While reprogramming resets a cell’s identity, Artan-102 restores the function of genes that are present but no longer translating into proteins, fixing cells that aren’t dead or senescent, just malfunctioning.
Data from a paper published in October 2024 show that normal DNA replication actively generates CpG C→T mutations that create stop codons over time. That means aging isn’t just damage or epigenetics, it’s progressive loss of protein execution.
Artan Bio is working with VitaDAO and other groups to bring a new gene therapy to market to address this problem.
Artan-102 directly addresses the biological consequence of the mutational mechanism described in the Nature Genetics (2024) paper. While the paper identifies how these mutations occur (DNA polymerase ϵ errors), Artan-102 focuses on mitigating the damage those mutations cause to cellular function.
The Connection: From CpG Mutations to Stop Codons
The paper establishes that the most common human mutations are C-to-T transitions at CpG dinucleotides, often occurring during replication by Pol ϵ. In many cases, these transitions transform a functional codon into a premature stop signal:
- The Mechanism: A CGA codon (Arginine) contains a CpG site. A C-to-T mutation at this site converts the DNA sequence to TGA, which transcribes into the UGA (opal) stop codon.
- The Result: This is a nonsense mutation. Instead of producing a full-length protein, the cell’s translation machinery (the ribosome) hits this “accidental” stop sign and stops prematurely, leading to truncated, nonfunctional proteins.
How Artan-102 Addresses the Problem
Artan-102 is an engineered nonsense suppression gene therapy designed to repair the “instruction set” of the cell while it continues to run.
1. Restoration of Translation
Instead of trying to fix the DNA mutation itself, Artan-102 uses an engineered suppressor system to recognize the UGA nonsense codon. It allows the ribosome to “read through” the accidental stop sign and insert an amino acid, thereby restoring the production of a full-length, functional protein.
2. Targeting the “Aging Mosaic”
The paper notes that these CpG>TpG mutations accumulate over time and across different tissues as a result of cell division. This creates a mosaic of cells that possess the right “identity” (genes) but fail in “execution” (translation). Artan-102 specifically restores protein output in these “partially broken” cells, potentially extending their functional lifespan without the risks associated with cellular reprogramming or deletion.
3. Complementary Action
Unlike other longevity approaches, Artan-102 focuses on the fidelity of protein production:
- Reprogramming resets the cell’s epigenetic state but does not fix the underlying genetic mutations described in the paper.
- Senolytics remove cells that have become dysfunctional, but they do not help cells that are still functional but producing truncated proteins.
- Artan-102 allows these cells to maintain their role in the tissue by repairing the faulty instructions at the translation layer.
Current Status and Safety
Recent in vivo data for Artan-102 in mouse models has shown that the therapy is capable of reaching multiple organs, including the brain, with zero reported adverse effects. By restoring protein levels in vital genes (such as tumor suppressors) that have been “silenced” by the mutations identified in the paper, this therapy offers a new path for tackling both aging and cancer simultaneously.