Kelch-like ECH-associated protein 1 (Keap1), leading to activation of nuclear factor erythroid 2-related factor 2 (Nrf2) [4]
AMP-activated protein kinase (AMPK) [4]
HDAC; Bax; Caspase-3

- In HT29 human colon cancer cells, Sulforaphane induced cell cycle arrest at the G2/M phase and apoptosis in a dose-dependent manner. It decreased the expression of cyclin B1 and cdc2, and increased the expression of p21. Apoptosis was associated with cytochrome c release from mitochondria, activation of caspases-3 and -9, and cleavage of poly(ADP-ribose) polymerase (PARP) [1]
- In rat H9c2 cells, Sulforaphane prevented doxorubicin-induced oxidative stress and cell death. It increased the activities of superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx), reduced reactive oxygen species (ROS) production and malondialdehyde (MDA) levels, and inhibited doxorubicin-induced apoptosis by upregulating Bcl-2 and downregulating Bax and cleaved caspase-3 [2]
- In various cancer cell lines (including breast, colon, and lung cancer cells), Sulforaphane exhibited anticarcinogenic activity by inhibiting cell proliferation and inducing apoptosis. It also inhibited the activity of phase I enzymes (e.g., cytochrome P450 1A1) and induced phase II detoxifying enzymes (e.g., quinone reductase) [3]
- In pancreatic cancer cells under high glucose conditions, Sulforaphane activated Nrf2, which in turn inhibited cell proliferation, migration, and invasion, and promoted apoptosis. This effect was mediated through AMPK-dependent signaling, as Sulforaphane increased AMPK phosphorylation, and the effects were reversed by AMPK inhibition [4]
In a dose-dependent manner, sulforaphane causes cell cycle arrest and eventual cell death. Higher expression of cyclin A and B1 was linked to this sulforaphane-induced cell cycle halt. Sulforaphane causes apoptosis, which is the process by which cells die. Sulforaphane is less harmful to differentiated CaCo2 cells and slows the return of growth in quiescent colon cancer cells (HT29), while also reducing their cell viability [1]. Sulforaphane pretreatment of H9c2 rat myoblasts decreased the amount of apoptotic cells and pro-apoptotic protein expression (Bax, caspase-3, and cytochrome c), as well as the increase in mitochondrial membrane potential that doxorubicin caused. Furthermore, sulforaphane decreases doxorubicin-induced levels of reactive oxygen species (ROS, as determined by MitoSOX Red reagent) in mitochondria via increasing the mRNA and protein expression of heme oxygenase-1 [2].

In mice, Sulforaphane showed anticarcinogenic activity by inhibiting the formation of carcinogen-induced preneoplastic lesions in the colon. It also induced phase II detoxifying enzymes in various tissues, including the liver, colon, and small intestine [3]
Sulforaphane reduces mammary tumor growth in Sprague-Dawley rats treated with a single dose of 9,10-dimethyl-1,2-benzanthracene. Administration of sulforaphane lowers the incidence, multiplicity, and weight of breast tumors generated by a single dose of DMBA in female Sprague-Dawley rats and slows their progression [3].

- For HT29 colon cancer cells: Cells were cultured in medium and treated with Sulforaphane at different concentrations (0-40 μM) for various times. Cell cycle analysis was performed by propidium iodide staining and flow cytometry. Apoptosis was assessed by annexin V-FITC/PI staining, TUNEL assay, and detection of caspase activity. Western blot analysis was used to measure the expression of cell cycle-related proteins (cyclin B1, cdc2, p21) and apoptotic markers (cytochrome c, caspases-3/-9, PARP) [1]
- For H9c2 cells: Cells were pretreated with Sulforaphane (0-5 μM) before doxorubicin exposure. Oxidative stress markers (ROS, MDA, SOD, CAT, GPx) were measured using respective assay kits. Cell viability was determined by MTT assay, and apoptosis was analyzed by western blot for Bcl-2, Bax, and cleaved caspase-3 [2]
- For pancreatic cancer cells: Cells were cultured under high glucose conditions and treated with Sulforaphane. Cell proliferation was assessed by CCK-8 assay, migration and invasion by transwell assays, and apoptosis by flow cytometry. Western blot was used to detect Nrf2, HO-1, NQO1, p-AMPK, and other related proteins. Nrf2 nuclear translocation was analyzed by immunofluorescence [4]

Mice were administered Sulforaphane via oral gavage at a dose of 200 μmol/kg body weight. After treatment, mice were sacrificed, and various tissues (liver, colon, small intestine) were collected. The activity of phase II detoxifying enzymes (quinone reductase) was measured in tissue homogenates. For carcinogen-induced preneoplastic lesion models, mice were treated with carcinogens and Sulforaphane concurrently, and the number of lesions was counted histologically [3]

[1]. 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.
[2]. Sulforaphane prevents doxorubicin-induced oxidative stress and cell death in rat H9c2 cells. Int J Mol Med. 2015 Jul;36(1):53-64.
[3]. Anticarcinogenic activities of sulforaphane and structurally related synthetic norbornylisothiocyanates. Proc Natl Acad Sci U S A. 1994 Apr 12;91(8):3147-50.
[4]. Activation of Nrf2 by Sulforaphane Inhibits High Glucose-Induced Progression of PancreaticCancer via AMPK Dependent Signaling. ell Physiol Biochem. 2018;50(3):1201-1215

- Sulforaphane is a naturally occurring isothiocyanate found in cruciferous vegetables. Its anticarcinogenic activity is partly attributed to the induction of phase II detoxifying enzymes, which enhance the detoxification of carcinogens, and the inhibition of phase I enzymes, which reduce the activation of procarcinogens [3]
- In colon cancer cells, the induction of apoptosis by Sulforaphane involves the mitochondrial pathway, characterized by cytochrome c release and caspase activation [1]
- The protective effect of Sulforaphane against doxorubicin-induced cell damage is related to its antioxidant properties, reducing oxidative stress and inhibiting apoptotic pathways [2]
Sulforaphane is an isothiocyanate having a 4-(methylsulfinyl)butyl group attached to the nitrogen. It has a role as an antineoplastic agent, a plant metabolite, an antioxidant and an EC 3.5.1.98 (histone deacetylase) inhibitor. It is a sulfoxide and an isothiocyanate.
Sulforaphane is under investigation for the treatment of Autism Spectrum Disorder. It is a naturally occurring isothiocyanate found in high concentration in a variety of broccoli.
Sulforaphane has been reported in Brassica oleracea, Brassica oleracea var. sabauda, and other organisms with data available.
Sulforaphane is a naturally-occurring phytochemical belonging to the class of isothiocyanates. As the aglycone metabolite of glucosinolate glucoraphanin (sulforaphane glucosinolate), sulforaphane acts as an antioxidant and potent stimulator of endogenous detoxifying enzymes. This agent displays anticarcinogenic properties due to its ability to induce phase II detoxification enzymes, such as glutathione S-transferase and quinone reductase, thereby providing protection against certain carcinogens and toxic, reactive oxygen species. Broccoli sprouts contain large amounts of sulforaphane, which is also found in other cruciferous vegetables including cabbage and kale. (NCI04)

C6H11NOS2

177.3

177.028

C, 40.65; H, 6.25; N, 7.90; O, 9.02; S, 36.17

4478-93-7

142825-10-3 (R-isomer); 155320-20-0 (S-isomer); 4478-93-7 (racemic);

5350

Colorless to light yellow liquid

1.2±0.1 g/cm3

368.2±25.0 °C at 760 mmHg

176.5±23.2 °C

0.0±0.8 mmHg at 25°C

1.567

0.23

0

4

5

10

152

0

O=S(CCCCN=C=S)C

SUVMJBTUFCVSAD-UHFFFAOYSA-N

InChI=1S/C6H11NOS2/c1-10(8)5-3-2-4-7-6-9/h2-5H2,1H3

1-isothiocyanato-4-(methylsulfinyl)butane

Sulforafan; Sulforaphane; BroccoPhane; sulforaphane; 4478-93-7; 1-Isothiocyanato-4-(methylsulfinyl)butane; Sulforafan; 1-isothiocyanato-4-methylsulfinylbutane; Sulphoraphane; Butane, 1-isothiocyanato-4-(methylsulfinyl)-; CHEBI:47807; Detoxophane; Broccoli sprout extracts; 4-methyl-sulfinybutyl isothiocyanatel

2934.99.9001

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

Note: (1). Please store this product in a sealed and protected environment (e.g. under nitrogen), avoid exposure to moisture and light.  (2). This product is not stable in solution, please use freshly prepared working solution for optimal results.

Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)

DMSO : ≥ 62.5 mg/mL (~352.53 mM)
H2O : ~50 mg/mL (~282.02 mM)

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.
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 corn oil and mix evenly.

---

Solubility in Formulation 4: 10 mg/mL (56.40 mM) in 30 % SBE-β-CD (add these co-solvents sequentially from left to right, and one by one), clear solution; with ultrasonication.

---

 (Please use freshly prepared in vivo formulations for optimal results.)