Urolithin B

Urolithin B at a Glance

Urolithin B is what is left at the end of the line. Dietary ellagitannins — the big hydrolysable tannins of pomegranate, walnut, raspberry, chestnut and oak — are barely absorbed at all; they are hydrolysed in the gut to ellagic acid, which colonic bacteria then strip of hydroxyl groups one at a time. Urolithin B is the terminal, most dehydroxylated product of that sequence: a small, flat dibenzo-α-pyrone (C₁₃H₈O₃, 212.2 Da) carrying one phenolic hydroxyl where the starting material had six.

That makes it a microbial metabolite, not a plant product. There is no herb you can extract urolithin B from, no leaf that contains it, no assay of its content in a root. It exists because bacteria in a human colon made it, which is why its “abundance” is a fact about a person rather than a species — and why the compound that matters most for pomegranate pharmacology cannot be found in a pomegranate.

The second thing to know is that it is the junior partner of a famous molecule. Urolithin A, the 3,8-dihydroxy member of the same series, carries a commercial supplement, a mitophagy mechanism and genuine human RCTs. Urolithin B has none of those. PubMed carries roughly 687 papers naming urolithin A against 151 naming urolithin B (51 with it in the title), and no clinical trial has ever administered urolithin B to a human being. This page exists to say what is genuinely known about B — including the handful of places where it beats A — without borrowing A’s evidence to do it.

Urolithin B vs. Urolithin A

The structural difference is one atom’s worth of chemistry. Urolithin A is 3,8-dihydroxy-6H-dibenzo[b,d]pyran-6-one; urolithin B is 3-hydroxy only — the same scaffold minus the 8-hydroxyl. Formula C₁₃H₈O₄ (228.2 Da) versus C₁₃H₈O₃ (212.2 Da). Because B has one fewer polar group it is the more lipophilic of the pair (calculated XLogP 2.7 vs. 2.3), and it has one fewer site available for phase-II conjugation.

The obvious question is whether losing that hydroxyl costs it potency. The honest answer, across every head-to-head that has actually been run, is: it depends entirely on the target, and there is no consistent winner.

Assay (both molecules, same experiment)	Urolithin A	Urolithin B	Winner
LPS-stimulated macrophages — TNF-α ↓, IL-10 ↑ 8Reference 8Bobowska A et al. · 2021Comparative studies of urolithins and their phase II metabolites on macrophage and neutrophil functionsView study →	most active of the series	weaker	A
Triglyceride accumulation, human adipocytes & hepatocytes, 30 µM 23Reference 23Kang I et al. · 2016Urolithin A, C, and D, but not iso-urolithin A and urolithin B, attenuate triglyceride accumulation in human cultures of adipocytes and hepatocytesView study →	attenuates	no effect	A
Melanogenesis in B16 cells, 10 µM 26Reference 26Wang ST et al. · 2017Antimelanogenic effect of urolithin A and urolithin B, the colonic metabolites of ellagic acid, in B16 melanoma cellsView study →	to 55.1% of control	to 76.4%	A
Oesophageal squamous carcinoma viability 28Reference 28Shojaee M et al. · 2025In vitroEvaluation and comparison of the anti-proliferative and anti-metastatic effects of urolithin A and urolithin B against esophageal cancer cells — an in vitro and in silico studyView study →	lower IC50	higher IC50	A
Human neutrophils — IL-8 and MMP-9 release, 20 µM 39Reference 39Piwowarski JP et al. · 2014Influence of gut microbiota-derived ellagitannins’ metabolites urolithins on pro-inflammatory activities of human neutrophilsView study →	inactive on these	the only active urolithin	B
Human neutrophils — ROS, elastase, myeloperoxidase 39Reference 39Piwowarski JP et al. · 2014Influence of gut microbiota-derived ellagitannins’ metabolites urolithins on pro-inflammatory activities of human neutrophilsView study →	ROS ↓ 42.6–53.7% at 1 µM	inactive	A (elastase: C)
Recombinant human MMP-9, IC50 27Reference 27Houssein-Zadeh N et al. · 2025Ellagitannins (ellagic acid, urolithin A, urolithin B) inhibit the catalytic activity of human recombinant metalloproteinase 9View study →	33.29 µM	13.17 µM	B
Recombinant human MAO-A, IC50 24Reference 24Singh R et al. · 2020Microbial metabolite urolithin B inhibits recombinant human monoamine oxidase A enzymeView study →	weaker	0.88 µM, best of the series	B
Diabetic rat myocardium, ↑dP/dt max 11Reference 11Savi M et al. · 2017AnimalIn vivo administration of urolithin A and B prevents the occurrence of cardiac dysfunction in streptozotocin-induced diabetic ratsView study →	+18%	+31%	B

Two patterns are worth extracting. First, A dominates the broad endpoints — cytokine suppression, oxidative burst, lipid handling, pigmentation — which happen to be the ones the field cared about first, and which is a large part of why A became the commercial molecule. But even inside a single experiment the split can be endpoint-by-endpoint rather than molecule-by-molecule: testing four urolithins on human neutrophils, urolithin A was the best ROS inhibitor, urolithin C the only one active on elastase release, and urolithin B the only one that inhibited IL-8 and MMP-9 production and blocked CD62L shedding ^{39Reference 39Piwowarski JP et al. · 2014Influence of gut microbiota-derived ellagitannins’ metabolites urolithins on pro-inflammatory activities of human neutrophilsView study →}. “Urolithin A is the active one” is a summary of averages, not a rule.

Second, B’s wins cluster around targets it reaches: in the diabetic-rat study, both urolithins were given by the same route, and urolithin B and its sulfate accumulated in myocardial tissue at higher concentration than urolithin A, which the authors offered as the explanation for B’s slightly better functional result ^{11Reference 11Savi M et al. · 2017AnimalIn vivo administration of urolithin A and B prevents the occurrence of cardiac dysfunction in streptozotocin-induced diabetic ratsView study →}. That is a distribution argument, not a receptor-affinity one, and it is the most credible mechanism anyone has proposed for why the missing hydroxyl sometimes helps.

The third pattern is the uncomfortable one. Most of the 151 urolithin-B papers are not head-to-heads at all — B appears as a co-analyte in a urolithin-A study, or as one row in a panel. The two molecules are studied unequally far more than they are compared, so most apparent “differences” between them are differences in who bothered to look.

Metabotype B — Who Actually Makes It

Urolithin B is the defining metabolite of one of the three reproducible human urolithin metabotypes, and getting the definition right matters because it is easy to state backwards.

• Metabotype A (UM-A) — produces urolithin A only as the final metabolite.
• Metabotype B (UM-B) — produces isourolithin A and/or urolithin B in addition to urolithin A ^{1,2Reference 1Tomás-Barberán FA et al. · 2014Ellagic acid metabolism by human gut microbiota — consistent observation of three urolithin phenotypes in intervention trials, independent of food source, age, and health statusView study →Reference 2Selma MV et al. · 2017Isolation of human intestinal bacteria capable of producing the bioactive metabolite isourolithin A from ellagic acidView study →}.
• Metabotype 0 (UM-0) — produces essentially none of the final urolithins.

The correction is the “in addition to”. Metabotype B is not an alternative to urolithin A — it is urolithin A plus two further metabolites. The bacteria of a UM-B gut carry the extra dehydroxylation steps that convert urolithin A (3,8-dihydroxy) onward to isourolithin A (3,9-dihydroxy) and urolithin B (3-hydroxy) ^{2Reference 2Selma MV et al. · 2017Isolation of human intestinal bacteria capable of producing the bioactive metabolite isourolithin A from ellagic acidView study →}. Saying that UM-B people “make urolithin B rather than urolithin A” is a common shorthand and it is wrong.

Prevalence. The original cross-trial stratification gave wide ranges: phenotype A 25–80% of volunteers, phenotype B 10–50%, phenotype 0 5–25%, consistent across food sources, ages and health states ^{1Reference 1Tomás-Barberán FA et al. · 2014Ellagic acid metabolism by human gut microbiota — consistent observation of three urolithin phenotypes in intervention trials, independent of food source, age, and health statusView study →}. A later Caucasian cohort of n = 839 spanning 5–90 years resolved the spread: the split is mostly age. UM-A falls from about 85% in childhood to roughly 55% in adulthood while UM-B rises from about 15% to about 45%, both stabilising from around age 35–40; UM-0 sits at roughly 10% and barely moves across the whole lifespan ^{3,4Reference 3Cortés-Martín A et al. · 2018The gut microbiota urolithin metabotypes revisited — the human metabolism of ellagic acid is mainly determined by agingView study →Reference 4García-Villalba R et al. · 2022Urolithins: a comprehensive update on their metabolism, bioactivity, and associated gut microbiotaView study →}. Metabotype B is also over-represented in people with metabolic syndrome or colorectal cancer — conditions associated with gut dysbiosis ^{1Reference 1Tomás-Barberán FA et al. · 2014Ellagic acid metabolism by human gut microbiota — consistent observation of three urolithin phenotypes in intervention trials, independent of food source, age, and health statusView study →}.

So a fair summary is: urolithin B is a metabolite of middle age and later, produced by something like two in five adults, and rarely by children.

Does being metabotype B help or hurt? This is the only place where metabotype has been tied to a human outcome, and the two available results point in opposite directions. In the POMEcardio randomised crossover trial, 49 overweight-obese adults took pomegranate extract at 160 or 640 mg phenolics/day; at the higher dose, total cholesterol fell 15.5%, LDL 14.9%, small LDL 47%, non-HDL 11.3%, apolipoprotein B 12% and oxidised LDL 24% — all of it only in UM-B subjects, partly correlated with urolithin production and rising Gordonibacter levels ^{40Reference 40González-Sarrías A et al. · 2017RCTClustering according to urolithin metabotype explains the interindividual variability in the improvement of cardiovascular risk biomarkers in overweight-obese individuals consuming pomegranate — a randomized clinical trial (POMEcardio)View study →}. Against that, the oak-extract surgical trial found lower post-operative pain associated with metabotype A ^{25Reference 25Volpp L et al. · 2020Constituents and metabolites of a French oak wood extract (Robuvit®) in serum and blood cell samples of women undergoing hysterectomyView study →}. UM-B individuals also started POMEcardio with the highest baseline cardiovascular risk ^{40Reference 40González-Sarrías A et al. · 2017RCTClustering according to urolithin metabotype explains the interindividual variability in the improvement of cardiovascular risk biomarkers in overweight-obese individuals consuming pomegranate — a randomized clinical trial (POMEcardio)View study →}, so the lipid result may be regression toward a worse mean rather than a benefit of the metabolite.

The honest position: metabotype B is a marker that changes who responds to an ellagitannin food, and it is not established as either a good or a bad thing to be. Neither result isolates urolithin B as the agent — UM-B people also make isourolithin A, and more urolithin A overall.

The organisms are partly identified. Gordonibacter species (Eggerthellaceae) perform the early steps to the intermediates urolithin M-5 and urolithin C but stop there; the first pure culture capable of making isourolithin A — the other metabotype-B metabolite — was isolated in 2017 and later named Ellagibacter isourolithinifaciens ^{2Reference 2Selma MV et al. · 2017Isolation of human intestinal bacteria capable of producing the bioactive metabolite isourolithin A from ellagic acidView study →}; and in 2023 a single new faecal isolate was shown to produce both urolithins A and B and the intermediates, with defined co-cultures reproducing the UM-A and UM-B patterns in vitro ^{5Reference 5Iglesias-Aguirre CE et al. · 2023Gut bacteria involved in ellagic acid metabolism to yield human urolithin metabotypes revealedView study →}. Urolithin B sits one dehydroxylation beyond urolithin A, which is why a UM-B gut yields A and B rather than B alone. That work is the basis for the current interest in urolithin-producing probiotics — the logic being that UM-0 individuals get nothing at all from an ellagitannin-rich diet.

What It's Used For

Urolithin B has a real and growing preclinical literature — around fifty papers with it in the title, covering muscle, heart, bone, brain, joint, gut and tumour models, most of them using the isolated molecule rather than an extract. What it does not have is a single human dose. Read every row below as an animal or cell result at concentrations that need checking against the exposure section.

Evidence by IndicationStrength of support · Beta

Support is an experimental score — weighted by study type (human > animal > in vitro) and volume. A beta, not a validated metric. Every row here is capped by the same two ceilings: no human has been dosed, and the circulating form in a person is a conjugate, not the aglycone tested in these assays.

01Cardiovascular protectionShaky38%Four independent rodent models + a tissue-distribution rationale; all parenteral dosing ^{11,13,14,15Reference 11Savi M et al. · 2017AnimalIn vivo administration of urolithin A and B prevents the occurrence of cardiac dysfunction in streptozotocin-induced diabetic ratsView study →Reference 13Zhao W et al. · 2019AnimalA novel candidate for prevention and treatment of atherosclerosis: urolithin B decreases lipid plaque deposition in apoE⁻/⁻ mice and increases early stages of reverse cholesterol transport in ox-LDL treated macrophagesView study →Reference 14Zheng D et al. · 2020Urolithin B, a gut microbiota metabolite, protects against myocardial ischemia/reperfusion injury via p62/Keap1/Nrf2 signaling pathwayView study →Reference 15Gao H et al. · 2020AnimalUrolithin B improves cardiac function and reduces susceptibility to ventricular arrhythmias in rats after myocardial infarctionView study →}

02Muscle mass & anti-atrophyShaky32%One well-built isolate study with cell + hypertrophy + denervation arms; no replication in nine years ^{6Reference 6Rodriguez J et al. · 2017Urolithin B, a newly identified regulator of skeletal muscle massView study →}

03Anti-inflammatory & antioxidantShaky32%Broad, consistent, mechanistically detailed — but A outperforms B head-to-head and conjugates are inert ^{8,17,19Reference 8Bobowska A et al. · 2021Comparative studies of urolithins and their phase II metabolites on macrophage and neutrophil functionsView study →Reference 17Qu Z et al. · 2022Urolithin B suppresses osteoclastogenesis via inhibiting RANKL-induced signalling pathways and attenuating ROS activitiesView study →Reference 19Lee G et al. · 2019Anti-inflammatory and antioxidant mechanisms of urolithin B in activated microgliaView study →}

04Bone & jointShaky28%Two osteoclast studies with an OVX in-vivo arm, plus osteoarthritis and peri-implant models ^{16,18,30,31Reference 16Li Y et al. · 2022Urolithin B suppressed osteoclast activation and reduced bone loss of osteoporosis via inhibiting ERK/NF-κB pathwayView study →Reference 18Xiao L et al. · 2024Urolithin B inhibits the differentiation of M1 macrophages and relieves the inflammation around the implants under osteoporosis via down-regulating the phosphorylation of VEGFR2View study →Reference 30Xue H et al. · 2024Urolithin B reduces cartilage degeneration and alleviates osteoarthritis by inhibiting inflammationView study →Reference 31Li Y et al. · 2025Gut microbiota metabolite urolithin B inhibits chondrocyte ferroptosis by rewriting iron homeostasis via the FGFR3/NCOA4/FTH1 axis, alleviating osteoarthritisView study →}

05Neuroprotection & CNSShaky24%Aging-mouse cognition, microglial inflammation, MAO-A inhibition at 0.88 µM ^{19,20,24Reference 19Lee G et al. · 2019Anti-inflammatory and antioxidant mechanisms of urolithin B in activated microgliaView study →Reference 20Chen P et al. · 2021AnimalThe gut microbiota metabolite urolithin B improves cognitive deficits by inhibiting Cyt C-mediated apoptosis and promoting the survival of neurons through the PI3K pathway in aging miceView study →Reference 24Singh R et al. · 2020Microbial metabolite urolithin B inhibits recombinant human monoamine oxidase A enzymeView study →}

06Metabolic & gutShaky20%Positive in HFHS mice via Akkermansia, but explicitly negative on the isolated cell endpoint ^{22,23Reference 22Chen P et al. · 2024AnimalUrolithin B protects mice from diet-induced obesity, insulin resistance, and intestinal inflammation by regulating gut microbiota compositionView study →Reference 23Kang I et al. · 2016Urolithin A, C, and D, but not iso-urolithin A and urolithin B, attenuate triglyceride accumulation in human cultures of adipocytes and hepatocytesView study →}

07AnticancerShaky18%Multiple tumour models, all preclinical, mostly µM cytotoxicity without a selectivity index ^{28,29,32Reference 28Shojaee M et al. · 2025In vitroEvaluation and comparison of the anti-proliferative and anti-metastatic effects of urolithin A and urolithin B against esophageal cancer cells — an in vitro and in silico studyView study →Reference 29Wang L et al. · 2023The gut microbiota metabolite urolithin B prevents colorectal carcinogenesis by remodeling microbiota and PD-L1/HLA-BView study →Reference 32Yu Z et al. · 2023AnimalUrolithin B alleviates Helicobacter pylori-induced inflammation and oxidative stress in miceView study →}

Mechanisms

The last row governs all the others. Every mechanism above except the microbiota ones was demonstrated on the free aglycone, and the free aglycone is not what circulates.

Pharmacokinetics

This is where urolithin B stops being a molecule and starts being a person.

It is only produced by some people. Nothing reaches the circulation unless the individual’s colonic microbiota carries the full dehydroxylation chain — roughly 45% of adults, and almost no children ^{3,4Reference 3Cortés-Martín A et al. · 2018The gut microbiota urolithin metabotypes revisited — the human metabolism of ellagic acid is mainly determined by agingView study →Reference 4García-Villalba R et al. · 2022Urolithins: a comprehensive update on their metabolism, bioactivity, and associated gut microbiotaView study →}. In the same trial, one participant will show urolithin B and the next will show none from an identical dose.

The levels are low, and they are conjugated. Urolithins circulate as glucuronide and sulfate conjugates at total concentrations in the 0.2–20 µM range ^{10Reference 10Espín JC et al. · 2013Biological significance of urolithins, the gut microbial ellagic-acid-derived metabolites — the evidence so farView study →}; unconjugated aglycones are found in faeces, not plasma ^{21Reference 21González-Barrio R et al. · 2011UV and MS identification of urolithins and nasutins, the bioavailable metabolites of ellagitannins and ellagic acid in different mammalsView study →}. For urolithin B specifically, a controlled human trial of 300 mg/day French oak-wood extract for 8 weeks in 66 hysterectomy patients measured a median serum urolithin B of 22.3 ng/mL (~105 nM), against urolithin A at 14.0 ng/mL and urolithin C at 2.66 ng/mL — with only urolithins A and B detectable inside blood cells ^{25Reference 25Volpp L et al. · 2020Constituents and metabolites of a French oak wood extract (Robuvit®) in serum and blood cell samples of women undergoing hysterectomyView study →}. After a single ellagitannin meal the numbers are far lower still: maximum plasma urolithin B around 0.01 µmol/L against urolithin A at 0.14 µmol/L ^{21,4Reference 21González-Barrio R et al. · 2011UV and MS identification of urolithins and nasutins, the bioavailable metabolites of ellagitannins and ellagic acid in different mammalsView study →Reference 4García-Villalba R et al. · 2022Urolithins: a comprehensive update on their metabolism, bioactivity, and associated gut microbiotaView study →}.

Put those two facts together and most of the in-vitro literature is out of reach. Typical urolithin-B cell experiments run at 10–50 µM of free aglycone. Peak human plasma urolithin B is roughly 100 nM, as a conjugate — two to three orders of magnitude below, in a chemically different form. And the conjugation is not a formality: when urolithin A, isourolithin A and urolithin B were tested beside their glucuronides on human and murine immune cells, none of the conjugates had any activity at all ^{8Reference 8Bobowska A et al. · 2021Comparative studies of urolithins and their phase II metabolites on macrophage and neutrophil functionsView study →}, and the same held for eicosanoid pathways ^{9Reference 9Giménez-Bastida JA et al. · 2020Inhibition of 5-lipoxygenase-derived leukotrienes and hemiketals as a novel anti-inflammatory mechanism of urolithinsView study →}.

Two honest qualifications. The colon is different — luminal urolithin concentrations of 1–15 µM are physiological ^{9Reference 9Giménez-Bastida JA et al. · 2020Inhibition of 5-lipoxygenase-derived leukotrienes and hemiketals as a novel anti-inflammatory mechanism of urolithinsView study →}, so gut-directed effects (microbiota remodelling, Salmonella virulence, colorectal models) sit at plausible exposures and are the most defensible results here. And the conjugates are not always inert: urolithin B-glucuronide fully restored TMAO-damaged cardiomyocyte function ^{12Reference 12Savi M et al. · 2018Trimethylamine-N-oxide (TMAO)-induced impairment of cardiomyocyte function and the protective role of urolithin B-glucuronideView study →}, and urolithin B sulfate modulated ABCA1/SR-BI ^{13Reference 13Zhao W et al. · 2019AnimalA novel candidate for prevention and treatment of atherosclerosis: urolithin B decreases lipid plaque deposition in apoE⁻/⁻ mice and increases early stages of reverse cholesterol transport in ox-LDL treated macrophagesView study →}. Tissue deconjugation is also real — urolithin A glucuronide has been shown to be hydrolysed back to free urolithin A in tissue after an inflammatory (LPS) stimulus, which would deliver aglycone precisely where it is wanted ^{41Reference 41Ávila-Gálvez MÁ et al. · 2019Tissue deconjugation of urolithin A glucuronide to free urolithin A in systemic inflammationView study →}. That has been demonstrated for urolithin A, not for urolithin B; whether the same happens to urolithin B glucuronide is untested and is one of the more consequential open questions here.

Finally, distribution favours B in at least one organ: in the diabetic-rat head-to-head, urolithin B and urolithin B-sulfate accumulated in myocardium at higher concentrations than urolithin A, which the authors used to explain B’s better functional result ^{11Reference 11Savi M et al. · 2017AnimalIn vivo administration of urolithin A and B prevents the occurrence of cardiac dysfunction in streptozotocin-induced diabetic ratsView study →}. It is the only tissue where a distributional advantage for B has been demonstrated.

Clinical Trials

None. No registered or published clinical trial has administered urolithin B to a human being. Searching the trial registry for urolithin B returns only studies that measure it — walnut and pomegranate-extract interventions that quantify urolithin B as a microbiota biomarker (NCT04066816, NCT02095145), and metabotype-stratification studies (NCT07182370). Every trial that actually doses a urolithin doses urolithin A (Mitopure), for muscle, immune or mitochondrial endpoints.

The nearest thing to human data are two trials that stratified by metabotype without dosing the molecule, and they disagree. The oak-wood-extract surgical trial measured serum urolithins alongside outcomes and found lower post-surgical pain associated with metabotype A ^{25Reference 25Volpp L et al. · 2020Constituents and metabolites of a French oak wood extract (Robuvit®) in serum and blood cell samples of women undergoing hysterectomyView study →}. The POMEcardio crossover trial found pomegranate extract’s cholesterol, LDL, small-LDL, apoB and oxidised-LDL improvements only in UM-B subjects ^{40Reference 40González-Sarrías A et al. · 2017RCTClustering according to urolithin metabotype explains the interindividual variability in the improvement of cardiovascular risk biomarkers in overweight-obese individuals consuming pomegranate — a randomized clinical trial (POMEcardio)View study →} — the strongest human signal anywhere near urolithin B, and still not attributable to it, since UM-B individuals also produce isourolithin A and urolithin A.

Last checked: August 2026.

Isolate vs. Plant Studies

The usual version of this axis does not apply, because urolithin B has no plant to be isolated from. The equivalent question — and it is sharper — is whether findings obtained by administering urolithin B tell you anything about eating an ellagitannin-rich food, and the answer is mostly no.

The molecule genuinely is studied as an isolate. Unlike most of the tannin literature, the urolithin-B papers overwhelmingly use pure synthetic or purified compound rather than an extract: the muscle study, the four cardiovascular studies, the two osteoclast studies, the MAO-A and MMP-9 enzymology. That is a real methodological strength and it is why so many of the mechanisms above are crisply defined.

But the route is wrong in almost every case. The muscle result used a subcutaneous osmotic pump ^{6Reference 6Rodriguez J et al. · 2017Urolithin B, a newly identified regulator of skeletal muscle massView study →}; the cardiac, atherosclerosis and bone results used intraperitoneal injection ^{11,13,14,15,16Reference 11Savi M et al. · 2017AnimalIn vivo administration of urolithin A and B prevents the occurrence of cardiac dysfunction in streptozotocin-induced diabetic ratsView study →Reference 13Zhao W et al. · 2019AnimalA novel candidate for prevention and treatment of atherosclerosis: urolithin B decreases lipid plaque deposition in apoE⁻/⁻ mice and increases early stages of reverse cholesterol transport in ox-LDL treated macrophagesView study →Reference 14Zheng D et al. · 2020Urolithin B, a gut microbiota metabolite, protects against myocardial ischemia/reperfusion injury via p62/Keap1/Nrf2 signaling pathwayView study →Reference 15Gao H et al. · 2020AnimalUrolithin B improves cardiac function and reduces susceptibility to ventricular arrhythmias in rats after myocardial infarctionView study →Reference 16Li Y et al. · 2022Urolithin B suppressed osteoclast activation and reduced bone loss of osteoporosis via inhibiting ERK/NF-κB pathwayView study →}. Only the lung-tumour study dosed orally ^{35Reference 35Sun J et al. · 2026Dietary urolithin B suppresses lung tumorigenesis correlating with autophagy induction and gut microbiota remodelingView study →}. Injected urolithin B delivers free aglycone systemically; dietary ellagitannins deliver, at best, ~100 nM of conjugate to a metabotype-B adult ^{25Reference 25Volpp L et al. · 2020Constituents and metabolites of a French oak wood extract (Robuvit®) in serum and blood cell samples of women undergoing hysterectomyView study →}. Those are not the same experiment.

And the plant’s own metabolite is usually A. The most pointed evidence is internal to the muscle group’s own work: fed punicalagin-rich pomegranate extract, mice showed urolithin A as the only detectable plasma metabolite, and the muscle protection was attributed to A ^{7Reference 7Rodriguez J et al. · 2017AnimalPomegranate extract prevents skeletal muscle of mice against wasting induced by acute TNF-α injectionView study →}. A year later the same group reported urolithin B as a muscle regulator using a pump ^{6Reference 6Rodriguez J et al. · 2017Urolithin B, a newly identified regulator of skeletal muscle massView study →}. Both results can be true; what cannot be inferred is that eating pomegranate delivers the urolithin-B mechanism.

The practical reading: treat the gut-luminal and microbiota results as the transferable ones — those happen at concentrations a diet produces, in the compartment where the molecule is actually made — and treat everything systemic as pharmacology of an injected drug candidate that no one has yet given to a person.

A Microbial Metabolite, Not a Plant Product

Urolithin B does not occur in plants. Searching for it alongside a botanical binomial returns metabolism studies, never phytochemical isolations: "urolithin B" AND "Punica granatum" returns 2 records, both on human or animal conversion of pomegranate ellagitannins rather than on pomegranate content. No herb monograph here can list urolithin B as a constituent, and none should.

What plants supply is the precursor. The chain runs:

ellagitannins (punicalagin, sanguiin H-6, castalagin, vescalagin, geraniin, corilagin, tellimagrandin II, lambertianin C) → hydrolysis in the gut → ellagic acid → colonic microbial dehydroxylation → urolithin M-5 → urolithin C → urolithin A → isourolithin A / urolithin B ^{2,4,5Reference 2Selma MV et al. · 2017Isolation of human intestinal bacteria capable of producing the bioactive metabolite isourolithin A from ellagic acidView study →Reference 4García-Villalba R et al. · 2022Urolithins: a comprehensive update on their metabolism, bioactivity, and associated gut microbiotaView study →Reference 5Iglesias-Aguirre CE et al. · 2023Gut bacteria involved in ellagic acid metabolism to yield human urolithin metabotypes revealedView study →}.

Precursor Sources

Dietary source	Ellagitannins present	On this site
Pomegranate	punicalagins, punicalins — the classic study food	(monograph pending)
Walnut	pedunculagin and relatives; the most-used urolithin research food	English walnut
Raspberry & other Rubus	sanguiin H-6, lambertianin C	raspberry leaf
Strawberry	casuarictin, sanguiin H-6	—
Oak- and chestnut-aged drinks	castalagin, vescalagin	—
Camu-camu, jabuticaba, Kakadu plum	castalagin, vescalagin	camu-camu

Two consequences follow. First, the source barely matters — metabotype assignment is reproducible across walnuts, berries, strawberries and pomegranate alike ^{1Reference 1Tomás-Barberán FA et al. · 2014Ellagic acid metabolism by human gut microbiota — consistent observation of three urolithin phenotypes in intervention trials, independent of food source, age, and health statusView study →}, so choosing a “better” ellagitannin food does not convert a UM-A person into a UM-B one. Second, which precursor you eat may still shift the yield: more highly polymerised ellagitannins are converted more slowly, so the same polyphenol intake does not produce the same urolithin output.

Urolithin B is not confined to humans. Comparative work across rodents, pigs, squirrels, beavers, sheep, cattle and birds found that all mammals studied produced urolithins, each species with a characteristic hydroxylation pattern, with glucuronides and sulfates dominant in plasma and urine and the free aglycones confined to faeces, ruminal content and beaver castoreum; insects and birds released ellagic acid but made no urolithins at all ^{21Reference 21González-Barrio R et al. · 2011UV and MS identification of urolithins and nasutins, the bioavailable metabolites of ellagitannins and ellagic acid in different mammalsView study →}.

Discovery & Synthesis

The compound family was found long before anyone knew what it was, and the name is a piece of veterinary pathology. In 1964, G. S. Pope isolated two benzocoumarins from “clover stone” — a type of renal calculus found in sheep grazing subterranean clover — and it is from that urolith that urolithins A and B take their name and their letters ^{38Reference 38Pope GS · 1964Isolation of two benzocoumarins from “clover stone”, a type of renal calculus found in sheepView study →}. An earlier member of the series had been described around 1949 as a pigment of beaver castoreum, the dried scent glands of Castor fiber; free urolithins are still recoverable from castoreum today ^{21Reference 21González-Barrio R et al. · 2011UV and MS identification of urolithins and nasutins, the bioavailable metabolites of ellagitannins and ellagic acid in different mammalsView study →}. For decades they were a veterinary curiosity with no known origin.

The modern understanding is recent. Their identity as human gut-microbial metabolites of dietary ellagitannins was established by the CEBAS-CSIC group in Murcia in the 2000s, followed by the comparative mammalian survey that mapped species-specific hydroxylation patterns in 2011 ^{21Reference 21González-Barrio R et al. · 2011UV and MS identification of urolithins and nasutins, the bioavailable metabolites of ellagitannins and ellagic acid in different mammalsView study →}, the three-phenotype stratification in 2014 ^{1Reference 1Tomás-Barberán FA et al. · 2014Ellagic acid metabolism by human gut microbiota — consistent observation of three urolithin phenotypes in intervention trials, independent of food source, age, and health statusView study →}, the isolation of isourolithin-A-producing bacteria in 2017 ^{2Reference 2Selma MV et al. · 2017Isolation of human intestinal bacteria capable of producing the bioactive metabolite isourolithin A from ellagic acidView study →}, the age-resolved metabotype cohort in 2018 ^{3Reference 3Cortés-Martín A et al. · 2018The gut microbiota urolithin metabotypes revisited — the human metabolism of ellagic acid is mainly determined by agingView study →}, and the first pure strains reproducing both metabotype patterns in 2023 ^{5Reference 5Iglesias-Aguirre CE et al. · 2023Gut bacteria involved in ellagic acid metabolism to yield human urolithin metabotypes revealedView study →}.

Synthesis is straightforward — unusually so for this database. Urolithin B is a small dibenzo-α-pyrone with a single phenol, and it is routinely prepared by chemical synthesis for research use; it was used as the structurally simplest model phenol for optimising a glucuronidation route that also produced the first synthesis of urolithin B-O-β-D-glucuronide in very high yield ^{36Reference 36Lucas R et al. · 2009A concise synthesis of glucuronide metabolites of urolithin-B, resveratrol, and hydroxytyrosolView study →}. That accessibility is why so much of the preclinical work uses genuinely pure material, and it is also why urolithin A could be commercialised as a supplement: these molecules are made, not extracted. There is no such product for urolithin B.

Patents: not yet researched.

Toxicity & Safety

Urolithin B carries an unknown flag, and the reasoning is worth stating because the reflex here is to assume it must be safe.

It is true that urolithin B is formed endogenously in roughly two in five adults after ordinary meals, which is a genuine, long-standing dietary exposure. But endogenous formation at ~100 nM is not a tolerability dataset for a dosed isolate, and there is no repeat-dose study, no genotoxicity battery, no reproductive-toxicity work, no CYP or transporter data and no human tolerability trial for urolithin B. Urolithin A’s safety package — including its first-in-human safety study — does not transfer; they are different molecules with demonstrably different targets. And there is one genuinely positive finding that argues against a clean bill.

Safety at a Glance

❔ Toxicity unknown

• Formed naturally in about 45% of adults from ordinary foods — pomegranate, walnuts, berries, oak-aged drinks — with no signal of harm from that dietary exposure.
• Androgen-receptor activity is its signature mechanism. The muscle effect runs through the androgen receptor ^{6Reference 6Rodriguez J et al. · 2017Urolithin B, a newly identified regulator of skeletal muscle massView study →}, and in prostate cancer cells urolithin B impaired the PSA-lowering effect of bicalutamide while urolithins A and C reduced DHT-driven PSA ^{37Reference 37Stanisławska IJ et al. · 2018The effects of urolithins on the response of prostate cancer cells to non-steroidal antiandrogen bicalutamideView study →}. That is an antagonistic interaction with an antiandrogen drug, not a theoretical concern.
• No toxicology of any kind on the isolated molecule — no repeat-dose, genotoxicity, reproductive or interaction study. Silence is not a clearance.
• Your exposure is set by your microbiome, not your dose. Antibiotics, age and dysbiosis change which urolithins you make; metabotype B is over-represented in metabolic syndrome and colorectal cancer ^{1Reference 1Tomás-Barberán FA et al. · 2014Ellagic acid metabolism by human gut microbiota — consistent observation of three urolithin phenotypes in intervention trials, independent of food source, age, and health statusView study →}.

Full Safety & Interactions Detail

The androgen-receptor signal. This is the finding that keeps urolithin B off a low-toxicity badge. The muscle hypertrophy result is explicitly androgen-receptor-dependent ^{6Reference 6Rodriguez J et al. · 2017Urolithin B, a newly identified regulator of skeletal muscle massView study →}, and a separate study of urolithins against prostate cancer cells found that while urolithins A and C reduced DHT-induced PSA secretion, urolithin B did not — and actively impaired bicalutamide’s PSA-lowering effect ^{37Reference 37Stanisławska IJ et al. · 2018The effects of urolithins on the response of prostate cancer cells to non-steroidal antiandrogen bicalutamideView study →}. Combinations of bicalutamide with urolithin A or B also had attenuated pro-apoptotic activity relative to the drug alone. The authors’ own conclusion was to advise caution about ellagitannin preparations as complementary therapy in prostate cancer. Anyone taking an antiandrogen has a mechanism-based reason to be careful with high-dose ellagitannin supplementation, and metabotype B is precisely the group that would generate urolithin B from it.

No isolate toxicology. There is no acute or repeat-dose toxicity study, no Ames or micronucleus data, no reproductive or developmental study, and no identification of a CYP isoform or transporter for urolithin B. The molecule is a UGT and SULT substrate — conjugation is its dominant fate ^{8,10Reference 8Bobowska A et al. · 2021Comparative studies of urolithins and their phase II metabolites on macrophage and neutrophil functionsView study →Reference 10Espín JC et al. · 2013Biological significance of urolithins, the gut microbial ellagic-acid-derived metabolites — the evidence so farView study →} — which raises the theoretical possibility of competition with other heavily glucuronidated drugs, but this has not been tested.

MAO-A inhibition deserves flagging as a hazard as well as a mechanism. Urolithin B inhibits recombinant human MAO-A at IC50 0.88 µM, selectively over MAO-B ^{24Reference 24Singh R et al. · 2020Microbial metabolite urolithin B inhibits recombinant human monoamine oxidase A enzymeView study →}. That potency is in the range where, if it were achieved in vivo, interactions with serotonergic drugs and tyramine-rich foods would become a real question. Nothing has established that it is achieved in vivo — plasma levels are ~100 nM as a conjugate — but a sub-micromolar MAO-A inhibitor forming inside the human colon is not a finding to leave unremarked. See MAO inhibitors for what that class of interaction looks like.

Microbiome dependence cuts both ways. Whether you make urolithin B at all is determined mainly by age and gut microbiota composition ^{3,4Reference 3Cortés-Martín A et al. · 2018The gut microbiota urolithin metabotypes revisited — the human metabolism of ellagic acid is mainly determined by agingView study →Reference 4García-Villalba R et al. · 2022Urolithins: a comprehensive update on their metabolism, bioactivity, and associated gut microbiotaView study →}. Antibiotics abolish urolithin production; ageing shifts the population from metabotype A toward B; and metabotype B is enriched among people with metabolic syndrome and colorectal cancer, and carried the highest baseline cardiovascular risk in the one trial that stratified for it ^{1,40Reference 1Tomás-Barberán FA et al. · 2014Ellagic acid metabolism by human gut microbiota — consistent observation of three urolithin phenotypes in intervention trials, independent of food source, age, and health statusView study →Reference 40González-Sarrías A et al. · 2017RCTClustering according to urolithin metabotype explains the interindividual variability in the improvement of cardiovascular risk biomarkers in overweight-obese individuals consuming pomegranate — a randomized clinical trial (POMEcardio)View study →}. Those associations are correlational, and there is no evidence that urolithin B causes any of them. The two controlled trials that tied metabotype to an outcome disagree: pomegranate’s lipid benefits appeared only in UM-B subjects ^{40Reference 40González-Sarrías A et al. · 2017RCTClustering according to urolithin metabotype explains the interindividual variability in the improvement of cardiovascular risk biomarkers in overweight-obese individuals consuming pomegranate — a randomized clinical trial (POMEcardio)View study →}, while lower post-surgical pain was associated with UM-A ^{25Reference 25Volpp L et al. · 2020Constituents and metabolites of a French oak wood extract (Robuvit®) in serum and blood cell samples of women undergoing hysterectomyView study →}. “Having metabotype B” is not established as either favourable or unfavourable.

Reproductive and developmental (prose only). No reproductive or developmental study of urolithin B exists. Urolithins have been detected in human breast milk ^{4Reference 4García-Villalba R et al. · 2022Urolithins: a comprehensive update on their metabolism, bioactivity, and associated gut microbiotaView study →}, which means an infant of a metabotype-B mother is exposed, but nothing follows from that either way. Decisions about ellagitannin-rich foods or supplements in pregnancy belong on the food or product page, not on a metabolite page.

Selectivity signal. Where cytotoxicity has been reported, selectivity indices are mostly absent. The one comparison that reported it found urolithins A and B less toxic to normal HFF fibroblasts than to oesophageal carcinoma cells ^{28Reference 28Shojaee M et al. · 2025In vitroEvaluation and comparison of the anti-proliferative and anti-metastatic effects of urolithin A and urolithin B against esophageal cancer cells — an in vitro and in silico studyView study →} — reassuring in direction, from a single study, and not a toxicology dataset.

Dosage

There is no human dose of urolithin B, and no product supplies it. Commercial “urolithin” supplements are urolithin A. The figures below are research doses, for orientation only.

The gap between the middle rows and the last one is the whole problem. Milligram-per-kilogram injections into rodents produce free-aglycone exposures perhaps a thousandfold above what a person achieves by eating — and only if that person is metabotype B. These are doses used in research and are not a personal recommendation.

References

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2. Selma MV, Beltrán D, Luna MC, Romo-Vaquero M, García-Villalba R, Mira A, Espín JC, Tomás-Barberán FA (2017). Isolation of human intestinal bacteria capable of producing the bioactive metabolite isourolithin A from ellagic acid. Frontiers in Microbiology, 8, 1521. https://pubmed.ncbi.nlm.nih.gov/28824607/
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