US-based Kyverna Therapeutics has added a further $60m as part of its Series B extension, raising a total of $145m to be used to fund trials of its CAR-T therapies in Europe and the US.
The extension featured new investors from Bain Capital Life Sciences and GordonMD Global Investments LP, based on the 3 August announcement.
The company initially raised $85m as part of the Series B financing round led by Northpond Ventures in January 2022. Two years earlier, Kyverna obtained $25m through a Series A round.
While CAR-T therapies have been approved by regulators in select cancers, Kyverna investigates the potential use of this cell therapy in autoimmune conditions.
The company announced the recruitment of the first patient in a Phase I trial of its lead candidate KYV-101 in lupus nephritis in June. The trial will enrol up to 12 patients with the condition in the US.
Last month, Kyverna also announced the approval for conducting a Phase I/II trial of KYV-101 in lupus nephritis by German regulators.
KYV-101 is an autologous CAR-T therapy that was fast-tracked by the US Food and Drug Administration (FDA) in lupus nephritis in June 2023. It is designed to deplete B cells in autoimmune disease patients, per the 1 June announcement. Autologous CAR-T therapies are made of the patient’s own cells while allogeneic therapies are produced out of other donors.
Kyverna is also developing the allogeneic CAR-T therapy KYV-201 for use in B-cell-mediated autoimmune diseases. In January 2022, the company announced a collaboration and licensing agreement with Intellia Therapeutics for the further development of KYV-201. The agreement gave Kyverna exclusive rights to KYV-201, with Intellia receiving an option to co-develop and co-promote the therapy. This includes the option to lead its US commercialisation.
While past generations of anti-CD19 CAR-T cells have used mouse-derived CD19 binding domains, Kyverna’s therapies KYV-101 and KYV-201 both use fully human anti-CD19 CAR and costimulatory domains, based on the company’s website. This was done to minimise cytokine production as mouse-derived CD19 binding domains have been linked to high levels of cytokine production that translates to cytokine release syndrome (CRS).
CRS has often been reported as an adverse event linked to CAR-T therapies, causing complications such as fever, increased heart rate and swelling in patients.
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