Proxofim

Also known as: Senolytic peptide

Evidence: Anecdotal

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Overview

Proprietary FOXO4-DRI-type senolytic peptide sold for research; the parent peptide disrupts FOXO4-p53 binding to kill senescent cells in mice, but this analog itself is unstudied.

Proxofim is marketed as a next-generation analog of FOXO4-DRI, a D-retro-inverso peptide that disrupts the FOXO4-p53 interaction so that p53 relocates to the mitochondria and senescent cells undergo apoptosis. The published mouse data (improved renal function, fitness and fur density in aged mice) belong to FOXO4-DRI, not to Proxofim, for which no peer-reviewed pharmacology, efficacy or safety data exist.

Benefits

Senescent-cell clearance, restored fitness, fur density and renal function, all shown for FOXO4-DRI in aged and fast-aging mice at 5 mg/kg on alternate days. No published data of any kind for this compound

Dosing reference

Research dose: 5 to 20 mg: vendor convention with no published basis for this compound. FOXO4-DRI mouse studies used 5 mg/kg intravenously or intraperitoneally on alternate days
Range: 5000 to 20000 mcg, 1x daily (short cycles)
Reconstitution: 2 mL bacteriostatic water
Common vial sizes: 10 mg

No published data for this analog; doses are vendor/community convention extrapolated from mouse FOXO4-DRI studies. A p53-dependent apoptosis inducer with no human safety data - unknown risk to healthy proliferating tissue; use is experimental.

Mechanism

No pharmacology has been published for this compound, so the mechanism is the vendor's claim that it acts like FOXO4-DRI. For that peptide the mechanism is established: senescent cells retain p53 in the nucleus through an interaction with FOXO4, and a competing peptide causes p53 nuclear exclusion and cell-intrinsic apoptosis selectively in senescent cells (Baar 2017), with solution NMR later showing it binds the disordered second transactivation domain of p53 (Bourgeois 2025). Whether Proxofim shares that mechanism cannot be checked, because its sequence and structure are not published. Senolysis is also not uniformly beneficial: clearing senescent pulmonary endothelial cells worsened pulmonary hemodynamics in rodents (Born 2023).

Evidence

Anecdotal: no peer-reviewed data

Reference compound FOXO4-DRI killed senescent human fibroblasts while sparing controls, and in mice 3 doses of 5 mg/kg on alternate days restored fitness, fur density and renal markers in fast-aging and naturally aged animals (Baar et al., 2017)
Reference compound: solution NMR shows the peptide binds the disordered second transactivation domain of p53, with affinity increased by p53 phosphorylation (Bourgeois et al., 2025)
Reference compound in aged mice: apoptosis of senescent Leydig cells, reduced senescence-associated secretion and higher testosterone output (Zhang et al., 2020)
Contrary result for the mechanism: senolytic clearance of pulmonary endothelial cells with FOXO4-DRI or ABT263 raised right ventricular systolic pressure and worsened vessel remodeling in mice and rats (Born et al., 2023)
Human-trial status: nothing is published about Proxofim in any species, its sequence is not disclosed, and no trial of it or of FOXO4-DRI is registered on ClinicalTrials.gov. Every finding above belongs to FOXO4-DRI, catalog id 41

References

Side effects

No human safety data; effects unknown beyond animal studies. The mechanism is induction of p53-dependent apoptosis, so off-target killing of healthy cells is the principal theoretical risk. Any displayed dose is extrapolated from mouse protocols and is not validated in humans.

Storage

Storage: Refrigerate 2-8°C (36-46°F)
Lyophilized: 2+ years at room temp, 3+ years refrigerated
Reconstituted: 28-30 days refrigerated

Pharmacology

Half-life: No pharmacokinetic data exist for this compound, and none have been published for FOXO4-DRI either
Bioavailability: Not measured. No bioavailability or distribution study exists for this compound, and FOXO4-DRI animal dosing was intravenous or intraperitoneal, never subcutaneous