Jason Gerberry: Hi guys, thanks for taking my questions. I just wanted to clarify – so, as you’re thinking about a Phase 3 program for your KRAS overall in the frontline setting. So it sounds like in the sub 50% PD-L1 expressing that could move forward a little bit more quickly and that perhaps more wait and see on some of the other segments in monotherapy pending durability data in the second half. Just maybe any decisions as it pertains to moving into pivotal Phase 3 in the frontline outside of the sub 50% PD -L1 is a late 2023 decision on your end. And then just on PRMT5 TANGO is going to have some data here, Phase 1 data in first half with their agent. And so, just as you think about the molecules comparatively based on preclinical data that’s out there, just your expectations, how you differentiate the idea of your 70 fold selectivity, view sort of where the key differentiation resides in the approaches. Thanks.
David Meek: Great. I’ll start with the first line question and thanks for the question. I think, a couple of important points about the first line. You’re right that there are in essence almost three different subsets, the less than one, one to 49 and the greater than 50%. We have K7 which is the doublet that is showing – that has shown safety and also some preliminary efficacy in that particular setting and we will be taking another look at the data in K7 the second half of this year that will allow us to provide information regarding the durability and also increased numbers of patients so we have a more refined response rate, giving us a concept – an idea of how to move forward best in the Phase 3 space. With respect to the speed with which you talked about, we’re really excited and anxious to work on both areas.
The less than 50%, we were able to go a bit faster from an administrative perspective because that we modified K7 be an amendment to be a Phase 3 study in that less than 50%. From the greater than 50%, it requires creating protocol from scratch, but we are moving forward with administratively on both areas and are looking forward to the updated data in K7 as I mentioned in the second half of the year. So, we’ll be able to have a data-driven decision based on any and-or all of those particular cohort.
James Christensen: Yes, I think you touched on the PRMT5 question. Again what we believe is operative here for the second-generation molecules is the therapeutic index. And in our hands preclinically, we want to maximize the level of target inhibition in tumor tissue and really again what the biomarker here, we want to be almost at 98%, 99% plus inhibition level for the full dose goal to maximize the inhibition of the target and maximize anti-tumor activity. This is one area where we believe this 70 fold selectivity for MTAP-deleted tumor cells relative to other normal cells that don’t harbor the MTAP gene deletion is going to be very important to spare the mechanism based bone marrow toxicity as well as some other tolerability issues associated with the first generation inhibitors and that’s where we think we have an advantage over the published competitors at this point in time.
Probably just to note that we pleased in the clinical studies at the PK and tolerability for 1719 so far, this has been a very well behaved molecule with respect to solubility, formulation, PK and reproducibility and generally, we are continue to escalate in the Phase 1 study inching up hopefully towards dose levels where we’ll start expanding. But we are very pleased with what we see with respect to tolerability in our clinical studies so far.
Operator: The next question comes from Michael Ulz at Morgan Stanley. Please go ahead.
