The 130-Year-Old-Lifespan Trials - Mitrix Bio

From Tom Benson, Mitrix Bio.

Proud to announce “The 130-Year-Old-Lifespan Trials”. Our volunteers – mostly in their 70s and 80s – aim to be the first people in history to break past the current “Lifespan Barrier” for the human species, which stands at 122. We aim to give them average lifespans of 130 with the health, strength, and appearance of 50.

This trial will be conducted in our new division – Biotech Explorers www.explorers.bio. Because there will be very limited space to treat people in the early years, this treatement will be initially provided only to current and former astronauts, along with certain premature aging diseases in children.

We’ve known for the past year, from animal trials, that bioreactor-grown mitochondria transplantation had the potential to dramatically speed healing, fight infection, and extend lifespan. We could see in animal tests in the brain, muscles, immune system, and skin, that the effect was real. Other types of mitochondrial transplantation have already been safely used for in human patients for rare diseases.

The 130-year-old lifespan treatment will be based on Bioreactor-Grown Mitochondrial Transplantation - a technique that our parent firm Mitrix Bio has been developing for several years. We are now making animals in the lab younger routinely.

Now the job in front of us, is to make the leap with careful, rigorous human trials targeting a 130-year-old lifespan. There is so much work to be done, but our team - top scientists from Stanford, University Laval, UConn, and other top research groups - are ready to take on this challenge.

Full press release and information packet here: (see below)

For more details on Bioreactor-Grown Mitochondrial Transplantation see: Mitrix Bio

For more information on Biotech Explorers see www.explorers.bio

Disclaimer: this is purely experimental work. Not approved for human use. There is no guarantee of success of these trials.

More related reading:

Source of post above: Tom B. on LinkedIn: #mitochondria #longevity #aging #space #medicine #regenerativemedicine | 10 comments

bex_announcement_packet_04032024.pdf (3.3 MB)

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A recent presentation by Matrix Bio on their approach to longevity:

Mitochondrial Bioreactors, Space Travel, and Longevity (Webinar 2/12/2024)

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Does this mean I could put someone else’s mitochondria in my cells along with my own? They would not be targeted as “other”.

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I think you are correct in that, but I have not read deeply on this issue. This presentation may answer more of your question:

related:

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I think he answers your question at this point in the presentation: https://youtu.be/Ok1umoZ1rgA?si=cEgjImWHsBOceykz&t=1723

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Interestingly, this presentation talks about how they have transplanted large amounts of human mitochondria into animals with no immune response issues.

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And here is an investor-focused presentation by Tom Benson, on Mitrix:

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Regardless of the outcome, it’s so great that this is happening. If there’s any chance of moving the field forward then these are the kind of trials that need to happen. Crossing fingers it’s successful.

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I think there are only a limited number of mitochrondrial haplotypes. It would be possible to find a perfect or near perfect match for transplantation.

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Very interesting! This is a methodology I hadn’t even heard of before

The point about mitochondrial DNA is that each mitochondrion generally will have a number of copies of mitochondrial DNA and those copies are not going to be the same as each other. Within a cell there will be more mitochondria and again the DNA will be different.

How different is another issue.

This is called “heteroplasmy”.

If the DNA makes the mitochondria too inefficient then that means the cell does not function as well.

I talked about it with the hacking aging group and this links to the bit about mitochondria and heteroplasmy.

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What we don’t know is what good quality mitochondrial DNA is incompatible with what good quality nuclear DNA. There may be some, but we don’t know.

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I understood the body goes to some effort to make sure father mitochondrial DNA does not get used. I thought this was to make sure there was only one mitochondrial dna in the new person’s (the fetus’s) cells. I guess there is more to it.

It is true that the body gets rid where possible of the paternal mitochondria. That is why the age of the father is more varied than the age of the mother. However, there are still variations from the mother and the quality of the zygote mtDNA can be both better and worse than the mother’s original cells.

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So have they gotten any animals to break the lifespan barrier yet? (For their species?)

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I think there may be a bit of a click bait element to this. But, listening to all of the videos I think there’s reason to believe it could be beneficial. Tom benson said that they’ve physically seen age reversal in the animals they’ve tested it on. They probably don’t need to extend lifespan, improving healthspan would be enough.

The number 130 is clickbait, but underlying this are good principles. It is complex because dosing is not an easy calculation and there remain uncertainties about conflicts between mtDNA and nuclear DNA.

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I absolutely agree. This could be revolutionary, and it makes a ton of sense. From what I understand they’re able to grow your own mitochondria and grow them in a bioreactor. I assume the barrier is that the technology is in its infancy and prohibitively expensive at the moment.
However, my understand is that finding a match won’t be too challenging if they get enough samples.

I wonder how bio age prediction correlates with chron age late in life for animals?

It would be interesting to see if bio age at 1 year predicts lifespan in a mouse with or without intervention.

Also, would be interesting to see if bio age reduction correlates with rapa dose even as doses are pushed very high.

I’m amazed that the ITP program hasn’t gone full-in on biomarker testing as part of their longevity program. Given they are doing all these simultaneous lifespan tests, it seems like an ideal situation to gain and track biomarker data across the populations of animals and figure out what biomarkers are best for predicting lifespan and healthspan. A massive missed opportunity I think.

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