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Proceeds from the investment round will be used by the company to advance further its late preclinical stage Antisense OligoNucleotides (AON) lead platform for the development of therapies for different forms of Spinocerebellar Ataxia (SCA) and Huntington Disease (HD).
FREMONT, CA: Netherland-based biotech company focusing on the development of RNA modulating therapies for rare neurological disorders, Vico Therapeutics, secured USD 31 million in a Series A financing round led by Life Science Partners (LSP) and co-led by Kurma Partners, with participation from Pontifax, Droia Genetic Disease, Polaris Partners and Pureos Bioventures and Idinvest Partners. Proceeds from the investment round will be used by the company to advance further its late preclinical stage Antisense OligoNucleotides (AON) lead platform for the development of therapies for different forms of Spinocerebellar Ataxia (SCA) and Huntington Disease (HD) into first-in-human clinical trials in late 2021. Its early discovery RNA editing platform is directed towards RETT syndrome.
“This Series A funding will allow us to advance our lead program into the clinic and continue to build our capabilities as a leader in the development of novel therapies for serious CNS disorders. We see tremendous potential to advance the field and apply the breadth of our antisense oligonucleotide (AON) expertise to address severe neurological disorders. We are looking forward to accelerating the development of our platform technologies around AON technology and RNA-modulation/editing to bring best-in-class therapies to patients. The Vico team built this company around a unique synergy between state-of-the-art molecular biology, AON chemistry laboratories and industry experience in successfully developing drugs based on AON technology.,” said Luc Dochez, Founder and Chairman of Vico Therapeutics.
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The company’s lead asset is an investigational AON therapy targeting expanded (CAG) trinucleotide repeats that translate into abnormally long and toxic polyglutamine (polyQ) stretches in proteins that cause a series of neurodegenerative polyQ disorders like Spinocerebellar Ataxia type 1 (SCA1), type 3 (SCA3) and Huntington’s disease (HD). It has been demonstrated to preferentially reduce the levels of mutant polyQ compared to wildtype proteins. This was confirmed in several established mouse models for SCA1, SCA3 and Huntington Disease, with a long-term and widespread distribution of the compound throughout the central nervous system.
“Vico is building a leading team and has a cutting-edge infrastructure to engineer best-in-class therapies for severe neurological conditions and accelerate their advancement into human clinical trials. A major strength of Vico’s approach is the broad applicability to different polyQ diseases and the selectivity for mutant proteins,” said Martijn Kleijwegt, managing partner at LSP, lead investor and board member.
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