$ILNS The CONJUMAB-A technology Antibody drug

$ILNS >> The CONJUMAB-A technology

Antibody drug conjugates are a novel class of therapeutics with multiple applications to treat a broad spectrum of diseases.  While current immunotherapy approaches attack the antibodies, they do not appropriately guard against the side effects, such as inflammation, that often comes with treatment.  Most commonly seen in the treatment of certain types of cancer, Intellect Neurosciences’ newest treatment platform, CONJUMAB-A, applies the antibody drug conjugate approach to neurological disease.  Intended to overcome the limitations of current passive immunotherapy approaches, the CONJUMAB-A platform increases clearance of amyloid proteins while delivering cytoprotective molecules to areas of the brain and other organs that may have been damaged as a result of these infirmities.  One example of CONJUMAB-A’s cytoprotective mechanism is the reduction of inflammation caused by amyloidosis (the abnormal deposit of beta amyloid in the brain or other organs, which can result in plaque or lesions), while avoiding vasogenic edema, a common side effect of plaque dissolution that occurs in some patients.  This approach has applications both in the therapeutic arena in diseases such as Alzheimer’s, Parkinson’s, Huntington’s, Age-Related Macular Degeneration, Glaucoma, Cerebral Angiopathy, Frontotemporal Dementia, Progressive Supranuclear Palsy, Pick’s disease, Cortical Basal Degeneration and Peripheral Amyloidosis.  It also has tremendous potential for in vivo imaging of beta amyloid in the brain.

Intellect Neuroscience’s flagship CONJUMAB-A molecule, IN-N01-OX2, is  a non-activating, stabilized IgG4 humanized antibody specific for beta amyloid protein (IN-N01, Intellect’s lead ANTISENILIN molecule) conjugated to as small molecule with neuroprotective properties.  While lead testing and optimization is expected to be complete in 2012, IN-N01-OX2 is expected to enhance the clearing capacity of IN-N01, deliver on-site protection against beta amyloid neurotoxicity and prevent interaction with the melatonin receptor.