Retrophin sheds Shkreli connection with new name: Travere Therapeutics

Retrophin sheds Shkreli connection with new name: Travere Therapeutics

Retrophin may have ousted Martin Shkreli back in 2014, but he kept reappearing, last year suing—and settling with—the management of his former company, all from a prison cell. Now, the rare disease biotech is turning the page for good with a new identity: Travere Therapeutics.

Based on the Latin roots of the words “path” and “truth,” the new name is meant to signify the company’s mission to be a partner to patients and communities living with rare disease. Getting rid of a moniker associated with the “pharma bro,” infamous for hiking the price of the company’s kidney stone drug 2000%, doesn’t hurt, either. The company will start trading under its new ticker symbol, “TVTX,” on Thursday.

The rebrand has been in the works since CEO Eric Dube, Ph.D., took over from Stephen Aselage in early 2019, Dube wrote in a LinkedIn post. Aselage became CEO in 2014, when Retrophin’s board gave Shkreli the boot.

Shkreli has said the name Retrophin was a combination of “Replace dystrophin,” the protein missing in people who have the rare, muscle-wasting disease Duchenne muscular dystrophy, according to The Wall Street Journal.

But that name doesn’t fit the company’s work anymore, Dube told the WSJ.

“The original name no longer has any relevance to the science that we’re in or the diseases that we [address],” he said.

Travere’s pipeline includes sparsentan, which is in phase 3 studies for the rare kidney diseases focal segmental glomerulosclerosis and IgA nephropathy, both of which affect the kidney’s filtering units, the glomeruli. Both studies are expected to report top-line data in 2021.

And that’s not all—the company snapped up Orphan Technologies last month, adding a rare metabolic disorder program to its pipeline in a deal worth $90 upfront but that could exceed $500 million thanks to milestones and royalties. The program, OT-58, is an enzyme replacement therapy in phase 1/2 in development for classical homocystinuria, which can increase the risk of heart attacks and strokes, complications in the eye and bones as well as developmental delays.

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