Benjamin Zeskind: Sure. Yeah. Thanks for the question. I can take the first part, and I’ll maybe hand it over to Brett to speak a bit to the second part. But, again, we’re really pleased with the progress of the trial. And, I think, we’ve provided some really granular guidance today that should hopefully be helpful in really knowing when we’re going to share data. So, I think, that’s really what I’d say about the trial. And then, Brett, maybe you want to speak to some color on the PD model?
Brett Hall: Yeah, absolutely, happy to. So we’re looking at 2 orthogonal pharmacodynamic assays. One is an induction-based assay, PBMCs, and the other is oncogene driven PD assay, where we’re looking at reduction from baseline of a KRAS-driven model. And so the key thing that we’re looking for there, of course, is attenuation of the MAP kinase pathway at the level of MEK inhibitor . I believe that was my question. I’ll turn it back to you, Ben.
Unidentified Analyst: Yeah. Thank you. I guess, just a quick follow-up on safety. I know you guys are going to be sharing a lot of that data this year. Given that it’s like a cyclical MEK inhibition. What kind of tox profile are you guys looking to see that kind of gives you confidence around the hypothesis of cyclical inhibition, if you don’t mind?
Benjamin Zeskind: Yeah. Thank you. So, yeah, I mean, look, the tolerability that we’ve seen in preclinical models has been really quite good. So, we’ve described that across the multiple animal studies that we’ve run each of which have shown very strong tumor growth inhibition in different models with different mutations in the RAS pathway in each of those we’ve seen very little body weight loss and no more than 3% to 6% body weight loss, so really good tolerability. And I think that during my comments is really kind of the key thing and, I think, seeing a single short half life is really important to that as well, right. I mean, I think that’s fundamental to the deep cyclic inhibition mechanism is seeing the short half life, seeing the high CMAX, manyfold higher CMAX, and so these are some of the things. But let me just €“ let me see if Brett wants to add anything there.
Brett Hall: No, I think you covered a lot, Ben.
Benjamin Zeskind: Okay. Thanks again for that question. Let’s take the next one.
Operator: Thank you. One moment for our next question. Our next question comes from the line of Yaron Werber from Cowen.
Unidentified Analyst: Hi, this is Joyce on for Yaron. Thanks for taking our question. Maybe just a couple on IMM-6-415. What additional preclinical data are you collecting right now? How are you thinking about your clinical development program and the potential design of a Phase 1 trial? And how are you thinking about selection of focused tumor types versus what are you doing for IMM-1-104? Thanks.
Benjamin Zeskind: Yeah. Thanks, Joyce. And we look forward to seeing you at your conference tomorrow. So, yeah, I mean, we’re really excited about IMM-6-415 is on track to file the IND by the end of this year. And, just as we’re calling IMM-1-104, the universal-RAS program, we’re actually calling 415, a universal MAPK program. And that’s because we €“ really, one of the key differences is that 6415 has a shorter halfway. So we project that it’ll end up being the idea or twice a day in humans versus 104, which is, of course, once a day. And so, we think that just kind of like tuning the dial on old-fashioned radio tunes in a different station with a different frequency, we think that different cadence will be optimized for unique biology.
