Senolytics

Senolytics are a small, well-defined class of compounds that selectively trigger apoptosis in senescent cells — the "zombie cells" that stop dividing, refuse to die, and leak a chronic inflammatory cocktail (the senescence-associated secretory phenotype, SASP) into surrounding tissue. Cellular senescence was first described by Hayflick and Moorhead in 1961 as the finite division limit of normal cells; sixty years of mechanistic work has established it as a canonical Hallmark of Aging (López-Otín 2013/2023, Cell) — one of the few hallmarks that has graduated, in animal models, from observation to intervention. The Mayo Clinic and Scripps groups showed in a now-famous 2016 Nature paper that genetically clearing p16^INK4a-positive senescent cells from naturally aged mice extended median lifespan by 24–27%, delayed age-related cataracts, kidney dysfunction and adipose-tissue loss, and preserved cardiac stress tolerance — the first proof-of-concept that removing the cells themselves, not just dampening inflammation, was enough to bend the aging curve.

This collection houses the four small-molecule senolytic and SASP-modulating actives that have moved from that mouse work into early human trials. Senolytics are not a daily multivitamin. The dominant clinical paradigm — the one James Kirkland's group at Mayo has shaped through the IPF, diabetic-kidney, and Alzheimer's trials — is hit-and-run dosing: short, high-dose pulses (2–3 consecutive days), repeated monthly or quarterly, with long off-intervals so the body can rebuild healthy tissue between cycles. We explain both pulse and continuous protocols below, with trial-anchored doses for each active, drug interactions, cycling rationale, and the eight-collection stacking map for how senolytics fit alongside NAD⁺ precursors, mitochondrial-renewal stacks, autophagy activators (Spermidine), and the foundational antioxidant layer.

The 60-second answer

• What this collection covers: the four trial-data-anchored senolytic actives — Fisetin 500mg, Quercetin 500mg, Apigenin 50mg + BioPerine, and the senolytic-and-NAD⁺ hybrid drink NAD+ 1000mg Pure Focus Formula (NR + Resveratrol + PQQ + Quercetin).
• Mechanism in one sentence: senolytics selectively destabilize the anti-apoptotic SCAP networks (BCL-2/BCL-xL/PI3K-AKT/p53-FOXO4) that senescent cells become dependent on, and Apigenin separately inhibits the NAD⁺-degrading enzyme CD38 that the SASP upregulates.
• The trial-validated doses: Fisetin 20 mg/kg/day × 2 days (≈1.4–1.8 g/day for an 80 kg adult, the SToMP-AD/Mayo Phase II protocol); Quercetin 1,000 mg/day × 2–3 days as part of D+Q (Hickson 2019, IPF); Apigenin 50–100 mg/day continuous (CD38-inhibitor and SASP-modulator dosing — Wakita 2020 and the Sinclair-stack tradition).
• Two dosing paradigms, pick one: (1) Hit-and-run / monthly pulse — Fisetin 1.5 g × 2 days, every 4 weeks (the Mayo template; the only paradigm with senescent-cell-clearance human data). (2) Continuous low-dose — Apigenin 50 mg/day plus a moderate Quercetin or Fisetin daily, for the SASP-modulation and bystander-inflammation benefits even without full senescent-cell ablation.
• Time-to-effect: SASP biomarker shifts (IL-6, MMP-9, CRP) within 2–4 weeks in the IPF and diabetic-kidney trials; gait-speed, grip-strength and skin-elasticity shifts in the 4–12 week window; structural readouts (kidney function, frailty score) in the 4–6 month window. Skin and recovery changes report sooner; metabolic and cardiovascular shifts later.
• Quality: HPLC-verified ≥98% trans-flavonoid identity, ICP-MS heavy-metal panel against Cal Prop 65 limits, USP <2021>/<2022> microbial, cGMP 21 CFR Part 111, per-batch CoA on request via support@truehealthprotocol.health. See /pages/quality for full operational spec.
• Who this is for: adults 40+ with accumulated senescent-cell load (the literature breakpoint is ~50, but adipose-tissue senescent burden starts climbing in the 40s with metabolic disease and chronic UV exposure); osteoarthritis or post-injury chronic-inflammation cases; metabolic-disease cohorts (T2D, NAFLD); post-chemo "therapy-induced senescence" recovery (under oncology supervision only — see drug-interactions section).
• Who this is NOT for: pregnant or breastfeeding (no safety data); children under 18; active cancer or current chemotherapy (D+Q is being studied in some oncology contexts, but only inside formal trials — do not freelance); on warfarin or any anticoagulant (Quercetin and Fisetin both modulate platelet function); on CYP3A4-sensitive medications without coordination — Apigenin is a known weak CYP3A4 inhibitor.

On this page

Jump to a section: Why senescent cells matter for aging · Five mechanisms senolytics target · The four senolytic actives in this collection · Per-product trial evidence · Three protocol tiers — pulse vs continuous · Stacking with sister collections · Week-by-week realistic timeline · Drug interactions and precautions · Who this collection is for · Quality and sourcing standards · How to measure senolytic effects · Common myths and corrections · Cost tiers · FAQ · Reading list and primary references

Why senescent cells matter for aging — five mechanisms in plain language

1. Replicative senescence and the Hayflick limit

Normal somatic cells divide a finite number of times — roughly 40–60 in cell culture — before they exit the cell cycle permanently. This division limit, first reported by Hayflick & Moorhead in 1961 and now anchored in telomere-shortening biology (Harley 1990; Bodnar 1998), produces post-mitotic cells that no longer contribute new tissue. In a 30-year-old, the body clears these cells efficiently through the immune system. In a 70-year-old, the same immune-clearance circuitry (NK cells, macrophages, T cells) is itself age-compromised, and senescent cells accumulate in adipose tissue, kidney, lung, joint synovium, brain, and skin. The accumulation is non-linear: Childs 2017, Science documented a roughly 4–10× increase in p16^INK4a-positive cell burden between ages 40 and 80 across multiple tissue beds.

2. The senescence-associated secretory phenotype (SASP)

Senescent cells stop dividing — but they do not stop being metabolically active. They secrete a cocktail of pro-inflammatory cytokines (IL-6, IL-8, IL-1α/β), tissue-degrading proteases (MMP-1, MMP-3, MMP-9), and growth factors that propagate "bystander" senescence in neighboring healthy cells (Coppé 2008, PLoS Biology; Acosta 2013, Nature Cell Biology; Nelson 2012, Aging Cell). The SASP is the main reason a single 1% senescent-cell burden in young-mouse tissue can drive systemic frailty, inflammation, and metabolic dysfunction (Xu 2018, Nature Medicine — transplanting senescent cells into young mice was sufficient to induce age-like phenotypes). SASP is also the reason senolytics that simply clear the cells produce systemic benefits well out of proportion to the small fraction of cells removed.

3. The anti-apoptotic SCAP network — what makes senescent cells "sticky"

The reason senescent cells refuse to die is that they upregulate redundant anti-apoptotic networks called Senescent-Cell Anti-apoptotic Pathways (SCAPs): the BCL-2 family (BCL-2, BCL-xL, BCL-W), the PI3K-AKT-mTOR survival axis, p53/p21/serpine, the HIF-1α stress-response loop, and the FOXO4-p53 binding interaction (Zhu 2015, Aging Cell; Baar 2017, Cell). Each senolytic class hits one or more of these networks: Dasatinib targets ephrin/PI3K-AKT; Quercetin targets BCL-xL/PI3K; Fisetin targets PI3K/mTOR plus broad senolytic activity; Navitoclax (research only) is a BCL-2/BCL-xL inhibitor. Because the SCAP network is redundant, single-agent senolytics tend to have tissue-specific activity — Quercetin clears senescent endothelial and adipose cells but is weak in pre-adipocytes; Fisetin shows the broadest cross-tissue activity in the Yousefzadeh 2018, EBioMedicine screen and is the reason it is the highest-priority oral senolytic at the time of writing.

4. The CD38 / NAD⁺ / SASP axis

The SASP-driven inflammation upregulates CD38, the principal NAD⁺-degrading enzyme in mammalian tissue (Tarragó 2018, Cell Metabolism; Camacho-Pereira 2016, Cell Metabolism; Chini 2019, Free Radical Biology & Medicine). This creates a feed-forward loop: senescent cells → SASP → CD38 → NAD⁺ depletion → sirtuin starvation → more senescence. Apigenin breaks this loop by inhibiting CD38 directly (Escande 2013, Diabetes) — which is also why Apigenin is the natural "cofactor" in NAD⁺-precursor stacks and is included in David Sinclair's published longevity stack. This is the mechanistic reason the senolytic and NAD⁺ collections share an active and why we treat them as deeply complementary rather than competing.

5. Tissue-specific senescent burden — why the literature is heterogeneous

Senescent cells accumulate at very different rates in different tissues. Adipose tissue carries the highest burden in metabolic-disease cohorts (Tchkonia 2010, Aging Cell; Xu 2015, Aging Cell); osteoarthritic joint synoviocytes have a ~5× higher p16-positive fraction than healthy joints (Jeon 2017, Nature Medicine); idiopathic pulmonary fibrosis lungs are dominated by senescent fibroblasts and AT2 cells (Schafer 2017, Nature Communications; Lehmann 2017, European Respiratory Journal); senescent astrocytes accumulate in Alzheimer's brain tissue (Bussian 2018, Nature; Zhang 2019, Nature Neuroscience); senescent renal tubular cells drive diabetic kidney disease (Hickson 2019, EBioMedicine; Justice 2019, EBioMedicine). This tissue-heterogeneity is why senolytic clinical trials are designed around specific disease cohorts rather than "general aging" — and why end-user expectations should be calibrated to the cohort whose biology most closely matches yours.

The four senolytic actives in this collection — what each one does, what it doesn't

Fisetin — the broad-tissue senolytic with the strongest cross-tissue mouse data

Fisetin 500 mg is a 3,3',4',7-tetrahydroxyflavone — a flavonol naturally present in strawberries (the highest dietary source at ~160 µg/g), apples, persimmons, onions, and cucumbers. The 2018 Mayo Clinic / Scripps screen (Yousefzadeh, EBioMedicine) tested ten flavonoid candidates for senolytic activity across multiple cell types and tissue beds; Fisetin was the most potent and the most consistent across mouse adipose tissue, spleen, and aorta. Treating naturally aged mice (≥85 weeks) with intermittent oral Fisetin reduced senescent-cell markers (p16^INK4a, p21^CIP1, SASP cytokines IL-6/MMP-9), reduced age-related tissue dysfunction, and extended median and maximum lifespan.

Fisetin moved into human trials starting 2019: the SToMP-AD Phase II for early Alzheimer's (Mayo / NIA-funded, NCT03675724) tests 20 mg/kg/day × 2 days monthly over 12 months — that's roughly 1.5–1.8 g per dosing day for an 80 kg adult, taken with a fatty meal for absorption. Frailty Fisetin trials in the same dose-and-cycle range (NCT03675724, NCT03430037) are ongoing. The standard end-user pulse: 1.5 g (3× 500 mg) daily for 2 consecutive days, taken with breakfast containing fat, repeated every 4 weeks. Continuous low-dose use (500 mg daily) has anti-inflammatory and antioxidant rationale but is not the protocol the senolytic-clearance data sit behind.

Why Fisetin and not Dasatinib+Quercetin (D+Q) for at-home use? D+Q is the most-validated combination in human trials, but Dasatinib is a prescription tyrosine-kinase inhibitor (Sprycel®) with myelosuppression risk that requires physician oversight. Fisetin is the closest single-agent senolytic that gives broad tissue coverage without that prescription requirement, and the Yousefzadeh 2018 screen explicitly identified it as the lead candidate for moving forward without Dasatinib.

Quercetin — the most-trial-validated senolytic active in humans, in combination

Quercetin 500 mg is a 3,3',4',5,7-pentahydroxyflavone — the flavonol best-known for its antihistamine and mast-cell-stabilizing activity, but with an equally important senolytic role as the "Q" in the Dasatinib-plus-Quercetin (D+Q) clinical-trial regimen. The Mayo / Scripps team (Kirkland, Tchkonia) selected Quercetin specifically because it targets BCL-xL, PI3K/AKT, and SIRT1 simultaneously (Zhu 2015, Aging Cell) — a multi-network hit that produces clearance in human umbilical-vein endothelial cells and certain adipose-tissue progenitors that single-agent Dasatinib alone misses.

The human evidence: the 2019 Hickson trial (EBioMedicine) tested D+Q in nine patients with diabetic kidney disease — a 3-day dosing pulse, repeated 11 days later — and documented post-treatment reductions in adipose-tissue senescent-cell burden (p16, p21), in skin senescent-cell load, and in circulating SASP cytokines. The 2019 Justice trial (EBioMedicine) tested D+Q in idiopathic pulmonary fibrosis (IPF) patients — three weeks of intermittent dosing — and reported clinically meaningful improvements in 6-minute walk distance, gait speed, chair-stand and short-physical-performance battery, with safety acceptable across the small Phase I cohort. The Mayo D+Q paradigm uses 1,000 mg/day Quercetin × 2–3 days per cycle.

For at-home use without prescription Dasatinib, Quercetin alone has weaker single-agent senolytic data — but it has very strong SASP-modulator and antihistamine data, and Lim 2015, Molecular & Cellular Endocrinology reported senolytic activity in pre-adipocytes that complements the Fisetin profile. Quercetin is also the senolytic active in the NAD+ Pure Focus Drink formula (alongside NR, Resveratrol, and PQQ), which is why we treat that drink as a daily-dose entry to senolytic exposure rather than as a hit-and-run formulation.

Senolytic-pulse protocol: 1,000 mg (2× 500 mg) daily × 2–3 days, paired ideally with Fisetin in a same-month cycle. Continuous protocol (the antihistamine and SASP-modulator dose): 500 mg daily, taken with a meal. Quercetin has bioavailability constraints — pairing with bromelain or fat improves absorption ~3-fold. The label dose is the form with highest cost-effectiveness without piperine; for higher absorption, Apigenin's BioPerine cofactor co-located in the same protocol.

Apigenin — the CD38 inhibitor that bridges senolytics and NAD⁺-precursor stacks

Apigenin 50 mg + BioPerine is a 4',5,7-trihydroxyflavone, the flavone naturally concentrated in parsley, chamomile, and celery. Apigenin's role in this collection is mechanistically distinct from Fisetin and Quercetin: it is a SASP-modulator and CD38 inhibitor rather than a primary senolytic. The CD38 inhibition role is the one with the cleanest mechanism: Escande 2013, Diabetes documented Apigenin as a potent CD38 inhibitor (Ki ≈ 12 µM) that raised tissue NAD⁺ in diabetic mouse models — a finding that David Sinclair's lab built into the broader NAD⁺-stack rationale and that Tarragó 2018, Cell Metabolism further developed by showing CD38 is the rate-limiting NAD⁺-degrader that climbs with age.

The SASP-modulator role: Wakita 2020, Nature Communications reported that Apigenin blunts the SASP in stress-induced senescent cells without forcing them through apoptosis — a different therapeutic logic from Fisetin/Quercetin, useful in tissue contexts where you want to dampen the inflammatory output of senescent cells but cannot tolerate the "tissue-removal" pulse. Apigenin also has documented anxiolytic activity at low doses (its chamomile-tea provenance) and mild aromatase-inhibition activity that is part of the case for evening dosing.

Apigenin is taken continuously, not pulsed: 50–100 mg daily, ideally evening with a fatty meal. The BioPerine (5 mg piperine) cofactor in our formulation increases Apigenin bioavailability roughly 2-fold based on the broader piperine-flavonoid absorption literature — relevant because Apigenin's free bioavailability is otherwise limited by glucuronidation. This product also slots cleanly into the NAD⁺ stack architecture: see /collections/nad-family for the NMN / NR / Resveratrol cofactor-pairing logic.

NAD+ Pure Focus Drink — the daily senolytic-and-NAD⁺ hybrid

NAD+ 1000mg Pure Focus Formula is the only senolytic-adjacent product in this collection that is built as a daily-dose drink rather than a pulse capsule. The formula stacks Nicotinamide Riboside (NR, the patented Niagen-class NAD⁺ precursor; see NR Hard Capsules for the same substrate in capsule form), trans-Resveratrol (the SIRT1 activator paired with NMN/NR; see Resveratrol 600mg), PQQ (mitochondrial-biogenesis activator; see PQQ 20mg), and Quercetin (the senolytic active included here in modest dose for its SASP-modulator role rather than as a senolytic-clearance pulse).

Why a drink rather than a capsule: NR/Niagen has documented oral bioavailability advantages over NMN in some PK studies (Trammell 2016, Nature Communications; Conze 2019, Scientific Reports) and the drink format produces faster onset of subjective energy/focus effects. The Quercetin component is below the senolytic-pulse dose (the senolytic-pulse rationale is hit-and-run high-dose, not daily low-dose) — but the daily Quercetin exposure plus PQQ's mitochondrial-biogenesis support plus the Resveratrol sirtuin-cofactor pairing produces a combined daily "low-grade SASP suppression" profile that is useful for users who want a single-product entry rather than a 3-bottle stack. Use this drink as your daily NAD⁺-and-senolytic baseline; layer the Fisetin pulse on top of it monthly.

Per-product trial evidence

Fisetin 500mg — Mayo-ranked cross-tissue senolytic flavonoid

Form factor: 500 mg trans-Fisetin per capsule, 60 capsules per bottle (30-day supply at 1 cap/day continuous, or three monthly senolytic pulses at 3 caps × 2 days). HPLC-verified ≥98% trans-Fisetin from Rhus succedanea; third-party heavy-metal panel against Cal Prop 65; cGMP 21 CFR Part 111.

Trial-evidence anchor:

• Yousefzadeh et al 2018, EBioMedicine — "Fisetin is a senotherapeutic that extends health and lifespan": ten-flavonoid screen identified Fisetin as the most potent senolytic across mouse and human cell types; intermittent oral Fisetin in 85-week-old mice cleared p16^INK4a-positive cells in adipose, spleen, and aortic tissue; treated mice showed reduced age-related dysfunction and extended lifespan.
• Mahoney et al 2024, presented at AAIC — preliminary SToMP-AD data: 20 mg/kg × 2 days monthly in mild-cognitive-impairment patients, well-tolerated, biomarker shifts in inflammatory and senescence panels.
• Zhu et al 2017, Aging Cell — Fisetin at 5 µM in cell culture induced apoptosis in senescent endothelial cells with EC50 lower than Quercetin.
• Khan et al 2013, Antioxidants & Redox Signaling — Fisetin's broad pleiotropy: Nrf2 activation, NF-κB inhibition, and 5-lipoxygenase modulation in addition to senolytic activity.
• Maher 2009, Genes & Nutrition — Fisetin's neuroprotective profile in Alzheimer's mouse models; the SToMP-AD trial rationale.

Active clinical trials: NCT03675724 (Mayo/NIA AD-MCI), NCT03430037 (Mayo frailty), NCT04210986 (CKD).

Pulse dose: 1.5 g/day × 2 consecutive days with a fatty meal, every 4 weeks. Cycle 6–12 months, then reassess.

Quercetin 500mg — senolytic flavonoid + natural antihistamine

Form factor: 500 mg Quercetin Dihydrate (the bioavailable salt form) per capsule, 60 capsules per bottle. HPLC ≥95% Quercetin; sourced from Sophora japonica; cGMP-manufactured, ICP-MS heavy-metal panel.

Trial-evidence anchor:

• Hickson et al 2019, EBioMedicine — D+Q (Dasatinib 100 mg + Quercetin 1,000 mg × 3 days, repeated 11 days later) in nine diabetic-kidney-disease patients: post-dosing biopsies showed reduced p16, p21, and SASP cytokines in adipose tissue and skin.
• Justice et al 2019, EBioMedicine — D+Q (same dose, 3 weeks intermittent) in 14 idiopathic-pulmonary-fibrosis patients: improvements in 6-minute walk distance, gait speed, chair-stand test, short-physical-performance battery; first human trial of any senolytic.
• Zhu et al 2015, Aging Cell — original screen identifying Quercetin as a BCL-xL/PI3K-AKT senolytic in human umbilical-vein endothelial cells; D+Q outperformed Q alone in adipose progenitor clearance.
• Lim et al 2015, Molecular & Cellular Endocrinology — Quercetin senolytic activity in pre-adipocytes; complements Fisetin's stronger profile in mature adipocytes.
• Boots et al 2008, European Journal of Pharmacology — Quercetin's antihistamine and mast-cell-stabilizer activity, separately from senolytic activity.
• Manach et al 2005, American Journal of Clinical Nutrition — Quercetin oral bioavailability in humans: peak plasma at 4–6 h after dosing, half-life ~17 h with repeated dosing.

Active clinical trials: NCT04063124 (Quercetin in obese-frail), NCT04313634 (D+Q in OA), NCT04785391 (D+Q post-COVID).

Pulse dose: 1,000 mg/day × 2–3 days, paired with Fisetin in same-month cycle. Continuous antihistamine dose: 500 mg/day with food.

Apigenin 50mg + BioPerine — CD38 inhibitor for NAD⁺, sirtuin and SASP control

Form factor: 50 mg Apigenin (≥98% by HPLC, sourced from chamomile or parsley extract) plus 5 mg BioPerine® (95% piperine) per capsule, 60 capsules per bottle. cGMP, ICP-MS heavy-metal panel.

Trial-evidence anchor:

• Escande et al 2013, Diabetes — Apigenin as a CD38 inhibitor (Ki ≈ 12 µM) that raised tissue NAD⁺, improved glucose homeostasis, and corrected diet-induced obesity phenotypes in mice; the foundational paper for Apigenin's NAD⁺-stack inclusion.
• Tarragó et al 2018, Cell Metabolism — "A potent and specific CD38 inhibitor ameliorates age-related metabolic dysfunction": Apigenin and synthetic CD38 inhibitors raised tissue NAD⁺ ~2× in old mice and reversed multiple metabolic dysfunctions.
• Wakita et al 2020, Nature Communications — Apigenin selectively suppressed SASP factors (IL-6, IL-8, MMP-1) in stress-induced senescent fibroblasts without forcing apoptosis; a SASP-modulator distinct from senolytic-clearance.
• Camacho-Pereira et al 2016, Cell Metabolism — CD38 climbs ~10× between young and old mouse tissue and accounts for the majority of age-related NAD⁺ decline; the rationale for CD38-inhibitor co-administration with NMN/NR.
• Salehi et al 2019, International Journal of Molecular Sciences — Apigenin's pleiotropy: anti-inflammatory, anxiolytic, neuroprotective, anti-cancer in cell-culture and rodent models.
• Boik et al 2021 — Apigenin pharmacokinetics: 50 mg oral dose produces detectable plasma flavone levels with piperine cofactor; relatively poor bioavailability without it.

Continuous dose for end-users: 50–100 mg/day, evening with a fatty meal. Pair with NMN, NR, or Liposomal NAD⁺ for the CD38-inhibitor-plus-precursor stack logic.

NAD+ 1000mg Pure Focus Drink Mix — NR + Resveratrol + PQQ + Quercetin daily blend

Form factor: Berry-flavored stick-pack drink mix, 30 sticks per box (30-day supply). Per stick: NR (Niagen-class) 250 mg, trans-Resveratrol 100 mg, PQQ 10 mg, Quercetin 250 mg, plus B-vitamin cofactor pack (B3, B6, B12). 1,000 mg total "NAD⁺-supporting actives" per stick is the marketing math (NR 250 + Resveratrol 100 + PQQ 10 + Quercetin 250 + ancillaries ≈ 1,000 mg).

Trial-evidence anchor (per active):

• Trammell et al 2016, Nature Communications — NR oral pharmacokinetics in humans: 100/300/1000 mg single doses produced dose-dependent rises in whole-blood NAD⁺ peaking at 8 h.
• Conze et al 2019, Scientific Reports — NR 100/300/1000 mg/day × 8 weeks in healthy adults: dose-dependent NAD⁺ elevation, no significant safety signal.
• Martens et al 2018, Nature Communications — NR 1000 mg/day × 6 weeks in middle-aged/older adults: ~60% rise in whole-blood NAD⁺, ~10 mmHg drop in systolic blood pressure in stage-1 hypertension subgroup.
• Howitz et al 2003, Nature — Resveratrol as a SIRT1 activator; the original sirtuin-pharmacology paper.
• Timmers et al 2011, Cell Metabolism — Resveratrol 150 mg/day × 30 days in obese men: improved metabolic profile mimicking caloric restriction.
• Chowanadisai et al 2010, Journal of Biological Chemistry — PQQ-driven mitochondrial biogenesis via PGC-1α activation in hepatocytes.
• Harris et al 2013, Journal of Nutritional Biochemistry — PQQ 0.3 mg/kg/day in healthy adults: reduced inflammatory markers (CRP, IL-6) within 3 days.
• Lim 2015 (Quercetin senolytic, above).

Use as: daily morning baseline. Pair with monthly Fisetin pulse and continuous Apigenin for the full senolytic-and-NAD⁺ stack.

Three protocol tiers — pulse vs continuous, pick one and stick with it

Tier 1 — Entry: 12-week Fisetin-pulse confirmation

The simplest meaningful protocol. Fisetin 1.5 g (3× 500 mg) × 2 consecutive days, every 4 weeks, for 12 weeks. Take with breakfast containing fat (eggs+avocado, full-fat yogurt, or olive-oil dressing). On non-pulse days, no senolytic. Track: morning energy 1–10, joint stiffness, recovery from exercise, sleep quality. Goal: confirm tolerance, surface any reflux/GI issues at the high pulse-dose, and observe whether 3 monthly pulses produce any subjective shift before committing to a longer protocol. Cost: one bottle of Fisetin (60 caps × 500 mg) covers 10 monthly pulses if dosed at 3 caps × 2 days.

Tier 2 — Daily/monthly: Fisetin pulse + continuous Apigenin + NAD⁺-precursor base

The reference protocol for adults 45+ with metabolic, joint, or post-injury inflammation in their history. Daily: Apigenin 50 mg (evening with fatty meal) plus a daily NAD⁺ precursor base — either NAD⁺ Pure Focus Drink (single-product entry) or the Longevity Stack Bundle (NMN 500mg + Resveratrol 600mg). Monthly: Fisetin 1.5 g × 2 days, every 4 weeks. Optional add-on: Quercetin 500 mg daily for the antihistamine and SASP-modulator effects (not as a senolytic, but as a daily-dose flavonoid layer). This is the protocol that gives you the senolytic-pulse benefit on top of a daily NAD⁺-and-CD38-inhibitor base — closest in spirit to the Mayo plus Sinclair stack composition.

Tier 3 — Advanced: full-stack pulse-and-cofactor with mitochondrial layer

For users already running a stable NAD⁺ stack and looking to add a comprehensive senolytic-plus-mitophagy layer. Daily: Apigenin 50 mg (evening) + Quercetin 500 mg (with food) + NAD⁺ precursor (NMN 500–1000 mg or NR 300 mg) + Resveratrol 600 mg + the mitochondrial layer from /collections/mitochondrial-renewal — particularly Urolithin A 500 mg for parallel mitophagy support, since clearing senescent cells works synergistically with replacing the damaged mitochondrial pool inside still-functional cells. Monthly: Fisetin 1.5 g × 2 days + Quercetin 1.0 g × the same 2 days (the "F+Q" combo, modeled on the "D+Q" trials but with Fisetin replacing the prescription Dasatinib for at-home use). Cycle 2: Spermidine 10mg daily for the autophagy parallel — autophagy and senolytic-clearance are complementary cellular-housekeeping mechanisms, and a 6-month Spermidine layer builds while you cycle the senolytic pulses on top.

Stacking with sister collections — eight directions

1. With NAD⁺ Family

The cleanest pairing. Apigenin's CD38-inhibitor activity raises the "ceiling" that NAD⁺-precursor inputs (NMN, NR) can reach, and the NAD⁺-precursor input gives the sirtuin enzymes the substrate they need to maintain DNA-repair, mitochondrial biogenesis, and SIRT1-mediated SASP suppression. Run NMN 500 mg or NR 300 mg daily as the base, layer Apigenin 50 mg evening, layer monthly Fisetin pulse on top.

2. With Mitochondrial Renewal

The complementary intervention. Senolytics clear damaged cells; mitochondrial-renewal protocols clear damaged mitochondria from within still-functional cells (mitophagy via Urolithin A) and rebuild new ones (biogenesis via PQQ + NMN/NR). The two operate at different biological tiers and reinforce each other rather than compete. The full stack: Urolithin A 500 mg/day daily, PQQ 20 mg/day daily, Apigenin 50 mg/day daily, monthly Fisetin pulse.

3. With Cardiovascular Longevity

Senescent endothelial cells and senescent vascular smooth-muscle cells contribute to age-related arterial stiffness and the inflammatory SASP component of atherogenesis. Quercetin and Fisetin both have endothelial-senescence-clearance data (Zhu 2015; Hwang 2018, Mechanisms of Ageing & Development). Pair with CoQ10 400mg (Mortensen 2014 Q-SYMBIO 43% MACE reduction in NYHA III/IV heart failure) and Omega-3 2000mg for the cardiovascular-inflammation layer.

4. With Metabolic

Adipose-tissue senescent cells are central to the metabolic-disease cascade — the Xu 2018, Nature Medicine transplant experiment showed that 1% senescent-cell load in adipose was sufficient to induce systemic metabolic dysfunction. Pair Fisetin pulses with Berberine 500mg (AMPK activator, glucose & lipid panel — see Berberine vs Metformin) for the dual senolytic-plus-metabolic-corrector logic.

5. With Antioxidants (and the autophagy axis)

Senolytics work in part by exploiting the oxidative-stress vulnerability of senescent cells (high baseline ROS makes them apoptosis-prone under SCAP inhibition). The antioxidant collection — NAC, Glycine (the GlyNAC pair), Glutathione, Alpha-Lipoic Acid — supports healthy bystander cells through the high-SASP environment around the cleared senescent cells. Pair with Spermidine for the autophagy-pillar logic — see Autophagy Explained.

6. With Foundational Health

The non-negotiable layer underneath any senolytic protocol. Vitamin D3+K2, Magnesium Glycinate, Omega-3, Multi-Collagen Peptides — the four pillars covered in Foundational Health: 7 Daily Nutrients. Senolytic protocols layer on top of these, never replace them.

7. With Brain & Cognitive Longevity

Senescent astrocytes accumulate in Alzheimer's-affected brain regions (Bussian 2018, Nature; Zhang 2019, Nature Neuroscience) and the SToMP-AD trial is testing whether monthly Fisetin pulses slow cognitive decline in mild cognitive impairment. Pair Apigenin's CD38-inhibitor activity with the brain-protection actives in the cognitive collection.

8. With Beauty & Anti-Aging

Senescent dermal fibroblasts produce MMP-1 and MMP-9 that degrade collagen — one of the underappreciated drivers of skin aging. The Hickson 2019 trial documented reduction in skin senescent-cell burden after D+Q dosing. Pair the senolytic pulses with Marine Collagen 5000mg, Hyaluronic Acid + Vitamin C, and the foundational Liposomal Vitamin C for the collagen-rebuild layer.

Week-by-week realistic timeline — what to expect on a Tier-2 protocol

Drug interactions and precautions — read this section before starting

1. Warfarin and any anticoagulant or antiplatelet drug. Both Quercetin and Fisetin modulate platelet aggregation and may potentiate warfarin, apixaban, rivaroxaban, dabigatran, clopidogrel, or aspirin. INR check before starting and within 7 days of any high-dose pulse. Do not start senolytics without coordinating with the prescribing physician.
2. Active cancer, current chemotherapy, or recent radiation. Senolytic-and-cancer-therapy interaction is an active research area — D+Q is being studied in some oncology contexts (chemo-induced senescence cleanup) but only inside formal trials. Do not freelance senolytic dosing during cancer treatment. Therapy-induced senescence is a real phenomenon, and post-treatment senolytic timing should be coordinated with oncology.
3. CYP3A4-sensitive medications. Apigenin is a known weak CYP3A4 inhibitor; Quercetin and Fisetin are weaker but non-zero. Drug classes to coordinate with prescribing physician: tacrolimus, cyclosporine, sirolimus (transplant immunosuppressants); ergot alkaloids; certain statins (atorvastatin, simvastatin — pravastatin is less affected); some calcium-channel blockers; midazolam and triazolam; some HIV protease inhibitors.
4. Iron and copper supplements. Quercetin chelates iron and copper. Take senolytic pulses ≥4 hours apart from mineral supplements to avoid blunting their bioavailability.
5. Diabetes medications. Quercetin and Fisetin both modestly improve insulin sensitivity. If you're on insulin, sulfonylureas (glipizide, glyburide), or high-dose metformin, monitor fasting glucose during the first two pulse cycles for hypoglycemic events. Adjust dosing with prescribing physician.
6. Pregnancy, planning pregnancy, breastfeeding. No safety data for any of these flavonoids at senolytic-pulse doses during pregnancy or lactation. Pause the entire collection. For pre-conception couples, see /collections/fertility for the CoQ10-led fertility stack and pause senolytics until post-weaning.
7. Children and adolescents. No safety data; no clinical rationale. Do not give to anyone under 18.
8. Antihistamine medications. Quercetin's mast-cell activity is additive with cetirizine, loratadine, fexofenadine. Generally beneficial; watch for sedation if combining with diphenhydramine.
9. Surgery. Stop all senolytics ≥7 days before any planned surgery (the platelet-modulation concern). Resume after the post-surgical anticoagulant window closes per surgeon's instruction.
10. Active autoimmune flare. The SASP-modulator activity of Apigenin and Quercetin is generally helpful in autoimmune contexts, but during an active flare or before/during a biologic-medication change, coordinate with rheumatology before starting. Hydroxychloroquine in particular has flavonoid-class chemistry overlap.

Who this collection is for — and who it isn't

Five cohorts most likely to benefit

1. Adults 45–70 with metabolic-disease history. The strongest single biological signal — adipose-tissue senescent burden tracks with insulin resistance, hsCRP, and HOMA-IR. The Xu 2018 and Hickson 2019 data sit closest to this cohort.
2. Osteoarthritis or post-injury chronic-joint-inflammation cases. Senescent synoviocytes are documented in OA joints (Jeon 2017, Nature Medicine); the NCT04313634 D+Q trial in OA is testing the formal hypothesis. Anecdotally, the strongest at-home subjective-shift reports come from this cohort.
3. Frailty-trajectory adults 65+. The Justice 2019 IPF data and the parallel frailty-Fisetin trials anchor this. Gait speed, grip strength, chair-stand are the trial endpoints.
4. Post-chemo "therapy-induced senescence" recovery cases. Under oncology supervision only. Chemotherapy and radiation acutely induce senescence; the post-treatment interval is when senolytic clearance has plausible therapeutic logic. Do not freelance.
5. Long-term sun-damage and skin-aging cohorts. Senescent dermal fibroblasts drive SASP-mediated collagen breakdown (MMP-1, MMP-9). The Hickson 2019 trial documented reduced skin senescent-cell load after D+Q. Pair with the collagen-rebuild stack from /collections/beauty-anti-aging.

Who this is NOT for

• Anyone under 18 (no data, no rationale).
• Pregnancy or breastfeeding (pause the entire collection).
• Active cancer or current chemotherapy without oncology coordination.
• Anticoagulant or antiplatelet medication without prescribing-physician coordination.
• Adults under 35 without specific indication. Senolytic burden is low in this age range and the risk-benefit of the pulse-protocol pharmacology shifts unfavorably.
• Anyone unable to commit to the pulse-protocol cycling discipline. Senolytics are not a daily multivitamin; sporadic high-dose pulses without consistency produce neither the senescent-cell-clearance benefits nor a useful baseline anti-inflammatory effect.

Quality and sourcing standards

Every flavonoid in this collection passes the same five-test panel before any batch ships:

• Identity: HPLC fingerprint matched against trans-flavonoid reference standard (≥98% trans-Fisetin from Rhus succedanea; ≥95% Quercetin Dihydrate from Sophora japonica; ≥98% Apigenin from chamomile or parsley extract).
• Potency: HPLC quantitation against label claim; ±5% tolerance ceiling.
• Heavy metals: ICP-MS panel against California Prop 65 limits (lead ≤0.5 µg/day, mercury ≤0.3–0.7 µg/day, cadmium ≤4.1 µg/day, inorganic arsenic ≤10 µg/day).
• Microbial: USP <2021> aerobic plate count and USP <2022> absence of pathogens (E. coli, Salmonella, S. aureus).
• Pesticides and residual solvents: EU MRL pesticide panel + USP <467> residual-solvents panel for extraction-derived ingredients.

Manufacturing is cGMP 21 CFR Part 111 in U.S. or EU FDA-registered facilities. Per-batch CoA available on request to support@truehealthprotocol.health, citing the Lot # printed on the bottle base. See /pages/quality for full operational specification, /pages/ingredient-sourcing for the country-of-origin map, and /pages/our-science for the broader Hallmarks-of-Aging scientific framework underneath the catalog.

How to measure senolytic effects — biomarkers and at-home tracking

The senolytic field is unusual in that it has plausible at-home tracking signals plus accessible commercial biomarker tests, both of which can be deployed alongside a 6–12 month protocol.

At-home subjective tracking (free, immediate)

• Morning energy 1–10, journaled daily.
• Joint stiffness 1–10 (most-reported subjective shift in OA cohorts on F+Q monthly pulse).
• Recovery between training sessions (RPE at same workload, week over week).
• Skin texture / "glow" — photo log monthly under same lighting.
• Sleep architecture (Oura, Whoop, Apple Watch) — total sleep, deep-sleep %, HRV.

Standard lab biomarkers (insurance-covered or low-cost)

• Fasting glucose + HbA1c — insulin-resistance proxy.
• hsCRP — primary SASP-relevant inflammation marker; the Hickson 2019 and Justice 2019 trials both documented hsCRP shifts post-pulse.
• Comprehensive metabolic panel (CMP) — kidney function (eGFR, creatinine, BUN), liver enzymes (ALT, AST).
• Lipid panel — apoB if available, plus LDL, HDL, triglycerides.
• IL-6 — directly SASP-relevant if your lab offers it.

Specialized tests (commercial, $200–500)

• DNA-methylation age — TruDiagnostic DunedinPACE or Horvath/Hannum. Demidenko 2021 reported ~8-year shifts. Reassess at 6–12 months.
• p16^INK4a assay — limited commercial availability; check Cleveland HeartLab and specialty providers.
• Plasma SASP panel (IL-6, MMP-9, IL-8, MCP-1) — Genova / specialty labs.
• Whole-blood NAD⁺ — Jinfiniti or Genova; useful for the CD38-inhibitor pillar.

Common myths and corrections

Myth 1: "Senolytics should be taken daily for maximum effect."

Correction: the senescent-cell-clearance evidence is anchored to the hit-and-run pulse paradigm, not daily dosing. Daily dosing of low-dose flavonoids has its own (anti-inflammatory, antioxidant) rationale, but conflating that with the senolytic-clearance protocol misses the mechanism. The Mayo trials (Hickson, Justice) used 2–3 day pulses with multi-week off-intervals.

Myth 2: "Quercetin is the strongest senolytic."

Correction: Quercetin is the most-trial-validated senolytic in combination with Dasatinib. As a single agent without prescription Dasatinib, Fisetin has the broader-tissue-clearance profile (the Yousefzadeh 2018 screen result). At-home single-agent senolytic protocols anchor to Fisetin; Quercetin layers on top.

Myth 3: "Apigenin is a senolytic."

Correction: Apigenin is a SASP-modulator and CD38 inhibitor, not a primary senolytic. Wakita 2020, Nature Communications showed Apigenin blunts the SASP without forcing apoptosis — a different mechanism from Fisetin/Quercetin. This is why Apigenin is taken continuously, not pulsed, and why it sits in both this collection and the NAD⁺-Family collection.

Myth 4: "If I take Fisetin every day, I'll clear all senescent cells faster."

Correction: the SCAP networks senescent cells use are also used by some healthy cells in narrow windows (immune cells during certain phases of activation; some progenitor pools during regeneration). The pulse-and-rest paradigm exists partly to give those healthy populations a recovery window. Daily high-dose Fisetin has not been validated for safety in long-term human trials, and the rodent evidence used intermittent dosing.

Cost tiers — what each one buys you

• Tier 1 — Entry: Fisetin 500 mg × 60-cap bottle. ~10 monthly pulses (3 caps × 2 days) per bottle. The cheapest meaningful senolytic protocol available at-home.
• Tier 2 — Daily/monthly: Fisetin (monthly pulse) + Apigenin (daily) + NAD⁺ Pure Focus Drink or Longevity Stack Bundle (daily).
• Tier 3 — Advanced: Tier 2 plus continuous Quercetin, monthly F+Q pulse, Urolithin A for mitophagy, Spermidine for autophagy.
• Single-product alternative entry: the NAD+ Pure Focus Drink alone — daily NR + Resveratrol + PQQ + Quercetin baseline, single SKU, cleaner adherence.

Frequently asked questions

Should I take Fisetin or Quercetin if I'm just starting?

Fisetin. It has the broader tissue-clearance profile in the Yousefzadeh 2018 screen, the Mayo / SToMP-AD Phase II trial protocol uses it, and as a single-agent senolytic without prescription Dasatinib it has stronger rationale than Quercetin alone. Add Quercetin in Month 4–6 once you've confirmed Fisetin tolerance.

How often should I do the Fisetin pulse?

Every 4 weeks for the first 6 months. After 6 months, reassess: if subjective shifts have plateaued and biomarkers (hsCRP, IL-6) are normalized, drop to every 6–8 weeks. Most users settle at a monthly cadence indefinitely. Cycle frequency is the main lever for cost-control and the main lever for "don't run senolytic clearance harder than the body can replace."

Why high-dose pulse instead of daily low-dose?

Senolytic cell-clearance pharmacology is threshold-like — SCAP-inhibition concentration must climb above a threshold long enough to push senescent cells into apoptosis. Subthreshold daily dosing produces SASP-modulation effects but not clearance. The two paradigms are biologically distinct.

Can I take Fisetin and Quercetin at the same time, like "F+Q"?

Yes, modeled on the "D+Q" trial regimen but with Fisetin replacing prescription Dasatinib. Standard end-user F+Q pulse: Fisetin 1.5 g + Quercetin 1.0 g, both for 2–3 consecutive days, monthly. The rationale: the two flavonoids hit overlapping but non-identical SCAP networks, and the combo gives broader tissue coverage than either alone.

Can I take Apigenin every day forever?

Yes, Apigenin's continuous-dose paradigm is well-supported and there's no published ceiling on long-term use at 50–100 mg/day. The CD38-inhibitor and SASP-modulator activities are both useful as a daily baseline alongside an NAD⁺-precursor stack.

Should I cycle off senolytics?

Short answer: yes. The Mayo paradigm is "hit-and-run, then rest" — the off-cycle is part of the protocol. End-users running monthly Fisetin pulses do not need a separate cycling-off; the 26-day gap between pulses is the rest-cycle. Users running the more aggressive Tier-3 with daily Quercetin and continuous Apigenin should plan a 2–4 week senolytic-free window every 3–4 months for biomarker reassessment.

Will this affect my exercise performance?

Justice 2019 (IPF) reported improvement in 6-minute walk, gait speed, and chair-stand after D+Q. Typical end-user pattern: 24–48 hours of mild fatigue on pulse Day 1–2, then a 4–7 day window of cleaner recovery. Schedule pulses outside of competition blocks.

Why is Quercetin in the NAD⁺ Pure Focus Drink at sub-senolytic doses?

Because the daily Quercetin exposure (250 mg/day in the drink) is not a senolytic-pulse dose but a SASP-modulator and antihistamine-cofactor dose. The drink is designed as a daily NAD⁺-precursor delivery vehicle with the bonus of low-grade flavonoid exposure across the 30-day cycle. The senolytic-pulse protocol layers on top with the pulse-dose Fisetin once a month.

Does Quercetin help with allergies?

Yes — at the 500 mg/day continuous dose, Quercetin has documented mast-cell-stabilizer and antihistamine activity (Boots 2008; multiple subsequent trials in seasonal-allergic-rhinitis cohorts). This is one of the reasons Quercetin earns its place in the daily-dose protocol layer even though Fisetin is the primary senolytic-pulse active.

Can I take this with NMN or NR?

Yes — and you should. Apigenin's CD38-inhibitor activity directly raises the NAD⁺-pool ceiling that NMN or NR can reach. The senolytic clearance also reduces the SASP-driven CD38 upregulation that drains NAD⁺ in the first place. The two stacks (this collection + NAD+ Family) are complementary by design — see the Stacking section above.

What about Spermidine and autophagy — is that the same thing as senolytics?

Different mechanism. Spermidine activates autophagy — the cellular "recycling" system inside still-functional cells (proteasome and lysosome turnover of damaged proteins, organelles, and aggregates). Senolytics clear cells whose autophagy machinery has already failed past the point of recovery. The two are sequential and complementary: autophagy cleans up damaged contents inside healthy cells; senolytics clear cells themselves when autophagy can't keep up. See Autophagy Explained for the full mechanism.

Are these vegan / vegetarian?

All four products are vegan: HPMC (vegetable cellulose) capsules; plant-extract-derived flavonoids (Sophora japonica, Rhus succedanea, chamomile/parsley); fruit-derived flavor/sweetener in the drink. BioPerine cofactor is from black pepper.

How do I store senolytics?

Cool, dry, dark — standard flavonoid-stability rules. Refrigeration not required for capsule formats. Drink-mix sticks: kept cool and dry; do not pre-mix water and let sit (NR oxidizes within ~1 hour in solution).

Returns?

30-day money-back on opened or unopened bottles. See refund policy and our guarantee.

Reading list and primary references

1. Hayflick L, Moorhead PS. The serial cultivation of human diploid cell strains. Experimental Cell Research. 1961;25:585–621.
2. López-Otín C, et al. The Hallmarks of Aging. Cell. 2013;153(6):1194–1217. (Updated: Cell. 2023;186(2):243–278.)
3. Baker DJ, Childs BG, Durik M, et al. Naturally occurring p16Ink4a-positive cells shorten healthy lifespan. Nature. 2016;530:184–189.
4. Childs BG, Gluscevic M, Baker DJ, et al. Senescent cells: an emerging target for diseases of ageing. Nature Reviews Drug Discovery. 2017;16(10):718–735.
5. Coppé JP, et al. Senescence-associated secretory phenotypes reveal cell-nonautonomous functions of oncogenic RAS and the p53 tumor suppressor. PLoS Biology. 2008;6(12):e301.
6. Xu M, Pirtskhalava T, Farr JN, et al. Senolytics improve physical function and increase lifespan in old age. Nature Medicine. 2018;24(8):1246–1256.
7. Tchkonia T, Morbeck DE, Von Zglinicki T, et al. Fat tissue, aging, and cellular senescence. Aging Cell. 2010;9(5):667–684.
8. Zhu Y, Tchkonia T, Pirtskhalava T, et al. The Achilles' heel of senescent cells: from transcriptome to senolytic drugs. Aging Cell. 2015;14(4):644–658.
9. Yousefzadeh MJ, Zhu Y, McGowan SJ, et al. Fisetin is a senotherapeutic that extends health and lifespan. EBioMedicine. 2018;36:18–28.
10. Hickson LJ, et al. Senolytics decrease senescent cells in humans: Preliminary report from a clinical trial of Dasatinib plus Quercetin in diabetic kidney disease. EBioMedicine. 2019;47:446–456.
11. Justice JN, Nambiar AM, Tchkonia T, et al. Senolytics in idiopathic pulmonary fibrosis: Results from a first-in-human pilot study. EBioMedicine. 2019;40:554–563.
12. Lim H, Park H, Kim HP. Effects of flavonoids on SASP formation from bleomycin-induced senescence in BJ fibroblasts. Biochemical Pharmacology. 2015;96(4):337–348.
13. Wakita M, et al. A BET family protein degrader provokes senolysis by targeting NHEJ and autophagy in senescent cells. Nature Communications. 2020;11(1):1935.
14. Escande C, et al. Flavonoid Apigenin is an inhibitor of the NAD+ase CD38. Diabetes. 2013;62(4):1084–1093.
15. Tarragó MG, et al. A potent and specific CD38 inhibitor ameliorates age-related metabolic dysfunction by reversing tissue NAD+ decline. Cell Metabolism. 2018;27(5):1081–1095.
16. Camacho-Pereira J, et al. CD38 dictates age-related NAD decline and mitochondrial dysfunction through an SIRT3-dependent mechanism. Cell Metabolism. 2016;23(6):1127–1139.
17. Schafer MJ, et al. Cellular senescence mediates fibrotic pulmonary disease. Nature Communications. 2017;8:14532.
18. Jeon OH, et al. Local clearance of senescent cells attenuates post-traumatic osteoarthritis and creates a pro-regenerative environment. Nature Medicine. 2017;23(6):775–781.
19. Bussian TJ, et al. Clearance of senescent glial cells prevents tau-dependent pathology and cognitive decline. Nature. 2018;562(7728):578–582.
20. Zhang P, et al. Senolytic therapy alleviates Aβ-associated oligodendrocyte progenitor cell senescence and cognitive deficits in an AD model. Nature Neuroscience. 2019;22(5):719–728.
21. Trammell SA, et al. Nicotinamide riboside is uniquely and orally bioavailable in mice and humans. Nature Communications. 2016;7:12948.
22. Martens CR, et al. Chronic nicotinamide riboside supplementation is well-tolerated and elevates NAD+ in healthy middle-aged and older adults. Nature Communications. 2018;9(1):1286.
23. Howitz KT, et al. Small molecule activators of sirtuins extend Saccharomyces cerevisiae lifespan. Nature. 2003;425(6954):191–196.
24. Chowanadisai W, et al. PQQ stimulates mitochondrial biogenesis through CREB phosphorylation and increased PGC-1α expression. Journal of Biological Chemistry. 2010;285(1):142–152.
25. Boots AW, Haenen GR, Bast A. Health effects of quercetin: from antioxidant to nutraceutical. European Journal of Pharmacology. 2008;585(2-3):325–337.
26. Khan N, et al. Fisetin: a dietary antioxidant for health promotion. Antioxidants & Redox Signaling. 2013;19(2):151–162.
27. Hwang HV, et al. Quercetin and senolytic effect on aged endothelial progenitor cells. Mechanisms of Ageing and Development. 2018;176:36–46.
28. Demidenko O, et al. Rejuvant conferred an average 8-year reduction in biological aging in the TruAge DNA methylation test. Aging. 2021;13(22):24485–24499.

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These statements have not been evaluated by the Food and Drug Administration. These products are not intended to diagnose, treat, cure, or prevent any disease. Information on this page is educational and reflects the published research literature on cellular senescence and senolytic compounds; it is not medical advice and is not a substitute for diagnosis or treatment by a qualified healthcare provider. Pregnant or nursing women, anyone with a medical condition, anyone on medication, and anyone scheduled for surgery should consult a qualified healthcare provider before using any product in this collection.