Peptide targeting CD33 to treat cognitive decline in Alzheimer's Disease patients

This technology is a small peptide that disrupts the interaction between CD33 and CD45 transmembrane factors to treat Alzheimer’s Disease.

Unmet Need: Simple and specific drugs for treating Alzheimer’s Disease

Current treatments for Alzheimer’s Disease (AD) such as acetylcholinesterase inhibitors and NMDA antagonists, are able to somewhat alleviate certain symptoms of AD, but do not prevent, decrease, or stop the rate of cognitive decline. CD33 is a known genetic risk factor for AD and its expression is elevated in AD patients’ brains, currently there are no FDA approved therapeutics that target CD33.

The Technology: Stable, cost-effective peptide that stops CD33 activity in Alzheimer’s Disease

This technology describes a peptide molecule which readily bypasses the blood brain barrier and disrupts the interaction between CD33 and CD45 to facilitate microglia activation, thus reducing amyloid plaque buildup in the brain. This peptide possesses the potential to greatly reduces the rate of cognitive decline for AD patients.

This technology has been validated in in-vivo mouse models.

Applications:

• Treatment for Alzheimer’s disease
• Treatment for other neurodegenerative diseases where microglia activation offers therapeutic benefits
• Prevention of Alzheimer’s disease for individuals with genetic risk factors
• Treatment for acute myeloid leukemia Immune modulation for cancer therapy
• Research tool for protein-protein interactions and studying Alzheimer’s disease

Advantages:

• High-throughput platform for peptide synthesis
• Treats disease progression, rather than symptoms
• Cost-effective
• Uses specific targets of AD
• Can readily bypass blood brain barrier

Lead Inventor:

Elizabeth Bradshaw, Ph.D.

Patent Information:

Patent Status

Related Publications:

Tech Ventures Reference:

• IR CU20113, CU20215, CU21001

• Licensing Contact: Joan Martinez