Liver fibrosis is a scarring process that can lead to cirrhosis, which causes more than 1.4 million deaths per year. Geneticist Gary Peltz of Stanford University School of Medicine is using Co-Scientist to accelerate the search for drugs that can tardy, stop or reverse the process.
IN research published in Peltz’s team explored whether a co-scientist could support efforts to identify drugs from the extensive literature on existing drugs that could be repurposed to treat fibrosis. Peltz asked his co-scientist to propose three candidates and explain their reasoning. Sam also identified two drug candidates based on their notable presence in the liver fibrosis literature.
Peltz then subjected all five drugs to a fibrosis test in his lab, which consists of living human liver cells. His two drugs showed no benefit against fibrosis. In turn, of the three drug candidates selected by the co-scientist, two blocked fibrosis and promoted liver cell regeneration. Only a few articles linked one of these drugs to liver fibrosis, which represented a needle in a haystack of scientific literature.
The co-scientist’s outstanding choice was vorinostat, an anticancer drug. In Peltz’s experiments, it blocked 91% of the damage responses that can cause liver scarring. The co-scientist’s suggestions pointed to drugs that change the shape of gene activity, rather than a single fibrosis pathway. Peltz argues that such drugs deserve solemn consideration as treatments for liver fibrosis and could ultimately support bring a recent generation of antifibrotic drugs to market.