OSK Partial Reprogramming dosage and evidence

What is OSK Partial Reprogramming?

How does OSK Partial Reprogramming work?

This is shown in mice. Switching on OSK partly wipes and rewrites the chemical tags on a cell's DNA, called methylation. It shifts them toward a younger pattern, without pushing the cell all the way back to a stem cell. In the 2020 optic nerve work, the benefit needed TET1 and TET2, the enzymes that strip those tags off. That is direct evidence the effect runs through the DNA tags, not through some general gene effect. In human cells, the only work is in a dish. Skin cells given OSK showed tag markers of reversed age in the 2024 Cellular Reprogramming paper. Nothing about how it works has been shown in a living person.

What have studies in people found about OSK Partial Reprogramming?

Nobody has had OSK given to their whole body. One trial exists. It is an early safety study of a single shot into one eye, in about 18 people. It began signing people up in March 2026 and has posted no results. There is no evidence in people that it works.

• NCT07290244, Life Biosciences ER-100: an early study where nobody is picked by chance. Doses go up step by step. One person gets each new dose first, and a safety committee must sign off before others do. About 18 people, starting 2 March 2026, still signing people up. Adults with open angle glaucoma go first. Then a dose is picked for a group with a type of optic nerve stroke.
• The treatment is a virus carrying the OCT4, SOX2 and KLF4 genes, injected into the jelly of one eye. Doxycycline pills for 56 days act as the switch that turns the genes on. Follow-up runs up to five years. People give tears, saliva, stool and urine so the team can check where the virus goes and whether it is shed. That is standard for a first-in-people gene therapy of this kind.
• Both main measures are about safety: how many people get side effects, and how many hit a dose that is too toxic. These are checked from the start to day 56 and day 112. Nothing it measures first is about whether it works.
• A search of the US trial registry, done when this page was researched, found no reprogramming trials for Altos Labs, YouthBio Therapeutics, Turn Biotechnologies or Retro Biosciences. Altos Labs is the best-funded company in the field and has no trial in people on the registry.
• Human cells in a dish: skin cells given OSK showed tag markers of reversed age in the 2024 Cellular Reprogramming paper. That is a dish, not a person.

What this does not tell you: Nothing here tells you whether OSK does anything good in a person. An early safety study in 18 people, dosed into one eye, cannot reliably measure sight coming back, and it is not built to. It says nothing about whole-body dosing or ageing outside the eye. It also says nothing about the cancer risk seen in mice, because 18 people followed for a few years cannot pick up a tumour rate that matters. Every claim that partial reprogramming works rests, for now, on mice.

The state of the research

The evidence, in charts

The studies we cite

• Study in people2026
  Evaluating ER-100 for Safety in People With Glaucoma or Non-Arteritic Anterior Ischemic Optic Neuropathy

  One human trial of this reprogramming approach exists and it has not reported anything. Life Biosciences is injecting a gene therapy carrying the OSK factors into one eye of 18 people with glaucoma or a form of optic nerve damage. A doxycycline tablet switches it on for 56 days. Doses rise in sequence and nobody is assigned by chance. Both things the trial is built to measure are safety: side effects and doses that prove too toxic. No results are posted. Recruiting began in March 2026.

  The only registered human OSK reprogramming trial. Sponsor Life Biosciences Inc., phase 1, non-randomised sequential dose escalation, estimated enrolment 18, recruiting since 2 March 2026. AAV-delivered OSK injected into one eye, activated by oral doxycycline for 56 days. Both primary endpoints are safety: treatment-emergent adverse events and dose-limiting toxicities. No results posted.

  NCT07290244 ClinicalTrials.gov
• Animal study2020
  Reprogramming to recover youthful epigenetic information and restore vision

  In mice, switching on three of the Yamanaka genes in the nerve cells at the back of the eye made those cells look younger. The chemical tags on their DNA went back to a young pattern. Damaged optic nerves regrew. Sight came back in mice with glaucoma and in old mice. The benefit needed two enzymes, TET1 and TET2, which strip those tags off. Funded by the US National Institutes of Health with other support.

  Mouse. Ectopic expression of Oct4, Sox2 and Klf4 in mouse retinal ganglion cells restored youthful DNA methylation patterns and transcriptomes, promoted axon regeneration after optic nerve injury, and reversed vision loss in a mouse glaucoma model and in aged mice. The benefit required the DNA demethylases TET1 and TET2. NIH funded, with non-US government and non-PHS support.

  PMID 33268865 Nature
• Animal study2022
  In vivo partial reprogramming alters age-associated molecular changes during physiological aging in mice

  In normally ageing mice, not ones bred to age fast, long stretches of partial reprogramming changed the kidney and skin. The longer the treatment ran, the bigger the change. Ageing clocks read younger. Genes for inflammation, worn-out cells and stress were turned down. The authors did not claim these mice lived longer.

  Mouse, physiologically ageing wild-type rather than progeroid. Long-term partial reprogramming regimens produced duration-dependent effects in kidney and skin, with reversion of epigenetic clock measures and reduced inflammation, senescence and stress-response gene expression. The authors make no lifespan extension claim for wild-type mice.

  PMID 37118377 Nature Aging
• Animal study2024
  Gene Therapy-Mediated Partial Reprogramming Extends Lifespan and Reverses Age-Related Changes in Aged Mice

  In mice, a virus carrying a switchable OSK system was given to very old males, 124 weeks old, through the body rather than into one organ. Their remaining life was about twice as long as untreated males, and they scored better on frailty. Read that carefully. It is remaining life from very late in life, in males only, from one lab, in a specialist journal. No independent lab and no government testing program has repeated it.

  Mouse. Systemically delivered AAV encoding an inducible OSK system, given to 124-week-old male mice, extended median remaining lifespan by 109 percent over wild-type controls and improved frailty scores. Read the number carefully: this is remaining lifespan from very late life in male mice only, from one group, in a specialty journal, and it has not been replicated by the NIA Interventions Testing Program or any independent laboratory.

  PMID 38381405 Cellular Reprogramming
• Animal study2024
  Targeted partial reprogramming of age-associated cell states improves markers of health in mouse models of aging

  In mice, reprogramming aimed at specific worn-out cell types improved health markers in ageing mouse models.

  Mouse. Partial reprogramming targeted at specific age-associated cell states improved health markers in mouse ageing models.

  PMID 39259812 Science Translational Medicine
• Animal study2013
  Reprogramming in vivo produces teratomas and iPS cells with totipotency features

  In mice, this is the key safety finding for the whole field. Switching on all four Yamanaka genes briefly caused tumours called teratomas growing out of several organs. It also left half-reset cells in the stomach, gut, pancreas and kidney, and put stem-like cells into the bloodstream.

  Mouse, and the central safety finding for this whole field. Transitory induction of Oct4, Sox2, Klf4 and c-Myc in reprogrammable mice produced teratomas emerging from multiple organs, dedifferentiated NANOG-expressing cells in stomach, intestine, pancreas and kidney, and circulating induced pluripotent stem cells in the blood.

  PMID 24025773 Nature