Investor Relations

VBL Presents New Data on the Potential of its Novel VB-600 Platform for Nonalcoholic Steatohepatitis (NASH) and Rheumatoid Arthritis (RA)

February 26, 2019

TEL AVIV, Israel, Feb. 26, 2019 (GLOBE NEWSWIRE) -- VBL Therapeutics (Nasdaq: VBLT), (the “Company”) today announced new data implicating the potential of its VB-600 platform of antibodies targeting MOSPD2 (motile sperm domain-containing protein 2) for treatment of various inflammatory indications, including NASH and RA. Previously, the Company has demonstrated efficacy of anti-MOSPD2 monoclonal antibodies in multiple sclerosis (MS) models, and novel findings now implicate MOSPD2 as a potential target for NASH and RA as well.  VBL's study entitled “MOSPD2: Key Regulator of Myeloid Cell Migration and a Novel Target for Treatment of Inflammatory Diseases,” is being presented today at the Keystone Symposia on Myeloid Cells in Santa Fe, New Mexico. 

Figure 1
Figure 1


Monocytes are immune cells that play a pivotal role in the induction and progression of various inflammatory diseases. Studies have suggested that limiting their migration may improve clinical outcomes in chronic inflammatory diseases; however, thus far it has been a challenging goal, due to the complexity and redundancy of ligands and receptors that regulate the movement of these cells.

VBL has identified new biological findings, which position MOSPD2 as a critical pathway controlling monocyte migration and as a key regulator of disease pathogenesis in different inflammatory autoimmune settings. Company data show that inhibition of MOSPD2 by either knockdown, silencing or proprietary antibodies, results in a significant reduction in the ability of monocytes to migrate, regardless of the inflammatory signals employed to attract them. Accordingly, mice in which the MOSPD2 gene was knocked out, essentially do not develop disease in the widely used experimental autoimmune encephalomyelitis (EAE) model for MS or the Collagen Antibody-Induced Arthritis model for RA. Knockout of this gene also leads to significant reduction in fibrosis in a high-fat-high-carbohydrate model for NASH. VBL's proprietary monoclonal antibody drug candidates, for which we have demonstrated potency in MS and NASH models, have the potential to become a new therapy in multiple chronic inflammatory indications.

"We believe that we have identified a key pathway through which the body is recruiting monocytes to specific sites of inflammation," said Dror Harats, M.D., Chief Executive Officer of VBL Therapeutics. "Not only is this an important scientific finding, it strengthens the potential therapeutic scope of our VB-600 platform of monoclonal antibodies across inflammatory indications. We continue to advance our VB-600 program towards a first IND filing in 2020."

For a link to VBL's presentation at the Keystone conference, see: Keystone Presentation

About VBL's VB-600 Platform

VBL is conducting two parallel drug development programs that are exploring the potential of MOSPD2, a protein that VBL has identified as a key regulator of cell motility, as a therapeutic target for inflammatory diseases and cancer. Our VB-600 platform comprises classical anti-MOSPD2 monoclonal antibodies for inflammatory indications, as well as bi-specific antibody candidates for oncology.

About VBL

Vascular Biogenics Ltd., operating as VBL Therapeutics, is a clinical stage biopharmaceutical company focused on the discovery, development and commercialization of first-in-class treatments for cancer. The Company’s lead oncology product candidate, ofranergene obadenovec (VB-111), is a first-in-class, targeted anti-cancer gene-therapy agent that is being developed to treat a wide range of solid tumors. It is conveniently administered as an IV infusion once every two months. It has been observed to be well-tolerated in >300 cancer patients and demonstrated efficacy signals in an “all comers” Phase 1 trial as well as in three tumor-specific Phase 2 studies. Ofranergene obadenovec is currently being studied in a potential registration trial for platinum-resistant ovarian cancer.

Forward Looking Statements

This press release contains forward-looking statements. All statements other than statements of historical fact are forward-looking statements, which are often indicated by terms such as “anticipate,” “believe,” “could,” “estimate,” “expect,” “goal,” “intend,” “look forward to,” “may,” “plan,” “potential,” “predict,” “project,” “should,” “will,” “would” and similar expressions. These forward-looking statements include, but are not limited to, statements regarding our programs, including VB-111, including their clinical development, such as the timing thereof, therapeutic potential and clinical results, and the scope and protection of our intellectual property rights. These forward-looking statements are not promises or guarantees and involve substantial risks and uncertainties. Among the factors that could cause actual results to differ materially from those described or projected herein include uncertainties associated generally with research and development, clinical trials and related regulatory reviews and approvals, the risk that historical clinical trial results may not be predictive of future trial results, and that we may not realize the expected benefits of our intellectual property protection. A further list and description of these risks, uncertainties and other risks can be found in the Company’s regulatory filings with the U.S. Securities and Exchange Commission, including in our annual report on Form 20-F for the year ended December 31, 2017, and subsequent filings with the SEC. Existing and prospective investors are cautioned not to place undue reliance on these forward-looking statements, which speak only as of the date hereof. VBL Therapeutics undertakes no obligation to update or revise the information contained in this press release, whether as a result of new information, future events or circumstances or otherwise.

INVESTOR CONTACT:
Michael Rice
LifeSci Advisors, LLC
(646) 597-6979

A photo accompanying this announcement is available at http://www.globenewswire.com/NewsRoom/AttachmentNg/8c21d0b9-d807-4ed9-9d56-9dfc75216752

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