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Therachon, achondroplasia therapy developer, closes $35M Series A

Therachon has raised significant funding to support clinical proof of its soluable form of human fibroblast growth factor receptor 3. This could treat achondroplasia, a genetic mutation that is the leading cause of dwarfism.

Therachon announced today that it closed a $35 million Series A round. The company, which develops therapies for achondroplasia, reportedly plans to use the funding to advance its program surrounding clinical proof of its soluable form of human fibroblast growth factor receptor 3 (FGFR3).

Achondroplasia is a genetic disease in which a single point mutation in the gene encoding FGFR3 causes stunted bone growth and malformed cartilage. It’s the leading cause of dwarfism and reportedly affects one in every 15,000 children.

The financing was led by OrbiMed and joined by New Enterprise Associates (NEA), Inserm Transfert Initiative and Versant Ventures. Stephen Squinto, venture partner at OrbiMed, and Dr. Sara Nayeem, M.D., principal at NEA, have joined Therachon’s board of directors.

In a press release, Therachon shared some input from those involved with the deal:

“This financing validates the work we have been doing at Inserm for the last six years,” said Elvire Gouze, a senior researcher at Inserm and the University of Nice Sophia Antipolis and Therachon’s founder and scientific advisor. “We have discovered a novel protein therapy that has restored normal skeletal growth and reduced comorbidities in animal models of the disease. If we can show the same effects in humans, this could dramatically improve the lives of achondroplasia patients.”

“As we met Elvire and learned about her innovative approach, we became very excited at the prospect of working with her to develop a life-altering therapy for children with achondroplasia,” said Tom Woiwode, Therachon’s chairman and managing director at Versant Ventures, which seeded Therachon along with ITI in 2014. “We’re thrilled to have brought together an exceptional international syndicate to support the company as we advance the program towards clinical trials.”

This therapy was proven to be effective in mice back in 2013 when Gouze’s lab showed that a soluable decoy version of FGFR3 increased bone length in mice who had the same genetic mutation with achondroplasia.

Photo: Flickr user zack-attack