Urolithin B

Urolithin B belongs to the family of metabolites made when intestinal microbes process ellagitannins and ellagic acid from food. Whether it appears after a meal varies between people: in a small pomegranate feeding study, urinary urolithin B-glucuronide was detected in only a subset of volunteers [3]. It differs from Urolithin A by one hydroxyl group, and the two compounds produce different responses in muscle cells [1][2].

The muscle-growth evidence starts with mice. In the 2017 study, six male mice per group received vehicle or 10 µg/day through implanted pumps for 28 days. Urolithin B increased the weight of the tibialis anterior, soleus and quadriceps; tibialis anterior fiber cross-sectional area was 11.9% larger. The experiment measured muscle size and protein synthesis, not improvements in human strength or exercise performance [1].

A separate experiment in female mice used the same daily infusion after sciatic nerve section. After seven days, loss of muscle mass was reduced in several muscles, but the gastrocnemius did not benefit. Muscle size in the uninjured limb did not increase over that short treatment period [1].

Human cells are a useful next step, but not a clinical trial. The 2026 study grew myotubes from postmortem muscle samples from nine donors aged 55–96. After 24 hours at 5 µM, urolithin B altered 339 genes, compared with 1,918 for urolithin A. The patterns differed: B more strongly implicated lipid metabolism and muscle-related processes, while A more strongly implicated mitochondrial pathways. These were exploratory molecular findings; no participant took either compound as part of this experiment [2].

Protein synthesis and breakdown. At 15 µM in C2C12 mouse myotubes, urolithin B increased protein synthesis and reduced protein degradation. mTORC1-related phosphorylation increased, AMPK phosphorylation decreased, and expression of the atrophy-associated ubiquitin ligases MuRF1 and MAFbx fell. The measured autophagy markers were unchanged, so this result does not establish the mitophagy mechanism commonly associated with urolithin A [1].

Androgen-receptor dependence is not proof of a selective androgen drug. Both receptor knockdown and bicalutamide prevented the myotube growth response. The experiments support a role for androgen-receptor signaling, but do not establish a binding affinity or selective action in muscle over other organs. Plasma testosterone did not increase in the male mouse experiment; in denervated females it fell at day 3 and was unchanged at day 7 [1].

Hormone-related activity is broader than the muscle pathway. Urolithin B inhibited aromatase in enzyme and breast cancer-cell experiments [4]. A separate MCF-7 study found both estrogenic and antiestrogenic activity under different assay conditions, with weaker estrogen-receptor binding than urolithin A. These cell findings do not establish a treatment for high estradiol or a clinical testosterone-boosting effect [5].

Inflammation is context-dependent. In activated microglia, urolithin B reduced inflammatory mediators and oxidative stress, suppressed NF-κB signaling and increased Nrf2-associated antioxidant defenses. AMPK phosphorylation rose in those cells, in contrast to the muscle model; it should not be described as a universal AMPK inhibitor or activator [1][6]. The human muscle-cell study also found mixed responses: in RNA sequencing, B lowered PTGS1 but increased IL17B, and lowered NQO1 while A increased it. Those expression changes do not by themselves demonstrate either clinical benefit or toxicity [2].

A human adverse-event rate and a safe supplementation range cannot be estimated from the studies cited here. Dietary formation and detection of urolithin metabolites are evidence of exposure, not a safety trial of purified urolithin B [3].

A reproductive-organ signal should not be omitted. Male mice receiving 10 µg/day for 28 days had reduced testis weight alongside the muscle effects. The paper did not establish fertility impairment or test a human risk, and plasma testosterone was unchanged, but the organ-weight finding warrants follow-up [1]. Its estrogen-receptor and aromatase activity also makes an assumption of hormonal neutrality unwarranted [4][5].

A narrow negative toxicity result is available: in a 2026 experiment, the tested urolithins, including B, did not cause rat red-blood-cell lysis at concentrations up to 200 µM over four hours. That assay does not establish chronic, reproductive or whole-body safety [7].

No clinical drug-interaction study of purified urolithin B was identified in this review. Bicalutamide blocked its muscle-cell growth response, and rapamycin blocked the mTORC1 response; these are laboratory observations, not measured interactions in treated patients [1].

Cell experiments found effects on CYP1A1 and conjugating enzymes, but oral supplementation in rats did not reproduce CYP1A1 induction in the colon. This mismatch argues against turning the cell findings into a broad clinical CYP interaction warning [8].

Urolithin A's antiplatelet activity should not be assigned to B. In the 2026 ex vivo human-blood study, B did not inhibit arachidonic-acid-triggered aggregation at 80 µM; activity appeared only at the higher 160 µM concentration. None of the tested urolithins changed the coagulation times measured at 50 µM. These results neither establish an antiplatelet benefit nor prove that combinations with anticoagulants are safe [7].