Andrew Allen: Yes, thanks, Ted. We haven’t disclosed the details of that study. But it will follow the same playbook, as we’ve followed with GRANITE as you might expect. Clearly, vaccinating subjects as a last line therapy, and end of life therapy essentially is never the optimal place for a vaccine based immunotherapy. Everyone I think will acknowledge that. But of course, that’s where you need to begin in order to demonstrate safety and earn your way to move upstream. I think we’ve done that with GRANITE, I think we’ve now done that with SLATE. So we are intending to move upstream to a much earlier line of therapy likely newly diagnosed metastatic subjects. And one of the key questions for an off the shelf product is how to deliver as many antigens as possible that are relevant to each patient.
Because of course, the beautiful thing about the personalized vaccine is you’re delivering, in our case, your 20 candidate new antigens, of which we’ve got data to suggest that typically between 12 to 15 of them are real neoantigens. And that is a strength of a product because the same as with small molecule drug therapy for viruses, you want multiple lines of attack on a highly mutable target to reduce the probability of acquired resistance. So that’s the same for viruses as it is for tumors. We just think about multiple lines of attack to reduce acquired resistance. So with SLATE how can we deliver multiple antigens to try and achieve the same goal? And KRAS obviously, is a very good shared target, but it is one target and therefore, what can we add in that will enable us to have attack T cell attack on stone KRAS neoantigens plus perhaps some other specific targets.
So that’s the work that obviously we do pretty extensively at Gritstone. We have a large team in Cambridge, Mass. This is our Tumor Epitope Discovery Group. They have continued to iterate on our prediction model over the last several years since we’ve asked published from the platform, and one of the key areas they’re looking at is additional shared tumor antigens. So it’s an important question and it is one we’re paying a lot of attention to. Today is not the day for us to reveal more, but we will do so later this year as we disclose details around that SLATE randomized trial. Okay, thanks operator. I think we’re ready for the next question. Thank you Ted.
Operator: Our next question comes from the line of Mayank Mamtani with B. Riley Securities. Please proceed.
Mayank Mamtani: Good afternoon, and thanks for taking your questions and congrats on the progress. So just a couple of quick follow ups. So in the Phase 2/3 regimen if you compare against the Phase 1 data set. Could you just talk about that? And then secondly, did you say what the standard of compare — standard of care, molecular response you’re expecting? And then I just have one final question.
Andrew Allen: So I didn’t specify, we think it will be low. But as I said, the study’s power to detect a difference, rather than being focused on an absolute value, so over 20% difference between the two arms, I think is likely to be meaningful. In terms of the rationale for administering a second dose of the adenovirus, let me hand that question over to our adenovirus guru, Karin, our head of R&D. Karin, would you like to take that one?
Karin Jooss: Yes, we have. Thank you, Andrew, great question. So we have assessed in non-human primates, whether we could we vaccinate non-human primates, after several months with the chimpanzee adenovirus vector. The reason was we knew that adenovirus is highly biased to driving high CD8 T cell responses. And this is what we after in with our primate vaccine, and I had done in the past — in the past studies assessing the interval needed to be able to come back with the adenovirus vector because once you vaccinate this, this vaccine platform, there is neutralizing antibodies being generated against the code proteins. And so we introduced in non-human primates after six or seven months and also up to four months, the adenovirus vector and we saw a very, very strong boost effect.
