Sodium Butyrate
SCFA HDACi: Tumor-suppressor ↑, cell-cycle arrest; preclinical in colorectal/breast/pancreatic/lung.
Forms: Tributyrin capsules (colon-targeted, 500-1000 mg) · Dietary via resistant starch/fiber
Key Takeaway
SCFA and class I/IIa HDAC inhibitor that re-expresses tumor suppressors and can trigger cell-cycle arrest/apoptosis—strong preclinical data; human oncology trials are limited. Clinically, leverage diet/tributyrin/colon-targeted delivery rather than high-dose sodium butyrate.
Evidence at a glance
Preclinical HDAC/apoptosis dominance; small CRC phase II signals; meta-barrier/QoL modest; ongoing tributyrin trials; delivery key to systemic reach.
How it may work
Butyrate inhibits HDACs, increasing histone H3/H4 acetylation and transcription of p21, p27, and pro-apoptotic genes. It modulates NF-κB and fuels colonocytes, improving barrier function and dampening inflammation. Epigenetic reprogramming reduces proliferation, induces differentiation, and sensitizes to 5-FU and other agents in colorectal and breast models.
Targets & pathways
Curated mechanistic targets reported for this agent — how it may act on cells, not proof of a clinical effect.
- HDAC↓Class I/IIa inhibition for acetylation ↑
- Tumor-Suppressor↑p21/p27 re-expression
- Cell CycleArrestG1 phase via p21
- NF-κB↓Inflammation modulation
- Apoptosis↑Pro-apoptotic gene induction
Often studied / combined with
Combinations reported in the literature, not a protocol or a recommendation.
- 5-FU: Apoptosis and response in CRC models.
- Curcumin: HDAC/NF-κB co-inhibition in breast.
- Resveratrol: Epigenetic re-expression synergy in pancreatic.
Overlapping mechanisms
- HDAC ↓: Overlaps vorinostat; monitor acetylation.
- Cell Cycle Arrest: Redundant with sulforaphane; G1 saturation.
Safety & interactions
Severity and how well-established each signal is are shown separately. Verify everything with your oncologist or pharmacist — absence here does not mean safe.
- 5-FUSynergizeLowTheoreticalApoptosis enhancement in CRC.
- HDAC inhibitorsMonitorLowTheoreticalAdditive epigenetic effects.
- 5-FUSynergizeLowTheoreticalImproved response in colorectal cancer.
Timing
- With-meal: Reduces GI upset.
- BID: Divided for steady colonic exposure.
References
- PMC10919761: Butyrate HDAC inhibition in cancer
- 10.3390/medicina61010136: Epigenetic effects in colorectal cancer
- 10.1038/s41598-024-63993-x: Apoptosis induction mechanisms
- 10.3389/fcimb.2022.1023806: Microbiome and butyrate in gut health
- DOI 10.3390/nu12061619: Synergy with 5-FU in CRC models
- PMC10221542: Combination with curcumin in breast cancer
Research
No published studies for Sodium Butyrate yet
New studies appear here once they’ve been reviewed. Browse all studies.
Dose: as studied, not a recommendation
Ranges seen in adjunct / practice use: 300–1200 mg/day (po) divided BID; tributyrin preferred, Adjunct 600 mg/day butyrate equivalent; dietary 10-20 g fiber/day; monitor sodium in renal impairment..
Trials studying Sodium Butyrate
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