Jack Allen: Great. Thank you, so much. And then I just have two quick follow-ups. I guess on the first one, outside of oncology, how are you thinking about the timetable as it relates to development in graft versus host disease? And should we expect that that’s going to be a partnered indication at this point? And then outside of the broader MiNK portfolio, I was wondering if you had any comments on a recent clinical hold from one of your competitors on an autologous iNKT program and how we’re thinking about the safety of allogeneic versus autologous iNKTs?
Jennifer Buell: Okay. Great questions, Jack. So, on the first, as I mentioned, of course, we’re in a really dynamic market where we need to be quite thoughtful. And for GvHD, we see an enormous potential there, and we have some supportive data to indicate a quick path forward to bring benefit to patients, both not only for GvHD, but also for engraftment success. This is an area where we have — we are looking at ways of advancing this into the clinic in ways that would not result in additional extent from our balance sheet right now, and that’s through strategic collaborations and investigators sponsored support as well. So, we’ll be talking more about that soon. We’ve designed the program, and it is designed in a way that we believe can bring the cells forward to a potential very rapid approval, and we’ll be making some announcements about that program in the upcoming weeks.
Our connectivity you’re referring to, that was a patient who had a fatality on the clinical trial. This is a patient with neuroblastoma. And that patient actually had metapneumovirus, which is commonly seen and it’s fatal in pediatric patients who are lymphodepleted. And as you can see from the trial with fast connect, they actually lymphodepleted their patients which is not something that we believe we need to do. We have not lymphodepleted. We’ve demonstrated that we could administer the allo-iNKTs very tolerably, no neurotox, no CRS, no related serious toxicity, of upgrade three. So, we’re in a position where I do believe that the cells can be administered and dosed really quite tolerably without lymphodepletion. And we also are seeing and we’ll be sharing an update about site of the cells, even in that setting.
So, I think that the case with is related to lymphodepletion and subsequent viral infection, secondary to the lymphodepletion that led to a very unfortunate circumstance for this patient. I don’t think that it reads through to the safety or tolerability of iNKT cells.
Operator: Our final question comes from the line of Matt Phipps from William Blair. Please proceed.
Matt Phipps: I was wondering on the FAP-CAR and the preclinical poster at SITC, some of the efficacy data was actually best combined with an NY-ESO one T cells. So how does that kind of preclinical data influence your thoughts around maybe combination development of this program? And then do you plan on trying to look at any biomarker for enrollment or like an immune-excluded phenotype? Or just how do you pick patient populations for that program?
Jennifer Buell: Well, that’s a great set of questions, Matt. Thank you. So, for that program, we actually set it up using the NY-ESO-TCR and that model to exemplify what a chronic antigen stimulated environment would look like. So, what happens when immune cells are constantly perturbed. And then can these cells actually overcome that perturbation and also reinvigorate CD8+ T cells to curing potential. And at our poster at we actually demonstrated that we could do that. So that model was to help us better understand what these cells can mechanistic review to reverse exhaustion and then carry CD8+ T cells into the stroma and invoke killing. Now the design of that molecule with seeing gives us opportunities for a potential biomarker selected population.
