Opexa Therapeutics presents key efficacy data on Tovaxin

Opexa Therapeutics, Inc. (NASDAQ: OPXA), a company developing a novel T-cell therapy for multiple sclerosis (MS), announced today that the Company presented key efficacy data at the American Academy of Neurology (AAN) 62nd Annual Meeting held in Toronto, Canada.

“We are pleased to have again been invited by the AAN to present key data on Tovaxin. The comprehensive data analyses of the TERMS Phase 2b trial have been progressing well and continue to provide strong evidence to support the further clinical development of Tovaxin”

Dawn McGuire, M.D., Chair of Opexa's Clinical Advisory Board and the Company's acting-Chief Medical Officer, presented data from the Phase 2b TERMS clinical trial which demonstrated promising efficacy and safety results in patients treated with Tovaxin®, the Company's lead therapy for MS. The presentation highlighted previously communicated efficacy data as well as new immunology data that appear to link Tovaxin's mechanism of action with observed clinical benefits.

The data show an increasing level of FoxP3+ T-Regulatory cells in patients treated with Tovaxin (a 23.4% increase from baseline to week 52) compared with a 6.3% increase among patients receiving placebo. The levels were statistically significantly larger (p<0.02) from baseline at each interval measured in the efficacy period (weeks 24-52) within the Tovaxin group, Additionally, the Tovaxin-treated patients who appeared to benefit the most clinically, as defined by an improvement or stabilization in disability (EDSS), also demonstrated the largest increase in the percentage of FoxP3+ cells. This correlation with clinical outcome is potentially quite relevant. FoxP3 is a marker identifying a subset of T-cells that regulate the immune system to prevent attacks against the body's own tissues. A reduction in these specific T-cells may contribute to the development of autoimmune diseases such as MS. It has been demonstrated in prior published studies that T-Regulatory cell function and FoxP3 expression are notably reduced in Relapsing Remitting MS patients as compared to healthy donors.

The trend towards a sustained increase of FoxP3+ cells suggests that Tovaxin may elicit regulatory T-cell-mediated effects in patients. The potential ability of Tovaxin to restore the percentage of FoxP3+ T-Regulatory cells supports the existing mechanism of action hypothesis whereby Tovaxin works, in part, by physically depleting and/or functionally inactivating pathogenic auto-reactive T-cells in MS patients.

"We are pleased to have again been invited by the AAN to present key data on Tovaxin. The comprehensive data analyses of the TERMS Phase 2b trial have been progressing well and continue to provide strong evidence to support the further clinical development of Tovaxin," stated Neil K. Warma, Opexa President and Chief Executive Officer. "To summarize our data analyses to this point, we have observed that among MS patients with active disease, defined as having at least one relapse per year at baseline, Tovaxin treatment has resulted in a post-treatment Annualized Relapse Rate (ARR) of approximately 0.20, which is at least as good as that observed with the best drug on the market. The associated reduction in ARR was 42% as compared to placebo, with 83% of Tovaxin treated patients remaining relapse free at the end of the 52 week study. Further, more than 16% of Tovaxin-treated patients in this group actually had sustained improvements in disability scores. Brain atrophy was substantially decreased in Tovaxin patients versus placebo patients, and fewer of their inflammatory lesions progressed to black holes, suggestive of less irreversible tissue loss. The additional new immunological data added to our previously-communicated clinical data provide a compelling case for linking Tovaxin's mechanism of action as we understand it thus far to clinical outcomes in MS patients. We will continue to evaluate the immunological data, its correlation to clinical benefit and continue to refine our understanding of Tovaxin's mechanism of action in our efforts to advance Tovaxin through clinical development," added Mr. Warma.