Cavion has developed a pipeline of best-in-class Cav3 antagonists


  • Neurology
  • Oncology
  • Discovery
  • Phase 1
  • Phase 2
  • Phase 3
  • Cav3 channels mediate neuronal firing and thalamocortical signaling
  • Cav3 has increased activity in pathologic conditions
  • Many neurologic disorders are characterized as “thalamocortical dysrhythmias (TCDs)” which are mediated by Cav3, a common pathophysiologic pathway
  • Cav3 antagonists have promising activity modulating Cav3 in multiple pre-clinical models and clinical studies of TCDs
  • Biomarkers support development of Cavion’s clinical-stage assets

Calcium and ion channels play a critical role in neuronal signaling.  T-type calcium channels (Cav3.1, 3.2, & 3.3) have unique characteristics whereby they respond to small membrane depolarizations and serve as pacemakers, gating the activity of additional ion channels whose activation results in the firing of neurons.  Cav3’s finely-tuned voltage-gated property and pacemaker function mediates the transition from tonic to bust-firing and  generates neural “oscillations” between brain nuclei and across their pathways.

Cav3 has increased activity in pathologic conditions.  The transition to burst-firing and abnormal oscillatory pattern (“dysrhythmia”) occurs in a number of neurologic disorders, including, but not limited to, essential tremor, Parkinson’s Disease, epilepsy, neuropathic pain, and schizophrenia and rare, pediatric genetic disorders, such as Angelman Syndrome and Dravet Syndrome.  Collectively referred to as “thalamocortical dysrhythmias (TCDs),” these diseases are mediated by Cav3, a common pathophysiologic pathway.  Central and peripheral biomarkers facilitate in vivo readouts of TCDs and target modulation with Cavion’s Cav3 antagonists.

Despite substantial interest in Cav3 as a target, to date there has been little chemistry progress made to improve upon existing, prototype Cav3 antagonists which demonstrate clinical validation, but are limited as chronic therapeutics. These limitations have hampered the full exploration of the utility of Cav3 antagonists to treat TCDs.   With CX-8998, Cavion possesses a potential best-in-class Cav3 antagonist with a superior potency and selectivity profile that is poised to enter Phase 2 clinical study.

  • Calcium is a central requirement for many biological functions, including proliferation
  • T-type calcium channels are up-regulated in a variety of cancer cell tissues
  • Inhibiting T-channel activity inhibits DNA double-strand break repair and leads to cell cycle arrest and apoptosis
  • Novel mechanism in oncology

Cavion discovered that the T-type calcium channel (Cav3) is essential for external calcium entry in cancer cells.  Inhibition of Cav3 hampers a cancer cell’s ability to repair double-strand DNA breaks and causes cancer  cell cycle arrest and apoptosis. 

Published Papers and Presentations

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