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Sanofi CEO outlines organizational overhaul

Mainstay therapeutic areas of diabetes and cardiovascular drug research are out

by Lisa M. Jarvis
December 12, 2019 | A version of this story appeared in Volume 97, Issue 48

A photo of Paul Hudson.
Credit: Sanofi
Paul Hudson is pulling Sanofi out of diabetes and cardiovascular drug development.

After just 100 days on the job, Sanofi CEO Paul Hudson has unveiled his plan for transforming the French pharmaceutical company over the next 3 years.

Among Hudson’s goals for Sanofi are devoting resources to six specific drug candidates, creating a stand-alone consumer health unit, and saving roughly $2.2 billion.

What the future does not include is diabetes and cardiovascular disease drug development. Sanofi markets the industry’s top-selling insulin treatment and for years relied on sales of Plavix, a now-generic blood thinner. But Hudson, who took over as CEO in September, told investors last week that while “our diabetes and cardiovascular portfolio is significant, we also have to recognize that it’s declining.”

As part of that decision, Sanofi won’t launch efpeglenatide, a long-acting GLP-1 agonist for diabetes that is in late-stage studies. Hudson noted that many of the diabetes and cardiovascular compounds in development don’t offer enough benefits. “We don’t think it’ll be appreciated by payers or physicians if it’s not going to transform lives,” he said.

Going forward, the firm will focus R&D on vaccines, immunology, rare diseases, rare blood disorders, neurology, and oncology. Sanofi will make bolt-on acquisitions to support those core areas.

To that end, Sanofi said it will buy Synthorx, a San Diego–based immuno-oncology firm, for $2.5 billion. Synthorx develops proteins featuring unnatural amino acids, which become handles for bioconjugation. Its lead drug candidate, THOR-707, is a variant of interleukin-2 engineered to allow a polyethylene glycol to be tacked onto a specific site, lengthening the life span of the drug in the body and stimulating proliferation of tumor-fighting effector T cells without ramping up immunosuppressive cells.



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