Vascular Biogenics Ltd (VBLT)

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Why is VB-111 better than current treatment options?

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The Fas ligand is highly expressed in non-tumoral normal tissues and the activation of Fas receptor by its ligand is associated with increase toxicities. Hepatotoxicity was observed to be bypassed by the specificity of the adenovirus modified promoter, which restricts activation of Fas pathway to angiogenic endothelial cells. The specificity is further improved as the Fas component of the transgene is activated via TNF-a ligand binding to TNFR-1 in the transgene – TNF-a is less prevalent in non-tumoral normal tissue. The transcription rate of small vasoconstriction peptide endothlin-1, which is known to aid in tumor growth and progression, is also augmented in the presence of TNF-a, which further suggests that VB-111 activity is specific to the tumor microenvironment.

VB-111’s mechanism of action is independent of tumor specific mutations, which may render it less susceptible to drug resistance.

http://blogs.shu.edu/cancer/2017/01/11/vb-111-a-novel-gene-therapeutic-agent-in-cancer-ashini-r-dias-contributor/