The stability and permeability of the BBB is modulated by brain endothelial cells that control tight junction integrity, immune signaling and vascular permeability
We are developing antibody-based therapeutics designed to restore endothelial stability and restore BBB function under disease conditions.
Phragma’s lead program is focused on restoring BBB integrity by correcting brain endothelial dysfunction.
The approach is based on monoclonal antibodies designed to:
This strategy addresses an upstream driver of neurological disease rather than downstream symptoms.
In multiple sclerosis, breakdown of the blood–brain barrier allows immune cells to enter the brain and attack myelin and neurons.
Although anti-inflammatory therapies exist, disease progression often continues, suggesting that upstream mechanisms remain insufficiently controlled.
By restoring BBB integrity, Phragma aims to target a fundamental mechanism contributing to disease progression.
BBB dysfunction also plays a role in numerous neurological conditions, including:
This creates the potential for broad therapeutic impact across CNS disorders.
One of the biggest challenges in neurology is that most therapeutics cannot cross the blood–brain barrier.
Approximately 98% of small molecules and nearly 100% of large molecules fail to penetrate the BBB effectively.
Phragma is developing monoclonal antibodies capable of transiently and selectively modulating BBB tight junctions, allowing therapeutics to enter the brain following standard systemic administration.
This approach could enable payload agnostic delivery of small molecules and biologics to the central nervous system.
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