Simba Gill: Yes. So on the AD data, we’ve given previous guidance but on the we’d be looking for around 40% PASI-50 — sorry, EASI-50 patients on active with EASI-50 or greater or placebo separation of 15%. So a separation in terms of percentage of patients with EASI-50 or greater of 15%. on the cohort 4 data. And that’s been consistent guidance for some time possible. On the data with EDP2939 first the remainder of the integrated profile but underpins everything we’re doing. Very uniquely, the potentially orally delivered drug that is very safe and well tolerated and has meaningful efficacy and can be priced with flexibility. What is something that has a Otezla-like efficacy or greater with safety and tolerability and level or greater would be a big win.
You’re aware, Gospel, so you guys have a forecast for Otezla that I think it’s most people consider on track to be a $3 billion a year drug with significant tolerability issues. So Otezla-like efficacy with safety and tolerability, we’ve got a major drug. We’re very close to that level of efficacy and I think we have strong conviction that, that is a likely result. What is even more exciting is what Mark talked about because of the fact that preclinically we’re seeing JAK or biologic there’s a big range between Otezla-like efficacy engaged at that level. But anywhere in that range is a win for us with EDP2939.
Operator: Our next question comes from the line of Kristen Kluska with Cantor.
Kristen Kluska: I just have one this morning. So I understand you haven’t necessarily discovered what has caused the high response in placebo, but I’m curious if there’s anything that you’re able to rule out at this time?
Simba Gill: So we have essentially ruled out the obvious possibility that there was a mix-up in supplier drug i.e. the patients took active instead of placebo and vice versa and we’ve worked through all of that, that does not seem to be . So that’s the one.
Operator: Our next question comes from the line of Peyton Bohnsack with Cowen.
Peyton Bohnsack: I guess just to start out, could you discuss what gives you the confidence to move forward with the lower dose in the psoriasis patients? And did you see any evidence of target engagement or biomarker changes in healthy volunteers in that study, in the 2939?
Simba Gill: Hi, Peyton. I’ll let Mark take those questions.
Mark Bodmer: So we’ve used actually a very conservative scaling factor to get from preclinical studies clinical studies with doses 4/10 of the 12 particles of the extracellular vesicle obey. Actually, based on the scaling factor by volume, if you know your PK/PD and pharmacology and allometry, that’s 100x higher than would be predicted. And the ability to do that is actually based on the small size of the EVs and their potency and that’s a big part of the EDP1815 as you go back to similar answer a moment ago to the question about the expected outcome in EDP2939, actually the whole point of what I was saying was to do with the estimated probability of getting above that baseline level of efficacy based on very, very basic principle of pharmacology in terms of potency and process goes forward.
So the we spent a lot of time for baking, how do we pick a single dose for a skinny study for a Phase 2a and the answer is we went . We went way above what we thought was likely to be the minimum effective dose.
Peyton Bohnsack: Great. And did you guys see a target engagement or biomarker changes in the healthy volunteers?
Mark Bodmer: We didn’t do that. So actually, you need to get me for an hour separately. So these drugs work in at-a-point stage it’s not to see unless there’s inflammation going on. It’s the same with these. So in the healthy volunteers, we don’t even look at that because
