Tezampanel or its Oral Prodrug (NGX426) for the Potential Treatment of Thrombotic Disorder
Research conducted at Johns Hopkins University (JHU) by Craig Morrell, D.V.M., Ph.D., and Charles Lowenstein, M.D. demonstrated the importance of glutamate release in promoting platelet activation and thrombosis. Research shows that platelets treated with an AMPA receptor antagonist such as tezampanel or NGX426 are more resistant to glutamate-induced aggregation than untreated platelets. This identifies the AMPA receptors on platelets as a new antithrombotic target with a different mechanism of action than Plavix®, aspirin or tPA. The studies also show that mice treated with an AMPA receptor antagonist have a prolonged time to clot formation and blood vessel occlusion compared with control mice.
Glutamate receptors mediate the functioning of glutamate, an important excitatory neurotransmitter. While normal glutamate production is essential, excess glutamate production, either through injury or disease, can have a range of pathological effects. By acting at both the AMPA and kainate receptor site to competitively block the binding of glutamate, both tezampanel and its oral prodrug, NGX426, have the potential to treat a number of diseases and disorders.
Development Status
Raptor has licensed the intellectual property of Tezampanel and NGX 426 for the treatment of thrombotic disorder from JHU and are in discussions with potential collaborators regarding the development of this product candidate.
Learn more about Raptor’s other preclinical programs:
- NeuroTrans™ for the potential delivery of therapeutics across the blood-brain barrier
- HepTide™ drug-targeting to the liver
- WntTide™ for the potential treatment of breast cancer