Martin Williams, the GlaxoSmithKline and Roche alum who helmed Tokai Pharma and co-founded Yuma Therapeutics, has a new gig—he's now the CEO of Caraway Therapeutics, a biotech working on treatments for neurodegenerative diseases that target the cell’s garbage disposal.
Williams joins Magdalene Moran, Ph.D., Caraway’s president and chief scientific officer, and Cristina Csimma, the company’s executive chair who signed on earlier this year. In his early career, he oversaw the development and commercialization of several flagship products at GSK, Roche and Lederle before it was snapped up by Wyeth, and then by Pfizer. After that, he jumped into biotech, serving as chief business officer at RNAi player Dicerna and cancer-focused Synta Pharma, which eventually merged with NASH biotech Madrigal.
“I’ve been very lucky in my career to [work in] lots of different important disease areas with high unmet need—oncology and things like that,” Williams told FierceBiotech. “Over the last 10 years or so, I’ve become increasingly passionate about neurodegeneration as a therapeutic area … If you look at the progress we’ve made treating cancer and other diseases, dementia lags significantly behind that and so, it remains a huge unmet need.”
He co-founded neuro-focused Yuma in 2009 and has been working in the space ever since. His move to Caraway was unexpected—”I wasn’t actively looking for a new role,” he said—but he knew some of the company’s investors and was intrigued by its approach targeting autophagy, the process by which cells clear out unwanted material such as proteins, organelles and pathogens.
“What Caraway is doing, looking at the cell’s garbage disposal system, is a really attractive approach with applications for multiple diseases. That, in a nutshell, drew me here. A great team and good investors filled out the picture,” he said.
Previously called Rheostat Therapeutics, Cambridge, Massachusetts-based Caraway is going after “targeted therapies that leverage the body’s natural ability to identify and clear toxic cellular materials,” Moran said. “These can be organelles and lipids in addition to proteins—really, anything that can cause cellular damage in their long-term accumulation.”
The company is prosecuting its lead program, which targets the lysosomal ion channel TRPML1, to figure out which diseases to advance it in.
Activating this channel would essentially ramp up the clearance and recycling processes in cells, Moran said, but in an agnostic fashion: “We’re not telling cells what to get rid of, but correcting defects that seem to be present in diseased and aging neurons.”
In 2020, the company aims to declare one development candidate and pick which neurodegenerative indication it will go after first, Williams said.
“We are also beginning to talk to various potential partners,” he said. “We’re getting a lot of inbound interest and we’re having some of those discussions. We will also think about fundraising probably toward the end of next year.”