Namely, for instance, homing and resisting the immunosuppressive signals in the tumor microenvironment. Those features were not built into FT538. They were not built into FT536. They are built into FT825. And we do think they are important features. As I mentioned, I do think that cell therapies can synergize with monoclonal antibodies in attacking solid tumors. And I would also note that our FT825 product dose include and is one of the first five candidates that I can think of does actually include while being a T-cell, it also includes our high affinity non-cleavable, CD16 receptor. So, we do have the potential with our 825 product candidate to actually through the CAR target HER2, but also leverage monoclonal antibody content to achieve dual antigen targeting with our T-cell product candidate.
So, in making some of the hard decisions that we were confronted with, we felt like advancing FT825 in solid tumors was the right approach, given the specific and additional functionality built into FT825. It wasn’t necessarily a decision about NK-cells versus T-cells, it is about what we think is a multitude of functionality that is going to be required to successfully have profound impacts in solid tumor.
Operator: Thank you. Our next question comes from Peter Lawson with Barclays. Your line is open.
Unidentified Analyst: Hey, good afternoon. This is Alex on for Peter. Thanks for taking our question. Just one on the 576 program here, do you plan to go to higher than a three-dose treatment regimen? And I am just trying to get a sense for how you are thinking about the dosing schedule. And if you feel that, the dosing schedule has been explored sufficiently here in this indication, multiple myeloma?
Scott Wolchko: Well, certainly in some of the dosing €“ some of the learnings we are taking from our lymphoma programs where we have dosed and typically dosed three doses from patient one starting with 576, sorry, with 516 in lymphoma, and obviously, with 596, we progressed from one to two to three doses. I think given just sort of the biological sort of properties of NK-cells and how they are different from T-cells, including their relatively short half life, and their inability to expand like a T-cell, I think a more high dose treatment schedule is important. And I think in multiple myeloma, we are excited to start the three-dose treatment schedule. We are starting at 1 billion cells, the protocol certainly allows us to continue to dose escalate beyond 1 billion cells.
Operator: Thank you. Our next question comes from Andrea Tan with Goldman Sachs. Your line is open.
Andrea Tan: Good afternoon. Thanks for taking my question. Scott, maybe just given the profiles you have seen to-date with your NK-cell programs and what’s been going on with your competitors. Can you help us understand your level of confidence in this modality? Do you see a scenario where you would become solely an iPSC derived T-cell company instead?
Scott Wolchko: Yes. I think honestly, with respect to NK-cells, I think what we have learned is that if you again, I do think NK-cells have significant activity. We have certainly seen that across multiple NK-cell programs. I think if you really want to develop a highly differentiated product though, especially in the context of competitive landscapes, like lymphoma, like myeloma, you need a unique product offering and that unique product offering I think will require sophisticated and multiplexed engineering. I think you will have to include multiple functional elements. I think you will have to potentially develop, deliver multiple mechanisms of action. And I think you potentially will, ideally with an off the shelf cell therapy need to begin to differentiate one of the modes of differentiation as well as moving away from intense chemotherapy conditioning.
