Lung Cancer Chemoprevention (Human RCT): A phase II randomized placebo-controlled trial in former smokers (high lung cancer risk) found that one year of oral sulforaphane (95 µmol/day) did not alter bronchial histopathology, but it significantly reduced cellular proliferation markers in airway biopsies pubmed.ncbi.nlm.nih.gov

Specifically, Ki-67 (a proliferation index) decreased by 20% in the SFN group versus a 65% increase in placebo (p=0.014), with even greater reductions in high-Ki67 areas pubmed.ncbi.nlm.nih.gov

No severe adverse events occurred, supporting further development of SFN as a lung cancer chemopreventive agent pubmed.ncbi.nlm.nih.gov

Breast Cancer and Therapy (Systematic Review): A 2025 systematic review (20 studies: 3 clinical trials, 5 animal studies, 12 cell studies) concluded that sulforaphane targets multiple breast cancer pathways pubmed.ncbi.nlm.nih.gov

Preclinical evidence shows SFN reduces tumor proliferation, induces cancer cell apoptosis, and inhibits metastasis, while sparing normal cells pubmed.ncbi.nlm.nih.gov

SFN also appeared to synergize with chemotherapy/radiation and protect healthy tissue from radiation damage, suggesting it could enhance breast cancer treatment outcomes pubmed.ncbi.nlm.nih.gov

Alzheimer's Disease Models (Animal Study): New evidence from an amyloid-beta induced mouse model of Alzheimer's disease (AD) demonstrated that a sulforaphane-rich broccoli sprout extract can improve cognition. Treated AD-model mice showed enhanced memory retention in maze tests and reduced amyloid plaque deposition in the brain cell.com

The SFN-rich extract also inhibited acetylcholinesterase activity (preserving acetylcholine levels) and reduced neuroinflammation, ultimately ameliorating AD-like neurobehavioral deficits cell.com

Tau Pathology and Cognition (Animal Study): Another 2025 in vivo study examined SFN in a transgenic mouse model expressing pathological, Caspase-3–cleaved tau protein (to mimic AD neurofibrillary tangles). Mice treated with SFN (50 mg/kg i.p. for 2 weeks) were protected from the memory deficits normally caused by toxic tau pubmed.ncbi.nlm.nih.gov

SFN treatment preserved cognitive performance (novel object recognition and maze tests) and prevented mitochondrial dysfunction in the hippocampus that was induced by the pathological tau pubmed.ncbi.nlm.nih.gov

These findings highlight SFN's neuroprotective action (likely via Nrf2-mediated antioxidant responses) against tau-mediated neurodegeneration.

Lifespan Extension in Worms (Preclinical Study): Emerging 2025 research suggests sulforaphane may have geroprotective effects. A C. elegans study (preprint) reported that continuous SFN exposure from early life extended worm lifespan by over 50% at optimal doses surfaceyourrealself.com

Treated worms also showed a ~20% lower "transcriptional age" (based on gene-expression aging clocks) compared to controls surfaceyourrealself.com

The longevity benefits of SFN were associated with activation of detoxification and stress-response pathways, consistent with a hormetic mechanism surfaceyourrealself.com

These results imply SFN triggers conserved pro-longevity networks, although translation to mammals remains to be seen (notably, C. elegans lack the Keap1 protein of the mammalian Nrf2 system surfaceyourrealself.com) (Study type: laboratory lifespan assay in nematodes – preprint, not yet peer-reviewed.)

Prediabetes Blood Sugar Trial (Human RCT): A double-blind RCT in 74 overweight adults with prediabetes tested broccoli sprout extract (rich in SFN) vs placebo for 12 weeks. SFN treatment led to modest but significant improvements in fasting blood glucose, with an average drop ~0.2 mmol/L greater than placebo (p≈0.04) nature.com

While the predefined primary endpoint was not fully met, a post hoc analysis identified a "responder" subgroup – individuals with mild obesity, lower insulin resistance, and particular gut microbiota – who experienced a larger ~0.4 mmol/L glucose reduction nature.com

Microbiome sequencing revealed that responders harbored higher levels of a Bacteroides gene cluster responsible for converting glucoraphanin to active sulforaphane, correlating with greater SFN blood levels nature.com

This suggests that gut bacteria and host metabolic profile together influence SFN's efficacy in improving glycemic control.

Fasting-Mimetic Effects (Cell Study): In vitro research in human cells found that sulforaphane can acutely activate cellular pathways reminiscent of caloric restriction. In cultured human retinal cells, SFN triggered multiple "starvation response" mechanisms pubmed.ncbi.nlm.nih.gov

Notably, SFN increased mitochondrial mass and antioxidant capacity, inhibited insulin/IGF signaling (with downstream suppression of mTOR nutrient-sensing activity), and upregulated autophagy and lysosome biogenesis pubmed.ncbi.nlm.nih.gov

SFN also transiently reduced glucose uptake and lactate production, with adaptive metabolic rebounding later observed pubmed.ncbi.nlm.nih.gov

These effects mirror known longevity-promoting pathways (AMPK/mTOR/autophagy activation), suggesting SFN may act as a caloric-restriction mimetic at the cellular level.

Anti-Inflammatory Actions (In Vitro): Sulforaphane's potent anti-inflammatory properties were reinforced by new cell-culture studies. For example, SFN exposure in LPS-stimulated macrophages significantly down-regulated key pro-inflammatory genes (coding for COX-2, IL-6, and TNF-α) cell.com

This demonstrates SFN's ability to blunt inflammatory signaling in immune cells, consistent with its known NF-κB inhibitory activity. Such in vitro findings align with SFN's broader antioxidant and Nrf2-driven anti-inflammatory profile.

Diabetic Wound Healing (Animal Study): A 2025 study in a diabetic mouse model showed that topical sulforaphane can accelerate chronic wound healing by resolving inflammation. In streptozotocin-diabetic mice with non-healing skin ulcers, SFN treatment improved closure rates, partly by enhancing efferocytosis (the clearance of dead cells) and shifting macrophages toward a pro-repair M2 phenotype pubmed.ncbi.nlm.nih.gov

Mechanistically, SFN-activated Nrf2/HO-1 signaling upregulated the MerTK receptor on macrophages, boosting their clearance of apoptotic cells and dampening local IL-6/TNF-mediated inflammation pubmed.ncbi.nlm.nih.gov

The net result was a reduction in persistent inflammatory burden and promotion of tissue repair. This preclinical finding suggests SFN as a potential adjunct therapy for chronic inflammatory conditions such as diabetic ulcers.

Cardiovascular Metabolism (Animal Study): In a Type 2 diabetic mouse model prone to diabetic cardiomyopathy, long-term sulforaphane supplementation conferred cardioprotective effects. Diabetic db/db mice gavaged with SFN for 16 weeks showed improved systemic metabolism (lower blood glucose, improved insulin sensitivity, and reduced dyslipidemia) and markedly healthier hearts pubmed.ncbi.nlm.nih.gov

SFN-treated diabetic mice had less cardiac fibrosis and injury, preserved diastolic function, and reduced lipid accumulation and oxidative damage in heart tissue pubmed.ncbi.nlm.nih.gov

At the molecular level, SFN normalized cardiac fuel use by down-regulating overactive fatty-acid uptake/metabolism pathways (e.g. reducing elevated CD36, CPT1B, and PPARα levels) and improving mitochondrial function pubmed.ncbi.nlm.nih.gov

These findings indicate SFN can mitigate diabetes-induced cardiac lipotoxicity and support heart metabolism, highlighting a potential role in preventing diabetic cardiac complications.