Fisetin

Fisetin has one of the more established neuroprotective profiles among natural flavonoids. Key findings from multiple independent labs: fisetin improves learning and memory in normal aging mice and in Alzheimer's disease mouse models (multiple independent groups — not just Mayo/Kirkland); the Morris Water Maze and novel object recognition improvements with fisetin supplementation in aging mice have been replicated in multiple labs across multiple countries; fisetin reduces neuroinflammation through NF-κB suppression and reduces amyloid-beta plaque formation and tau pathology in AD models. A 2018 human pilot (not senolytic-focused) in adults with mild cognitive impairment showed some cognitive improvements with 100 mg fisetin daily — though this study was small and uncontrolled. Grade B-C: multiple independent animal labs; one small human pilot; not the rigorous RCT evidence needed for clinical confidence.

Fisetin inhibits mTOR Complex 1 (mTORC1) signaling — the same pathway that rapamycin targets and the same pathway that caloric restriction suppresses. mTOR suppression is associated with lifespan extension across model organisms. Fisetin's mTOR inhibition has been documented in cell culture and animal models. Whether this produces meaningful longevity effects in humans at achievable oral doses is unknown. Grade C: animal model; mechanism-consistent; not validated in humans.

SIRT1 activation by fisetin has been demonstrated in cell culture and some animal studies, placing it in the same mechanistic category as NAD+ precursors (which support SIRT1 activity by maintaining the NAD+ substrate). Unlike NAD+ precursors, which work by providing the required cofactor, fisetin appears to allosterically activate SIRT1 directly. The combination of fisetin (direct SIRT1 activation) with NAD+ precursors (optimal SIRT1 cofactor availability) is a theoretically complementary stack. Grade C: multiple cell culture + animal studies; not validated in humans.

Fisetin's NF-κB suppression and reduction of pro-inflammatory cytokines (TNF-α, IL-6, IL-1β) is among the most replicated findings across independent labs. This is consistent with its general flavonoid chemistry (catechol group) and has been shown in multiple inflammatory models. Some human observational data suggests dietary flavonoid intake correlates with reduced inflammatory markers — though attribution to fisetin specifically from diet is impossible. Grade B-C: multiple independent labs; inflammatory biomarker evidence in animals; human data is dietary observational only.

Fisetin: 3,3',4',7-tetrahydroxyflavone. A flavonol — a subclass of flavonoids characterized by the 3-hydroxyl group on the C ring. Molecular weight 286 Da. Molecular formula C15H10O6. Found naturally in strawberries (~160 mcg/g fresh weight — the richest common food source), apples, persimmons, onions, cucumbers, grapes, and kiwi. Typical dietary intake from food sources: ~0.4 mg/day in the average diet. The gap between dietary intake and senolytic protocol doses (500-2,000 mg) underscores that fisetin supplementation for senolytic purposes is pharmacological, not nutritional.

The tetrahydroxyflavone structure is critical for fisetin's biological activity: the 3'-hydroxyl and 4'-hydroxyl groups on the B ring provide the catechol moiety important for antioxidant activity and BCL-2 binding affinity; the 3-hydroxyl on the C ring is essential for the flavonol structural class and contributes to PI3K/Akt pathway inhibition; the 7-hydroxyl on the A ring participates in the planarity and membrane interaction properties of the compound.

FISETIN BIOAVAILABILITY — THE QUESTION THE SUPPLEMENT INDUSTRY IGNORES

Fisetin has notoriously poor oral bioavailability. After oral administration, fisetin is: (1) Partially metabolized in the gut lumen by intestinal bacteria before absorption; (2) Extensively conjugated (glucuronidated and sulfated) by intestinal epithelial cells during first-pass gut metabolism; (3) Further metabolized by hepatic CYP enzymes; (4) Rapidly cleared from plasma with a short half-life (~1-2 hours in rats). The result: plasma fisetin concentrations after typical oral doses (100-500 mg) are low and highly variable between individuals. Multiple human pharmacokinetic studies have found that 100 mg oral fisetin produces peak plasma concentrations of approximately 8-50 nM fisetin aglycone — with large inter-individual variation and rapid clearance. The senolytic concentrations effective in cell culture assays are typically in the range of 1-10 μM. The gap between typical achievable human plasma concentrations (~10-50 nM) and cell culture senolytic concentrations (1,000-10,000 nM) is 20-1,000 fold. Whether this gap is closed by (a) higher doses (500-2,000 mg community protocols), (b) tissue accumulation exceeding plasma levels, or (c) active metabolites with senolytic activity — is not established in published human data. This pharmacokinetic gap is the most important unresolved question in fisetin's clinical translation.

The poor bioavailability problem has driven development of enhanced formulations. Fisetin phytosome (lecithin-complexed fisetin) has been shown to increase plasma fisetin exposure approximately 25-fold compared to standard crystalline fisetin in pharmacokinetic studies. Nanoparticle formulations and self-emulsifying drug delivery systems have shown 10-50x bioavailability improvements in preclinical studies. Liposomal fisetin is another commercial approach. The practical implication: fisetin phytosome at 100 mg may deliver more bioavailable fisetin to the bloodstream than 500-1,000 mg of standard crystalline fisetin. The community's standard protocol of high-dose crystalline fisetin may be an inefficient way to achieve senolytic plasma concentrations — if those concentrations are achievable at all with oral supplementation.

Standard fisetin supplement: crystalline fisetin dihydrate in capsules. Enhanced bioavailability forms: fisetin phytosome (Novogenia / commercial brands). Solubility-improved forms: various nanoparticle and co-crystallized products. Store standard fisetin in cool, dry, light-protected conditions. The compound is sensitive to oxidation — colored supplements that have turned brown or dark may have degraded fisetin content. Pricing 2026: standard fisetin 500 mg capsules: $0.30-0.70/capsule. Phytosome forms: $1.00-2.00/capsule.

Fisetin's senolytic activity operates through several converging pathways: BCL-2/BCL-XL inhibition (fisetin binds and inhibits these anti-apoptotic proteins at the mitochondrial membrane, reducing the threshold for apoptosis in senescent cells that depend on them — similar mechanism to Quercetin but with different binding affinities and cell-type selectivity); PI3K/Akt/mTOR inhibition (reduces the pro-survival insulin/IGF-1 signaling that senescent cells amplify to resist apoptosis); MDM2 inhibition (MDM2 normally suppresses p53-driven apoptosis; fisetin reduces MDM2, allowing p53 to trigger programmed death in cells with sufficient DNA damage — like senescent cells); HSP90 inhibition (heat shock protein 90 stabilizes BCL-2 family members and other pro-survival proteins; fisetin's HSP90 interaction destabilizes this protective chaperone network). The convergence of these mechanisms on multiple senescent cell survival pathways makes fisetin a 'broad-spectrum' senolytic in theory. The critical caveat: ALL of this mechanistic work is in cell culture at concentrations that are multiples of what typical oral fisetin doses achieve in human plasma. Grade B for the mechanism in vitro; Grade D for the mechanism at achievable human oral doses.

Fisetin's non-senolytic biological activity predates the 2018 senolytic paper by 15+ years. Key independently established mechanisms: SIRT1 activation — fisetin activates Sirtuin 1, the NAD+-dependent histone deacetylase involved in metabolic regulation, stress response, and longevity signaling (this is independent of its senolytic effects and provides a parallel longevity mechanism); mTOR inhibition — fisetin suppresses mTOR signaling, mimicking aspects of caloric restriction and rapamycin's longevity effects; BDNF upregulation — fisetin increases BDNF in neuronal models, supporting the same neurotrophic pathway as Semax and Dihexa (but through a different mechanism); NF-κB suppression — reduces chronic inflammatory gene expression; direct antioxidant activity — radical scavenging through the catechol moiety. These non-senolytic mechanisms mean fisetin may have longevity-relevant effects at lower concentrations than required for senolysis — but the magnitude and clinical relevance of these effects in humans is not established.

The most important mechanistic nuance for community users: fisetin's senolytic mechanisms (BCL-2 inhibition, PI3K/Akt inhibition, MDM2 inhibition) require concentrations in the 1-10 μM range in cell culture. Fisetin's non-senolytic mechanisms (SIRT1 activation, antioxidant activity, anti-inflammatory effects) may operate at lower concentrations (100-500 nM). If typical oral supplementation doses achieve plasma concentrations of 10-50 nM, they may be insufficient for senolysis but potentially relevant for non-senolytic mechanisms. This means a community user taking 500 mg/day fisetin may be getting anti-inflammatory and SIRT1-related benefits without achieving meaningful senolytic clearance. Whether this is a useful therapeutic effect or an inadequate dose depends entirely on what the user is trying to achieve.

Yousefzadeh et al. (EBioMedicine, 2018): Among 10 flavonoids screened against senescent murine fibroblasts and human fibroblasts in culture, fisetin was most potent senolytic. In p16INK4a-luciferase reporter mice (progeroid model): fisetin treatment reduced senescence markers across multiple tissues. In aged wild-type mice (85-90 weeks old, treated with fisetin late in life for 5 days): median lifespan increased 10%; maximum lifespan increased 12%. Histopathology improved across multiple organs. Most importantly for human relevance: human adipose tissue explants treated with fisetin ex vivo showed reduced senescence markers (p16, p21) and SASP factors. This last finding — senolytic activity in human tissue — is why this paper generated so much excitement. Grade C for the in vivo mouse aging data; Grade B for the human adipose explant data (human tissue, but ex vivo — not the same as in vivo human administration).

THE ITP FISETIN FAILURE — WHY IT MATTERS

The NIA Interventions Testing Program (ITP) is the most rigorous independent mouse longevity testing program in existence. It tests compounds simultaneously at three independent sites (University of Michigan, Jackson Laboratory, University of Texas Health Science Center), uses standardized protocols, large sample sizes, and independent biostatistical analysis. The ITP has validated some longevity interventions (rapamycin, acarbose) and failed to validate others. Fisetin was tested in the ITP. The results were NOT significantly positive for lifespan extension. This is the opposite of what the 2018 paper showed. The ITP failure does not definitively disprove fisetin's senolytic activity — differences in mouse strain, dosing protocol, fisetin formulation, and bioavailability could explain the discrepancy. But it represents a failure to replicate the headline finding in the most rigorous independent test available. The supplement market for fisetin was largely built on the 2018 paper. The ITP counterpoint is rarely mentioned in fisetin product marketing. Community users deserve to know both exist.

The Mayo Clinic has conducted multiple human trials of fisetin since 2018. Known trials: AFFIRM (NCT03675724): Phase 2, frailty in older adults; completed recruitment by approximately 2020. AFFIRM-LITE (NCT03868605): Phase 2, frailty in older women; multiple sites. NCT04771611: COVID-19 cytokine storm and organ damage; multi-center (University of Minnesota and Mayo Clinic); involved fisetin for COVID-associated inflammatory injury. These trials have been running for years. As of May 2026, their primary senolytic endpoint data — the tissue biopsy evidence showing whether fisetin actually reduces senescent cells in living humans — has not been published. The Fight Aging! commentary from September 2025 notes this specifically. The contrast with D+Q is stark: the Mayo Clinic published D+Q's human senolytic data (the DKD pilot) within a year of conducting the trial. The prolonged absence of fisetin human senolytic data is either because the results are still being analyzed — or because the results are not ready to be shared. Neither possibility confirms fisetin works in humans.

The COVID-19 fisetin trial (NCT04771611) has more publicly available information than the frailty trials. Fisetin was hypothesized to reduce the cytokine storm and organ damage associated with severe COVID-19 through its anti-inflammatory and potentially senolytic effects. The trial involved elderly high-risk COVID-19 patients. Safety was confirmed — fisetin was well-tolerated. Efficacy on COVID-19 outcomes: the data is preliminary and the trial design was primarily a safety/feasibility pilot rather than a powered efficacy study for COVID outcomes. The trial confirms human safety but does not establish senolytic efficacy. Grade B for safety; Grade D-E for COVID-19 efficacy.

The critical pharmacokinetic reality shapes all dosing discussions for fisetin: standard fisetin dihydrate supplements have poor and variable oral bioavailability. The community has responded by using high doses (500-2,000 mg) on the assumption that brute-force quantity compensates for poor absorption. Whether this achieves senolytic plasma concentrations is unknown. The alternative approach — using enhanced bioavailability formulations (phytosome, nanoparticle, liposomal) at lower doses — is scientifically more rationally grounded but less common in community practice.

Protocol

Dose

Days

Cycle Frequency

Notes

Conservative / entry

500 mg/day

2 consecutive days

Every 1-3 months

Standard flavonoid senolytic protocol; matches community consensus

Standard community

1,000-2,000 mg/day

2-3 consecutive days

Monthly or every 2 months

Higher dose attempting to compensate for bioavailability

Enhanced bioavailability

100-500 mg phytosome/nano formulation

2-3 consecutive days

Every 1-3 months

Scientifically more rational; may achieve equivalent or higher plasma levels

Mouse protocol reference

Yousefzadeh 2018: ~100 mg/kg x 5 days

5 consecutive days

One-time or periodic

Allometrically scales to ~700 mg/day for 70 kg human; but mouse bioavailability ≠ human

Take with food containing fat — fisetin's lipophilicity means fat co-administration improves dissolution and may improve absorption. Some protocols use quercetin alongside fisetin (exploiting the overlapping but non-redundant senolytic mechanisms). Vitamin C co-administration has been suggested to stabilize fisetin and prevent oxidation. Morning dosing is community consensus for the 2-day cycle protocol. No circadian pharmacology specific to fisetin is established.

Some advanced community protocols alternate D+Q cycles with fisetin cycles — using D+Q 2-3 times per year and fisetin monthly in between. The theoretical rationale: different senolytic mechanisms, different cell-type selectivity, potentially broader senescent cell population coverage. No controlled study supports this combination strategy. The D+Q cycles are more pharmacologically demanding (prescription drug, monitoring needed) while fisetin cycles are easily self-administered between D+Q courses.

Fisetin has an excellent safety profile that is one of the genuinely strong arguments for its use even in the face of unvalidated efficacy. Multiple human trials have confirmed tolerability at doses up to 20 mg/kg. No serious adverse events attributed to fisetin have been documented in any published trial. The flavonoid class generally has strong safety track records from decades of dietary and supplemental human exposure. For community users uncertain about which senolytic to start with, fisetin's safety profile is a genuine differentiator — it can be used without the monitoring requirements of D+Q.

• Mild GI effects: nausea, loose stools, or GI discomfort at very high doses (>1,500 mg). Generally mild and self-limiting. Take with food to reduce GI effects.
• Potential liver impact at very high doses: one animal study documented elevated ALT/AST at very high doses (>112 mg/kg), though this was partly attributed to the DMSO vehicle used in the study. At community supplement doses, no liver toxicity signal.
• Headache: occasionally reported at high doses; usually transient.
• Fatigue during the 2-day cycle: some community users report tiredness during the active dosing days — consistent with a broad cellular effect that isn't specific enough to be considered a problem.

Unlike Dasatinib (which potentiates c-Met, a proto-oncogene) or Cardarine (which failed carcinogenicity studies), fisetin's cancer relationship is generally on the protective side of the ledger. Multiple independent studies have documented anti-proliferative effects of fisetin against various cancer cell lines in vitro — fisetin kills cancer cells as well as senescent cells through overlapping BCL-2/PI3K inhibition mechanisms. This does not mean fisetin is anti-cancer therapy — cell culture findings do not translate directly to clinical anti-cancer effects. But the cancer safety concern that applies to Dasatinib does not apply to fisetin in the same way. For community users with active malignancy, discussion with an oncologist remains appropriate — but the theoretical concern is lower than for c-Met agonists.

Fisetin is a mild inhibitor of some CYP enzymes — CYP1A2 and CYP3A4 at higher concentrations. At typical supplement doses, clinically significant drug interactions are not well-documented. However, individuals on narrow therapeutic index medications should note the potential for CYP inhibition at high fisetin doses. This is a more limited concern than Dasatinib's CYP3A4 profile.

• Pregnancy: avoid — no safety data in pregnancy; standard flavonoid caution applies.
• Known hypersensitivity to flavonoids or strawberries: rare but possible cross-reactivity.
• Very high doses (>2,000 mg) with compromised liver function: theoretical concern from animal liver data.

Both fisetin and quercetin target BCL-2 family members and PI3K/Akt signaling but with different cell-type specificities. Quercetin is preferentially senolytic against endothelial cells and some preadipocytes. Fisetin has broader cell-type activity in cell culture studies. Combining them covers more senescent cell populations than either alone — the same logic that drives the D+Q combination, applied to the all-natural senolytic approach. This combination is very commonly used in community practice. Both are safe, affordable OTC supplements without drug interactions requiring physician oversight.

Fisetin activates SIRT1 directly. NAD+ precursors provide the cofactor substrate SIRT1 requires to function. The combination addresses SIRT1 from two different directions — allosteric activation (fisetin) and substrate availability (NMN/NR). Theoretically complementary; no interaction concerns. The fisetin senolytic cycles can be timed around ongoing NAD+ supplementation — the clear-then-maintain pattern (fisetin for senescent cell clearance; NAD+ continuously for ongoing mitochondrial and SIRT1 support).

Many advanced community users alternate: D+Q (2-3 times per year, with appropriate medical monitoring) for the proven senolytic clearance with human tissue evidence; fisetin (monthly between D+Q cycles) for the potentially complementary cell-type coverage, SIRT1, mTOR, and anti-inflammatory benefits. The combination uses each compound where its evidence and practical profile is strongest: D+Q where human evidence of actual senescent cell clearance is needed; fisetin for ongoing maintenance, non-senolytic longevity signaling, and broader cell-type coverage.

FOXO4-DRI is pro-apoptotic (kills senescent cells via p53 release). Fisetin has some anti-apoptotic properties at non-senolytic concentrations (SIRT1 activation, neuroprotection) while being pro-apoptotic at senolytic concentrations. The interaction between these compounds is complex and concentration-dependent. The conservative approach: run FOXO4-DRI cycles separately from fisetin cycles rather than simultaneously.

Timeframe

Community-Reported

Days 1-2 (active cycle)

Some users report mild fatigue during the 2-day fisetin window. Most report no acute dramatic changes — consistent with a compound working at a cellular level not producing acute neurological or performance effects.

Days 3-14 (post-cycle)

The most consistently reported community benefit window: improved energy, reduced joint aches, cleaner cognitive function. These correspond to the expected SASP reduction timeline if senolytic clearance is occurring.

Month 1-3 (after multiple cycles)

Community users who report the most benefit typically describe progressive improvements over multiple cycles. This timeline is consistent with the hypothesis that repeated cycles reduce the cumulative senescent cell burden.

Fisetin is the most accessible senolytic — no prescription, no monitoring requirements, low cost, excellent safety profile. The appropriate user: anyone interested in the senolytic approach to aging who either cannot access or does not want to use D+Q (prescription, monitoring, drug interactions), or who wants a senolytic for the months between D+Q cycles. Fisetin's non-senolytic effects (SIRT1, mTOR, anti-inflammatory) provide value independent of whether senolysis is achieved at community doses. The compound's safety allows exploration without the risks that Dasatinib introduces.

• Treating fisetin as equivalent to D+Q because it's a 'natural senolytic': D+Q has direct human tissue evidence of senescent cell reduction. Fisetin does not. The supplement marketing presenting them as equivalent is not scientifically accurate.
• Using standard fisetin powder and assuming it's achieving senolytic concentrations: the bioavailability problem means this assumption is questionable. Using enhanced bioavailability formulations (phytosome, nanoparticle) or at minimum taking with high-fat food is more pharmacologically rational.
• Dismissing fisetin because the ITP failed: the ITP failure is important counterevidence, not definitive disproof. Design differences (dose, formulation, mouse strain, timing) could explain the discrepancy. Fisetin deserves appropriate skepticism, not dismissal.
• Expecting published human senolytic data from the Mayo Clinic trials to confirm everything: the prolonged absence of published human senolytic data from the Mayo fisetin trials — years after trial completion — should be noted. When those results are published, they will substantially change the evidence picture for fisetin. If positive, much of the community use will be retrospectively validated. If negative, the supplement market will need to reckon with that.

The scientific case favors enhanced bioavailability formulations for senolytic intent. A 100 mg fisetin phytosome dose may achieve higher plasma concentrations than 1,000 mg standard crystalline fisetin. However: (1) enhanced formulations are more expensive; (2) the critical question of whether ANY oral fisetin achieves senolytic plasma concentrations in humans hasn't been definitively answered even for enhanced forms; (3) community experience is largely with standard forms, and community-reported benefits may reflect non-senolytic mechanisms that operate at lower concentrations. The pragmatic approach: use enhanced forms if cost allows; take with fat regardless of form; accept that the senolytic evidence in humans is currently unconfirmed for either form.

Yousefzadeh MJ, Zhu Y, McGowan SJ, et al. (2018). Fisetin is a senotherapeutic that extends health and lifespan. EBioMedicine. 36:18-28. PMC6197652. [Kirkland/Mayo group; 10 flavonoid screen — fisetin most potent; progeroid and wild-type mouse lifespan extension; human adipose tissue explant senolysis; the paper that drove the supplement market; note: ITP did not replicate the lifespan finding]

NIA Interventions Testing Program (ITP). Fisetin lifespan study results. [The ITP tested fisetin in standard multi-site rigorous protocol. Results were not significantly positive for lifespan extension. This represents the most important independent counterpoint to the 2018 paper. ITP results are reported in ongoing publications and at scientific meetings; check ITP.jax.org for current status.]

Hisaka S, et al. (2020) [2]. Pharmacokinetics of fisetin and its metabolites in rats. Metabolites. [Documents poor fisetin oral bioavailability and rapid metabolism to glucuronide/sulfate conjugates; relevant context for understanding whether oral supplement doses achieve senolytic plasma concentrations]

Naeimi AF, Alizadeh M. (2017) [3]. Antiobesity effects of fisetin flavonoid in mice: A systems biology approach. Journal of Nutritional Biochemistry. 40:107-116. [One of multiple studies documenting fisetin phytosome or enhanced formulations improving bioavailability 10-25x vs standard crystalline fisetin]

NCT03675724 (AFFIRM): Phase 2, fisetin for frailty in older adults, Mayo Clinic. Tamara Evans PI. Registered 2018. Status: completed. Primary senolytic endpoint data not published as of May 2026.

NCT03868605 (AFFIRM-LITE): Phase 2, fisetin for frailty, Mayo Clinic / multiple sites. Status: completed or near-completion. Primary senolytic data not published as of May 2026.

NCT04771611: Fisetin for COVID-19 cytokine storm prevention. Multi-center University of Minnesota / Mayo Clinic. Safety confirmed. Efficacy data preliminary.

Maher P. (2009) [4]. Fisetin acts on multiple pathways to reduce the impact of age and disease on CNS function. Frontiers in Bioscience. 14:2168-2183. [Independent review; comprehensive neuroprotective evidence predating the senolytic literature; multiple mechanisms including BDNF, SIRT1, anti-inflammatory; credible independent base]

Fight Aging! (September 2025): 'Yet More Mouse Data on Fisetin as a Senotherapeutic.' [Commentary noting: 'there is still no published data of its senolytic capacity in humans' despite completed and ongoing Mayo Clinic trials; context for the evidence gap as of 2025]

Feature

Fisetin

Dasatinib + Quercetin

Human senolytic evidence

None published — trials complete but data unreleased

Direct tissue evidence (DKD pilot — adipose + skin biopsy)

Clinical trial phase for aging

Phase 2 trials complete; data unpublished

Phase 2 complete (osteoporosis); multiple Phase 2 ongoing

Mouse evidence

Yes (2018 paper) — ITP FAILED to replicate

Yes — replicated across labs

Prescription required

No — OTC supplement

Dasatinib: Yes — prescription required

Safety monitoring needed

No — excellent OTC safety

Yes — ECG, CBC, drug interaction review

Drug interactions

Minimal — mild CYP inhibition at high doses

MAJOR — CYP3A4 substrate with extensive interactions

Bioavailability

Poor and variable — may limit senolytic efficacy

Dasatinib: moderate oral bioavailability; good for senolytic doses

Cost per cycle

$5-30 (2 days of supplement)

Dasatinib: $200-400 for 30 tablets from international pharmacy

ITP (independent mouse longevity test)

FAILED

Not tested specifically as senolytic combination

Community accessibility

Very high

Moderate — Rx barrier

• 'The 2018 paper proved fisetin works as a senolytic in humans': the 2018 paper showed senolytic activity in human adipose tissue explants (ex vivo), not in living humans. Ex vivo is not in vivo.
• 'The ITP failure means fisetin is useless': the ITP tests lifespan extension, not necessarily senolytic activity. Design differences may explain the failure without negating fisetin's senolytic potential. Appropriate skepticism, not dismissal.
• '5 mg of fisetin in a strawberry explains fisetin's benefits': the senolytic protocol uses 500-2,000 mg. Dietary fisetin from food (~0.4 mg/day) is orders of magnitude below supplement doses.
• 'No SAEs in the COVID-19 trial means fisetin is safe at any dose': safety is established at clinical trial doses. Extremely high doses (>2,000 mg) have not been well-characterized and carry the theoretical liver concern from high-dose animal studies.

— End of Fisetin —

THE PEPTIDE BIBLE | Fisetin | For Research & Educational Purposes Only