Sulforaphane — SFN (Isothiocyanate · Nrf2 Activation · Chemopreventive · Air Pollution)
| Compound | Sulforaphane (SFN) |
| Chemical class | Glucosinolate Hydrolysis Product — Isothiocyanate (4-Methylsulfinylbutyl isothiocyanate) |
| CAS | 4478-93-7 |
| Primary source | Enzymatic hydrolysis of glucoraphanin in Brassica oleracea (broccoli) by myrosinase |
| Key applications | Nrf2 activation, Phase-II detoxification, air pollution protection, chemopreventive, autism research |
| Claim strength | Moderate |
| Typical form | Broccoli extract (sulforaphane or glucoraphanin + myrosinase); sulforaphane isolate; broccoli sprout powder |
| Buy from Herbuno |
Name origin: Sulfo- (the methylsulfinyl group) + raphan- (from glucoraphanin) + -ane (organic compound suffix). Sulforaphane is an isothiocyanate — the —N=C=S functional group is directly responsible for its electrophilic reactivity with Keap1 (the Nrf2 repressor protein), which is the basis for its Nrf2-activating pharmacology. Traditional use: No traditional use of isolated sulforaphane; its parent compound glucoraphanin (in broccoli, cabbage) has ancestral food-as-medicine use. The significant research history of sulforaphane begins with Paul Talalay’s Johns Hopkins group identifying it as the primary Phase-II enzyme inducer in broccoli in 1992. Research trajectory: Sulforaphane is the most extensively studied dietary isothiocyanate globally, with approximately 3,000 published studies covering: Nrf2 activation, Phase-II enzyme induction, air pollution detoxification (China RCT), autism spectrum disorder symptom reduction (small but compelling RCTs at Johns Hopkins), COPD, type 2 diabetes, and cancer chemoprevention. It is arguably the most pharmacologically documented single phytochemical from cruciferous vegetables. Commercial source: Broccoli Extract Powder and Broccoli Liquid Extract from Herbuno deliver sulforaphane (if myrosinase-active) or glucoraphanin (sulforaphane precursor) depending on processing method. See sourcing options below.
Evidence for Sulforaphane Applications
Nrf2 activation and Phase-II enzyme induction — mechanism cornerstone: Sulforaphane covalently modifies cysteine residues on Keap1 (the Nrf2 repressor), releasing Nrf2 to translocate to the nucleus and activate antioxidant response element (ARE)-driven gene expression. This induces NQO1 (quinone oxidoreductase), GST (glutathione S-transferase), HO-1 (heme oxygenase), thioredoxin reductase, and ferritin. This mechanism is the basis for virtually all of sulforaphane’s pharmacological applications. Claim strength: High (mechanism; human biomarker RCTs).
Air pollution protection (China biomarker RCT): A landmark randomised trial in Qidong, China (Egner et al. 2014, n=291) demonstrated that daily consumption of a broccoli sprout beverage (delivering 600 µmol glucoraphanin/26 µmol sulforaphane) increased urinary excretion of benzene metabolites by 61% and acrolein metabolites by 23% over 12 weeks. This is among the most direct demonstrations of dietary intervention enhancing carcinogen detoxification in humans. Claim strength: Moderate (single RCT; strong biomarker outcomes).
Autism spectrum disorder (ASD) — pilot RCTs: A randomised trial (Singh et al. 2014, n=44, Johns Hopkins) showed that sulforaphane (50–150 µmol/day) significantly improved social interaction, abnormal behaviour, and verbal communication scores in young men with moderate to severe ASD over 18 weeks — with reversal of gains after washout. These are among the most unexpected and intriguing human RCT findings for any phytochemical. The mechanism is proposed to involve heat shock protein induction, oxidative stress reduction, and neuroinflammation modulation. Claim strength: Moderate (small RCT; needs replication at scale).
COPD and respiratory: A Phase II clinical trial (NCT01238263) with broccoli sprout extract (delivering 200 µmol sulforaphane/day) in COPD patients showed significant improvements in lung function and reductions in inflammatory markers (IL-8, TNF-α) over 4 months. Claim strength: Moderate.
Browse Standardised Extract Powders →
Dosage & Formulator Specification
Human RCT dose range: 30–200 µmol/day sulforaphane (approximately 5–35 mg sulforaphane or 25–125 mg glucoraphanin with active myrosinase). The China air pollution RCT used 600 µmol glucoraphanin/day (a high dose); the ASD RCT used 50–150 µmol sulforaphane/day (approximately 9–27 mg). Broccoli extract standardised to glucoraphanin is the most stable commercial form — specify myrosinase status (active or inactive). For guaranteed sulforaphane delivery without myrosinase dependency, sulforaphane isolate (GreenSelect® SFN or equivalent) or sulforaphane-cyclodextrin complex (more stable than free sulforaphane) are available from specialist suppliers. Sulforaphane itself is volatile, unstable, and strongly odorous — formulation as an enteric-coated capsule or with cyclodextrin complexation significantly improves stability and palatability.
Frequently Asked Questions — Sulforaphane
What is Keap1-Nrf2-ARE and why is sulforaphane uniquely effective at activating it?
Keap1 (Kelch-like ECH-associated protein 1) normally keeps Nrf2 tethered in the cytoplasm for ubiquitin-mediated degradation. Sulforaphane alkylates specific cysteine residues (Cys151, Cys273, Cys288) on Keap1 via Michael addition of the isothiocyanate group — a covalent, irreversible modification that disrupts Keap1’s ability to retain and degrade Nrf2. Free Nrf2 translocates to the nucleus and binds the Antioxidant Response Element (ARE), activating a battery of cytoprotective genes. Sulforaphane’s effectiveness reflects both its electrophilic isothiocyanate group (covalent Keap1 modifier) and its membrane permeability (reaches intracellular Keap1 efficiently).
Can sulforaphane supplements benefit individuals with BRCA mutations?
This is an area of active but preliminary research. Sulforaphane has demonstrated epigenetic activity (DNMT and HDAC inhibition) in BRCA-related cancer cell models, and some in vitro data suggest selective sensitisation of BRCA-mutant cells to sulforaphane-induced apoptosis. No human RCT has specifically evaluated sulforaphane supplementation for BRCA mutation carriers. The mechanistic rationale is plausible but the clinical evidence gap is significant. Standard advisory language for high-risk individuals to consult oncology specialists before supplement use applies.
Why was the autism spectrum disorder finding so surprising?
The Singh et al. 2014 ASD RCT used a dietary phytochemical (sulforaphane) to produce measurable improvements in core ASD symptoms (social interaction, communication, behaviour) in a condition without effective pharmacotherapy for behavioural symptoms. The proposed mechanism — sulforaphane inducing heat shock proteins that correct protein misfolding underlying ASD neuronal dysfunction — was novel and has generated significant research interest. The finding remains to be confirmed in larger trials. It represents one of the most clinically significant potential applications for a single dietary compound in neurological conditions.
Is sulforaphane safe at supplement doses long-term?
Sulforaphane from dietary broccoli consumption (providing 5–20 mg/day sulforaphane equivalent) has an impeccable safety record as a food constituent. At supplement doses (10–100 mg/day) in clinical trials, sulforaphane is well-tolerated with GI discomfort (flatulence, bloating) as the primary reported side effect. At very high doses (>400 µmol/day), potential pro-oxidant effects and GSH depletion are theoretical concerns. Standard pregnancy advisory applies; active thyroid conditions warrant monitoring given glucosinolate class thyroid considerations.
Related compounds: Glucoraphanin, Indole-3-Carbinol, Phenethyl Isothiocyanate, Allyl Isothiocyanate
Claim-strength scale – High = multiple human RCTs; Moderate = limited trials or strong preclinical convergence; Emerging = early-stage lab or animal data.
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