Arvelle Therapeutics raises $180m in Series A financing

It’s one of the largest Series A financings for a European biotech company. A global syndicate of investors led by LSP and including NovaQuest, BRV Capital Management, Andera Partners, and H.I.G. BioHealth Partners supported new company Arvelle Therapeutics with a $180m financing to acquire the exclusive rights from Korean SK Biopharmaceuticals to develop and commercialise cenobamate in Europe. Cenobamate (YKP3089) is a small molecule drug discovered at SK Biopharmaceuticals and further developed at SK Life Science, which has been filed for FDA approval, that is being investigated for the treatment of focal seizures in adult patients. Global trials for adults with partial-onset seizures are ongoing to evaluate Cenobamate’s safety.

Under an exclusive licensing agreement with SK Biopharmaceuticals, CNS specialist Arvelle Therapeutics will develop and commercialise cenobamate in Europe as treatment to prevent focal seizures.  SK Biopharmaceuticals will receive $100m upfront for the commercialisation rights and is eligible to receive up to $430m (€380.3m) in milestones plus royalties on net sales generated in Europe when approved. Arvelle intends to file a marketing authorisation application (MAA) for cenobamate for partial-onset seizures in adult patients based on the data generated from SK Biopharmaceuticals’ global clinical trial programme. Belgian UCB SA already markets Vimpat (lacosamide) for focal seizures.

“We launched Arvelle to bring truly innovative CNS products to patients suffering from serious neurological conditions and cenobamate is the perfect potential first portfolio product,” said Mark Altmeyer, President and CEO of Arvelle. “We believe cenobamate has the potential to be an important anti-epileptic drug treatment option for adult patients suffering from partial-onset seizures.”

Cenobamate’s mode of action is not fully understood, but it is believed to work through two separate mechanisms: enhancing inhibitory currents through positive modulation of GABA-A receptors and decreasing excitatory currents by inhibiting the persistent sodium current.