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Tbu2.0
Tributyrin Research
Mostly mechanism / observational
10 peer-reviewed studies
What the evidence says
Mostly mechanism / observational
Most Tributyrin studies are mechanism or observational rather than RCTs that measure a clinical effect — keep findings provisional.
Most evidence is from mixed-quality randomised trials published 1998–2026 with a typical study size of 17 participants.
Based on 10 studies · 1 RCT · 62 total participants
Confidence
Low confidence
By outcome
Butyrate delivery & target engagement
Mostly mechanism / observational8 studies
Cancer & antiproliferative effects
Mostly mechanism / observational4 studies
Neurological & psychiatric conditions
Too few graded studies2 studies
Inflammation
Too few graded studies1 study
Gut barrier & intestinal integrity
Too few graded studies1 study
Safety & dose-limiting effects
Too few graded studies1 study
By the numbers
Pulled from 10 studies with measurable effects
People studied
62
typical study: 17 people
Strongest designs
1
0 pooled, 1 randomised
How long studies ran
1–4 weeks
1
Populations Studied
Men with overweight/obesity1
Mice and rats1
People with Parkinson's disease plus normal controls1
Human visceral adipose tissue ex vivo1
Active research area
4 studies in the last 5 years
199820122026
1Postprandial plasma butyrate and hexanoateCrossovern=12 · very small study2022
In plain English: In the gut model, tributyrin was rapidly cleaved in the GASTRIC compartment — the direct contradiction of the distal-delivery claim.
van Deuren T et al. · Front Nutr (2022)
PubMed does NOT index this record as a Randomized Controlled Trial despite the title; treat the human portion accordingly
In the validated TIM-1 stomach-and-small-intestine model, tributyrin/caproin was rapidly cleaved in the GASTRIC compartment, whereas the long-chain-esterified comparator released short-chain fatty acids predominantly in the small intestine
The human portion tested Akovita SCT, a MODIFIED triglyceride designed to delay release — not tributyrin itself
In plain English: RODENT study. Oral sodium butyrate reached about 9 mM peak plasma butyrate in mice; oral tributyrin peaked around 1.75 mM — at a dose that killed roughly 10% of the animals.
Egorin MJ et al. · Cancer Chemother Pharmacol (1999)
RODENT pharmacokinetics (mice and rats) — not human data
Oral sodium butyrate at 5 g/kg produced peak plasma butyrate of about 9 mM in mice, exceeding 1 mM for 90 minutes
Oral tributyrin at 10.3 g/kg peaked at only about 1.75 mM and stayed above 1 mM for just 10-60 minutes
3Target engagement by [11C]butyrate PETOpen-Labeln=17 · very small study2026
In plain English: OPEN-LABEL, no control arm, no blinding — the PET imaging confirms the compound reaches tissue, and the clinical improvements are explicitly exploratory.
Bohnen JLB et al. · Neurotherapeutics (2026)
OPEN-LABEL with NO control group and NO blinding — the design cannot separate drug effect from expectation or natural variation
Fourteen people with Parkinson's disease and three normal controls completed 30 days (+/- 7) of 500 mg tributyrin orally three times daily
Ten subjects completed [11C]butyrate PET before and after, confirming organ-specific changes in brain, liver, heart and gastrointestinal butyrate uptake — genuine target engagement
5Plasma butyrate pharmacokinetics and tumour responseOpen-Labeln=20 · very small study2003
In plain English: No dose-limiting toxicity — and NO objective responses, with a median butyrate concentration of 52 micromolar, at the very bottom of the authors' own stated activity range.
Edelman MJ et al. · Cancer Chemother Pharmacol (2003)
20 patients with advanced solid tumours treated at 150-200 mg/kg three times daily; uncontrolled Phase I
NO objective responses were seen
Median butyrate concentration was 52 micromolar with considerable interpatient variability — the authors state in vitro differentiating activity requires levels above 50-100 micromolar
6Plasma butyrate pharmacokinetics and toxicityOpen-Labeln=13 · very small study1998
In plain English: Butyrate disappeared from plasma by 5 h after a dose, and peak concentrations did NOT increase in the three patients who had dose escalation.
Conley BA et al. · Clin Cancer Res (1998)
13 patients treated with escalating doses of 50 to 400 mg/kg/day, once daily for 3 weeks then a 1-week rest; uncontrolled Phase I
Peak plasma butyrate ranged 0 to 0.45 mM and butyrate had DISAPPEARED from plasma by 5 hours after a dose
Peak concentrations did NOT increase in the three patients who underwent dose escalation — the exposure did not scale with dose
7Intestinal tight-junction protein expressionAnimal2014
In plain English: MOUSE study — and the protective effect held for short-term and acute alcohol exposure but NOT after chronic ethanol feeding.
Cresci GA et al. · Alcohol Clin Exp Res (2014)
MOUSE model of ethanol-induced gut injury — no human equivalent has been run
All three ethanol protocols reduced tight-junction protein expression (ZO-1, occludin) and butyrate receptor/transporter expression in the ileum and proximal colon
Tributyrin supplementation protected against these changes
In plain English: A narrative review that concludes with a call for more work — 'despite the lack of data available in the literature, TB is a promising molecule'.
Heidor R et al. · Curr Drug Targets (2012)
NARRATIVE REVIEW, not a systematic review or meta-analysis — no pooled data and no quality appraisal
Summarises in vitro and in vivo work on apoptosis, cell differentiation and epigenetic modulation
Frequently cited as though it were evidence of efficacy; it is a summary of preclinical hypotheses