Uro-B, UroB, Uro B, 3-hydroxy-6H-dibenzo[b,d]pyran-6-one, 3-hydroxyurolithin · Evidence-based safety and harm-reduction overview.
| Also known as | Uro-B, UroB, Uro B, 3-hydroxy-6H-dibenzo[b,d]pyran-6-one, 3-hydroxyurolithin |
| Category | Research Chemical |
| Compound class | Dibenzo[b,d]pyran-6-one (dibenzopyranone); gut-microbial ellagitannin metabolite |
| Origin | Produced in the colon from ellagic acid / ellagitannins (pomegranate, walnuts, berries) |
| Relation to Urolithin A | Less-hydroxylated, downstream/minor metabolite; less studied sibling |
| Best-studied action | Skeletal-muscle anabolism via mTORC1 up, ubiquitin-proteasome down (preclinical) |
| Highest evidence level | In vitro (C2C12 myotubes) and mouse models; no robust human trials |
| Regulatory status (US) | Not FDA-approved; no independent GRAS; typically sold as a research chemical |
| US legal status | Not an FDA-approved drug and not an approved dietary-supplement ingredient in its own right. Urolithin B is a naturally occurring human gut metabolite, but as an isolated ingredient it has no independent GRAS notification or NDIN clearance in the United States, unlike its sibling Urolithin A (marketed as Mitopure, which received a favorable FDA GRAS review in 2018). In practice, Urolithin B is most often sold to labs and formulators as a "research chemical" / reference standard "not for human consumption," and it appears in some multi-ingredient longevity or muscle products where its regulatory footing is weaker than Urolithin A's. Because it is also produced endogenously from dietary ellagitannins, trace exposure from food (pomegranate, walnuts, berries) is unavoidable and unregulated; that is distinct from the legality of selling concentrated Urolithin B for supplementation. Status can change and varies by jurisdiction. Informational only, not legal advice. |
Urolithin B is one of the final gut-microbial metabolites of ellagitannins and ellagic acid, the polyphenols found in pomegranate, walnuts, chestnuts, and some berries. Structurally it is a dibenzo[b,d]pyran-6-one (a dibenzopyranone) bearing a single hydroxyl group, making it the least-hydroxylated and most reduced of the common urolithins. It sits downstream of Urolithin A and Urolithin C in the microbial conversion pathway, so it tends to be a minor or "terminal" metabolite whose production depends heavily on an individual's gut flora (the so-called urolithin metabotypes). It is the less-studied sibling of Urolithin A: where Urolithin A is characterized mainly as a mitophagy inducer, most Urolithin B interest centers on skeletal-muscle anabolism. The human evidence base is thin, and essentially all efficacy data are preclinical.
The best-characterized proposed mechanism is in skeletal muscle: Urolithin B is reported to stimulate protein synthesis through an mTORC1-dependent pathway while simultaneously suppressing the ubiquitin-proteasome degradation system, shifting net protein balance toward accretion. Signaling analyses in the Rodriguez 2017 work suggested crosstalk between the androgen receptor and mTORC1, possibly mediated by decreased AMPK activity. This is mechanistically distinct from Urolithin A, whose signature action is induction of mitophagy (clearance of damaged mitochondria) followed by mitochondrial biogenesis. Secondary mechanisms proposed from cell and rodent studies include Nrf2/ARE-driven antioxidant enzyme induction, NF-kB and MAPK inhibition producing anti-inflammatory effects, competitive/mixed aromatase inhibition, and in-vitro inhibition of monoamine oxidase A. All of these mechanisms are proposed from preclinical systems and have not been demonstrated to operate at physiologically achievable concentrations in humans.
Urolithins were first described as gut-microbial products of ellagitannin/ellagic-acid metabolism, with research initially concentrating on Urolithin A. Interest in Urolithin B specifically accelerated after Rodriguez and colleagues published their 2017 paper in the Journal of Cachexia, Sarcopenia and Muscle identifying it as a regulator of skeletal-muscle mass, which reframed it from a passive end-metabolite into a candidate anabolic agent. A 2022 Frontiers in Pharmacology review consolidated the scattered preclinical literature on Urolithin B (muscle, cardiovascular, anti-inflammatory, antioxidant, and anticancer signals), noting that no Urolithin-B-only review had previously existed and that it remained substantially less studied than Urolithin A. It has not followed Urolithin A into the GRAS-cleared consumer-supplement space.
The most cited primary finding is Rodriguez et al. 2017 (Journal of Cachexia, Sarcopenia and Muscle), which identified Urolithin B as a regulator of skeletal-muscle mass. In cultured C2C12 myotubes it increased protein synthesis and myotube diameter and repressed the ubiquitin-proteasome degradation pathway; in mice, continuous low-dose delivery (about 10 micrograms/day for 28 days via osmotic mini-pump) induced modest muscle hypertrophy and blunted the atrophy caused by sciatic-nerve denervation. Beyond muscle, in-vitro and rodent work reports anti-inflammatory effects (NF-kB and MAPK suppression, lower IL-6/TNF-alpha), Nrf2/heme-oxygenase-1 antioxidant signaling, aromatase inhibition and anti-proliferative activity in cancer cell lines, cardioprotection against TMAO-induced injury, and inhibition of recombinant human MAO-A in the enzyme assay (IC50 ~0.88 micromolar, mixed-mode). Every one of these is preclinical. There are no robust randomized controlled human trials of isolated Urolithin B for muscle, longevity, or any endpoint; human data are limited to it appearing as a measured metabolite in ellagitannin-feeding and bioavailability studies. Treat all mechanistic claims as hypothesis-generating rather than clinically established.
Informational only, not a protocol or recommendation. There is no established human dose for isolated Urolithin B, because no human efficacy or dose-finding trials have been conducted. The frequently cited animal figure, roughly 10 micrograms/day delivered continuously by osmotic pump over 28 days in mice, is a controlled-release research-model input and does not translate to an oral human dose. Human exposure in the published literature arises indirectly, as Urolithin B measured in plasma or urine after eating ellagitannin-rich foods, and those circulating levels are low and dominated by phase-II conjugates (glucuronides, sulfates) of reduced bioactivity. Any figures seen on vendor pages are marketing, not clinically validated ranges. A researcher should not infer a "human dose" from the mouse or in-vitro numbers.
This is general research/context information, not medical advice or a recommended protocol.
Stacking claims for Urolithin B are speculative and unsupported by human data. It is sometimes combined with Urolithin A on the theory that the two act through complementary pathways (Urolithin B on mTORC1-driven protein balance, Urolithin A on mitophagy), but no controlled human study has tested that combination or shown additive benefit; a person who consumes ellagitannins already produces a variable mix of both endogenously. Pairing with resistance training is the only genuinely evidence-based lever for the muscle outcome people are chasing, and its effect is established independent of any urolithin. Any "muscle stack" positioning should be read as marketing extrapolation from mouse and cell data, not a validated protocol.
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Get tested with Ulta Lab Tests →No. Both are gut-microbial metabolites of the same dietary polyphenols, but they are different molecules with different proposed actions. Urolithin A is characterized mainly as a mitophagy inducer and has a favorable FDA GRAS review as a supplement ingredient (Mitopure). Urolithin B is less hydroxylated, is a more downstream/minor metabolite, is studied mostly for muscle protein balance, and does not have that regulatory footing.
No robust human evidence. The muscle findings come from cultured muscle cells and mice (notably Rodriguez et al. 2017). There are no randomized controlled trials of isolated Urolithin B in people, so its human efficacy for muscle mass, strength, or atrophy is unproven.
We do not provide dosing guidance. There is no validated human dose, no human dose-finding study, and the cited mouse figure (about 10 micrograms/day by continuous pump) does not translate to an oral human dose. Anyone considering it should discuss it with a qualified clinician.
It is generally available to labs and formulators as a research chemical or reference standard, often labeled not for human consumption. As an isolated ingredient it lacks an independent US GRAS notification or NDIN, unlike Urolithin A. It is also produced naturally in the body from food, which is separate from the legality of selling concentrated material. This is informational, not legal advice.
Only in theory. One in-vitro study found it inhibits recombinant human MAO-A (IC50 near 0.88 micromolar). That has never been shown to happen in a living human at realistic exposures, but on mechanism alone anyone taking MAO inhibitors, SSRIs/SNRIs, or other serotonergic drugs should treat combination as unstudied and consult a clinician or pharmacist.
Urolithin A drew earlier and heavier attention for its mitophagy activity and moved into human trials and a GRAS-cleared consumer product. Urolithin B is a more downstream, often minor metabolite, and dedicated reviews of it only appeared recently (e.g. a 2022 Frontiers in Pharmacology review). Its literature remains largely preclinical.
Medical & legal disclaimer. This site is for informational and harm-reduction purposes only. It is not medical advice and is not a substitute for a licensed healthcare professional. The compounds discussed are largely not approved by the FDA for human use and many are sold strictly as research chemicals 'not for human consumption.' Nothing here is an endorsement to purchase, possess, or use any substance. Laws vary by jurisdiction. Always consult a qualified physician and follow the law where you live.
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