RemeGenix is developing its lead drug candidate MoBA as a disease modifying treatment for Alzheimer's disease (AD).

In the near term, the Company is focused on completing the pre-clinical studies required by the FDA prior to submitting an Investigational New Drug Application (IND). The Company is also working to design the most efficient and effective clinical trials, leveraging the data generated in our pre-clinical studies.

The Company's ultimate goal being submission of an application for market authorization. The Company is positioning itself to more successfully raise the funds necessary to complete such milestones via the public markets, and where possible via non-dilutive funding such as grants and partnerships.

Near term value and our corporate and commercial goals will be achieved several ways:

  • Leveraging grants and international funding initiatives in order to minimize dilution and allow completion of our pre-clinical and clinical milestones;
  • Cultivating relationships and business opportunities with larger pharmaceutical companies;
  • Expanding the company's intellectual property portfolio;
  • Progressing its core therapeutic technology MoBA into human clinical trials;
  • Securing early revenues through commercialization of our drug development and discovery pipeline NoMAD; and
  • Presenting at various investor and industry trade conferences and publishing papers on the scientific developments.
RemeGenix is developing MoBA; a disease modifying drug to treat Alzheimer's disease. MoBA has one of the best possible safety and efficacy profile, among all of the drug candidates currently in development. The Company's therapeutic and platform technologies were developed from a comprehensive understanding of the relationship between a protein named BRI2 and Amyloid Precursor Protein (APP). BRI2 was found, by Dr. D'Adamio, to be the natural binding partner of APP, and is responsible for protecting APP from being cleaved (cut into smaller pieces) by a variety of different proteins/secretases including the beta and gamma secretases.
Importantly, individuals who have a lack of functional BRI2 have been found to have significant cognitive deficits, and similarly the mice Dr. D'Adamio created, the basis for our NoMAD platform technology, demonstrated the same cognitive deficits that are also associated with Alzheimer's disease.

Recovery of this cognitive decline was observed in all of the following scenarios:

  • Increasing the levels of BRI2 in models of dementia
  • Decreasing the levels of APP in our NoMAD models
  • Administering MoBA in models of dementia

This proof of concept data is the basis for the further pre-clinical and clinical development of RemeGenix lead candidates. RemeGenix technology has several competitive advantages over current solutions:

  • Our MoBA pipeline represents a new therapeutic approach that has been shown to specifically modulate beta secretase access to APP, for example limiting the production of byproducts of APP such as:
    • C99,
    • Abeta,
    • AICD,
    • sAPPBeta, and others
  • The mechanism of action of our pipeline is specific and is less likely to inhibit normal, ongoing biological processes. Current alternatives focusing on divergent pathways will more likely have side effects when administered to patients, and have shown such side effects in recent clinical trials.
  • RemeGenix' technology has the potential to compete on a cost and efficacy basis with other products in this disease space.
  • RemeGenix' technology is potentially applicable to multiple types of dementia and cognitive disorders.
  • RemeGenix' approach has been validated in animal models of disease as well as a human disease.