Head to head
Dimethyl fumarate against Sulforaphane
An approved multiple sclerosis drug that is the cleanest available NRF2 activator, next to the supplement version of the same idea. Dimethyl fumarate did not extend mouse lifespan, and the paper reports the delivered dose averaged only 35 percent of target.
Column A
Dimethyl fumarateDimethyl fumarate (Tecfidera), NRF2 pathway activator
An approved multiple sclerosis drug and the cleanest available NRF2 activator. It did not extend mouse lifespan, and the paper reports the dose delivered averaged only 35 percent of target, which the authors say may explain that.
Column B
SulforaphaneSulforaphane, an isothiocyanate released from broccoli glucoraphanin
Three randomised trials with prespecified primary endpoints, three misses: PSA slope in 78 men after prostatectomy, fasting glucose in 74 adults with prediabetes, and the autism replication in 45 children. The cleanest positive human result is a urinary detoxification biomarker, a 63.2 percent rise in benzene mercapturic acid excretion in Qidong, China.
Side by side, on the facts we can check
| Attribute | Dimethyl fumarate | Sulforaphane |
|---|---|---|
| Category | Antioxidant | Antioxidant |
| FDA status | FDA-approved as Tecfidera for relapsing forms of multiple sclerosis. Not approved for any ageing indication. | Not an approved drug for any indication. Sold as a dietary supplement, usually as broccoli seed or sprout extract standardised to glucoraphanin rather than to sulforaphane itself. |
| Half-life | Very short as the parent compound, which is rapidly hydrolysed to monomethyl fumarate, the active metabolite, with a half-life of roughly one hour. | Roughly 2 hours in plasma after an oral dose, with most urinary metabolite excretion complete within about a day. |
| Molecular weight | 144.1 Da. A small molecule, not a peptide. | 177.3 Da. An isothiocyanate, not a peptide. |
| Mechanism | An electrophile that modifies cysteine residues on KEAP1, the protein that normally tags NRF2 for degradation. Disabling KEAP1 lets NRF2 accumulate and enter the nucleus, where it drives transcription of antioxidant response element genes including glutathione synthesis enzymes, NAD(P)H quinone dehydrogenase 1 and haem oxygenase 1. It also depletes glutathione acutely and has immunomodulatory effects independent of NRF2, including lymphocyte reduction, which is relevant to its multiple sclerosis efficacy and its main risk. | Sulforaphane modifies cysteine residues on KEAP1, which releases the transcription factor NRF2 to enter the nucleus and drive a large battery of phase 2 detoxification and antioxidant genes, including glutathione S-transferases and NAD(P)H quinone dehydrogenase 1. This is why its most reproducible human effect is on the conjugation and excretion of electrophilic toxicants rather than on any disease process: the pathway it activates is literally a disposal system. Separate work identified sulforaphane by matching a type 2 diabetes liver gene expression signature against a library of 3,800 drug signatures, and found it suppressed hepatic glucose production through NRF2 nuclear translocation with reduced expression of gluconeogenic enzymes. In the plant it does not exist. Broccoli stores the stable glucosinolate glucoraphanin in one compartment and the enzyme myrosinase in another, and sulforaphane is generated when the tissue is damaged, which is the relevance of chewing, chopping and of whether a capsule contains active enzyme. |
| Human studies cited | 0 | 7 |
| Legal status, US | FDA-approved, prescription only | Sold as a supplement |
Frequently asked questions
What is the difference between Dimethyl fumarate and Sulforaphane?
Dimethyl fumarate: An approved multiple sclerosis drug and the cleanest available NRF2 activator. It did not extend mouse lifespan, and the paper reports the dose delivered averaged only 35 percent of target, which the authors say may explain that. Sulforaphane: Three randomised trials with prespecified primary endpoints, three misses: PSA slope in 78 men after prostatectomy, fasting glucose in 74 adults with prediabetes, and the autism replication in 45 children. The cleanest positive human result is a urinary detoxification biomarker, a 63.2 percent rise in benzene mercapturic acid excretion in Qidong, China.
Which has stronger research evidence, Dimethyl fumarate or Sulforaphane?
This database does not grade compounds. It counts what was run in people: 0 of the 1 studies cited on the Dimethyl fumarate profile were human work, against 7 of 7 for Sulforaphane. Those counts are of our own citation lists and understate any larger literature, and neither is a recommendation.
Are Dimethyl fumarate and Sulforaphane FDA-approved?
Dimethyl fumarate: FDA-approved as Tecfidera for relapsing forms of multiple sclerosis. Not approved for any ageing indication.. Sulforaphane: Not an approved drug for any indication. Sold as a dietary supplement, usually as broccoli seed or sprout extract standardised to glucoraphanin rather than to sulforaphane itself..
Reviewed Sep 2026. This page sets two published records side by side. It is educational, it is not medical advice, and it contains no dosing protocols or recommendations for personal use.