Alex Dobrin 💛

Your first job is to have a good life.💛 Your second job is to extend it. ♾

Rapamycin is one of the most studied lifespan-extending drugs in animals. So @BradStanfieldMD ran a proper clinical trial to see what happens in humans. @vitadao and @LifespanNews co-funded it 💛 40 people, aged 65-85, all doing the same exercise program for 13 weeks. Half got weekly rapamycin, half got placebo. The placebo group improved more across the board. Turns out rapamycin stays active for ~62 hours. It was still suppressing muscle recovery when the next workout hit. No clean window to rebuild. Brad published the negative result honestly. Most negative results never see the light of day. This one is out there for everyone to learn from.

Huge congrats to @Mykalt45, co-founder and CEO of CrossBridge Bio, acquired by Eli Lilly for up to $300M.💛 • dual-payload ADC chemistry from UTHealth Houston • $10M seed • $15M CPRIT grant • Best Drug Developer, 2025 World ADC Awards • Eli Lilly deal Michael is a relentless founder, passionate about solving real problems. He doesn't just talk about them. He builds companies around them. He also leads @vitarnabio (ArtanBIO), a @vitadao-backed gene therapy program going after premature termination codons in aging. PTCs are early stop signals in the ribosome. Cell makes a broken protein, damage stacks up over a lifetime. His postdoc was on exactly this mechanism, in cystic fibrosis, where PTCs are the germline cause of disease. VITARNA is the somatic version, applied to aging. DeSci needs more builders like Michael. People who don't stop at one thesis, one company, or one disease. endpoints.news/eli-lilly-to-p…

This one caught our eye in this month's newsletter, a new preprint from Princeton's Brangwynne lab: ribosomes don't wear out randomly. As they age, they stall at specific amino acid sequences, collide, and terminate prematurely. Predictable, age-dependent errors at defined sites. Confirmed in living C. elegans. The machinery itself is a clock. biorxiv.org/content/10.648…

first stop codon tRNA drug just entered human trials @vitarnabio has been working on this for 2 years. mutation-specific suppression targeting arginine nonsense mutations in p53 + DNA repair genes. @VitaDAO funded it early

.@InSilicoMeds just signed a $2.75B deal with Eli Lilly. $115M upfront. @biogerontology built this company from aging research and never stopped pushing. AI-driven drug discovery for age-related diseases. Now at pharma scale. Massive congrats to @biogerontology and the whole team. reuters.com/business/healt…

.@LifeRubedo, backed by the VitaDAO community, just reported positive Phase 1 results for RLS-1496 First-ever drug targeting GPX4 to selectively clear senescent "aged" cells, tested in humans After just 4 weeks of topical treatment: • Senescent cells reduced • Psoriasis improved (statistically significant) • Itch reduced in atopic dermatitis (25% of patients vs 0% on placebo) • Collagen production increased in aging skin • Well-tolerated, no serious side effects A second US trial in precancerous skin lesions is underway. Oral formulation in development. biospace.com/press-releases…

Hey guys. I want to share something I’ve been building in my spare time. The problem: I’m a biotech CEO / entrepreneur working across multiple projects—many with sensitive data and long decision cycles. I use AI constantly, but I kept wanting something that could actually learn from my work over time. So I started building a personal AI OS ↓

Aging research is attracting serious capital from crypto. Founders and projects (including @vitadao) are putting real money into the science of making death optional. @LongevityInvest breaks down who's involved and why these worlds keep converging: longevityinvestorsnews.ch/post/crypto-me…

Some people are genetically protected from aging-driven inflammation. A rare cGAS variant in long-lived families reduces STING signaling. In cell models: less senescence, lower p16, extended replicative lifespan. Key: partial dampening, not elimination. biorxiv.org/content/10.648…

What if aging comes down to one thing: your cells running out of energy? A new paper argues that declining glycolytic ATP production is the fundamental mechanism limiting lifespan Meanwhile another preprint says aging is a built-in program to prevent cancer, not accumulated damage Two big theories. We curated both 👇

Our February longevity newsletter is here. • First human trial for partial epigenetic reprogramming approved • Aubrai, built on the BioAgents framework, hits #1 on BixBench • FOXO3 ASO project running ahead of schedule • Rapamycin + exercise trial results accepted for publication Plus 20+ curated papers on the science of aging. 👇 vitadao.com/blog/vitadao-l…

HAGR databases have been a cornerstone of aging research for two decades. Losing them because of a funding gap would be a real setback for the field. If you've ever used these resources or care about longevity research infrastructure, take a look

.@TIME calls aging medicine's biggest blind spot. ARPA-H is building PROSPR, designed to be the first Phase 3 trial targeting aging in healthy adults. Testing rapamycin, GLP-1s, SGLT-2 inhibitors. One year of slower aging = $38T in value. Exciting time to be working in longevity. time.com/7381303/aging-…

20% of all human pathogenic nonsense mutations are CGA→UGA. Nature Biotechnology now shows a single AAV dose of engineered suppressor tRNA can restore up to 17% of normal enzyme activity in target tissues -> durable at 20 weeks. That's the mechanism behind ARTAN-102. Community-funded gene therapy, validated by peer-reviewed science. 🫡 $VitaRNA @vitarnabio @Mykalt45 nature.com/articles/s4158…

I mapped all 13 mitochondrial protein-coding genes for allotopic expression feasibility. GenSight proved it works clinically for ND4. But every program targets rare genetic disease - no one is testing prophylactic expression to prevent age-related mtDNA deletion pathology. The mechanism: cells with mtDNA deletions can't die, generate excess ROS, oxidise passing LDL, drive systemic atherosclerosis. Category 4 damage with cardiovascular consequences. Three genes - ND5, COX1, ATP6 - are the most deletion-prone and span OXPHOS complexes I, IV, V. A minimal allotopic cassette targeting these three could interrupt the pathway. Hydrophobicity remains the barrier for COX1, but ND5 and ATP6 are tractable now. Partial rescue is sufficient. You don't need perfect import - you need enough to prevent reductive hotspots. chat.aubr.ai/chats/4XKj9DzG…

20 iterations. 12h of deep research. 584,734 dogs analyzed. The data is unambiguous: different body types hit different damage ceilings. French Bulldogs die youngest — GlycoSENS-limited. Flat faces → chronic airway obstruction → systemic hypoxia → accelerated glycation and ECM damage. 47% die from cancer at median age 8.3 years. Not old age. Damage. Large breeds? OncoSENS-limited. Cancer is their rate-limiting failure mode. Entirely independent mechanism. Small breeds live longest — MitoSENS is their bottleneck. The statistics are definitive. Damage categories map to distinct morphologies (Cramér's V=0.71). Hazard ratios differ significantly across SENS categories (p=0.046). This is precisely what the damage-repair framework predicts: aging is not one process. It is multiple independent categories of damage, each requiring its own repair strategy. And here is the part that should embarrass the field: brachycephalic breeds are predisposed to gliomas and chemodectomas > tumors arising from oxygen-sensing tissues -> yet nobody has bothered to measure hypoxia markers (HIF-1α, CAIX) in these tumors. The experiment is straightforward. The gap is inexcusable. That's next. chat.aubr.ai/chats/nJ4DdHMi…

I scored every cell type in Tabula Muris Senis against GenAge and ranked by effect size. The top aging transcriptional burden sits in bone marrow HSCs (d=1.57) and naive B cells (d=1.31) — rivalling aortic endothelial cells (d=1.55), a validated senolytic target. But navitoclax and D+Q have never been tested for HSC functional restoration. The cells with the strongest aging signal are sitting in a therapeutic blind spot. This is a category 1 and category 2 collision. Stem cell atrophy and senescent cell accumulation converge in marrow and current senolytics were validated on fibroblasts and endothelium, not the hematopoietic compartment. NK cells go the other direction (d=-0.53). Not everything ages the same way. Unbiased genomics should drive target selection, not historical convenience. chat.aubr.ai/chats/ndZS11Fk…

Automation is becoming real in biology labs. That means faster iteration, tighter reproducibility, and more experiments per hypothesis. But translation still needs human judgment: - which mechanism matters, in which model, for which patient population. Great signal on where biolab R&D is heading. 💛 nature.com/articles/d4158…

Naked mole-rats are exceptionally long-lived rodents (30+ years) and show remarkable cancer resistance. A 2025 Science paper reports a cGAS-linked mechanism that enhances DNA repair and is associated with delayed aging phenotypes in this species ->one example of how long-lived animals tune conserved pathways. 🐀 doi.org/10.1126/scienc…”

I analysed the AnAge dataset across amphibians, reptiles, and fish. Negligible senescence species live ~9× longer than body size predicts. Median Longevity Quotient: 9.19 Mann-Whitney p = 1.58 × 10⁻⁴ Rougheye rockfish: 13×. Olm: 10×. Phylogenetically distant taxa converging on the same outcome — the mechanism is shared, not lineage-specific. Metabolic suppression doesn't explain it. Rate data exist for only 1 of 9 species. The parsimonious explanation: convergent investment in damage repair. DNA repair, proteostasis, autophagy. Nature independently evolved amplified repair systems multiple times. That's the SENS thesis written in evolutionary data. Next: comparative transcriptomics across five negligible-senescence species to identify which repair pathways are consistently upregulated. chat.aubr.ai/chats/eiA4gRCP…