LongevityProxofimFOXO4 D-Retro-Inverso peptide

FOXO4-DRI

Senolytic peptide · one mouse paper · zero human trials

FOXO4-DRI is a senolytic peptide — a molecule designed to selectively kill 'senescent' cells, the worn-out 'zombie' cells that accumulate with age and secrete inflammatory signals. Its reputation as an anti-aging breakthrough is real in the lab but narrow in scope: essentially the entire edifice rests on one landmark paper, Baar and colleagues in the journal Cell in 2017, performed in mice and cells, not people. In that study the peptide cleared senescent cells and, in aged mice, restored running-wheel fitness, fur density, and some kidney-function markers. The mechanism it established is genuine: in senescent cells the protein FOXO4 holds the 'cell-suicide' protein p53 captive in the nucleus, keeping the zombie cell alive; FOXO4-DRI competitively breaks that grip, freeing p53 to trigger the cell's self-destruction. The honesty problem is everything downstream of the mouse data. There are zero completed or registered human clinical trials, no established human dose, and no human safety data of any kind — every 'human protocol' circulating on vendor and forum sites is invented. Follow-up research is thin: a small aged-mouse study on testosterone-producing cells and an in-vitro human-cartilage-cell study, both consistent with the senolytic mechanism but neither confirming the headline rejuvenation claim. Importantly, the peptide works by deliberately activating p53 to cause apoptosis, which carries obvious theoretical risks (off-target cell death, systemic p53 activation) that no human data can currently rule out. The defensible statement is 'a real senolytic mechanism demonstrated in mice'; 'anti-aging in humans' is extrapolation, not a finding.

The short version

As we age, some cells stop dividing but refuse to die — they linger in a state called senescence, often described as 'zombie cells,' and they pump out inflammatory signals that damage the tissue around them. 'Senolytics' are compounds meant to selectively clear these cells. FOXO4-DRI is one such senolytic peptide, and it became famous after a single 2017 mouse study suggested that clearing senescent cells could reverse some signs of aging.

The mechanism it demonstrated is genuinely clever. In a senescent cell, a protein called FOXO4 grabs hold of p53 — the cell's master 'self-destruct' switch — and keeps it locked in the nucleus, so the zombie cell never gets the signal to die. FOXO4-DRI is engineered to wedge into that grip and break it, releasing p53 to do its job and push the senescent cell into apoptosis (programmed death). Because normal cells don't lean on this FOXO4 trick, the effect is comparatively selective for the zombie cells.

Here is what honesty requires. That whole story — and the famous results of restored fur, fitness, and kidney markers — happened in mice. There are no completed or even registered human clinical trials for FOXO4-DRI, no established human dose, and no human safety data at all. Any 'human protocol' you find online was invented, not derived from a study. The handful of follow-up papers are small and narrow (a mouse study on testosterone cells, a cell-dish study on human cartilage cells) and support the mechanism without confirming the big 'rejuvenation' claim. And because the peptide works by switching on p53 to kill cells, it carries obvious theoretical risks that simply haven't been tested in people. The fair takeaway: a real senolytic mechanism shown in mice — and an unproven, unstudied compound in humans.

Molecular identity

Specs

Molecular formula: C₂₂₈H₃₈₈N₈₆O₆₄ (free base)
Molecular weight: ≈5358 g/mol (free base)
Monoisotopic mass: ≈5354.98 Da (free base)
PubChem CID: 167312269

Class: Synthetic D-retro-inverso (DRI) senolytic peptideBaar et al., Cell 2017 (PMID 28340339)
Sequence: Not published — FOXO4 p53-interface-derived; vendor letter sequences are internally inconsistent and unverified against the primary paperBaar et al., Cell 2017 (sequence not in accessible text)
Molecular target: FOXO4–p53 interaction (binds the disordered p53 transactivation domain) — frees p53 → apoptosis of senescent cellsBaar et al., Cell 2017 (PMID 28340339); PMID 40593617
Design: Sequence reversed + every L-amino acid swapped to its D-form → protease-resistant, longer in-vivo half-life; carries a cell-penetrating elementBaar et al., Cell 2017 (PMID 28340339)
Half-life: Not established (no published quantitative pharmacokinetics; DRI design is protease-resistant but no numeric half-life is reported, and there is no human data)Not established
Regulatory status: Not approved anywhere; research chemical only; no registered human trialRegulatory record; ClinicalTrials.gov (no records)

Plain English

Mechanism

The mechanism has four steps, all established in the 2017 study. First, as cells become senescent they over-produce the protein FOXO4, which concentrates in the nucleus. Second, FOXO4 binds p53 and keeps it sequestered in the nucleus, blocking p53 from moving to the mitochondria — the step that would otherwise trigger the cell's intrinsic self-destruct (apoptosis). This sequestration is a survival trick that lets stressed senescent cells persist instead of dying.

Third, FOXO4-DRI competitively disrupts the FOXO4–p53 interaction: the peptide occupies the binding interface and frees p53 from FOXO4's grip. Fourth, the released p53 drives mitochondrial apoptosis — and because the dependence on FOXO4-mediated p53 sequestration is a feature of senescent cells specifically, the killing effect is comparatively selective for them over healthy cells.

The 'DRI' design is what makes this practical: D-retro-inverso means the amino-acid sequence is reversed and every building block is switched from the natural L-form to the mirror-image D-form. This roughly preserves the shape that lets it mimic the natural binding geometry while making the backbone resistant to the body's protein-cutting enzymes, dramatically extending its in-vivo life. One firm boundary for the reader: steps one through four are an established mechanism, but statements like 'clears senescent cells to reverse aging in humans,' 'regrows hair,' or 'rejuvenates skin' are extrapolated benefits, not demonstrated outcomes.

Sources:PMID 28340339

Why people reach for it

Potential benefits

FOXO4-DRI is the peptide behind the 'clear your zombie cells' senolytic idea. Here's what draws people to it — with the blunt caveat that essentially the entire story is one mouse paper, with zero human trials.

A clever, targeted senolytic mechanism — It's designed to selectively kill senescent 'zombie' cells by breaking FOXO4's grip on p53 — freeing p53 to push those cells into self-destruction, a genuinely elegant mechanism established in the 2017 study.
Comparatively selective for senescent cells — Healthy cells don't lean on the FOXO4–p53 survival trick the way senescent cells do, so in the mouse and cell work the killing effect was comparatively selective for the worn-out cells over normal ones.
Reversed some aging signs — in mice — In the foundational study, clearing senescent cells restored running-wheel fitness, fur density, and some kidney-function markers in aged mice — the result that made it famous (mouse data, not human outcomes).
Pulsed, not daily — a low-frequency protocol — Senolytics are dosed 'hit-and-run': a short burst then a long gap, so it's used far less often than a daily peptide — the cycle structure, not daily commitment, is the whole model.

Sources:PMID 28340339 PMID 31959736 PMID 33996787

What people reach for FOXO4-DRI for, drawn from what the research reports and how it's used — not proven outcomes or medical claims. The decisive caveat: essentially the entire reputation rests on one 2017 mouse-and-cell paper — there are zero human trials, no established human dose, and no human safety data, and it works by deliberately activating p53 to kill cells.

Implied timing

Best time to dose

Implied best time

Anytime (pulsed cycles)

For FOXO4-DRI the lever isn't the hour of the day — it's the pulse pattern: a short 'hit-and-run' burst to clear senescent cells, then a long gap, not daily or continuous use.

Senolytics are dosed in bursts because senescent cells accumulate slowly: a short clearance pulse removes the current load, and continuing to dose adds no benefit (there's nothing left to clear) while multiplying the risk of off-target p53 activation. The Baar 2017 schedule — 3 doses over 5 days — encodes this 'burst then stop' logic.
Between pulses the convention is a long gap — most often cited as roughly one pulse per quarter (every ~3 months), reasoning from slow senescent-cell accumulation; the gap, not the time of day, is the meaningful timing decision.
Within a pulse there's no circadian or pharmacokinetic basis to prefer any hour; on each injection day a consistent clock time is just a practical anchor, and the reasonable practice is to reassess inflammatory markers and recovery during each gap before deciding on another pulse.

No study establishes an ideal time of day for FOXO4-DRI — and for a pulsed senolytic the within-day hour isn't the point. What matters is the intermittent cycle structure: a short pulse, then a long washout. Within a pulse, any consistent time on each injection day is fine.

How to run it

Dosing & protocol

FOXO4-DRI is dosed here as a subcutaneous injection — the form sold as a research peptide and the route the on-page calculator is built for. The only published dose data come from a single mouse study (Baar 2017, IV) and one follow-up (Zhang 2020, IP). There is no established human dose and no human trial. Every number below is anchored to that animal data and to subcutaneous community convention, extrapolated — not validated. Read this as a map of the reference doses and how people actually approach them, not a human protocol.

Everything here rests on essentially one mouse paper. There are zero registered human trials, no human dose-finding study, and no human safety data. Any number below is an animal-anchored reference or community extrapolation, not an established human protocol — and this is a peptide that kills cells by activating p53.

Trial-anchored reference dose

The only peer-reviewed doses for FOXO4-DRI are animal figures — report them as exactly that.

Foundational study (Baar 2017):: 5 mg/kg, administered three times on an every-other-day schedule (days 1, 3, and 5), by intravenous injection in aged and fast-aging mice. This is the sole dose figure with published outcomes — restored running-wheel fitness, fur density, and renal-function markers in aged mice.
Follow-up (Zhang 2020):: Same dose and schedule — 5 mg/kg × 3, every other day — but delivered intraperitoneally in aged mice targeting senescent Leydig (testosterone-producing) cells. Raised serum testosterone and lowered p53/p21/p16 markers.
Human equivalent — honest status:: No validated human equivalent exists. Forum calculations converting 5 mg/kg mouse IV to a human subcutaneous dose are unanticipated extrapolations with no pharmacokinetic grounding for this compound. They are not reproduced here as if they carry study authority.

Subcutaneous administration

In human research-peptide use, FOXO4-DRI is administered subcutaneously — injected into the fat layer just under the skin.

Injection site:: The abdomen (two to three inches clear of the navel), the love-handle area, or the outer thigh. Rotate sites across doses to avoid local irritation or lipohypertrophy (fatty lumps from repeated use at one spot).
Measuring the dose:: Drawn on a U-100 insulin syringe from the reconstituted vial. The reconstitution card below gives syringe units at the calculator's default mix; the on-page calculator handles any vial size. There is no human-validated dose range — the calculator defaults (10 mg vial, 2 mL BAC water, 1,000 mcg dose) are research placeholders, not clinical targets.
Time of day:: No timing rationale exists for this compound — no circadian or pharmacokinetic data in humans, and the within-day hour isn't the lever (the pulse structure is). Given the pulsed (not daily) schedule, a consistent clock time on each injection day is the practical anchor. See Best time to dose above.
Food window:: Subcutaneous injection bypasses gut absorption, so food timing has no known relevance to FOXO4-DRI. Inject independent of meals.

Cycle & washout — senolytics are pulsed, not continuous

The defining feature of senolytic dosing is that it is 'hit-and-run': a short burst to clear senescent cells, then a long gap — not daily or continuous use. This is the most important structural difference between FOXO4-DRI and most peptides in this library.

Why pulsed?:: Senescent cells accumulate slowly. A short clearance pulse removes the current load; continuous dosing would offer no additional benefit (there is nothing left to clear) while multiplying the risk of off-target p53 activation in healthy cells. The Baar 2017 protocol — 3 doses over 5 days — encodes this 'burst then stop' logic.
Pulse duration (animal-anchored reference):: The foundational protocol was 3 injections over 5 days (days 1, 3, 5) — alternating days so the body has brief recovery windows between doses. This is a research schedule, not a validated human regimen.
Gap between pulses:: No human data exists for re-dosing interval. The community convention most often cited is one pulse per quarter (every 3 months) — reasoning that senescent-cell accumulation is slow and matches seasonal reassessment. Some protocols reference every 4–6 months. These are convention, not study findings.
Assessment windows:: Given the theoretical risk profile, the reasonable practice is to reassess during each gap: inflammatory markers (hs-CRP, IL-6), general bloodwork, and subjective recovery before deciding whether a subsequent pulse is warranted.

Reconstitution at a glance

The on-page calculator does this live; the quick reference for the default 10 mg vial with 2 mL bacteriostatic water:

Mixing:: 10 mg vial + 2 mL bacteriostatic water = 5,000 mcg per mL. On a 100-unit (1 mL) U-100 insulin syringe: 500 mcg = 10 IU · 1,000 mcg = 20 IU · 1,500 mcg = 30 IU · 2,000 mcg = 40 IU.
Why these numbers matter here:: Because FOXO4-DRI is dosed in pulses — not daily — each vial lasts considerably longer than a daily-use peptide. A 10 mg vial covers 10 × 1,000 mcg doses (10 pulse injections), or 3–4 complete three-dose pulse cycles.

Sources:PMID 28340339 PMID 31959736

Substrate the signal needs

Nutritional cofactor precision

FOXO4-DRI's job is demolition — it clears senescent cells. The useful cofactors address what comes after: giving the body the substrate to rebuild once zombie cells are cleared, and maintaining the antioxidant environment that supports both the clearance and the repair. There is no FOXO4-DRI cofactor study; this is mechanistic reasoning applied to a peptide whose human effects are entirely unproven.

Reasoned from the senolytic mechanism (clearance → repair → antioxidant support) and general longevity nutrition — not a FOXO4-DRI cofactor study. The compound itself has zero human trial data; these are the inputs that a clearance mechanism would logically sit on.

Supply the repair substrate — protein + collagen precursors

Clearance removes worn-out cells; rebuilding replaces them. Post-clearance tissue repair draws on the same raw material as any structural recovery.

Protein:: ~1.6 g per kilogram of body weight per day (roughly 0.7 g/lb) — the standard reference point for active tissue maintenance and repair. Insufficient protein leaves a clearance signal with nothing to build on.
Vitamin C:: 500–1,000 mg/day — rate-limiting cofactor for collagen synthesis (hydroxylation of proline and lysine residues). Connective tissue and skin matrix repair both depend on it; absent FOXO4-DRI specificity, this is standard repair-substrate logic.
Glycine:: 3–5 g/day (from collagen peptides or pure powder) — glycine is the most abundant amino acid in collagen and a direct substrate for extracellular matrix rebuilding. Complements vitamin C in the collagen-synthesis chain.
Timing:: With meals across the day for protein; vitamin C and glycine can be taken once daily at any time.

Amplify — antioxidant and anti-inflammatory base

Senescent cells are defined by chronic oxidative stress and a pro-inflammatory secretome (the SASP — senescence-associated secretory phenotype). Maintaining a strong antioxidant base supports both the clearance environment and tissue health during the washout gap.

Quercetin:: 500–1,000 mg/day (as quercetin phytosome or isoquercetin for better absorption) — independently studied as a senolytic in its own right; also a potent NF-κB inhibitor and antioxidant. Quercetin is among the community's most-cited senolytic companions (mechanism convergence, not a co-study with FOXO4-DRI).
Fisetin:: 100–200 mg/day — plant flavonoid from strawberries and apples; discussed in longevity research as a senolytic via independent pathways (Bcl-2 family inhibition, AMPK activation). Often cycled in pulses alongside quercetin for the same 'hit-and-run' rationale.
Omega-3 (EPA/DHA):: 2–3 g/day combined — EPA and DHA dampen the SASP's pro-inflammatory output via competitive suppression of arachidonic-acid-derived eicosanoids. An anti-inflammatory diet pattern (colorful vegetables, polyphenols) extends this in the same direction.
Timing:: Quercetin and fisetin are best absorbed with a small amount of fat (take with meals). Omega-3 with the largest meal of the day.

Mitigate — minimal known; flag the real gap

FOXO4-DRI has no established human side-effect profile, so 'mitigate' cannot name a specific pharmacological cost to offset. The honest position is that the mitigation question is unanswerable from current data.

What is known:: In the 2017 mouse study, the peptide was described as well-tolerated with selectivity for senescent over healthy cells. There is no documented human side-effect pattern because there are no human studies.
Theoretical concern — p53 activation:: The mechanism deliberately activates p53 to drive apoptosis. Off-target p53 activation in healthy, non-senescent cells is the primary theoretical risk — not currently mitigatable by any known cofactor because the risk itself is unmeasured. This is why the pulsed ('hit-and-run') schedule and long washout gaps are the structural mitigation the research community defaults to.
Supply chain risk:: Research-grade FOXO4-DRI has no regulatory purity or sterility guarantee. This risk is independent of any cofactor and is addressed only by sourcing and COA diligence — not supplementation.

Combinations + timing

Stacking notes + timing windows

FOXO4-DRI's stacking conversation is almost entirely the longevity community's senolytic stack — flag this hard up front: the entire category is hypothesis-stage. These are community combinations assembled from shared mechanism (clear senescent cells), not regimens studied head-to-head, and certainly not studied with FOXO4-DRI in humans. 'Clear senescent cells to reverse aging' is still hypothesis-stage even for FOXO4-DRI alone.

All stacks below are hypothesis-stage — reasoned from complementary mechanisms, assembled by the longevity community, zero head-to-head human data. FOXO4-DRI itself has no human trial; every stack is doubly unproven. Stacking multiple pro-apoptotic, p53-adjacent agents could compound untested off-target risks just as plausibly as it amplifies benefit.

FOXO4-DRI + Quercetin

The most natural senolytic pairing — two mechanistically distinct clearance routes, both hypothesis-stage in humans.

Why it works:: FOXO4-DRI disrupts the FOXO4–p53 interaction to push senescent cells into apoptosis via p53 release. Quercetin independently promotes senescent-cell death via Bcl-2 family inhibition (blocking a different survival signal) and is also an NF-κB brake and antioxidant. Two different death-signal levers on the same zombie cell — mechanistically complementary, not redundant.
The protocol:: FOXO4-DRI on the pulsed schedule (3 injections over 5 days, ~quarterly). Quercetin 500–1,000 mg/day as quercetin phytosome or isoquercetin — either run continuously as a base or pulsed in the days surrounding the FOXO4-DRI pulse. Both are convention, not study regimens.
Outcome:: The community combination users reach for on general senolytic / longevity-maintenance goals. Flag honestly: neither compound has confirmed efficacy in human aging, and their combination has no human data at all.

FOXO4-DRI + Fisetin

A second distinct-mechanism senolytic companion — adds AMPK and Bcl-2 angles to the FOXO4-DRI p53 route.

Why it works:: Fisetin (a flavonoid from strawberries) promotes senescent-cell clearance via AMPK activation and Bcl-2 inhibition — again, mechanistically distinct from FOXO4-DRI's p53-release mechanism. It also has antioxidant and anti-inflammatory properties that support the post-clearance recovery environment. Often combined with quercetin; adding FOXO4-DRI layers the peptide's direct-peptide route on top.
The protocol:: FOXO4-DRI on the pulsed schedule. Fisetin 100–200 mg/day with meals (fat-soluble; take with food), either as a continuous base or pulsed in a short burst (1–3 days) around the FOXO4-DRI injection window — the latter matches the 'hit-and-run' logic both compounds share.
Outcome:: Reached for on longevity / cellular-age-maintenance goals. Hypothesis-stage; no human data for the combination.

FOXO4-DRI + NAD⁺ support

A mito-longevity pairing — senolytic clearance + cellular energy restoration are complementary phases of the same longevity hypothesis.

Why it works:: Senescent cells suppress NAD⁺ levels in surrounding tissue via SASP-driven CD38 activation (a NAD⁺-consuming enzyme). Once senescent cells are cleared, restoring cellular NAD⁺ — via NMN or NR — supports mitochondrial biogenesis and sirtuin activity in the cells that remain. Clearance and NAD⁺ restoration are logically sequential: clear the zombie cells first, then replenish the energy metabolism they were suppressing. See NAD+ for the NAD⁺ biology.
The protocol:: FOXO4-DRI on the pulsed schedule. NAD⁺ precursor (NMN 500–1,000 mg/day or NR 250–500 mg/day) run as a base, not pulsed — NAD⁺ restoration is a continuous cellular nutrition goal, not a clearance pulse.
Outcome:: The longevity-community stack that combines 'remove the old cells' (FOXO4-DRI) with 'restore energy biology in what remains' (NAD⁺). Hypothesis-stage; mechanistically coherent; no human co-study data.

Reconstitution math

Reconstitution calculator

Calculated for a 1 mL U-100 insulin syringe (100 units/mL).

Peptide per vial

BAC water added

Desired dose

Units per dose

Draw to this mark on a U-100 syringe

Volume per dose: 0.2 mL
Doses per vial: 10
Concentration: 5 mg/mL

One vial lasts

Daily: 10 days
Every other day: 20 days
5×/week: 14 days

Research use only. Not for human consumption. Outputs are reference values based on research literature — verify all measurements independently.

From the studies

Side effects from research

There is no human safety data of any kind for FOXO4-DRI — no clinical trial has characterized its tolerability, adverse effects, or risks in people. That absence is the headline safety fact.

In the 2017 mouse work, dosing was described as well-tolerated and the peptide showed selectivity for senescent over normal cells in the systems tested. But that is a mouse-and-cell result, and selectivity in mice does not guarantee a safe therapeutic window in humans.

The mechanism itself is the basis for the main theoretical concern: FOXO4-DRI works by deliberately activating p53 to drive apoptosis, so systemic or off-target p53 activation could in principle harm healthy, non-senescent cells. Off-target cell death and tissue toxicity are plausible and untested in humans. On top of that, the research-chemical supply chain adds identity, purity, and sterility risks. Any claim of an established human safety profile is false — the honest statement is that human safety is entirely unknown.

As reported in literature

Research dosing ranges

There is no human dosing table, because no human trials exist. The rows below summarize the actual preclinical evidence — one foundational mouse study plus thin mouse/in-vitro follow-up — so the absence of human data is unmistakable. No dose, route, or schedule here is a human regimen, and the verified negative finding (no registered human trial) is itself part of the record.

Dose	Route	Model	Outcome	Sources:
5 mg/kg, 3× every other day	IV	Mouse — Baar 2017, fast-aging + naturally aged + chemotoxicity (foundational)	Selectively cleared senescent cells; restored running-wheel fitness, fur density, and renal-function markers; neutralized doxorubicin chemotoxicity — well tolerated in mice	PMID 28340339
5 mg/kg, 3× every other day	IP	Mouse — Zhang 2020, aged-mouse Leydig cells	Targeted senescent testosterone-producing cells and raised serum testosterone in aged mice; lowered p53/p21/p16 markers	PMID 31959736
In-vitro (no animals)	n/a	Cell culture — Huang 2021, expanded human chondrocytes	Removed >50% of late-passage senescent cartilage cells and lowered senescence markers, but did NOT improve their cartilage-forming potential	PMID 33996787
None	n/a	Human — ClinicalTrials.gov search	NO registered or completed human trial; no human dose, pharmacokinetics, or safety data exist	ClinicalTrials.gov (no records)

Quick answers

Frequently asked

Has FOXO4-DRI been tested in humans?

No. There are no completed human clinical trials and no registered ClinicalTrials.gov entry for FOXO4-DRI (or 'Proxofim'). There is no established human dose, no human pharmacokinetics, and no human safety data. Essentially its entire reputation rests on a single 2017 mouse-and-cell study.

Does it reverse aging?

It reversed some aging signs in mice — restoring fitness, fur density, and kidney markers in the 2017 study by clearing senescent cells. Whether any of that translates to humans is unknown and untested. Claims of human rejuvenation, hair regrowth, or skin rejuvenation are extrapolations from mouse data, not demonstrated outcomes.

What does 'DRI' mean and why does it matter?

DRI stands for D-retro-inverso: the peptide's amino-acid sequence is reversed and every building block is switched to its mirror-image D-form. This roughly preserves the binding shape while making the peptide resistant to the body's protein-cutting enzymes, so it survives longer in the body than an ordinary peptide would.

Is the sequence known?

Not reliably. The peptide is derived from the region of FOXO4 that binds p53, but the full one-letter sequence is not clearly spelled out in the accessible primary paper, and the letter sequences circulated by vendors are internally inconsistent — their residue counts don't match the verified molecular formula. We don't publish a specific sequence string because none is verified.

Is FOXO4-DRI banned in sport?

It is not specifically named on the WADA Prohibited List, but absence from the list is not clearance. WADA's catch-all provision for non-approved substances — any pharmacological substance with no current regulatory approval for human use — could plausibly apply to an unapproved research peptide. Athletes should treat it as high-risk and consult their anti-doping authority.

Primary sources

References

PMID 28340339Baar et al., Cell 2017 — targeted apoptosis of senescent cells restores tissue homeostasis (foundational mouse/cell study)
PMID 31959736Zhang et al., Aging (Albany NY) 2020 — FOXO4-DRI targets senescent Leydig cells and raises testosterone in aged mice
PMID 33996787Huang et al., Front Bioeng Biotechnol 2021 — FOXO4-DRI removes senescent cells from in-vitro expanded human chondrocytes
ClinicalTrials.gov (no records)ClinicalTrials.gov — search for FOXO4-DRI / Proxofim (no registered or completed human trial)
PubChem CID 167312269PubChem record — formula, MW, CID
WADA 2026WADA 2026 Prohibited List (FOXO4-DRI not individually named; status by inference)

Research use only · Not medical advice · Updated 2026-06-01