
CEO @artan_bio · Codon Therapy for the mutations of aging · Bay Area ↔ St. Pete · Science, longevity, family
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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…
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
Brian Bodemann retweeted
The big banks are catching on. What we’re doing in the desci space is different! @vitarnabio @vita_dao @artan_bio
Younger generations realize that health maxing will significantly impact their future quality of life. At @artan_bio, we develop health solutions for consumers who want to maximize their potential. Aging is a program we can refactor for longer, healthier lives.
Half of 500 Americans surveyed would pay for one app that handles their records, labs, wearable data, and booking care.
That's the race to become the "healthcare home," one of six trends identified. The others:
- Non-toxic everything, from water filters to organic mattresses
- Peptides beyond GLP-1s
- Cholesterol treatment that can reverse some of the plaque in your arteries
- Wearables that measure far more than steps
- Brain-computer interfaces and wearables for the brain
Across all six, consumers are ready to act. They're seeking out tests, trying new products, and spending their own money on health. The opening for founders is helping them follow through.
"As AI makes answers and interpretation cheaper, value will migrate to the companies that can figure out the action layer."
Full piece from a16z's Daisy Wolf and Eva Steinman: a16z.news/p/the-state-of-lon…
Brian Bodemann retweeted
What would happen if we could stop the functional consequences of somatic mutations we know accumulate over time?
Let's walk through what the data say. 🧬👇
@vitarnabio @vita_dao @artan_bio @Bodeeeman @aschwartzphd
An underappreciated aspect of the longevity sector is the fiscal opportunity for aging nations. Just as GDP growth can cover for poor fiscal policy, so can longevity and healthspan medicines cover for underfunded social security and national pension programs. Nations need solutions that extend the useful working life of their citizens to delay a tsunami of future obligations.
At @artan_bio, we (@Mykalt45 and @aschwartzphd) are working on transformative biology to address this problem, backed by the $VITARNA Community.
Brian Bodemann retweeted
Attention $vitarna token holders and longevity enthusiasts. As we go into @Jefferies London, we’re sharing more the science behind Artan. You’ll see how we’re different.
The problem:
One C→T change at a CGA codon turns arginine into a premature stop. It happens on its own, and it builds up with age.
Here's how it works and why it's the stop we built around. 🧬👇
@vitarnabio @vita_dao @artan_bio @Bodeeeman @aschwartzphd
Brian Bodemann retweeted
1/6 🧬 A single genetic letter can stop a critical protein from being made.
What if we could restore it?
Human genetic research in Parkinson’s disease highlights exactly the class of mutations ARTAN Bio’s VitaRNA technology is designed to address.
Here’s why this matters for $VITARNA. 🧵 @vitarnabio @vita_dao @artan_bio @Bodeeeman @aschwartzphd
It is. And part of what it has to beat is chemistry: methylated CpG cytosines deaminate with age, turning CGA into a TGA stop.
By 80, ~1 in 9 blood stem cells carries one. 31.6% of premature stops in human HSCs land at CGA.
Our codon suppressor is designed to address them all. @artan_bio $VITARNA
CR cuts somatic mutations. Did it specifically drop CGA→TGA (Arg→stop) from cytosine deamination? Those trash the proteome.
That’s the exact class we’re silencing with codon suppressors at @artan_bio.
Eating 30% Less Food Has an Unexpected Effect on DNA, Study Finds | NYU Langone Health / NYU Grossman School of Medicine, SciTechDaily
A study reveals that calorie restriction affects genetic mutations differently across tissues and regions of DNA.
Eating fewer calories may do more than slow certain aspects of aging. Scientists have found that mice consuming 30 percent less food accumulated fewer DNA mutations across several tissues, suggesting that diet can influence how genetic damage builds up over time.
The study, published in Cell, examined mutations across a large portion of the genome rather than focusing on individual genes. The results showed that calorie restriction affected different organs and regions of DNA in surprisingly different ways.
How Eating Less Affects DNA Mutations
DNA mutations develop throughout life as cells experience genetic damage or make mistakes while copying and repairing their DNA. Most mutations are harmless, but some interfere with normal gene function and can contribute to cancer and other diseases. Although animal studies have established that calorie restriction can extend lifespan and slow certain effects of aging, its broader influence on mutation accumulation has remained unclear.
To investigate, researchers led by NYU Langone Health and University Hospitals Cleveland worked with scientists at the University of Texas Southwestern Medical Center and the National Institutes of Health. Using highly accurate DNA sequencing technology, they examined genetic changes in mice fed 30 percent fewer calories than animals allowed to eat freely.
The restricted diet reduced several types of mutations, including substitutions, which occur when one DNA letter is replaced by another, and insertions and deletions, which add or remove DNA letters. However, the reductions differed across tissues, with liver cells showing a stronger response than kidney or brain cells.
“While links between diet and lifespan have been established in animals, our results show that diet and mutations across the genome are also linked,” said co-corresponding study author Gilad D. Evrony, MD, PhD, a researcher at NYU Langone Health and associate professor at NYU Grossman School of Medicine. “Mice on a calorie-restricted diet are healthier for longer, but this diet is too challenging for humans. Nevertheless, considering the role mutations play in cancer and many other diseases, it’s exciting to have found a way to decrease mutations, which we can now work to understand.”
The Unexpected Pattern Hidden Across the Genome
The researchers also discovered that calorie restriction did not affect all regions of DNA equally. In liver and kidney cells, the greatest reductions in mutations occurred in the least active portions of the genome. These regions contain either no genes or genes that are not being used by the cells.
One possible explanation involves differences in DNA repair activity. Regions containing actively used genes already undergo frequent DNA repair, which may limit how much additional protection they receive if calorie restriction reduces DNA damage. Less active regions, where repair occurs less frequently, could experience a larger reduction in accumulated mutations. The researchers have not yet established whether this mechanism explains the pattern.
“We didn’t expect to find this asymmetry across the genome,” said co-corresponding author Jonathan Shoag, MD, an associate professor in the Department of Urology at University Hospitals Cleveland and Case Western Reserve University School of Medicine. “By profiling more dietary interventions and mutations in additional tissues and cell types, we hope to learn what drives the connection between diet and mutations.”
Could Genetic Damage Be Reduced Without Extreme Dieting?
The findings establish a connection between calorie restriction and lower mutation levels in mice, but they do not demonstrate that people would experience the same benefits. Sustained, substantial calorie restriction is also difficult to maintain and can carry health risks.
Researchers now hope to identify the biological processes responsible for the reduction in mutations. Understanding those processes could help scientists investigate approaches that protect DNA without requiring people to follow severely restricted diets.
“Understanding these mechanisms could eventually reveal new ways to reduce mutations – without the challenges and risks of an extreme diet—to counter diseases of aging,” said first study author Marta Grońska-Pęski, PhD, a postdoctoral fellow in Evrony’s laboratory.
The research relied on a specially established group of mice used to study the biological effects of calorie restriction. “We were fortunate to have collaborated with Dr. Victoria Acosta-Rodríguez, Dr. Joseph Takahashi, and Dr. Carla Green, who established this mouse caloric restriction cohort,” said Dr. Evrony.
scitechdaily.com/eating-30-l…
Train more. Live longer. Recover faster. Tall guy life hack from my favorite cardiologist and NBA team doctor ➡️ @Hyperice every single day
St Petersburg, Florida is where the future takes flight. This is why we chose it as the headquarters for @artan_bio.
Replying to @ARKInvest
@ARKInvest is excited to attend @jobyaviation’s flight from our doorstep in St. Petersburg, Florida, across Tampa Bay. Joby is retracing the route of the first commercial airline flight in the world in 1914.
We believe eVTOL technology will transform urban air mobility, offering travel at a fraction of the time and, at scale, a price comparable to a taxi ride.
Excited to execute on the next phase for @artan_bio and the base:0x2b09be2a00cfc7787d0e3ec332d514f9a43a6469 community! Working with @vita_dao and @artan_bio team (@Mykalt45 and @aschwartzphd) on the next phase of the project.
Our Asian tour continues. Fresh back from South Korea 🇰🇷, our COO @aschwartzphd heads to the @lanternsummit in Shanghai 🇨🇳. If you're interested in making investments that transform the aging journey, let's connect. @artan_bio @Mykalt45 @vita_dao
Excited to speak about @artan_bio at the @lanternsummit in Shanghai next week.
I'll be discussing our Condon Therapy for age-related diseases. @Mykalt45 @Bodeeeman @vitarnabio
Brian Bodemann retweeted
No success so far in using fusion to turn mercury into Bitcoin, thankfully.
Last month, we demonstrated high-rate alchemy: turning mercury into real, stable gold, beating CERN’s record by a factor of 10.
Last week, we enriched isotopes in the world’s most powerful plasma centrifuge, beating the Soviet record that stood for 40 years.
Now, we’re building a fusion reactor in San Francisco to achieve record power density.
Waving goodbye 👋 to offshore dollar creation….
The GENIUS Act marks a watershed moment in American finance, further cementing the United States as the crypto capital of the world. Just as President Abraham Lincoln’s National Currency Act of 1863 established a national framework for bank-issued currency, the GENIUS Act establishes a federal framework for payment stablecoins in the digital age.
The @USOCC's final rule carries that landmark legislation forward, providing a clear, practical foundation for private-sector innovation, competition, and American leadership in digital assets.
California politics of the last decade specialized in first order thinking and second order decline. 🥇 for meaning well.
this California wealth tax thing is just incredible.
so in October 2025, a California healthcare union proposed a "one time" 5% tax on any billionaire's wealth. the ballot measure will be voted on next month. In early December 2025, California announced that it would be a retroactive tax if passed, applying to anyone with CA residency as of Jan 1, 2026. The objective is to pay for Medi-Cal, California's incredibly dysfunctional healthcare system. (which also functions as a glorified welfare apparatus, but that's a discussion for another time).
polls reveal that the CA electorate is split around 50/50 on the tax, but prediction markets only give Prop 40 a ~23% chance of passing (there are competing measures on the ballet that would nullify it).
there are 200 billionaires in CA, worth collectively somewhere between $2.3 and $2.6 trillion. 5% of that is around $100b, accounting for a small amount of attrition. proponents of the tax forecasted a significant windfall, assuming only a 10% departure rate.
supporters thought they were being clever with the retroactive concept. no billionares would leave CA in the few short months between the tax being proposed and the residency cutoff date, without the tax even having passed yet, right?
well as it turns out, they did.
a new paper [1] from two academics at Stanford called "The Net Present Value of the California Billionaire Tax Act", argues that not only did more billionaires leave due to the proposed tax than its proponents expected, but that the value of the tax, if it does pass, is actually negative.
proponents of the tax only assumed 10% avoidance, that is, only 10% of the taxable base of targeted billionaires would leave CA within the very short Oct-Dec 2025 window. Jaros and Rauh, the Stanford academics, find that a lower bound of 28.6% of the taxable base managed to leave.
just based on known departures, those departures total $577b in net worth, or $28.8b in potential tax lost. this of course does not capture everyone (many left without announcing their departure), so the authors normalize to departure rates estimated from other wealth tax events, and apply other discounts for litigation, arriving arrive at a figure of only $28-$36b in forecasted tax revenues.
but this isn't all! all of the income taxes paid by the departed billionaires are also forsaken. the authors estimate that CA billionaires pay $3.3- 5.8b in annual income taxes. they assume a midpoint of $2b lost in annual collections from departed billionaires. the net present value of that lost income stream is -$68.9 billion.
so when you add it all up you get:
+ $30b one-time tax windfall (estimated)
- $69b in present value of lost future income taxes
= - 38.9b overall net present value of the tax
of course, this analysis is highly estimate driven. the authors simulate the parameters 100k times and find a negative NPV of the implemented tax 85 percent of the time.
and if the tax doesn't pass, which it's not looking like it will, California still ended up losing at least $577b in departed net worth, and they have permanently poisoned the well with entrepreneurs who will now worry about future wealth taxes.
[1]: nber.org/system/files/workin…





















