Project Immortality
A genomic platform targeting the cellular mechanisms of aging in end-stage organ disease.
Overview
Project Immortality applies iPSC-derived cellular systems and CRISPR-Cas9 genomic editing to the problem of aging-related organ failure.
Every available treatment for aging-related organ failure — whether a drug, a supplement, or a surgical intervention — addresses a downstream consequence rather than the cause. The evidence points to a single upstream convergence point: the lifelong accumulation of unrepaired DNA damage. When cells lose the ability to maintain their genome, every other hallmark of aging follows.
Project Immortality takes a different approach. Rather than managing the consequences of cellular aging, we engineer cells that are intrinsically resistant to its causes — modifying iPSC-derived stem cells at the genomic level before transplantation, with differentiation programmed to activate only upon reaching the target tissue. The goal is not to slow the clock. It is to replace the mechanism that winds it down. Initial indications: ESRD, HFrEF, and IPF.
Key Capabilities
- iPSC line generation with GFP/PiggyBac ITR CRISPR-Cas9 constructs
- Single-cell sorting and clonal expansion via multiple instruments (Cytena C.SIGHT 2.0, MACSQuant Tyto)
- Primary indications: ESRD, HFrEF, IPF — high unmet need, aging-driven prevalence
- NIH SBIR Phase I targeting September 2026
Strategic Motivation
Aging is not a single disease — it is a convergent failure of cellular maintenance. The tools to interrogate and intervene at that level now exist. The question is whether they can be assembled into a tractable clinical platform. That is the work.
Why aging is a DNA damage problem
The table below catalogs every known mechanism of DNA damage that accumulates with age — from oxidative lesions to replication errors — alongside the non-DNA hallmarks they drive. Toggle the complexity level to explore.
How Project Immortality addresses this
Every intervention currently available for aging-related organ failure — whether pharmacological, behavioral, or surgical — addresses a downstream consequence rather than the initiating event. Senolytic drugs clear cells that have already senesced. Rapamycin suppresses a signaling pathway already dysregulated. Mitochondrial supplements compensate for an organelle already failing. The evidence increasingly points to a single upstream convergence point: the progressive, lifelong accumulation of unrepaired DNA damage across every cell in the body. When cells lose the ability to faithfully maintain and express their genome, every other hallmark of aging follows — proteostasis collapses as chaperone synthesis is impaired, mitochondria fail as their own genome is corrupted and biogenesis genes are silenced, epigenetic programs drift as repair proteins are redistributed away from chromatin maintenance, and the immune system shifts from surveillance to inflammation as genomic debris activates innate sensing pathways. No drug introduced into a systemically damaged organism reverses this process; it merely manages it.
Project Immortality takes a different approach. Rather than treating the downstream consequences of cellular aging, we engineer cells that are intrinsically more resistant to the causes. Using iPSC-derived cellular systems, we modify stem cells at the genomic level — introducing enzymatic reinforcements to DNA repair pathways, mitochondrial maintenance systems, and proteostatic networks — before transplantation into the target tissue. The transplanted cells are programmed to remain quiescent during delivery and to differentiate only upon reaching their destination organ, where they gradually repopulate the tissue with a population that carries a substantially higher DNA damage tolerance than the native aging cells they replace. The ambition is not to slow the clock — it is to replace the mechanism that winds it down.