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Beskrivning
Land | Danmark |
---|---|
Lista | Small Cap Stockholm |
Sektor | Hälsovård |
Industri | Bioteknik |
Saniona (OMX: SANION), a clinical stage biopharmaceutical company, marks a significant epilepsy pipeline milestone by selecting SAN2355 as the first clinical candidate from its Kv7 epilepsy program. SAN2355, a subtype-selective activator of Kv7.2/Kv7.3 channels, represents a promising new generation of effective and well-tolerated epilepsy medicines. Having successfully passed critical candidate selection steps and secured a favorable opinion from the European Patent Office (EPO), Saniona is poised to advance SAN2355 into the preclinical development phase.
“We announced in November that we had initiated the candidate selection program with a subtype-selective frontrunner from our highly successful Kv7 lead optimization program. I am pleased to announce that SAN2355 has surpassed all critical steps in this process and is now ready for preclinical development. We already experience large commercial interest in the program, and we believe that the candidate selection will increase the level of interests further”, says Thomas Feldthus, CEO of Saniona.
“SAN2355 is a unique molecule with an unprecedented subtype selectivity profile among Kv7 channels. We firmly believe it will preserve highly efficacious anti-epileptic activity while mitigating adverse effects that limit the therapeutic use of non-selective Kv7 channel activators in clinical settings. I have high expectations for SAN2355 in treating not only treatment-resistant adult epilepsies but also inherited childhood epilepsies”, says Palle Christophersen, Executive VP, Research.
More about Kv7 channels and epilepsy
Epilepsy, a brain disorder characterized by recurrent seizures, affects millions of people worldwide. Approximately 30 percent of patients are unresponsive to current medicines, emphasizing a substantial unmet need in the field.
Kv7 channels play a crucial role in mediating potassium ion transport across the cell membrane of neurons, reducing the likelihood of generating uncontrolled bursts of nerve impulses. The Kv7 channel family comprises five subtypes, with channels consisting of Kv7.2 and Kv7.3 subunits selectively expressed in the brain. Activators of Kv7.2 and Kv7.3 channels effectively dampen overactive neurons, aiding in the prevention of epileptic seizures.
Mutations in the Kv7.2 and Kv7.3 subunits are the second most common cause of inherited, severe childhood epilepsies, underscoring the importance of Kv7.2/Kv7.3 channels in controlling nerve cell activity.
The non-selective Kv7 activator retigabine has provided clinical and commercial proof-of-concept for treating patients with resistant focal onset seizures. However, it has been withdrawn from the market due to compound-specific and non-target-related side effects.
For more information, please contact
Thomas Feldthus, CEO, +45 22109957; thomas.feldthus@saniona.com
About Saniona
Saniona (OMX: SANION) is a clinical-stage biopharmaceutical company leading the way in ion channel modulation for the treatment of epilepsy and other neurological disorders. Saniona’s epilepsy pipeline features SAN711, a Phase 2-ready candidate drug targeting absence seizures, SAN2219 for acute repetitive seizures, and SAN2355, addressing refractory focal onset seizures. Beyond epilepsy, Saniona oversees three clinical programs poised for collaboration. Tesofensine, Saniona’s most advanced candidate, is progressing towards regulatory approval for obesity in Mexico through a partnership with Medix. Tesomet™ is ready for Phase 2b, targeting rare eating disorders, while SAN903 is set for Phase 1 for inflammatory bowel disease. Saniona has esteemed partners, including Boehringer Ingelheim GmbH, Productos Medix, S.A de S.V, AstronauTx Limited, and Cephagenix ApS. Saniona is based in Copenhagen and listed on Nasdaq Stockholm Main Market. For more information, please visit www.saniona.com.
This information is information that Saniona AB (publ) is obliged to make public pursuant to the EU Market Abuse Regulation. The information was submitted for publication, through the agency of the contact persons set out above, at 2023-12-27 08:00 CET.