CEO @artan_bio · Codon Therapy for the mutations of aging · Bay Area ↔ St. Pete · Science, longevity, family
San Francisco Bay Area
Joined May 2025
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As we age, our cells accumulate somatic mutations, a feature of aging that touches everyone. At @artan_bio we're building therapies + cosmetics to address it. Today we announced a $1M seed, and I'm stepping in as CEO. Advancing toward NHP studies now. prnewswire.com/news-releases…
Dario believes in zero liability for AI products, so cures for all diseases in 10 years isn’t a stretch. Just AI away that pesky clinical development process and regulatory burden.
If they had cures for all diseases today, they still wouldn’t get them all to market in 10 years.
Anthropic CEO predicts cancer, Alzheimer's, heart disease, mental illness will be cured in less than 10 years
ACCELERATE
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Brian Bodemann retweeted
Clonal hematopoiesis isn't only about age.
Cancer therapy can select for it, and new data show the same after CD19 cell therapy. 🧬👇
@vitarnabio @vita_dao @artan_bio @Bodeeeman @aschwartzphd
It would be very effective and altruistic to open source your capsid designs and in vivo delivery data @claudeai
Gene therapies can be delivered in a protein shell called a capsid. Mythos 5.2 found a new way to predict a whole capsid’s structure.
In our tests, it accurately modeled 28 of the 34 capsids it attempted. Biologists could use it to design capsids faster and more cheaply.
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Brian Bodemann retweeted
Topical RNA has a barrier problem. One classic paper shows how hard it is. A new one shows engineered carriers can still get RNA into skin. 🧬👇
@vitarnabio @vita_dao @artan_bio @Bodeeeman @aschwartzphd
Brian Bodemann retweeted
Amazing time in Boston. Blessed to be a part of an amazing community working to do good. #twitter instagr.am/p/DfiFBGomVgw/
Brian Bodemann retweeted
Where do premature stops in human disease come from? Many come from one codon.
Two papers, and a number from our own analysis. 🧬👇
@vitarnabio @vita_dao @artan_bio @Bodeeeman @aschwartzphd
Share your opinions on advancing longevity medicines through early trials 👇
Montana and the Bahamas now let people try some longevity drugs before full approval.
Done well, that's real-world data on how aging drugs work in people. Done badly, it's unmonitored self-experiments.
Which matters most to you: the safety bar, the monitoring, or getting your own data back?
3-min survey with Infinita, LARTA & Wildcreek 👇
longevity-survey-share-vita-…
Brian Bodemann retweeted
Different body sites, different mutation burdens.
Fowler et al. mapped skin clones across body sites. Most mutations were UV-related. 🧬
doi.org/10.1158/2159-8290.CD…
@vitarnabio @vita_dao @artan_bio @Bodeeeman @aschwartzphd
Brian Bodemann retweeted
Saturday reading.
Martincorena et al., Science 2015: in sun-exposed eyelid skin, over a quarter of cells carried cancer-causing mutations, and the skin still worked normally. Aged skin is a patchwork of thousands of clones. 🧬 ethereum:0x7b66e84be78772a3afaf5ba8c1993a1b5d05f9c2 @artan_bio @vitarnabio @Bodeeeman @aschwartzphd @vita_dao
doi.org/10.1126/science.aaa6…
Brian Bodemann retweeted
Our community funded the science. Now $VITARNA holders help decide the next experiment.
The bet underneath this vote: you don't have to repair every broken letter in your DNA. You just have to get the cell to read past it.
VRNAP-6 asks whether that changes how a mouse ages -> carried in every cell from birth, aged beside unedited littermates, judged on lifespan and healthspan.
@vitarnabio proposes testing it, starting with tolerability. No new raise.
👉Read the proposal and cast your vote.
snapshot.org/#/s:vitarna.eth…
As we age, cells pile up "stop" errors in their DNA that cut proteins short.
@artan_bio's Codon Therapy is built to read through them.
VRNAP-6 asks: do we test it for a whole lifetime?
🐭 Mice carry the fix from birth
📊 We track lifespan, frailty, grip, balance, gait 👇
Brian Bodemann retweeted
More insight into @artan_bio and our vitabeauty project.
Sunlight's signature mutation is C→T, and at methylated CpG sites it's especially easy to make. In a CGA codon, that creates a stop.
The chemistry, in the papers: 🧬👇
@vitarnabio @vita_dao @Bodeeeman @aschwartzphd
Investors don’t need to feed the AI capital cookie monsters to solve longevity. Invest in real biotech teams developing real solutions built for the reality of the actual onerous regulatory process for novel therapies. @artan_bio
OpenAI’s Greg Brockman says "death becoming a choice" is possible, and predicts AI will make real strides on curing diseases in the next 12 to 18 months
“I think that you look at something like biology, and that’s not something that’s unique to just humans. I think that we all suffer, that the question of even just thinking about death becoming a choice. All of this is possible.”
“Having cures for diseases is something that’s become also a trope in this field, but I think that you’re gonna see real delivery and real significant strides and impacts on biology, health, and curing of diseases over the next 12 months, 18 months.”
“I think it’s gonna take time to really deliver on the full impacts, just by the nature of this field. But I think it’s all possible and doable, and it’s exactly the kind of thing we have these models that are solving these unsolved problems. Clearly, we need to apply it to biology and life sciences.”
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Brian Bodemann retweeted
Attention $VITARNA token holders:
We want your feedback on a proposed experiment! Token holders actually have a say! Vote below. This is #desci in action!
snapshot.org/#/s:vitarna.eth…
@vitarnabio @vita_dao @Molecule_sci @BioProtocol @Bodeeeman @aschwartzphd
Brian Bodemann retweeted
For those interested, we share updates on the Vitarna Telegram thread here:
t.me/vitarna
Brian Bodemann retweeted
Attention $vitarna token holders. Here’s another thread on the data of our therapeutic:
Does the codon suppressor reach tissue? We dosed mice once with AAV9 and measured codon suppressor expression 14 days later. 🧬👇
@vitarnabio @vita_dao @artan_bio @Bodeeeman @aschwartzphd
There's another way aging marrow hurts bone: clonal hematopoiesis.
As we age, mutant blood stem cell clones grow. In the UK Biobank, people with those clones had a 44% higher osteoporosis risk. The biggest DNMT3A clones tracked with weaker bone.
In mice, losing Dnmt3a in blood cells ramps up IL-20, which makes osteoclasts chew bone faster. Block IL-20 or use a bisphosphonate, and bone recovers.
doi.org/10.1084/jem.20211872
If those clones fuel bone loss, the direct move is to shrink them. Our HSPC-targeted codon suppressor is built for that. @artan_bio $VITARNA
These bone scans came from old female mice of the same age.
The only difference was a cholesterol pill millions of people already take.
Left, a few broken struts. Right, a dense lattice of bone.
A second cholesterol drug, evolocumab, did nothing for bone, so lower cholesterol alone doesn't explain it.
Atorvastatin pushed cells in the marrow, including stem cells, to build bone, and only when estrogen was low. Old male mice got no benefit.
Two small groups of women past menopause who took statins also lost bone more slowly than women who didn't.
Randomized studies haven't shown a consistent drop in fractures, so this is still a lead.
A pill prescribed for the heart may have been doing a second job in women's bones all along.
Brian Bodemann retweeted
Attention $vitarna token holders:
Artan-102 restores full-length p53 in Calu-6 cells with R196X on both alleles.
R196X is a CGA→TGA stop. The Artan-102 band runs stronger than the G418 control. Not quantitative. 🧬
@vitarnabio @vita_dao @artan_bio @Bodeeeman @aschwartzphd
