Operator: Our next question comes from Yanan Zhu with Wells Fargo.
Yanan Zhu: First on the lupus study for FT819, I was wondering — I think you mentioned that lympho depletion regimen is standard. I’m wondering, how does it compare with the German group’s lympho depletion regimen and also if…
Scott Wolchko: It’s exactly the same regimen.
Yanan Zhu: And another question on FT522, and for the non-lympho depletion regimen, I was wondering 300 million times three, that dose regimen at the starting dose, what’s your expectation in terms of how much T cells can that dose remove? Do you think it’s — it could be possible that that’s enough to remove all the T-cells or you might need to dose escalate simply on the basis of clearing more T cells as opposed to optimizing for anti-tumor activity?
Scott Wolchko: Difficult for me to answer that question today. We’re certainly going to prioritize translational data in understanding differences between the doses. Keep in mind that, this is not all about, at the end of the day, it’s not really about lympho conditioning through ADR, it’s about the ADR technology, potentiating the NK cell. And so, the mechanism of action is not necessarily here to condition and remove all T-cell. Not all T-cells express 4-1BB in fact only, for instance, the alloreactive T-cell compartment is the primary expressor of 4-1BB. So this is not really a lympho conditioning approach. It’s meant to defend the cell from potential forces of rejection. It’s also a receptor. It is a CAR against 4-1BB, so it potentiates the NK cell and provides additional activating signal. And at least in preclinical models, we’ve seen synergistic activity between NK cells and T-cells and increased anti-tumor activity.
Yanan Zhu: Got it. That’s very helpful. And then lastly, in terms of your consideration for FT522 for autoimmune disorders, I was wondering what might be the catalyst that prompt that decision? Would it be the observation in this cancer study, and see how the non-lympho depletion regimen is doing? Or is it something else? Thank you.
Scott Wolchko: Yes, I think the 522 study in oncology certainly can inform how we design the study in autoimmunity or study in autoimmunity with 522. I think, quite honestly, at least as I sit here today, I could imagine a study with 522 in autoimmunity that actually would test something very similar to what we’re doing in oncology plus or minus cy/flu.
Operator: Our next question comes from Etzer Darout with BMO Capital Markets.
Etzer Darout: Just a question here on the systemic lupus program. Are you — the preclinical data that I’m assuming you’ve generated, when could we see the data there if you are indeed generating that type of data, and then ultimately just getting us trying to get a sense of how you think that the platform here with 819 compares to sort of some of the emerging data around other assets that are exploring sort of systemic lupus. Thank you.
Scott Wolchko: Sure. I mean, there is a slide in our presentation deck or investor deck. It’s in vitro, but it does look at, and I’ll let Bob talk to it a little bit. It does certainly look at, for instance, the b-cell depletion with both 522, and 819 compares them head-to-head against, for instance, a primary T-cell, if I’m not mistaken.
Bob Valamehr: So our initial study doesn’t apply to that. It’s taken samples from healthy patients or healthy donors, SLE patients and lymphoarthritis patients, and we can clearly see a very distinct and specific elimination of the B-cell compartment within those three populations. But I would also reference you back to Michel Sadelain, the collaboration publication that we have had about a year ago now in Nature Biomedical Engineering where there is a whole slew of in vitro and in vivo studies showing the durability of the activity of FT819 in targeting B-cell.
Scott Wolchko: And then the final thing that we talked — the other thing that we talked to in the past, which we have not presented yet publicly, but are looking for an opportunity to do that. In terms of clinical proof-of-concept, we have looked at cohorts of patients in both the 819 oncology study as well as the prior 596 study in oncology, wherein some of those patients, we were able to detect T-cells cells in those patients at baseline. And we were able to go back and look at, for instance, the kinetics and depth of B-cell depletion in oncology receiving a 819 and/or receiving FT596.
Operator: Thank you. And our last question comes from Mara Goldstein with Mizuho. Your line is open.
Mara Goldstein: Great. Thanks. So I just wanted to go back to the autoimmune question and really maybe to understand not so much FT819 versus 522, but 819 versus the rest of the field of cars. And then the other question is, do you think of 819 as a bridge into looking at other constructs in autoimmune in the same way, you went through that us with NKs.
Scott Wolchko: I think it’s a little too early to know. I mean, the field is very enthused by the potential of taking cell therapies into autoimmunity. And in a small number of patients, and I would potentially say in a carefully selected number of patients, into academic studies, we have seen some pretty remarkable results. I think it is really early for the field. And ultimately, what are the therapeutic requirements that best serve patients and induce long-term drug free remissions, which I think is the excitement in particular about cell therapies. I think we are all going to learn a lot about that, quite honestly, in the next three, six, 12, 18 months as we explore — it is the first versions of autologous and allogeneic CD19 targeted CAR T-cell therapies.
Mara Goldstein: And just on the on the autoimmune study, how many sites are you going to start in the U.S?
