FOXO4-DRI: what the studies show, status and safety
Summary
FOXO4-DRI is a lab-made peptide designed to kill senescent cells, meaning cells that have stopped dividing but do not clear themselves away. Everything known about it comes from cells in dishes, from isolated tissue and from rodents, and above all from a single paper published in 2017. No study in people has ever been registered or published, and nobody has tested whether the peptide extends life in any species. A 2023 study found that clearing these cells in this way made blood flow through the lungs of mice worse.
Key findings at a glance
- A single mouse study from 2017 carries the whole field. It reported lower levels of the waste products urea and creatinine in the blood, denser fur and livelier reactions, both in old mice and in mice that age unusually fast [1].
- Not one registered study in people. A registry search on 6 September 2026 found nothing under FOXO4-DRI, Proxofim, Cleara Biotech or senolytic peptide [2].
- In a dish it hit worn-out cells about twelve times harder than healthy ones. The measured selectivity factor was 11.73 in human lung cells, and the same peptide built the ordinary way did nothing at all [1].
- Nobody has measured lifespan. Not in mice, not in any other creature. The founding paper looked at markers in tissue, not at how long the animals lived [1].
- A 2023 study reported harm. When senescent cells were cleared, with this peptide among the methods used, blood flow through the lungs of mice got worse and the animals lost cells from the lining of their lung vessels [3].
- Banned in sport around the clock. Category S0 covers substances that no health authority anywhere has approved [4].
- A 2026 review calls it clinically unproven. It notes that the cell-killing effect was shown in laboratory models and has never been confirmed in patients [5].
What it is
FOXO4-DRI is a fully lab-made peptide, a chain of 46 building blocks that are mirror images of the natural ones and are strung together back to front (D-amino acids in reverse order). One half copies a stretch of a human control protein called FOXO4. The other half is the TAT sequence from HIV, a positively charged module that ferries whatever is attached to it into cells [1]. Nothing of this kind occurs in the body.
A group at Erasmus University Medical Center in Rotterdam first described the peptide in March 2017, working together with laboratories in Graz and at the Buck Institute for Research on Aging [1].
Proxofim is a trade name used by sellers of research chemicals, and it carries no scientific or regulatory weight. It appears in no journal: a search of the PubMed literature database returns nothing for it. The entire scientific literature on the peptide itself amounts to 19 PubMed entries [6].
Quick facts
| Field | Value | Ref |
|---|---|---|
| Class | Lab-made peptide meant to kill senescent cells, built as a mirror image in reverse order (D-retro-inverso) | [1] |
| Structure | 46 mirror-image building blocks; a piece copied from FOXO4, joined to the TAT shuttle from HIV | [1], [7] |
| Sequence | ltlrkepaseiaqsileaysqngwanrrsggkrppprrrqrrkkrg, all in the mirror-image D-form | [1], [7] |
| Formula and mass | C228H388N86O64, 5,358 g/mol as calculated by PubChem | [7], [8] |
| CAS registry number | 2460055-10-9, listed on both PubChem entries | [7], [8] |
| PubChem CID | 168431240 and 167312269 | [7], [8] |
| UNII | None assigned | [7], [8] |
| Wikidata | Q136955527 | [9] |
| Trade designation | Proxofim, used by sellers, absent from the literature | [6] |
| How long it lasts in the body | No published value | [1] |
| Status | Laboratory stage only; no approval and no registered study in people | [2] |
| Where it came from | Erasmus MC Rotterdam, with Graz and the Buck Institute | [1] |
How it works
The whole idea rests on one single contact between two proteins, and that contact has never been measured inside a living person.
- FOXO4 keeps p53 locked away. In senescent cells, FOXO4 appears to hold the self-destruct protein p53 in small clumps inside the nucleus, so that it can no longer set off the cell suicide programme. That would make FOXO4 a kind of survival switch [1], [10].
- The peptide muscles in. Because it looks like FOXO4, the peptide may compete for the same spot on p53 and prise the pair apart. The freed p53 would then leave the nucleus and start the cell suicide programme, known as apoptosis [1].
- The target is a floppy piece of protein. Structural measurements in solution, using a method called NMR, place the binding site on a loose, shapeless stretch of p53 rather than on its firmly folded part, and the positively charged TAT module helps that binding along [11].
- A chemical tag acts as a switch. When p53 carries a small phosphate tag, it seems to bind both FOXO4 and the peptide more tightly, which may explain why cells carrying a lot of that tag at the spot called serine 15 respond [11].
- What happens next. Work on the main artery of aged mice describes the tagged p53 leaving the nucleus and then switching on the killer proteins BAX and caspase-3 [12].
- Getting inside the cell. The TAT module is described as carrying the peptide in without the cell spending energy on it; the peptide can be detected inside cells after two to four hours and stays there for at least 72 hours [1].
- Why the mirror-image build. Reversing the chain and using mirror-image building blocks keeps the shape the peptide needs, while making it much harder for the protein-cutting enzymes of the body to chop it up [1], [13].
This works quite differently from the growth factor and hormone-like peptides that fill most of this register. FOXO4-DRI imitates no messenger and switches on no receptor. It was built to prise apart a pair of proteins inside the cell.
What the studies found
Everything below comes from cells in a dish, from isolated tissue or from rodents. There is no line for people to report.
Counts as of 6 September 2026. The laboratory publications are the 19 PubMed entries found under the substance name. Sources [2], [6].
Senescent cells in culture
Cell culture Human lung cells, known as IMR90 fibroblasts, were pushed into senescence with radiation or with the chemotherapy drug doxorubicin. The peptide killed them while largely sparing the healthy comparison cells, roughly twelve times more selectively (a factor of 11.73), and the effect appeared after 24 to 36 hours. Two comparison peptides did nothing: the same sequence built in the ordinary way, and an unrelated peptide called FOXM1-DRI [1].
Aged and progeroid mice
Animal data In mice that age unusually fast, called XpdTTD/TTD mice, and in normal mice from 110 weeks of age, the waste products urea and creatinine dropped in the blood. The authors read the value measured 30 days after dosing as a sign that the kidneys were filtering properly again [1]. The fur of the animals also grew denser and they reacted more readily to gentle touch. Those last measures are soft ones that can only partly be put into numbers.
Chemotherapy toxicity in mice
Animal data In mice bred to glow wherever senescent cells build up, called p16::3MR reporter mice, and given two doses of doxorubicin, the peptide dimmed that glow. The rise of a liver enzyme in the blood, AST, and the weight loss were both less pronounced. The measurement of the glow rests on five animals [1].
Testis and fertility in rodents
Animal data Two papers from related groups report that the senescent cells which produce testosterone, called Leydig cells, died off in old mice [14], [15]. The same papers describe less of the age-related shortfall in testosterone and better sperm quality in those animals. Note which organ this is: these are studies of the testes, not of the prostate. No independent group has repeated them.
Lung, vessel and tumour models
Animal data Other groups report less scar tissue in mice whose lungs had been scarred with the drug bleomycin, on a par with the approved drug pirfenidone [16], and tumours that responded better to radiation while the surrounding lung scarred less [17]. In newborn rats kept in 95% oxygen, dosing on four days after birth lowered the markers of senescence [18]. A correction to the 2022 lung scarring paper was published in 2024 [16].
Animal data In naturally old mice and in fast-ageing mice, injections held back the ageing of the main artery and improved how well it worked [12]. In laboratory work on the brain tumour glioblastoma, the peptide served as a tool to strip out senescent tumour cells alongside the chemotherapy drug temozolomide [19].
Human tissue, not humans
Ex vivo Overgrown scar tissue, known as keloid, kept alive in the laboratory, and the cells grown from it, showed dying cells and fewer cells resting between divisions, with the form of p53 tagged at serine 15 pushed out of the nucleus [20]. This is donated tissue in a dish. No patient was treated.
Negative and contrary results
Ex vivo In human cartilage cells that had been multiplied many times in the laboratory, the peptide removed more than half of the most-divided cells while leaving the fresher ones alone. The hoped-for benefit did not follow: treating the cells beforehand did not improve their ability to form cartilage, and the authors call the value of the approach for cartilage an open question [21].
Animal data The clearest signal pointing the other way comes from 2023. In several mouse models of high blood pressure in the lung vessels, clearing senescent cells, this peptide among the methods, changed the blood flow for the worse and cost the animals cells from the lining of those vessels. The authors conclude that removing senescent cells from the lung lining can make blood flow through the lungs worse [3].
What is still unknown
- Everything about people. Nothing is known about how the body takes the peptide up and clears it again, what dose a person could tolerate, where it ends up in the body or what it does to any measurable outcome in a patient [2], [5].
- The guard against tumours. The mechanism cuts straight into p53, the protein that keeps damaged cells in check. A 2026 review asks explicitly for that risk to be examined; nobody has done it [5].
- Long-term toxicity. No such study exists in any species. The original authors themselves named a thorough analysis as still missing [1].
- Independent repetition. No group unconnected with the original authors has repeated the 2017 animal work in the same way.
- Immune reactions. A construct of 46 building blocks that carries a sequence from a virus has never been tested for the immune response it might provoke.
- The lung signal. The 2023 finding has never been followed up systematically in another model [3].
Side effects and safety
There is no list of side effects, because nobody has taken the peptide in a study. That no harm has been reported here means only that nobody has looked, not that the substance is safe [2].
- How well mice tolerated it was only a first impression. Body weight and kidney weight stayed the same, and the authors themselves wrote that a more thorough analysis is required [1].
- Blood flow through the lungs got worse. In one mouse strain, clearing senescent cells with this peptide among the methods changed that blood flow and destroyed cells from the lining of the vessels [3].
- p53 is the brake the body puts on tumours. Disturbing it again and again has unknown consequences for cancer risk, and no study has looked [5].
- The TAT module carries a strong positive charge. Shuttle sequences of that kind are known to tear holes in cell membranes once they get concentrated enough. No systematic toxicity work covers this particular construct [1], [11].
- Nobody has checked the material sold under this name. No authority has examined the purity, the impurities, the bacterial residues or the shelf life of anything on the market [22].
The gaps in the data are the safety picture. There is no work on effects on fertility or offspring, nothing on interactions with other substances, no cancer study and no pharmacopoeia entry. Nothing on record supports a judgement about the risk to people, in either direction.
Doses used in studies
These are the doses used in the cited studies, listed for reference. They are not a recommendation.
Every line in the table comes from a rodent, from a piece of tissue or from a dish of cells. There is no human dose for this substance, because there is no human study [2].
| Study | Model | Dose | Route | Frequency | Ref |
|---|---|---|---|---|---|
| Baar 2017, fast-ageing mice | XpdTTD/TTD mice, p16::3MR reporter strain | 5 mg/kg | Intraperitoneal | Days 1, 3 and 5 | [1] |
| Baar 2017, naturally aged mice | p16::3MR mice from 110 weeks | 3 × 5 mg/kg | Intraperitoneal | Every other day, readout at 30 days | [1] |
| Baar 2017, chemotherapy damage | p16::3MR mice after doxorubicin | 5 mg/kg | Intraperitoneal | Every other day over five days | [1] |
| Baar 2017, cell culture | Human IMR90 fibroblasts | 25 µM | Culture medium | Single addition | [1] |
| Baar 2017, kidney slices | Slices from mice aged 130 weeks | Not stated in mg/kg | Added to tissue outside the body | Once, read after three days | [1] |
| Baar 2017, competition measured by NMR | Purified protein, no cells | 300 and 600 µM | In vitro sample | Titration | [1] |
| Jing 2024, bronchopulmonary dysplasia | Sprague-Dawley rat pups | Not stated in the abstract | Intraperitoneal | Postnatal days 4, 6, 8 and 10 | [18] |
Two numbers are regularly misread. The 25 mg/kg that appears in the same paper belongs to a comparison drug called ganciclovir, not to the peptide [1]. And the micromolar figures describe how concentrated the liquid in a dish or in a measuring tube was, not a dose given to an animal.
Milligrams per kilogram in mice cannot simply be scaled up to people. Such a conversion needs data on how the body takes a substance up and clears it again, and for this peptide there are none [5].
Development and approval status
Nine years, no clinic
- 2017First description in the journal CellData from mice and from cells in dishes, with a commentary in the same issue, refs [1], [10]
- 2020-2024Follow-up work in other organsModels covering testes, lung, cartilage and newborn animals, refs [14], [17], [18], [21]
- 2023Safety signal in the journal CirculationClearing senescent cells made blood flow through the lungs of mice worse, ref [3]
- 2025Structure of the target pair measuredFunded by the company, with conflicts of interest declared, ref [11]
- 2026Still in the laboratoryNo registered trial; the spin-out company lists other candidate molecules, refs [2], [23], [24]
The peptide has never entered clinical development. Cleara Biotech, the company in Utrecht that grew out of the laboratory of the senior author, works on the same pair of proteins [23]. Its own website names CL04177 and CL04183 as its lead candidates, aimed at cancers in which p53 no longer works properly. FOXO4-DRI is not listed there, and the company has no study registered [2], [23], [24].
| Market | Status | Note | Ref |
|---|---|---|---|
| United States | Not approved | Not reviewed for pharmacy compounding either | [22] |
| European Union | Not approved | No entry, and no special status for rare diseases | [25] |
| Germany | Not approved | Follows the European route | [25] |
| United Kingdom | Not approved | No marketing authorisation | [26] |
| Australia | Not approved | Not in the register of medicines, and not named in the Poisons Standard | [27] |
| Canada | Not approved | A search of the ingredient database returns nothing | [28] |
| Switzerland | Not approved | No marketing authorisation | [29] |
One point about the United States deserves care. The FDA advisory committee that looked at peptides in July 2026 considered BPC-157, KPV, TB-500, MOTS-c, emideltide, epitalon and semax. FOXO4-DRI does not appear anywhere in that document, so there is no decision in either direction [22]. Every register search behind this table was run on 6 September 2026.
Anti-doping
FOXO4-DRI is prohibited in sport at all times, in and out of competition. Category S0 of the 2026 Prohibited List covers "any pharmacological substance which is not addressed by any of the subsequent sections of the List and with no current approval by any governmental regulatory health authority for human therapeutic use" [4]. In plain words, that covers anything drug-like that no health authority anywhere allows doctors to use.
The substance is not printed on the list by name, and that is not a loophole. The ban follows automatically from the fact that no authority has approved it. No tested routine method for detecting it in athletes has been published. The wider picture is at peptides banned in sport.
Compared with related peptides
Substances that kill senescent cells, called senolytics, are a field of research rather than a group of treatments. The table shows what each of the comparisons has actually been through in people.
| Compound | Type | Human evidence in the cited record | Overlap with FOXO4-DRI |
|---|---|---|---|
| FOXO4-DRI | Peptide that targets the contact between FOXO4 and p53 | None; no registered study [2] | — |
| Dasatinib plus quercetin | A cancer drug plus a plant compound | Small open pilot study in 14 people with lung scarring over three weeks; they walked further and faster, while lung function did not change [30] | Same idea of killing senescent cells, different mechanism |
| Fisetin | A plant compound | Early data in people at high doses, cited in a 2026 review [31] | Often mixed up with the peptide data in the same reviews |
| Navitoclax, also called ABT-263 | A drug that blocks the survival proteins of the BCL-2 family | Not reported here | Tested in the same mouse lung models, and made things worse in the same way [3] |
| MOTS-c | A peptide that comes from the cell powerhouses | No verified trial of the natural peptide in people [32] | Sold alongside it as a longevity peptide, but works in a completely different way |
Two differences matter. Dasatinib with quercetin, and fisetin as well, are small molecules swallowed by mouth, and both have made it into first pilot studies in people, which FOXO4-DRI has not [30], [31]. MOTS-c is a peptide, which is why the two are often marketed side by side, but it acts on the signals of the cell powerhouses and never touches p53 [32].
The navitoclax line carries the sharpest lesson. In the models of high blood pressure in the lung vessels, three different ways of killing senescent cells all made matters worse in the same way [3]. That points at the idea itself rather than at any single molecule.
Common misconceptions
- "Proxofim is a drug that someone developed." It is nothing more than a seller name for the same peptide, missing from journals, from pharmacopoeias and from registries. A search of the PubMed literature database returns nothing [6].
- "It reverses ageing." No lifespan study exists in any creature. The 2017 paper measured fur, kidney values and how briskly the mice reacted, and its title talks about keeping tissue in order [1].
- "Cleara is about to run trials of it." The company works on the same pair of proteins, but it names two other molecules as its lead candidates and has no study registered [2], [23].
- "ES2 is an improved version." ES2 is a separate compound from another research group, designed on the computer, tested in other models and covered by different patents [33].
- "Clearing out senescent cells is safe in itself." In mice it made blood flow through the lungs worse and cost the animals cells from the lining of their vessels. In some tissues, senescent cells appear to have jobs that keep things running [3].
- "It weighs about 4.8 kDa." Sellers often state that figure. The PubChem database calculates 5,358 g/mol for the structure deposited there. Nobody has resolved the difference, so anyone calculating with the number should say where it came from [7], [8].
Frequently asked questions
Has FOXO4-DRI ever been given to humans in a study?
No. A search of the ClinicalTrials.gov registry on 6 September 2026 turned up no study at all under FOXO4-DRI, under Proxofim, under Cleara Biotech or under senolytic peptide, and no results in people have been published elsewhere either. Everything that is known comes from cells in dishes, from tissue and from rodents.
What is FOXO4-DRI?
It is a lab-made chain of 46 building blocks that are mirror images of the natural ones and are strung together back to front (D-amino acids in reverse order). One part copies a stretch of a human protein called FOXO4, and the other part is a shuttle sequence borrowed from HIV, known as TAT, which carries the chain into cells. Nothing like this molecule occurs in the body.
Does FOXO4-DRI extend lifespan?
No study has looked at that question. There is no published lifespan study in mice or in any other creature. The 2017 paper measured how dense the fur of the mice was, what their kidney values looked like and how briskly they reacted, and even its title talks about keeping tissue in order rather than about a longer life.
Is Proxofim a different substance?
No. Proxofim is simply the name that sellers of research chemicals use for the same peptide. It appears in no journal, in no pharmacopoeia and in no regulatory register, and a search of the PubMed literature database for the name returns nothing at all.
Is FOXO4-DRI approved anywhere?
No. There is no approval in the United States, the European Union, Germany, the United Kingdom, Australia, Canada or Switzerland. It was also not one of the peptides the FDA advisory committee looked at in July 2026, so no decision on pharmacy compounding exists in either direction.
What is the safety profile?
There is none, because nobody has taken it in a study. In mice, the original authors described how well it was tolerated as a provisional impression and asked for a more thorough analysis. A 2023 paper in the journal Circulation reported that blood flow through the lungs got worse after senescent cells were cleared, with this peptide among the methods used.
Is FOXO4-DRI banned in sport?
Yes, at all times. Category S0 of the 2026 Prohibited List covers any drug-like substance that no health authority anywhere has currently approved for people. FOXO4-DRI is not printed on the list by name; it falls under the ban because of that status, so its absence from the list is not a loophole.
Is Cleara Biotech running trials of FOXO4-DRI?
No trial is registered. Cleara Biotech is the company that grew out of the laboratory of the senior author of the 2017 paper, and it works on the same pair of proteins. Its own website names two other molecules, CL04177 and CL04183, as its lead candidates, not FOXO4-DRI.
How does it differ from ES2?
ES2 is a separate compound from a different research group, designed on the computer to fit the same spot on the protein. It is shorter, was tested in other models and belongs to different patents. What is found for the one says nothing about the other.
What would have to happen before human use could be assessed?
A review published in 2026 lists what is missing: proof that the peptide really hits the intended form of the protein in the intended tissue, studies of how the body takes it up and gets rid of it, long-term toxicity work, and a clear look at whether disturbing p53 weakens the guard the body keeps against tumours. None of that exists today.
Sources
- Baar MP et al. (2017). Targeted apoptosis of senescent cells restores tissue homeostasis in response to chemotoxicity and aging. Cell 169(1):132-147.e16. PMID 28340339. DOI 10.1016/j.cell.2017.02.031
- ClinicalTrials.gov API v2. Queries for "FOXO4-DRI", "FOXO4 DRI", "Proxofim", "Cleara Biotech" and "senolytic peptide"; each returned totalCount 0. Retrieved 6 September 2026. https://clinicaltrials.gov/api/v2/studies
- Born E et al. (2023). Eliminating senescent cells can promote pulmonary hypertension development and progression. Circulation 147(8):650-666. PMID 36515093. DOI 10.1161/CIRCULATIONAHA.122.058794
- World Anti-Doping Agency. The 2026 Prohibited List, in force from 1 January 2026, section S0. Full-text checks for "FOXO" and "senolytic" returned no match. Retrieved 6 September 2026. https://www.wada-ama.org/en/prohibited-list
- Mateescu DM et al. (2026). FOXO4 as a redox-sensitive regulator of antioxidant defense and cellular senescence. Antioxidants 15(7):842. PMID 42510573. DOI 10.3390/antiox15070842
- PubMed. E-utilities searches: "proxofim" returned count 0; "FOXO4-DRI" returned 19 records. Retrieved 6 September 2026. https://pubmed.ncbi.nlm.nih.gov/?term=proxofim
- PubChem. Compound CID 168431240, "FOXO4-DRI", full residue listing in D-configuration. Retrieved 6 September 2026. https://pubchem.ncbi.nlm.nih.gov/compound/168431240
- PubChem. Compound CID 167312269, "Foxo4-dri", trifluoroacetate salt form, registry number 2460055-10-9. Retrieved 6 September 2026. https://pubchem.ncbi.nlm.nih.gov/compound/167312269
- Wikidata. Item Q136955527, FOXO4-DRI. Retrieved 6 September 2026. https://www.wikidata.org/wiki/Q136955527
- Krimpenfort P, Berns A (2017). Rejuvenation by therapeutic elimination of senescent cells. Cell 169(1):3-5. PMID 28340347. DOI 10.1016/j.cell.2017.03.014
- Bourgeois B et al. (2025). The disordered p53 transactivation domain is the target of FOXO4 and the senolytic compound FOXO4-DRI. Nature Communications 16(1):5672. PMID 40593617. DOI 10.1038/s41467-025-60844-9
- Hu Z et al. (2026). FOXO4-DRI regulates endothelial cell senescence via the P53 signaling pathway. Frontiers in Bioengineering and Biotechnology 13:1729166. PMID 41625068. DOI 10.3389/fbioe.2025.1729166
- Guichard G et al. (1994). Antigenic mimicry of natural L-peptides with retro-inverso-peptidomimetics. PNAS 91:9765-9769. PMID 7937888
- Zhang C et al. (2020). FOXO4-DRI alleviates age-related testosterone secretion insufficiency by targeting senescent Leydig cells in aged mice. Aging (Albany NY) 12(2):1272-1284. PMID 31959736. DOI 10.18632/aging.102682
- Li Y et al. (2024). FOXO4-DRI improves spermatogenesis in aged mice through reducing senescence-associated secretory phenotype secretion from Leydig cells. Experimental Gerontology 195:112522. PMID 39025385. DOI 10.1016/j.exger.2024.112522
- Han X et al. (2022). FOXO4 peptide targets myofibroblast and ameliorates bleomycin-induced pulmonary fibrosis in mice. Journal of Cellular and Molecular Medicine 26(11):3269-3280. PMID 35510614. DOI 10.1111/jcmm.17333. Erratum 2024, J Cell Mol Med 28(16):e18502
- Meng J et al. (2021). Targeting senescence-like fibroblasts radiosensitizes non-small cell lung cancer and reduces radiation-induced pulmonary fibrosis. JCI Insight 6(23):e146334. PMID 34877934. DOI 10.1172/jci.insight.146334
- Jing X et al. (2024). Cellular senescence contributes to the progression of hyperoxic bronchopulmonary dysplasia. American Journal of Respiratory Cell and Molecular Biology 70(2):94-109. PMID 37874230. DOI 10.1165/rcmb.2023-0038OC
- Ning N et al. (2026). Acylglycerol kinase sensitizes glioblastoma to temozolomide via limiting mitochondrial damage related cellular senescence. Molecular Carcinogenesis 65(9):1092-1104. PMID 42391447. DOI 10.1002/mc.70134
- Kong YX et al. (2025). FOXO4-DRI induces keloid senescent fibroblast apoptosis by promoting nuclear exclusion of upregulated p53-serine 15 phosphorylation. Communications Biology 8(1):299. PMID 39994346. DOI 10.1038/s42003-025-07738-0
- Huang Y et al. (2021). Senolytic peptide FOXO4-DRI selectively removes senescent cells from in vitro expanded human chondrocytes. Frontiers in Bioengineering and Biotechnology 9:677576. PMID 33996787. DOI 10.3389/fbioe.2021.677576
- FDA. Briefing document, Pharmacy Compounding Advisory Committee, meeting of 23 to 24 July 2026; full-text search for "FOXO" returned no match. Retrieved 6 September 2026. https://www.fda.gov/media/193342/download
- Cleara Biotech B.V., Utrecht. Company website, lead development candidates CL04177 and CL04183. Retrieved 6 September 2026. https://www.clearabiotech.com/
- Fight Aging! People are still working on the senolytic peptide FOXO4-DRI. 16 February 2026. https://www.fightaging.org/archives/2026/02/people-are-still-working-on-the-senolytic-peptide-foxo4-dri/
- European Medicines Agency. Medicines search for FOXO4 and FOXO4-DRI; no entry, no EPAR, no orphan designation. Retrieved 6 September 2026. https://www.ema.europa.eu/en/medicines
- MHRA. Product search; no marketing authorisation identified. Retrieved 6 September 2026. https://products.mhra.gov.uk/
- Poisons Standard (SUSMP), Australia. Full-text check; the only "FOXO" match is afoxolaner, a veterinary antiparasitic. No ARTG entry. Retrieved 6 September 2026. https://www.tga.gov.au/resources/artg
- Health Canada. Drug Product Database API, active ingredient queries for FOXO4, FOXO4-DRI and Proxofim; all empty. Retrieved 6 September 2026. https://health-products.canada.ca/api/drug/activeingredient/
- Swissmedic. Swiss medicinal product information; no entry identified. Retrieved 6 September 2026. https://www.swissmedicinfo.ch/
- Justice JN et al. (2019). Senolytics in idiopathic pulmonary fibrosis: results from a first-in-human, open-label, pilot study. EBioMedicine 40:554-563. PMID 30616998. DOI 10.1016/j.ebiom.2018.12.052
- Alameen AAM et al. (2026). Targeting the FOXO4-p53 axis by retro-inverso peptide senolytic agents. Naunyn-Schmiedeberg's Archives of Pharmacology 399(10):14659-14676. PMID 42024235. DOI 10.1007/s00210-026-05309-6
- ClinicalTrials.gov. NCT07505745, registry entry claiming a phase 2 study of MOTS-c for insulin sensitivity in adults with prediabetes and overweight or obesity; sponsor Hudson Biotech, whose further entries describe themselves as mock, example or fictional records, so the entry is not counted here as a trial. Retrieved 6 September 2026. https://clinicaltrials.gov/study/NCT07505745
- Le HH et al. (2021). Molecular modelling of the FOXO4-TP53 interaction to design senolytic peptides for the elimination of senescent cancer cells. EBioMedicine 73:103646. PMID 34689087. DOI 10.1016/j.ebiom.2021.103646
Cite this page
The facts on this page were checked on 6 September 2026, and every register search behind the status table was run on that date. For a substance with no clinical record at all, the date on which those searches came back empty is part of the finding itself.
myPeptides Research & Editing. (2026). FOXO4-DRI: what the studies show, status and safety. Version 1.0, 6 September 2026. myPeptides Peptide Register. Retrieved from https://mypep.app/peptides/foxo4-dri
How pages in this register are compiled and graded is described under methodology; the full register is at peptides.