Researchers have developed an enzyme named CMLase, capable of reversing an age-related protein modification called Nε-carboxymethyl-lysine (CML). In laboratory experiments involving arterial tissue from a 75-year-old individual, CML levels were significantly reduced by more than 70%.
This innovative enzyme targets advanced glycation end products (AGEs), which accumulate on long-lived proteins such as collagen and elastin throughout a person’s lifespan. The potential of CMLase challenges the long-held belief that the molecular damage associated with AGEs is irreversible, indicating that it may be possible to repair rather than just slow biological aging.
Conducted by scientists at Revel Pharmaceuticals in collaboration with Calico and the University of Colorado Anschutz Medical Campus, the study marks a significant advancement in aging research. Previous efforts to combat AGEs focused on preventing their formation rather than addressing existing damage, often by neutralizing the reactive molecules responsible for their creation.
The new approach represents a paradigm shift, as it enables the repair of already accumulated CML damage. To create CMLase, the research team analyzed approximately 45,000 protein structures and underwent five rounds of directed evolution, testing over 500 million variants to enhance the enzyme's oxidase activity. The enzyme effectively oxidizes CML modifications, returning proteins to their original lysine state.
Revel's CEO stated, “We believe you can remove CML damage enzymatically.” While the current experiments were conducted ex vivo on excised human tissue, the researchers envision further studies that could take place within living organisms. This breakthrough could lead to new therapeutic strategies targeting aging at a molecular level, shifting the narrative from slowing aging processes to actively repairing damage.
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