Dror's compared avastin vs VB-111 by saying:
"Avastin blocks one anti-angiogenic factor (VEGF), while the tumor cells have redundancy and can overcome VEGF blockade by secreting one or more alternative pro-angiogenic factors. The MOA of VB-111 is completely differentiated from Avastin or TKIs, and is not limited to a certain factor or mutated pathway. In fact, in ovarian cancer, we have seen responses with VB-111 even post failure on Avastin and TKIs, including in women whose tumors were platinum-resistant/refractory. The added value coming from VB-111’s immune effect further enhances its anti-tumoral activity. Currently, there are very limited options for recurrent-GBM or platinum-resistant ovarian cancer patients, especially treatments that can prolong patients’ survival."
This is what I have consistently heard. Don't recall him saying one is general and the other is specific.