Sulforaphane (SFN) is an antioxidant agent that exerts protective effects against cell damage by activating Nrf2; protects RLE?6TN cells from oxidative damage, potentially via increasing Nrf2 expression and reducing ROS levels; reduces lens epithelial cell growth, migration and viability, and promotes ER stress and autophagy in lens cells; also inhibits class I and II HDAC activity and suppresses tumor growth by inducing cell cycle arrest and apoptosis selectively in various cancerous prostate epithelial cells without affecting normal cells.Breast Cancer Phase 2 Clinical(In Vitro):Sulforaphane induces a cell cycle arrest in a dose-dependent manner, followed by cell death. This sulforaphane-induced cell cycle arrest was correlated with an increased expression of cyclins A and B1. Sulforaphane induces cell death via an apoptotic process. Sulforaphane inhibits the reinitiation of growth and diminishes cellular viability in quiescent colon carcinoma cells (HT29) and has a lower toxicity on differentiated CaCo2 cells. Pre-treatment of H9c2 rat myoblasts with sulforaphane decreases the apoptotic cell number and the expression of pro-apoptotic proteins (Bax, caspase-3 and cytochrome c), as well as the doxorubicin-induced increase in mitochondrial membrane potential. Furthermore, sulforaphane increases the mRNA and protein expression of heme oxygenase-1, which consequently reduces the levels of reactive oxygen species (ROS, measured using MitoSOX Red reagent) in the mitochondria which are induced by doxorubicin.(In Vivo):Sulforaphane can block the formation of ammary tumors in Sprague-Dawley rats treated with single doses of 9,10-dimethyl-1,2-benzanthracene. Administration of sulforaphane reduces the incidence, multiplicity, and weights and delays the development of the mammary tumors evoked by a single dose of DMBA in female Sprague-Dawley rats.

Sulforaphane induces a cell cycle arrest in a dose-dependent manner, followed by cell death. This sulforaphane-induced cell cycle arrest was correlated with an increased expression of cyclins A and B1. Sulforaphane induces cell death via an apoptotic process. Sulforaphane inhibits the reinitiation of growth and diminishes cellular viability in quiescent colon carcinoma cells (HT29) and has a lower toxicity on differentiated CaCo2 cells. Pre-treatment of H9c2 rat myoblasts with sulforaphane decreases the apoptotic cell number and the expression of pro-apoptotic proteins (Bax, caspase-3 and cytochrome c), as well as the doxorubicin-induced increase in mitochondrial membrane potential. Furthermore, sulforaphane increases the mRNA and protein expression of heme oxygenase-1, which consequently reduces the levels of reactive oxygen species (ROS, measured using MitoSOX Red reagent) in the mitochondria which are induced by doxorubicin.

Sulforaphane can block the formation of ammary tumors in Sprague-Dawley rats treated with single doses of 9,10-dimethyl-1,2-benzanthracene. Administration of sulforaphane reduces the incidence, multiplicity, and weights and delays the development of the mammary tumors evoked by a single dose of DMBA in female Sprague-Dawley rats.

SFN

Nuclear Receptor/Transcription Factor

Keap1-Nrf2

Keap1-Nrf2

Cancer

——

4478-93-7

177.28

C6H11NOS2

>98% (HPLC)

DMSO : ≥ 62.5 mg/mL 352.53 mM

O=S(CCCCN=C=S)C

1-isothiocyanato-4-(methylsulfinyl)-butane

(-20℃)

With Ice Pack

≥ 2 years