Anti-fibrotic drug associated with lower biological age in human blood proteins
A drug developed to treat scarring of the lungs has shown an unexpected signal in an early human trial: it appears to lower participants’ biological age as measured by proteins in the blood.
Rentosertib is an experimental medicine tested in a phase 2a trial in people with idiopathic pulmonary fibrosis, a condition in which lung tissue gradually becomes replaced by scar tissue. Researchers analyzed blood samples from that trial using six different proteomic aging clocks. A proteomic aging clock is a mathematical model that estimates how old the body is biologically, based on the levels of specific proteins in the blood. The analysis was published in Nature Biotechnology.
What six independent clocks found
All six aging clocks consistently predicted a lower biological age in participants who had received rentosertib compared with the control group. This is notable because the clocks were developed independently and yet consistently pointed in the same direction.
The researchers themselves note that protein-based aging clocks cannot separate the effects of aging from those of disease. Pulmonary fibrosis itself alters blood protein profiles. It is therefore uncertain whether the lower biological age the clocks recorded reflects slowed aging or simply the anti-fibrotic effect of the drug. Through additional pathway analyses, the researchers found signals suggesting effects on cellular senescence and metabolic processes alongside the anti-fibrotic activity.
Still far from proof of anti-aging in humans
Rentosertib is not an approved drug. This was a small phase 2a trial in a specific patient group. The findings are preliminary. Follow-up studies are needed to determine whether effects on aging clocks also occur in people without pulmonary fibrosis and whether they are clinically meaningful.
Search terms to explore further: proteomic aging clock biological age, TNIK inhibitor pulmonary fibrosis, blood protein profile anti-aging