OSKM Cyclic Partial Reprogramming dosage and evidence
Written by Aaron CuhaReviewed Sep 2026
The short answer
OSKM Cyclic Partial Reprogramming is all four Yamanaka genes, switched on in short bursts. It made a mouse bred to age too fast live longer, not a normal mouse. The same move in living mice causes tumours, including in the kidney.
Evidence grade for OSKM Cyclic Partial Reprogramming: Animal or lab only. The rule: only animal or lab studies on this page. No study in people yet. The sum on this page: 6 animal studies, no human study. A grade counts how much has been done to people, not whether it works.
- People given it
- 0
- Human studies
- 0
- Found nothing
- 0
Dose
No human dose established
No published study on this page has given this compound to people and reported a result.
6 animal studies, no human study
5 effects reported, 4 unwanted, 1 wanted, by people using it, not a trial
Goal pages: Brain, memory and mood, Ageing and longevity, Heart and circulation, Immune system and inflammation
In plain English
In plain English, from Aaron
This is how I would explain it to a friend. The evidence, with the numbers, is further down the page.
This switches on all four of the famous reset genes, in short bursts. The fourth one, c-Myc, can drive cancer. This is the founding experiment of the whole reprogramming field.
What people take it for
- Reversing ageing, off that founding mouse paper.
- Nothing else. There is no product and no clinic offering it.
What studies in people showed
Nobody has had this. No trial of the four gene version is registered anywhere in people. The one registered trial in the world uses the three gene version, in one eye. In mice, the 2016 paper used animals bred to age too fast. Short bursts improved signs of ageing and those mice lived longer. In older normal mice, the same treatment helped them recover from metabolic disease and muscle injury. It did not claim they lived longer. Leaving out the words bred to age too fast is the most common mistake in coverage of this field.
What people report
Reports, not study results
The good
- We have not collected user reports on this one yet.
- Nothing is sold, so nobody is reporting on a product.
The bad
- Briefly switching on all four genes caused tumours in the stomach, gut, pancreas and kidney of mice.
- Switching them on and then off caused kidney tumours like a childhood cancer.
- Leaving the genes on all the time kills mice.
- Anyone offering this as a treatment is offering something that does not exist.
Where these come from: The mouse lifespan and tumour findings come from the studies on this page. No user reports exist and no human has been dosed.
My bottom line
The paper everyone quotes, in mice bred to age too fast, with a real cancer signal attached. Nobody should be selling this.
An opinion, not a finding. I am a coach, not a doctor.
What it has been measured to do
Animal and lab work, not yet tested in people
Real results, but from animals or cells, not people. What works in a mouse often does not work the same way in a person. Nobody can patent this, so nobody would ever earn back the cost of a study in people. That is usually why there is none. The record on this one is set out below.
- Living longer2 animal or lab studies
- Kidney function1 animal or lab study
- Cancer and tumours1 animal or lab study
- Memory and thinking1 animal or lab study
32 of the 36 indexed goals have no study of any kind behind OSKM Cyclic Partial Reprogramming
No study in people, animals or cells on this page reports a result for these. That does not prove OSKM Cyclic Partial Reprogramming does nothing for them. It does mean anything you have heard about OSKM Cyclic Partial Reprogramming and one of these did not come from a study cited here.
Show full evidence
What is OSKM Cyclic Partial Reprogramming?
OSKM Cyclic Partial Reprogramming is all four Yamanaka genes, switched on in short bursts. It made a mouse bred to age too fast live longer, not a normal mouse. The same move in living mice causes tumours, including in the kidney.
Nobody has been given OSKM. There is no registered trial of four-gene reprogramming in people anywhere. The one registered human reprogramming study in the world uses OSK, the three-gene set with c-Myc taken out, injected into one eye.
The 2016 Cell paper from the Izpisua Belmonte lab started this whole field, and what it found is narrower than how people quote it. The mice were progeroid, meaning bred to age too fast. Switching on Oct4, Sox2, Klf4 and c-Myc in short repeated bursts improved signs of ageing in their cells and bodies, and they lived longer. In older normal mice, the same treatment helped them recover from metabolic disease and from muscle injury. The paper claims recovery and repair in normal mice. It does not claim they lived longer. Writing that partial reprogramming makes mice live longer, without the word progeroid, is the most common mistake in coverage of this work.
Why c-Myc was dropped is on the record. In 2013, briefly switching on all four genes in mice caused tumours called teratomas growing out of the stomach, gut, pancreas and kidney, plus stem-like cells in the blood. In 2014, switching the genes on and then off caused tumours in several mouse tissues. The kidney ones looked like Wilms tumour, a childhood cancer. Those tumours were driven by the chemical tags on DNA, not by damage to the genes themselves. The team proved it by taking stem cells from the tumours and growing normal kidney cells from them. So starting and then stopping reprogramming in a living animal is itself cancer-causing in mice. That is exactly the move partial reprogramming depends on.
How does OSKM Cyclic Partial Reprogramming work?
Shown in mice only. Short bursts of Oct4, Sox2, Klf4 and c-Myc push cells part way back toward being stem cells. That resets the chemical tags on DNA that go with age. If the burst is short enough, it stops before the cell loses what it is. Leaving the genes on all the time kills mice, through tumours and organ failure. That is why every method uses short bursts. How long and how much set the safe zone, and it has only been mapped in mice. None of this has been worked out in a person.
What have studies in people found about OSKM Cyclic Partial Reprogramming?
None. Nobody has had OSKM reprogramming, and no four-gene trial is registered on the US trial registry. The whole evidence base is mouse work plus cells in a dish.
What this does not tell you: Because nobody has been dosed, nothing is known about whether four-gene reprogramming does anything in a person. Nothing is known about whether the tumours seen in mice would happen in people. Those mouse safety findings are why the only product to reach a trial in people uses three genes instead of four, and stays in one eye.
The state of the research
Two things get blurred in coverage of the 2016 paper, and both matter. The first is which mouse. The lifespan result is in a mouse bred to age too fast because of one specific fault. Delaying that fault helps that animal live longer. It shows nothing about normal ageing. In the older normal mice in the same paper, what got better was recovery from metabolic disease and muscle injury, not lifespan. The second is that this field's safety papers are as strong as its good-news papers, and they point the other way. Nature in 2013 and Cell in 2014 both show that switching reprogramming on and then off in a living mouse causes cancer.
Companies have moved on from OSKM for exactly that reason. c-Myc can drive cancer, and the four-gene set is the one with the tumour studies attached. Every programme near the clinic uses the three-gene OSK set instead. This page exists because OSKM is the founding experiment everyone cites, not because anyone plans to give it to a person.
The evidence, in charts
Fig. 1a · how many people
0people have taken this in any study cited here
0 people · 0 studies in people
What this page cites instead is 6 animal studies. None of them gave the compound to a person.
Counted from the list of sources on this page. We draw this chart only when a study in people is cited. An empty one is the answer, not a gap in the page.
Fig. 1b · evidence mix
None of the 6 sources here are studies in people.
- Animal study · done in animals6100%
Counted from the list of sources on this page. It counts only what we cite, so there may be more studies out there. A review counts once, however many studies it sums up.
Fig. 2 · evidence over time
The studies cover 5 different years, 2013 to 2024, counted from the list of sources on this page.
Fig. 3 · legal status at a glance
US
Not approved
UK
Not approved
AU
Not approved
CA
Not approved
Not approved in any of the four countries shown. This is what the law says, not a verdict on the science. See Legal status below for the full text and any notes.
Fig. 4 · how much does what
Nobody has tested different amounts in people
This chart would show how the effect changes as the amount goes up. For this compound, nobody has measured that in people. So we leave it empty. We will not borrow an animal chart and pretend it works the same in people.
Fig. 5 · what the molecule is
- Kind of compound
- Biologic
- Molecule weight
- Not on file
- Half-life
- None on file
- Chain length
- None on file
No amino acid sequence is on file for OSKM Cyclic Partial Reprogramming, so none is drawn rather than guessed from a name.
The studies we cite
- Animal study2016In Vivo Amelioration of Age-Associated Hallmarks by Partial Reprogramming
In mice bred to age too fast, short repeated bursts of all four Yamanaka genes improved signs of ageing in their cells and bodies, and they lived longer. In older normal mice, the same treatment helped them recover from metabolic disease and muscle injury. The paper made no claim that the normal mice lived longer.
Mouse. In a PROGEROID model of premature ageing, short-term cyclic expression of Oct4, Sox2, Klf4 and c-Myc ameliorated cellular and physiological hallmarks of ageing and prolonged lifespan. In older WILD-TYPE mice the same treatment improved recovery from metabolic disease and muscle injury, with no lifespan claim made for those animals.
- Animal study2013Reprogramming in vivo produces teratomas and iPS cells with totipotency features
In mice, briefly switching on the four genes caused tumours called teratomas growing out of several organs. It left half-reset cells in the stomach, gut, pancreas and kidney, and put stem-like cells into the blood. Those cells inside the animal were closer to embryo stem cells than the ones usually grown in a dish, and they formed embryo-like lumps when injected into the belly.
Mouse. Transitory induction of the four factors 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. Those in vivo cells were transcriptionally closer to embryonic stem cells than standard cultured iPS cells and generated embryo-like structures when injected intraperitoneally.
- Animal study2014Premature termination of reprogramming in vivo leads to cancer development through altered epigenetic regulation
In mice, from the Yamada and Yamanaka labs. Switching the reprogramming genes on and then taking the doxycycline switch away caused tumours in several tissues. The tumour cells were unformed and abnormal, with big changes to the chemical tags across their DNA. The kidney tumours looked like Wilms tumour, a childhood cancer. Stem cells taken from those tumours grew into normal kidney cells, which proves the tumours came from the tags, not from damaged genes.
Mouse, from the Yamada and Yamanaka laboratories. Transient expression of reprogramming factors followed by doxycycline withdrawal produced tumours in various tissues, consisting of undifferentiated dysplastic cells with global DNA methylation changes. Kidney tumours shared characteristics with Wilms tumour. Stem cells derived from those tumour cells gave rise to non-neoplastic kidney cells, proving the tumours were epigenetically rather than genetically driven.
- Animal study2024In vivo cyclic overexpression of Yamanaka factors restricted to neurons reverses age-associated phenotypes and enhances memory performance
In mice, switching the four genes on in bursts, only in nerve cells, reversed signs of ageing and improved memory. Limiting the genes to one cell type is one way researchers are trying to make this safer.
Mouse. Cyclic four-factor expression restricted to neurons reversed age-associated phenotypes and improved memory performance. Restricting expression to one cell type is one of the strategies being used to narrow the safety window.
- Animal study2024Expansion of the neocortex and protection from neurodegeneration by in vivo transient reprogramming
In mice, brief reprogramming in the living animal grew the outer layer of the brain and protected against nerve cell loss.
Mouse. Transient in vivo reprogramming expanded the neocortex and protected against neurodegeneration.
- Animal study2022In vivo partial reprogramming alters age-associated molecular changes during physiological aging in mice
In mice, the authors name the gap head on. Partial reprogramming makes mice bred to age too fast live longer, but nobody knew what longer stretches of it would do in normally ageing mice. Their answer is that cells and tissues looked younger and the method was tolerated. They did not measure lifespan.
Mouse. The authors open by naming the gap directly: partial reprogramming extends the lifespan of a premature ageing mouse model, but the effects of longer-term partial reprogramming in physiologically ageing wild-type mice were unknown. Their result is molecular and tissue-level rejuvenation plus protocol safety, not lifespan.
Common questions
Has OSKM Cyclic Partial Reprogramming been tested in people?
Not in any study cited here. OSKM Cyclic Partial Reprogramming is all four Yamanaka genes, switched on in short bursts. It made a mouse bred to age too fast live longer, not a normal mouse. The same move in living mice causes tumours, including in the kidney.
What is the OSKM Cyclic Partial Reprogramming dosage?
No human dose established. No published study on this page has given this compound to people and reported a result. 6 animal studies, no human study
Is OSKM Cyclic Partial Reprogramming FDA-approved?
Not approved anywhere. ClinicalTrials.gov lists no human study of OSKM reprogramming, which uses four genes. The only registered human reprogramming study uses the three-gene OSK set.
Did partial reprogramming extend lifespan in mice?
In a mouse bred to age too fast, yes. The 2016 Cell paper found short repeated bursts of the four genes made those mice live longer. In older normal mice in the same paper, what got better was recovery from metabolic disease and muscle injury, and no claim was made about lifespan. Missing that difference is the most common mistake in coverage of this field.
Is OSKM dangerous?
In mice, yes, and the evidence is direct. Briefly switching on all four genes caused tumours growing out of the stomach, gut, pancreas and kidney, and put stem-like cells into the blood. Switching the genes on and then off caused kidney tumours like Wilms tumour, a childhood cancer. Those were driven by the chemical tags on DNA, not by damage to the genes. Leaving the genes on all the time kills mice.
Why do companies use OSK instead of OSKM?
Because c-Myc can drive cancer, and the four-gene set is the one with the tumour studies attached. Dropping it leaves the three-gene OSK set. That is what the only registered trial in people uses, injected into one eye with a switch that can be turned off.
Can I get this?
No. Nobody has had OSKM by any route, no four-gene trial is registered anywhere, and nothing in this area is sold. Anyone offering reprogramming as a treatment is offering something that does not exist in the clinical record.