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December 12, 2016 Issue



Novel Drugs Targeting A-Beta in the Brain Offer Hope in the Treatment of Alzheimer’s Disease



Dr. Nazneen Dewji

President & Founder


Cenna Biosciences, Inc.



Nazneen N. Dewji, Ph.D.

(858) 456-0821


Interview conducted by:

Lynn Fosse, Senior Editor, CEOCFO Magazine, Published – December 12, 2016


CEOCFO: Dr. Dewji, would you tell us about Cenna Biosciences?

Dr. Dewji: We are trying to develop disease-modifying drugs for Alzheimer’s disease. There is close to twenty years of academic research at the University of California at San Diego (UCSD) into this disease-modifying drug. Our target is A-Beta, which is the primary toxic insult in Alzheimer’s disease. It is now generally regarded as the first thing that goes wrong. We are able to inhibit the production of A-Beta using a novel technology that addresses some of the problems encountered with previous attempts by others.


CEOCFO: Would you explain the technology and how it differs from what is available?

Dr. Dewji: A-Beta is a small peptide that aggregates in the brain. It comes from a much larger precursor protein - so it is cleaved out of the precursor by two enzymes, which are like molecular scissors, the beta and the gamma-secretase. All the current approaches, apart from monoclonal antibodies, that are trying to inhibit the production of A-Beta have focused on these two enzymes. Researchers have tried to inhibit the catalytic activities of these proteases. That approach has been successful in reducing A-Beta, but the problem is that enzymes work on more than one substrate and these particular enzymes have something like fifty or sixty other substrates that they cleave. So whereas people have been very successful in using these approaches in inhibiting A-beta production, they also inhibited fifty or sixty other reactions in the cell. Some of those reactions are very important to the cell, such as the cleavage of Notch by gamma-secretase.  What several other groups are working on now is try to modulate the catalytic activity of the enzymes so that they make a shorter A-Beta fragment rather than the current 40 and 42 amino acid fragment.  It is a variation to the same theme.


CEOCFO: What are you doing at Cenna?

Dr. Dewji: What we are doing is different. Our peptide is derived from the amino terminal domain of one of the proteins that make up the gamma-secretase complex. We have an 8 amino acid peptide, which binds to the amyloid precursor protein but not at either of the secretase cleavage sites. The binding of the peptide to the precursor stops the processing of the precursor protein to A-Beta. It leaves the catalytic activities of both the enzymes completely intact, a huge advantage over previous approaches.


CEOCFO: What gave you the idea that this would work?

Dr. Dewji: We have been working on this line of thinking since 1996 and it has evolved. We first published the idea in 1996 and then some data in 2006 when we had the first inkling that this could work in vitro. In 2015 we published our technology along with the peptide data in vitro and in an animal model of Alzheimer’s disease.


CEOCFO: What has been the response from those that should know about this?

Dr. Dewji: Ours is the only approach that can reduce A-Beta without targeting the beta and gamma secretases. It is the only one that spares the catalytic activities of the enzymes. The other approach is the use of monoclonal antibodies, which is completely different. So people are excited. To date the pharmaceutical companies have focused heavily on the beta or the gamma-secretase inhibitors - although I do not think anyone is still working on the gamma-secretase inhibitors. A few pharmaceutical companies are still pursuing the beta-secretase inhibitors, which are less toxic than the gamma-secretase inhibitors. However, even if they are less toxic now, in short-term toxicology studies, we do not know how they will behave with long-term use. Any Alzheimer’s drug would probably be taken for a long time – perhaps over twenty years- so even if these inhibitors do not show much toxicity right now, twenty years is a long time to inhibit fifty or sixty reactions in the cell without consequences.


CEOCFO: Is the science relatively easy to understand for the medical people?

Dr. Dewji: Yes, the science is easy to follow. What we have shown is that Cenna’s peptides bind the amyloid precursor protein and we have shown that A-Beta is reduced following that binding. Further detailed mechanisms at the molecular level following the binding of the peptide to the precursor and A-Beta being reduced are being studied. Those are things that are going to be sorted out in time. Cenna’s drug, we hope, will stop Alzheimer’s disease in its tracks and if taken early enough, will prevent the onset of the disease.


CEOCFO: What are the next steps for Cenna?

Dr. Dewji: What we are doing now is to complete the preclinical studies. We are about a year to IND. We function entirely on NIH money - so far we have had no investor money at all. We have been able to get this far entirely on money from the NIH and small amounts from the founders, myself and my partner, Professor S. Jonathan Singer Ph.D. from UCSD. We were both professors at UCSD when we started this work. We should be able to complete the toxicology studies within a year. We will then get permission from the FDA to start Phase 1 clinical trials.


CEOCFO: How do you handle the frustration with the length of time to get moving?

Dr. Dewji: I think it is the passion that I have. I have been working on Alzheimer’s disease since 1986 - that is when George G. Glenner first discovered that A-Beta was involved in Alzheimer’s disease! I need to see a therapy for this terrible disease. You keep going just like with everything else. We are at actually a very happy stage right now. After all these years we have something that looks so promising.


CEOCFO: Why is Cenna Biosciences important and why pay attention to the company right now?

Dr. Dewji: We have the only technology which can reduce A-Beta substantially and specifically without targeting the secretases, that can potentially produce a disease modifying drug for Alzheimer’s disease. Not only would our drug be useful for all stages of Alzheimer’s disease, it would essentially arrest the disease at whatever stage, because it would stop the further production of A-Beta. One of the reasons why all the Alzheimer’s therapies have failed so far in clinical trials is that they have been given too late in the game. Our approach is the earliest, to intervene even before A-Beta is produced. Our target to stop the disease in its tracks, but also to give the drug to people before the symptoms are apparent. It takes as many as twenty years of A-Beta deposition and subsequent events in the brain before symptoms appear. With this technology you really have the opportunity of intervening before people get dementia and to stop the disease in its tracks. Another reason is that Alzheimer’s is a huge market, which should be of interest to the investor community. The cost of Alzheimer’s disease is about $200 billion a year right now and this market is expected to grow at about 19% a year. So I think people need to pay attention to us.



“Cenna’s drug, we hope, will stop Alzheimer’s disease in its tracks and if taken early enough, will prevent the onset of the disease.”- Dr. Nazneen Dewji


Cenna Biosciences, Inc.



Nazneen N. Dewji, Ph.D.

(858) 456-0821

Cenna Biosciences, Inc.

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