Steve, safety is clearly a very important consideration in the management of chronic diseases such as autoimmune disorders. I will note, however that even as we await those initial human data in multiple myeloma with 2644. We are in parallel performing preclinical studies to understand how this molecule could differentiate not only from imvotamab, but also other potential competitors in this space. So in summary, a lot of activity and we await that human data.
Stephen Willey: Great. Thanks for taking the questions.
Fred Schwarzer: Thanks Steven.
Operator: Thank you. And our next question is from Greg Harrison with Bank of America. Your line is open.
Greg Harrison: Hey, good afternoon. Congrats on the progress and thanks for taking the questions. First off maybe could you give some additional color on the transition towards autoimmune indications for imvotamab? What was the decision process that led to the choice of lupus and RA, and how broadly do you think imvotamab could be applied across autoimmune disease?
Fred Schwarzer: Well, Mary Beth, I think that’s probably a question for you. It’s one we spend a lot of time thinking about, and it’s very broad. So I’ll leave you to go at it Mary Beth.
Mary Beth Harler: Indeed, and thank you for that question. Again, the CD20 as a target in autoimmune disease well established and a very broad dataset out there in the literature with respect to how various approaches to CD20 and B-cell depletion may look in the management of different B-cell and auto €“ auto-antibody mediated diseases. As I think back to the conversations that were taking place, as our company contemplated the choice of continued investment in NHL versus beginning to invest in autoimmunity, you heard the key points of that rationale earlier in the presentation given the level of competition, given the change in the regulatory and therefore the commercial environment in the lymphoma space, right? The upside on the autoimmune front, again given that this is a well-characterized target and one that could absolutely benefit from deeper B-cell depletion.
Those are the things that really got us excited. If you have not seen the publication from Georg Schett at all from the University of Erlangen in September of 2022, looking at an anti-CD19 CAR-T in five patients with severe lupus that really catalyzed a deeper look at what is possible through deep B-cell depletion, right? And we think that imvotamab, which we believe will enable deeper B-cell depletion than currently available anti-CD20, because we are not dependent upon local complement and local NK cells. We know from our preclinical data that imvotamab will deplete in the spleen, in the lymph nodes, in the bone marrow, where reservoirs of pathogenic B-cells can sometimes hide and basically continue to drive autoimmune disorders. So our hope is that imvotamab will deliver that level of deep B-cell depletion that was suggested by the CAR-T data, but do so with an off-the-shelf product, with a better safety profile, clearly lower cost and fewer logistical considerations, so we’re quite excited and moving quickly.
Chris Takimoto: So I might add there that in terms of Greg, to your question, why lupus and RA as the first two indications and where might we go beyond that? Lupus obviously as Mary Beth mentioned you’ve got the proof of concept with Georg Schett and that paper of real immune modulation, that’s obviously a great place for us to start because we think we’ve got advantages over CD19 CAR-Ts there. RA is a place where we think we can get a signal very quickly in terms of biomarkers, and so forth. But in terms of where we go after those two, I think, you can think more broadly first any place where CD20 has shown signs of clinical activity or efficacy. Those are good places and any place across the entire landscape of autoimmune diseases where you got autoantibodies implicated in, in disease.
