Intellect Neurosciences Inc. (fka ILNS)

[montanus]

ILNS PIPELINE UPDATE

Our current focus is to establish proof of concept for TauC3, a therapeutic monoclonal antibody licensed by Intellect from Northwestern University on an exclusive basis, targeting a truncated form of tau protein.  We believe that this truncated protein is a key driver of neurodegeneration in tauopathies, which causes irreversible damage to nerve cells and propagates pathology throughout the brain.
Several groups have observed that amyloid beta accumulation and tau itself, under certain circumstances, can activate enzymes known as “caspases” and that caspase-cleaved tau (TauC3, aka delta tau) may have biological properties that could compromise neurons (Guillozet-Bongaarts  et al., 2005, Stoothoff et al., 2009, de Calignon et al., 2012,  Plouffe  et al., 2012; Lee  et al.., 2012). For example, it has been demonstrated that TauC3 is a likely precursor for neurofibrillary tangles. More recently, it was suggested that tau (or potentially a misfolded or post-translationally modified tau) can be released from neurons, be taken up by other neurons, and act as a nidus for a new tangle – i.e. leading to “propagation” of tau species across neuronal pathways Fulga et al., 2007, Quintanillaet al., 2012, Yanamandra et al., 2013). Tau C3, along with hyperphosphorylated forms, appears to be preferentially secreted and to enhance misfolding and aggregation. Because misfolding and secretion are two prerequisites for uptake and propagation, we hypothesize that TauC3 may be a potent agent in terms of propagation of tau pathology from one neuron to the next. 
In 2011, we filed a patent claiming therapeutic potential of antibodies targeting truncated forms of tau.  In 2012, we licensed a TauC3 antibody from Northwestern University, acquiring exclusive global development and commercialization rights to the TauC3 antibody.
In January 2014, we announced top line data showing proof of concept in a preclinical Alzheimer's model indicating the antibody’s potential to be disease modifying. The study was conducted in collaboration with University of California, Irvine's Dr. Frank LaFerla, Chancellor's Professor and Chair, Neurobiology and Behavior School of Biological Sciences, Director, Institute for Memory Impairments and Neurological Disorders. The data showed that the TauC3 antibody effectively engaged the target and reduced certain phosphorylated pathological forms of Tau, indicating that the treatment with the peripherally administered antibody had an effect in the brain and is potentially disease modifying. 
We have developed a detailed plan to corroborate these preliminary findings in additional models. This work will be outsourced to specialist contract research organizations and will involve collaboration with a leading AD investigator who has developed sophisticated models that are particularly well suited to test the TauC3 antibody. 

http://www.intellectns.com/internal-pipeline