And then from there, over time, we’ll build the cumulative evidence about its superiority. I think to emphasize the big picture here in the G12C space, it’s very likely that combination therapy is really where the puck is going to be. We’re already moving there, as you know. And so focusing too much on trying to prove differentiation around monotherapy isn’t probably the wisest thing for us to do, although we certainly believe mechanistically, that’s the case and we think we will accumulate some data pointing in that direction. But the real impact for patients is going to come from those combinations. And so demonstrating that Pharmacy-6291 can be combined effectively, tolerably, safely with the other agents will be extremely important and that can only come after we get to reach a recommended Phase II dose and schedule and then we can move forward from there with those combinations.
Eric Joseph: Okay, got it. And then a follow-up, if I could, on the G12D RMC-980, I guess, looking to starting patient dosing in mid-next year, how should we be thinking about the therapeutic window for this compound? And I guess relatedly, are you able to characterize the PK of the compound relative to the multi-RAS and the G12C candidates?
Mark Goldsmith: I’ll try to process the second part of your question. But for the first part of it, is it mutant selective Well, it’s highly mutant selective. And it is a covalent compound. It’s the only own KRAS-G12 covalent compound and it carries all of the benefits of covalence C which is that even after you take away drug from the system, there’s still covalently bound inhibitor that’s blocking G12D in the own state. So it’s highly mutant selective compared to, let’s say, RMC-6236 which is served by definition, equipotent against all RAS , including wild type. So there certainly is going to be a ceiling for dosing RMC-6236, at which point you would start to see on pathway, normal tissue, RAS, media side effects and there shouldn’t be the same dose ceiling for RMC9805.
But those are just different to some degree, technical characteristics. What really matters is can you dose either of them sufficiently to achieve the desired anti-tumor effect safely and tolerably and we project the answer to that is yes based on preclinical results but I have to demonstrate that in the clinic. The second part of your question, maybe you could unpack that a little bit for me which is PK. I wasn’t quite sure what you were trying to get at from the PK question. I’d like to understand that .
Eric Joseph: Yes, absolutely. Some competitors in this space have noted challenges in coming up with an oral formulation, similar to your approach with 9805. So I guess just looking for a little more color around the PK properties of your compound, how you feel about how investors get comfortable with a favorable oral bioavailability with that compound. I guess are there — is there a contrast with 6291 that might be informative here?
