While Oren could be right, the phase II data argue otherwise.
In the limited exposure cohort, progress ors on VB-111 went onto Avastin... total overall overall survival was 8 months, average time to progression on VB-111 was 2 months, so patients might have averaged something less than 6 months on Avastin--probably just 3-4.
In the continuos exposure cohort, progressors on VB-111 went onto combination therapy with avastin.... time to progression on VB-111 was 2 months, overall survival was 14 months... that means several more months of Avastin exposure.... since the average number of VB-111 dosages was like 4.4, so by definition the continuous cohort received much more avastin than the limited exposure group.
Oren's argument appears to be Avastin is harming patients. There is no data that shows the placebo outperforms avastin in rGBM. There is also no data showing the converse.
But if you examine the phase II data, looking at the swim lanes of both cohorts, the continuous cohort received twice as much VB-111, lived twice as long as the limited cohort, AND received twice as much Avastin than the limited disease cohort. How do we know, the continuous cohort received Avastin and VB--111 on progression, lived twice as long as the limited cohort.
If you look at the phase II data carefully, if anything there appears to be some synergy b/w Avastin and VB-111. That's not to say that Oren's is wrong, but the phase II data suggests he is.
