Liver fibrosis is a scarring process that can lead to cirrhosis, which causes more than 1.4 million deaths each year. Geneticist Gary Peltz at Stanford University School of Medicine is using Co-Scientist to accelerate the hunt for medicines that can slow, stop, or reverse it.

In research published in Advanced Science, Peltz’s team explored whether Co-Scientist could support efforts to identify drugs from the vast literature of existing medicines that could be repurposed to treat fibrosis. Peltz asked Co-Scientist to propose three candidates and explain its reasoning. He also identified two candidate drugs himself, based on their notable presence in the liver fibrosis literature.

Then Peltz put all five drugs through his lab’s fibrosis testbed, which consists of live human liver cells. His two drug picks showed no benefit against fibrosis. By contrast, of the three drug candidates selected by Co-Scientist, two blocked fibrosis and promoted the regeneration of liver cells. One of these drugs had only been linked to liver fibrosis in a handful of papers – a needle in the haystack of scientific literature.

Co-Scientist’s standout pick was the cancer drug vorinostat. In Peltz’s experiments, it blocked 91% of a damage response that can drive liver scarring. Co-Scientist’s suggestions pointed toward drugs that reshape gene activity, rather than targeting a single fibrosis pathway. Peltz argues that such drugs deserve serious consideration as treatments for liver fibrosis, and could ultimately help launch a new generation of anti-fibrotic medicines.

Co-Scientist feels like a collaborator that’s read everything available about biomedical science, with the reasoning capabilities to find the connections that we’re currently missing.

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