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NEW YORK, N.Y. –  CereSpir™ Incorporated, a company with a novel approach to treat neurodegenerative diseases by harnessing the innate immune system, today announced the company has obtained a new patent from the United States Patent and Trademark Office (USPTO) covering the optimal synthetic route for the commercial manufacture of CSP-1103 in late stage development to slow the progression of Mild Cognitive Impairment (MCI) due to Alzheimer’s disease (AD).  CereSpir has exclusive rights to the patent (US 9,056,818) as part of the intellectual property related to CSP-1103 it obtained under a worldwide license agreement with Chiesi Farmaceutici S.p.A.

The novel chemistry disclosed in this patent offers an efficient chemical process for the preparation of CSP-1103 and other CSP-1103 analogues that are also covered under this patent.  This US patent provides protection for the innovative chemistry disclosed, and ensures exclusive rights to CereSpir’s preferred manufacturing process for CSP-1103 and related compounds for the lifetime of the patent.

“The issuance of this new patent by the USPTO enhances our strong patent portfolio which already includes patents related to composition of matter, processes, prodrugs and therapeutic uses of CSP-1103”, said Dr. Daniel Chain, President and Chief Executive Officer of CereSpir.  “Of special importance, the patent covers the optimal, most efficient, process for commercial manufacture of the compound until October 2031, long after the compound is anticipated to reach the market pending successful Phase 3 trials.”

CereSpir recently announced its submission of a Special Protocol Assessment (SPA) request to the U.S. Food and Drug Administration (FDA) to initiate detailed design discussions for a Phase 3 clinical study of CSP-1103 to test its ability to slow the Progression of Mild Cognitive Impairment (MCI) due to Alzheimer’s disease (AD).

About Mild Cognitive Impairment due to AD

AD is the most common cause of dementia and represents an enormous and growing global public health challenge.  It is a uniformly fatal neurodegenerative disorder with no cure or substantially effective treatment.  AD currently affects more than 5 million Americans, 7 million Europeans and, in total, about 44 million people worldwide according to the most recent report by the Alzheimer’s Association. Mild Cognitive Impairment (MCI) causes cognitive changes that are serious enough to be noticed by the individuals experiencing them or to other people, but the changes are not severe enough to interfere with daily life or independent function; therefore, they do not meet diagnostic guidelines for dementia.  Just over half of people with MCI progress to an AD dementia diagnosis. This proportion is significantly increased in people who also have measurable brain amyloid. Thus people who have this combination are considered to have MCI due to AD. Although several symptomatic treatments have been developed and approved in various countries for AD dementia, they result in only small cognitive and functional benefits in this disease stage that are not sustained.  Acetylcholinesterase inhibitors (rivastigmine, galantamine, donepezil) and N-methyl d-aspartate receptor antagonists (memantine) have a minimal impact and target late aspects of the disease.  Although these treatments and others have been tested in the pre-dementia disease stage, none have been approved.  Moreover, no truly disease-modifying treatments have been approved for either the early or late disease stages.

About CSP-1103

CSP-1103 is an orally available, small molecule which is the first among a new class of pharmacologic agents, combining the reduction of pro-inflammatory cytokines and enhancement of phagocytosis.  Both properties should be therapeutically beneficial for AD, and the combination might be especially valuable.  The Phase 2 clinical program generated preliminary safety and efficacy data in approximately 100 people half of whom received CSP-1103 for up to 2 years.  Data from this study were presented at the Alzheimer’s Association International Conference in 2013 and 2014.  CSP-1103 has been shown to inhibit brain amyloid beta (Aβ) plaque deposition, reduce tau pathology and neuro-inflammation and reverse associated memory deficits in AD transgenic mouse models. These changes associated with the observation that CSP-1103 can restore normal microglial function which is impaired in AD by increasing phagocytosis and decreasing production of pro-inflammatory cytokines. Chronic dysfunction of microglia is increasingly believed to play an important role at the very beginnings of AD with several newly discovered genetic risk factors supporting this idea.  These effects of CSP-1103 may translate into preventing the memory loss that is the hallmark of MCI due to AD.