So we think these are off target for both, the NIMBUS compound and for deucravacitinib. We have speculations and ideas about potentially what may be happening, hitting some other targets that are involved in these side effects. But from our perspective, we don’t expect to see these. They are not picture driven, and so they are off target. I think that’s the most relevant conclusion for our compound, VTX958. The other question was about €“ about the €“ go ahead.
Bill Sandborn: Yeah, the viral infection was specifically COVID, and there did seem to be a treatment and an imbalance between placebo and the treatment groups, although it wasn’t very dose dependent as I recall. We don’t really see that with the €“ and I interfere on alpha antibody, and lupus patients and so I’m not quite sure what to make of that.
-: And also to note that this really hasn’t been seen to any meaningful degree in the way that the COVID was seen in the Takeda Phase 2 study. That really wasn’t seen in the Phase 2 and Phase 3 trials across multiple indications with Deucravacitinib, at doses that are getting up to overlapping with some of the numbers Takeda doses. And so I €“ in terms of IC-50 and 70 coverage for the TYK targets. So I’m going to guess in the fullness of time that, that safety issue won’t be replicated, but time will tell.
Raju Mohan: So back to the newer oral L-17 and oral IL-23. So let’s just take oral IL-17 first. So look, we had a discussion about PASI-75, we are PASI-90, we are talking about PASI-100 possibilities with drugs that can achieve the coverage that we do, biologic-like coverage to talk about a drug, where there was absolutely no PASI-75. I just don’t think it’s relevant to this discussion today and we can have more discussions subsequently if and when we see better effects with an oral IL-17, so I’ll put that to rest there. In terms of oral IL-23 and I’m assuming you’re referring to some of the protagonist Janssen PR that has come out, it’s very hard to speculate on data that we haven’t seen and we expect to see this data in the latter half of the year, and we can have a discussion just like we’re having today with €“ compared to the compound is certainly very hard to speculate on PR, generic PR that came out.
But I think more in context of opportunities that we have, with our approach, with the 958 across a broad range of autoimmune indications, and perhaps a lack of opportunity for some of these newer oral IL-23 and I’d like to hear Bill’s perspectives on that, because I think that’s more important to us broadly. Today we can discuss and talk about data that we haven’t seen Bill.
Bill Sandborn: So we’ll need to see, as Raju said, what the data looked like in psoriasis. But as I mentioned earlier, you really €“ to unlock the inflammatory bowel disease market, you really need to have doses that mimic optimally dose IL-23 antibody in psoriasis. So doses that would give you PASI-75 up to 85% or 90% and 60% to 70% PASI-90’s and sort of 33% to 40% or 50% PASI-100’s, and the IBD doses are often a bit higher than that. Part of that is a couple of reasons. You know antibodies and I think peptide antagonists are going to be the same. You’re basically binding already secreted cytokine and different disease settings can give different amounts of cytokine and you can have differences in target mediated clearance.
