NRF2 covalent switch vs indirect inflammation modulation
What this is
Head-to-head evidence table: Sulforaphane vs Curcumin (compound).
Why it matters
Sulforaphane covalently modifies KEAP1, releasing NRF2 to drive 200+ cytoprotective genes. Curcumin modulates NF-κB and inflammation but has poor bioavailability and weaker NRF2 activation data.
What to do next
Use the verdict row to pick a primary compound, then open both deep-dives and /shop verification checklists.
Sulforaphane covalently modifies KEAP1, releasing NRF2 to drive 200+ cytoprotective genes. Curcumin modulates NF-κB and inflammation but has poor bioavailability and weaker NRF2 activation data.
NRF2 activation mechanism
Sulforaphane
KEAP1 covalent modification — direct
Curcumin
Indirect; weak KEAP1 data
Bioavailability
Sulforaphane
Requires myrosinase conversion
Curcumin
Poor native; needs piperine/phytosome
hs-CRP evidence
Sulforaphane
Strong when paired with lifestyle + GlyNAC
Curcumin
Mixed meta-analyses
Gene programs induced
Sulforaphane
NQO1, GST, HO-1, proteasome subunits
Curcumin
NF-κB, COX-2 modulation
TNiC stack role
Sulforaphane
Core NRF2 Defense compound
Curcumin
Not in TNiC presets
Buyer verification
Sulforaphane
GR + myrosinase quantified
Curcumin
Curcuminoid % + absorption tech
TNiC verdict
Sulforaphane wins for NRF2-primary stacks and hs-CRP reduction paired with GlyNAC. Curcumin is adjunct anti-inflammatory — not a substitute for KEAP1 pathway activation.
Choose Sulforaphane when
Choose Curcumin when
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