Overview
Transforming the Treatment of Neurodegenerative Diseases
Neurodegeneration is increasingly understood as driven by complex, multi-factorial biology — including immune dysfunction and chronic neuroinflammation — that existing protein-targeting approaches do not fully address. ImmunoBrain’s strategy is designed to tackle these upstream drivers.
"…We propose that activating the peripheral immune system, specifically through modulating immune checkpoint pathways (e.g. the PD-1/PD-L1 pathway), has the potential to provide a novel and effective means of combating neurodegenerative disorders."
At ImmunoBrain, we are pioneering a paradigm shift, building on the groundbreaking discovery that the peripheral immune system, particularly monocytes and T cells, plays a crucial role in maintaining brain health and function. We propose that activating the peripheral immune system, specifically through modulating immune checkpoint pathways (e.g. the PD-1/PD-L1 pathway), can provide a novel and effective means of combating neurodegenerative disorders, enhancing the immune system’s ability to clear pathogenic factors in the brain. This innovative approach potentially opens new avenues for the treatment of neurodegeneration.
This includes the active recruitment of immune cells to the brain, where these cells contribute to multiple beneficial activities, including reduced local brain neuroinflammation, removal of toxic or misfolded protein compounds, and supporting neuronal rescue and tissue repair. In preclinical studies using different amyloid and tau pathology mouse models, this approach led to significant improvements in cognitive performance.
ImmunoBrain’s approach is based on immune checkpoint biology that has transformed oncology, applied here in a fundamentally distinct mechanism, with a molecule engineered specifically for chronic neurological disease settings, not derived from oncology protocols
Our therapeutic approach, rooted in over two decades of studies out of the lab of Professor Michal Schwartz at the Weizmann Institute of Science, has shown that transient intermittent blockade of the PD-1/PD-L1 pathway reinvigorates the adaptive immune response, enabling it to effectively recruit reparative immune cells to the brain.
Phase 1b data confirm that IBC-Ab002 is engaging the intended biological pathways in humans, with a favorable safety and tolerability profile and directionally favorable changes in key CSF biomarkers at the 30 mg/kg dose. IBC-Ab002 is now in clinical development for Phase 2 in Alzheimer’s Disease and in additional indications.
