Unlike the competition, RemeGenix' lead drug in its pipeline is a Modulator of Beta secretase processing of APP (MoBA) and, as such, can reduce APP processing without having the potential for side effects that have been seen when using various secretase inhibitors (see here for an overview of the activities of MoBA in comparison with the competitive products). Thus, MoBA provides the most specific protection, and therapeutic recovery from the negative biological processes that cause cognitive dysfunction.

In early proof of concept animal studies, the company's scientific founder, Luciano D’Adamio, at the Albert Einstein College of Medicine, demonstrated that the therapeutic approach (of which MoBA is now the lead candidate) can act to alter the progression of the disease, possibly even after manifestation of a memory deficit, and MoBA has been shown to directly modulate APP processing. Taken together, RemeGenix' lead drug candidates represent a novel disease altering mechanism, and have the potential to treat both early (asymptomatic) and late stage (symptomatic) disease.

In discovery efforts, unsatisfied with existing animal models for dementia, Dr. D’Adamio created our Novel animal Models of Alzheimer's and dementia (NoMAD), and then used these models to advance our scientific understanding of the disease. NoMAD was also used to establish proof of principle of MoBA in direct comparison with several competitive drugs acting in the APP pathway. NoMAD is now patent pending and licensed to RemeGenix, and represents the first biological model of AD that faithfully replicates a human dementia. We anticipate, as more and more people review NoMAD, and as the industry's understanding of the biology of AD increases, that they will realize the need for such a model in their own discovery efforts (see here for an overview of the type of discovery tools possible with NoMAD).

The Company feels strongly, and has openly stated, that many of the competitive products in development have failed clinical trials because they were designed and tested on animal models that are not biologically relevant, meaning that they do not genetically match any possible form of human dementia, and thus the results achieved with models other than NoMAD are almost guaranteed to fail once translated into human studies.

Pipeline ID	Research & Development	Lead Optimization	Clinical Development	Commercialization
MoBA
NoMAD

RemeGenix' scientific founder, Dr. D'Adamio has developed an innovative and novel suite of therapeutic product candidates for use in treating neurodegenerative diseases such as Alzheimer's and dementia. Our lead technology, MoBA, derived from the BRI2 protein, has demonstrated commercial potential in several animal models, and has provided evidence that MoBA can work therapeutically. Therapeutic Overview of MoBA MoBA's Value Proposition

Preclinical studies of MoBA and its parent protein BRI2, have demonstrated significant efficacy and safety. MoBA's specificity in binding APP provides us with hints of a promising long-term safety profile. So far, MoBA has shown the following results: a reduction in APP processing by beta-secretase, without inhibition of Beta-secretase a rescue of the synaptic plasticity deficits and cognitive decline associated with aberrant APP processing In a related proof of concept study using mice overexpressing BRI2 (the parent protein of MoBA), Dr. D'Adamio saw a reduction in common diagnostic measures of AD, when crossed with a widely accepted model of AD. We believe this was accomplished by the increased levels of our target protein BRI2.

Collectively, our research efforts provide significant evidence of safety and efficacy of our product portfolio, and the Company is solidly moving forward on two primary initiatives: MoBA: RemeGenix' lead peptide for AD MoBA-SM: R&D Stage Small molecule program (undisclosed targets).

RemeGenix Alzheimer’s animal model will serve as a drug development platform for not only its internal needs, but will also serve as a catalyst for a number of different partnership opportunities. The Company’s co-founder has recently published several manuscripts discussing the most recent and compelling data, and the Company will work diligently to ensure that this model will become one of the preferred animal models used in the development of a variety of Alzheimer’s and/or dementia drug development efforts.
We feel interest in this model is gaining momentum, especially since the animal models currently being used in the field are lacking significant biological relevance to the human disease, and have been translating lackluster clinical results. Our models were specifically created to be biologically relevant (mimicking a human model of dementia, versus creating a biologically impossible genetic mutant), and thus facilitating more rapid translation of drug candidates to the clinic. NoMAD models have shown: an increase in APP processing a reduced cognitive function, similarly to humans with the same genetic mutation, and a recovery of cognitive function (as opposed to other studies which have only shown a drugs ability to reduce the speed of cognitive decline over time) that gamma secretase inhibitors actually make the cognitive decline worse In some of Dr. D'Adamio's earlier studies, he also showed BRI2's ability to reduce Amyloid plaque size and number in a widely accepted model of AD (if you are of the school of thought that plaque is important to the disease). Collectively, the data generated thus far has provided us with significant proof of concept as to the safety and efficacy of our therapeutic and platform technology. With this data, the Company is moving forward with the studies required for an IND submission and is seeking collaborative and business development opportunities for its NoMAD platform.