VBL Therapeutics is a publicly traded (NASDAQ: VBLT), late-stage clinical biopharmaceutical company focused on the discovery, development and commercialization of first-in-class treatments for cancer. 

VBL’s clinical pipeline is based on two distinct, proprietary platform technologies that leverage the body’s natural physiologic and genetic regulatory elements.  To date, VBL has developed two programs based on these platforms – an oncology program and an anti-inflammatory program.

The Company’s lead oncology product candidate, VB-111, is a targeted anti-cancer gene-therapy agent that is positioned to potentially treat a wide range of solid tumors.  VB-111 is conveniently administered as an IV infusion once every two months. It has been observed to be well-tolerated in >300 cancer patients.  The mechanism of VB-111 combines blockade of tumor vasculature with an anti-tumor immune response. This mechanism may retain activity regardless of baseline tumor mutations or the identity of the pro-angiogenic factors secreted by the tumor.

VB-111 has received orphan drug designation in both the United States and Europe and was granted Fast Track designation by the FDA for prolongation of survival in patients with glioblastoma that has recurred following treatment with standard chemotherapy and radiation. VB-111 has also received an Orphan Designation for the treatment of ovarian cancer by the European Medicines Agency (EMA).

In December 2017,  VBL Therapeutics has launched OVAL, a Phase 3 Study, of VB-111 in Platinum Resistant Ovarian Cancer in Collaboration with the GOG Foundation, Inc.

VBL’s oncology program is based on the Company’s proprietary Vascular Targeting System™ or VTS platform technology which utilizes genetically targeted therapy to destroy newly formed or angiogenic blood vessels.

VBL has also developed a proprietary platform of investigational orally-available small molecules, designated Lecinoxoids, for the treatment of chronic immune-related indications.

Founded in 2000, VBL is based in Modiin, Israel.