Operator: Jack Allen with Baird. Your line is open.
Jack Allen : Great. Thank you so much. And congratulations to the team on the progress made over the course of the quarter. I think everyone is excited about the SITC presentation. So maybe I’ll start by asking a little bit about that. You mentioned these transitional biomarkers in the response to the last question. I was hoping you could dive a little bit more deeply into exactly what measures we’ll be looking towards? And then as it relates to the idea of this study being a combination trial, can you provide some context around what you’re looking at as far as the bars for success of the study?
Jennifer Buell : So to your first question, I think what is known about these cells is they actually are incredibly active at secreting tumor killing cytokines like interferon gamma and immune regulatory cytokines on the tumor side of things. We will be showcasing data in which we’ve evaluated both peripheral as well as local information on the biology of these cells that will give us signals of persistence, some of the underlying mechanisms that we believe are supporting the clinical efficacy that was observed in the autologous setting, but also being observed in our allogeneic setting. So I would say there are some known mechanisms of these cells in which they can directly block and kill. They can tumors. They can recruit T cells and NK cells for direct attack as well as for durable memory responses.
And they do so through a series of mechanisms, some of which can be elucidated looking at cytokine profile, other immune markers and we’ll be sharing that data. I think you’ll be enthusiastic about some of the mechanisms that we’ve been elucidating here and some data in which we can show how these cells help other immune cells like CD8 T cells actually traffic and function. This is a very important part, and I’m hesitant to say much more because of our restrictions with the data presentation at SITC, but our data will reveal some very important interactions between iNKT cells and other very important cells and their function that will help us better understand how these cells are working and eliminating disease. I think that you had another question which escapes me right now.
Jack Allen : Yes. I was wondering if you could help contextualize what the thought for success is in the study, given that it’s going to be a combination regimen with an immune checkpoint as well.
Jennifer Buell : So we actually €“ in negotiation with the agency, we were able to go into a setting in which patients have been treated as standard of care with KEYTRUDA or OPDIVO. Those patients progress on those agents. And in some cases, there is nothing more for those patients so they remain on the approved checkpoint. In the case of non-small cell lung cancer, patients progress on KEYTRUDA and then the only option for them really now is docetaxel, which has about a 9% response rate. And so those patients, many of whom will actually €“ if they can tolerate it €“ they remain on KEYTRUDA. We were able to see, based on the mechanism of these cells, if we can add these on to that regimen and actually reverse the progression and expand the benefit of the approved agents.
So the bar here is really any signal. These patients are progressing on standard of care, commercially available standard of care, and we’re adding ourselves to actually change the disease trajectory in those patients and that means, first, certainly, we want to look at tolerability. But next, we’re looking at very, very low response rates in patients with thymomas, cholangiocarcinoma, non-small cell lung cancer, hepatocellular carcinoma, once they’re refractory to checkpoint modulating antibodies. So the bar is low. We will be showcasing what these cells can do both clinically and translationally as well as are they tolerable. And that’s an important marker for what we then can take these cells into based on these features.
Jack Allen : Great. Thanks, so much.
Operator: Kalpit Patel with B. Riley Securities. Your line is open.
Unidentified Analyst: Good morning. This is Andy on for Kalpit. Thank you for taking questions and congratulations on the progress. Looking forward to the upcoming SITC posters and R&D Day. We’ve seen other emerging cell types such as gamma delta T cells, garner more partnership interest surrounding engineered cell products as opposed to unedited cells. Are you seeing a similar trend with your pipeline candidates? And any more general commentary regarding your approach to partnerships would be helpful. Thank you.
Jennifer Buell : Thank you for the question, Andy. I’ll tell you, we are the most advanced company bringing an allogeneic iNKT that’s not engineered into the clinic. So this is really first of its kind data and observations compared to what we see with some other cell types. We also have, of course, the capabilities and the engineering construct, which is, I believe, best-in-class here. And I’ll tell you, just as a reminder, MiNK was born out of a long-standing immune-oncology company, Agenus, which boasts really one of the most productive R&D pipeline. Mark Van Dijk, who’s our Chief Scientific Officer, had joined through an acquisition. Was a part of the leadership team at Agenus and he’s Chief Scientific Officer of MiNK. Mark had designed the antibody discovery platforms at Genmab, Medarex, Agenus.
And he’s been able to actually engineer some extraordinary platforms for MiNK. And that includes our ability through the CARDIS platform to engineer cells, which you’re going to hear much more about at the SITC conference. Also to apply the technology to create iNKT engager technology, which you’re also going to hear more about. And we’ve previously disclosed the platform’s capability to reproducibly generate high-quality TCRs. The productivity of our research engine sets us up for an opportunity to actually leverage that research productivity for partnerships. We have already engaged a number of strategic discussions on leveraging partners who could help us accelerate the advancement of some of these technologies as well as continue to support and expand our financial capability.
So that will allow us to take advantage of molecules and engineering capabilities and our research productivity, not only to finance the business, but also to accelerate the development of our innovations. So you’ll hear more about these conversations as we continue to advance them. What we have disclosed on the infectious disease side, we do have an opportunity, and we are in contract negotiations with DARPA. We were selected as fundable to advance these cells in their native form as a variant agnostic approach to emerging viral and infectious threats. That is an important partnership for us, not only to support our clinical €“ our preclinical progress, but also to expand the clinical benefit of these advancements. So the cells in their native form, there is no comparator because we’re class leading here.
And the cells in their engineered form certainly have quite a bit of interest. There’s a lot of interest in both directions, the native as well as the engineered, both of which we will take advantage of through less dilutive financing opportunities.
