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Tbu2.0
Tributyrin Research
Mostly mechanism / observational
11 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 11 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
5 studies in the last 5 years
199820122026
1Review2026
In plain English: This framework provides a testable model and supports interventional studies to determine whether restoration of SCFA signaling-such as through early administration of butyrate-producing microbes or tributyrin (a stable butyrate triglyceride)-can favorably alter immune trajectories and improve clinical outcomes.
Yip YY, Ho KM. · Journal of critical care (2026)
These pathways provide a mechanistic bridge between these seemingly opposing states.
They are not merely consequences of sepsis but active determinants of immune trajectory.
Loss of SCFA- producing microbiota may impair immune regulation and promote dysregulated cell death, sustaining both hyperinflammatory and immunosuppressive states.
2Postprandial 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
4Target 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
6Plasma 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
7Plasma 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
8Intestinal 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
The authors explicitly note the LACK of data available in the literature and call for additional preclinical AND clinical studies