And then practical observed challenges if you apply that principle, to a therapy designed to expand lesion size. So RECIST is a problem. I think the agency kind of knows this. And the question is whether the modification to RECIST, could iRECIST that use that permits essentially one cycle of so called pseudoprogression, whether that adequately addresses the nature of efficacy that we observed with our vaccine based immunotherapy. And we simply don’t know the answer. And that’s why we’re collecting the data in the phase 2 study. So that will be part of the discussion. And then obviously, there’s much interest in ctDNA it is clearly something that a lot of people are working on. Our view is that it will become an accepted surrogate in metastatic disease.
But the question is, when will that come and obviously, the agency needs to see a body a significant body of validating data that so far has not been generated and presented. And so there is uncertainty as to when that window crossed the line and start to accept ctDNA change as a surrogate endpoint. I think they’re holding the bar appropriately high. Obviously, we don’t want to approve drugs, with endpoints that actually lead to approval of drugs that ultimately don’t extend survival. Parenthetically, we’ve seen quite a bit of that with checkpoints and the use of RECIST, as a basis for accelerated approvals. Hence the advisory committee last year on that notion of dangling approvals, some of which led to sponsors withdrawing, approvals. So it’s a complicated topic.
It’s one that can only really be answered with data. We’re generating the data, and we’ll be discussing those data with the agency first half of 2024. And as I say, there’s always going to be an endpoint for phase 3 that we will be very happy with which will be able to survival. The question on table is whether there’s a proximal endpoint that might enable an earlier perhaps accelerated approval. So more to come on that topic. Thanks for the question.
Mayank Mamtani: Thank you. Looking forward to it.
Operator: The next question comes from the line of Arthur He with H. C. Wainwright. Please proceed.
Arthur He: Hey, good afternoon, Andrew and team. This is Arthur on for Sean. Thanks for taking my question. I apologize because I get on the call late. And I apologize if this topic has been discussed. So regarding your COVID vaccine program, I noticed there’s a data update expecting the second quarter of this year. Could you tell us what kind of data result can expect here?
Andrew Allen: Sure, yes. Thanks for the question. I’ll turn it that question has not been asked before. So happy to take it. The key issue with self-amplifying mRNA is whether it is better than mRNA. Because if it isn’t, then obviously I think we have some pretty good mRNA vaccine players out there. But they are not perfect. And one of the key challenges has proven to be the durability of mRNA vaccine elicited neutralizing antibodies. And if you had a vaccine platform that generated antibodies that were more persistent, that I think would be a materials advanced because it would reduce the need for repeated boosting, which obviously has bedeviled the field of mRNA vaccines as we all know. And we have early data in the boost setting from our U.K. study suggesting that some RNA elicits neutralizing antibodies that have high stability in the blood, meaning that the cause concentrations of antibody doesn’t materially change over six months.
That’s what we observed in a small number of subjects. And therefore, we need to confirm that finding in a much larger end, ideally of subjects who have not been previously primed and vaccinated but are vaccine naive. And that’s the dataset that we’ve been generating in South Africa in our CEPI funded study of several different SARS-CoV-2 constraints in a vaccine naive population in South Africa. So six months antibody data is what we anticipate sharing at the ECCMID Conference in Copenhagen in April. And that will be from over 100 subjects, that we’re looking at some different dose levels, slightly different types of subjects, some are virus naive, or we’re trying to determine virus nature, which can be a little bit challenging, but let’s label them virus naive versus clearly virus convalescent folks.
