Operator: Our next question comes from Bill Maughan from Canaccord Genuity. Please proceed.
Bill Maughan: Good morning and welcome Mike. So, two questions for me. When you cite the 57 accounts to DANYELZA, is that all, that have written and currently set up to write DANYELZA or is there sort of a time cut off to weed out any who may be inactive? And then a question on the SADA platform. Looking forward to potentially trying to read through the GD2 targeting to the CD38 targeting, are there any unique challenges to targeting CD38 versus GD2 that might prevent a seamless read through from that data? Thank you.
Sue Smith: Bill, thank you. I appreciate the question. I will take the first part of that, and I will ask Sue to address the accounts that are set up for DANYELZA.
Sue Smith: Thanks. Thanks, Bill for the question. So those 57 accounts are set up to use our product. And to give you some perspective, in the United States, only a 152 accounts have ever used any anti-GD2 therapy. So we are well on our way to over a third of those accounts, who are using DANYELZA. And as we mentioned before, we are seeing deeper penetration of those accounts and also the repeat use in 22 accounts with two or more patients. We are also seeing an increase in the Tier 1 accounts. So we are making good headway from a breadth and a depth standpoint.
Sue Smith: And Bill, as far as your second question goes on the GD2 versus CD38, I’m going to pass that to Steve. But understanding that, our team has a very deep and domain knowledge in CD38, which actually makes it very interesting for us moving forward and being able to target the CD38 receptor. So Steen?
Steen Lisby: Yes, there are some differences between the two because going to the CD38, we are entering the hematological space. And of course, with a two step procedure, we also need to make sure that we don’t have too much bone mar involvement, which is part of the protocol development that we have some limits on how much bone marrow involvement the patient can have in order for us not to put radioactivity directly on the T-cells. So there is some slight difference in the protocol development and the inclusion exclusion criteria, but else most of those lymphoma patients also have like the lymph nodes of course involved in which we are quite comparable reaching those areas as compared to solid tumors. We are see now with GD2.
Operator: Our next question comes from – from BMO Capital Markets.
Unidentified Analyst: And Mike congrats on the role here, as CEO. Just one quick question for me, going back to some of the comments in the 10-Q around the interval of dosing of two to five days for GD2 – where you ultimately think would be sort of an optimal dosing schedule for the technology sort of moving forward as you kind of go through sort of Part A into potentially the Part B expansion.
Michael Rossi: Thank you for your question and I will pass that to Steen, as he is the majority of the work on the targeting.
Steen Lisby: So I think, it is too early to say what you could see on the curves, I shared with you earlier on this call. There was a slight shift to the right when you get wind up in the protein concentration. So likely the dose interval will be longer than the two days, depending on how high we can dose up the protein. And this is a safety precaution, so we will have to wait until we see the B and 10 milligram dose cohorts to see how the blood PK behaves. And this will also together with the absorption into the tumor. So bio distribution, tumor symmetry will dictate the sweet spot where the best relationship between the free drug in the blood and tumor uptake would count. So for now at least we can say that we actually worse in a good position here in the early part of the trial, but likely they could be longer than two days.
Operator: Our next question comes from Mike Ulz from Morgan.
Mike Ulz: Maybe just a follow-up on the ADA program. You are in the process of advancing the CD38 program, but just curious, thinking about advancing some of those earlier programs such as the HER2 program. And will you be waiting to see more of insured data from GD2 potentially before deciding to advance some of those programs?
Michael Rossi: I appreciate the question. As we start looking at this, we have committed to submitted IND every year and we are going to continue to do that and advance some of the early programs on. We are extremely confident in ADA and what it can do and the problems that it actually addresses in the radiopharmaceutical therapeutic market. So we are going to continue to invest in the early programs and look to introduce IMEs on an annual basis in order to continue the events, the overall side Next question, operator.
Operator: Our next question comes from Robert Burns from HC Wainwright.
Robert Burns: Congrats on the quarter and congrats Mike, on your appointment as CEO. Just two questions, maybe two and a half-ish from me. So since the point of the SADA platform is to reduce radiation associated toxicities and enable greater doses of radiation to be received, I was curious to know whether or what – at what level of radiation would you start seeing dose DLTs and toxicities that would put patients off of therapy if you weren’t given the SADA platform specifically associated with the lutetium? So I want, I’m essentially trying to get at what is the incremental dose level you think you could get given that a base level radiation with SADA?
