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Cerebral cavernous malformations (CCMs) are clusters of abnormal blood vessels in the brain and spine. CCMs can bleed and cause strokes, seizures, and headaches. CCM proteins have important effects on the blood brain barrier (BBB) and the loss of those effects in both Sporadic and Familial CCM result in BBB disruption and bleeding.

The structural and functional integrity of the BBB is one of the most critical factors for maintaining brain homeostasis. Alterations in these cellular components have been implicated in the progression and development of many neurodegenerative disorders and is likely a driving force in the development of all neurodegenerative disorders presenting with symptomatic disease.

CCM progression is driven by inflammation and oxidative stress. TNF-α is a the main driver of inflammation and lesion formation in CCM. Increased TNF-α contributes to the development and rupture of CCM lesions.

There is no current drug intervention for CCM and both surgery and radiosurgery present with poor outcomes and significant risks. Accordingly, there is an unmet need for a safe, non-toxic approach to treating the underlying pathology of CCMs.

MBM-02 represents a potential breakthrough treatment for CCM by preventing lesion formation and bleeds

  1. MBM-02 inhibits  TNF-α and other pro-inflammatory cytokines via upregulation of ADIPOQ;
  2. MBM-02 preserves and repairs blood brain barrier structural integrity.
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