Thank you for coming to GS Healthcare Conference, Matt, and I want to welcome you representing Gritstone, and want to hear some updates about what's been going on with the company. So maybe to start, could you provide an overview of the Gritstone approach and pipeline with a focus on the key drivers over the next 12 months -24 months? Yeah, I'm happy to. So Omari, thanks for, thanks for the invite on behalf of Gritstone. I'm happy to be here. I'm excited to talk about, you know, our story in both oncology as well as infectious diseases. And so, you know, there's a lot going on. I think it's a really, really exciting time. And maybe I'll start with the oncology, which I think is the key value driver for the, for the company right now. So, you know, maybe just as a little bit of a reminder and as perspective, you know, we, we founded the company back in 2015, originally as Gritstone Oncology, now Gritstone Bio, of course, as we've expanded. To really realize our vision, to bring, you know, tremendous benefit and see, you know, a profound impact with cancer immunotherapy via cancer vaccine. So, at that time, when we started the company, there were a couple of papers that had been published from some of our founders in the New England Journal and Science, basically showing when you activate T cells with checkpoint inhibitors, those T cells are recognizing neoantigens on the surface of the tumor. That was a key insight that really was a, you know, one of the key moments where we realized, and I think frankly, others in the field realized, that cancer vaccines could be an interesting and exciting new modality. And so we started it, and we've really, you know, we built over a number of years, a number of different elements. So you know, a prediction platform, next generation vectors and chimpanzee adenovirus, as well as self-amplifying mRNA. We built our manufacturing facility, and we also brought other capabilities, which we think are important for this as well, which is, the ability to take these immunogens or antigens and put them together in the right way, in the cassette, in our vectors, and also, you know, learning. You know, going from bench to bedside, back to bench, back to bedside. That kind of cyclical approach is something that we... You know, it's very near and dear to us, and I think we've seen the benefits of that. So, you know, we've built this company and you know, to bring the most potent vaccines forward into the clinic to help you know, unmet needs, whether those are oncology or infectious diseases. And I think these are you know, it's now a really exciting time for cancer vaccines. I think we've seen exciting data over the last now couple of years, but from Moderna, but even most recently, as last week at ASCO. And I think it's a watershed moment for the field, and I think you know, this is a exciting new modality for cancer immunotherapy that I think is here to stay. I think, coming in Q3, our mature PFS data from the GRANITE study will be key, I think, for the field and something that we're super excited about, and happy to, you know, dig more into it as this dialogue continues. Definitely. So you talked about a lot of learnings- Sure ...and being sort of like a cyclical process. And so cancer vaccines have been a challenging modality to kind of develop therapeutics in. So can you talk about what makes the GRANITE platform different, and how it's able to overcome some of these challenges that you experienced? Yeah, I appreciate the question. It's a great question. So, you know, when we started, and again, I'll put it into context. When we started the company, you know, we couldn't look to a cancer vaccine success, really. There was, you know, no cancer vaccines that had really worked, so we think we needed to figure this out, and we looked to infectious disease as really our benchmark of how, you know, because vaccines have been used in infectious disease for many, many years. And so the things that we thought were important, first off, you got to put the right targets in, and neoantigens are non-self, those are important. Second, you want to drive T cell responses, robust, you know, high magnitude T cell responses, and we think you needed to do that with viral vectors and deploy those viral vectors in a way that would maximize T cell responses, so a heterologous prime boost. And then the third piece, which I think made it the right time, is to combine it with checkpoint inhibitors. So I think all the players right now are definitely combining. But those first two pieces, I think we can talk about and talk about maybe some of the differences I see in the space. So I think there's largely a couple players that are all in the clinic right now with their personalized cancer vaccine or individualized cancer vaccine, really an N of 1 therapeutic that's manufactured individually for each patient, in randomized phase II trials. We have Moderna, which clearly presented some data, most recent data last week. BioNTech, who also presented some... So Moderna with adjuvant melanoma, Right ...... Moderna, BioNTech with some adjuvant PDAC, pancreatic, and then Gritstone, we presented some preliminary data in Q1, and we'll have mature randomized phase II data in Q3. So how do we think about these different players? Well, first, there's... You have to put the right targets in, right? And so that's something that Gritstone, we've invested a lot of time and resources in to build a platform we call EDGE, which is our epitope identification platform. Over a number of years with real-world tumor samples, and we think that's important for a variety of different real reasons. It has a positive predictive value of well over 80% right now, covers lots and lots of alleles across the whole globe. And we've been very deliberate, and we're a very science-oriented company, so we've published it in a peer-reviewed manuscript in Nature Biotechnology. So, we've put it out there, and I, you know, I tend to think of it... I like the three Ps. We've published it, we've patented it, and we've partnered it. There's a deal, we partnered with a biotech company a number of years ago, bluebird bio, now 2seventy bio. So, you know, we feel very good about that, but that's one piece. Looking at BioNTech and Moderna, I think it's not entirely clear to us how Moderna achieves their prediction. They haven't published it yet, so I can only talk about what we do. I would say that BioNTech acquired a small biotech company called Neon a number of years ago, which had also invested in... We knew them quite well. They had put information out there about their platform. We thought it was quite good. I think there's a number of advantages that Gritstone has compared to that approach. It's unclear how, if, and how they're using it, but I think it's a fair representation that they're probably leveraging that technology in some ways. That's, you know, a antigen identification. The next piece being the vectors, right? So delivery of this payload. And so at Gritstone, we are big believers in, you know, you have to have very high T cell levels you want to drive, and we think that's best accomplished with viral vectors. And we do that with an adenovirus and a self-amplifying mRNA. And our samRNA is derived from an alphavirus, so again, virus delivery. And, you know, all things point to the adenovirus is one of the best vectors for driving CD8 T cell responses, and that's... You know, when we built the company, that was our goal, and we were unshackled, or we were- we weren't shackled by an existing platform. So we can go out and determine what's the best platform for that application. Mm-hmm. Obviously, we're all familiar with the Moderna mRNA as well as BioNTech mRNA. Right. So I think there is some distinction there. And then maybe the last piece is the different context, indications by which we're pursuing our randomized studies. So obviously, we have our study in first line metastatic MSS microsatellite stable colorectal cancer, and randomized, and we'll have mature data in Q3. Moderna has just presented the data, again, three-year follow-up, quite exciting for the field, I believe, in adjuvant melanoma. And then BioNTech their randomized study is in first-line metastatic melanoma. Now, we haven't seen, as far as I know, that data from that first-line metastatic study yet. I think it was originally supposed to be in 2023, and I think we have-- I don't... I'm not aware of their latest guidance about if or when they will publish that or present it at a scientific meeting. We have seen some data from BioNTech with their pancreas, the pancreas study, the PDAC. I think it's a small number of patients, but it's a study being run by Vinod Balachandran, and I think it's exciting, even in those, I think, 16 patients, in the data they saw. So I think that those are some of the differences between our platforms. Mm-hmm. You know, again, I think I'm waiting to see some of the data from BioNTech, and obviously, I think the field is waiting to see some data from Gritstone later this year. I think those are two really important moments this year. So I think in many ways, this is a year of the neoantigen cancer vaccine. Yeah. Cancer immunotherapy. No, right. Yeah. It's gonna be big, it's gonna... big year for us. Yeah. It's a very, you know, great overview of the thus far. Maybe to level set the conversation, could you just walk us through the data you... in colorectal cancer, and, you know, what are the key takeaways from that data set? Yeah, I'd be happy to. Great question. Obviously data that we were very scared. You know, we looked at the preliminary data, needed to see this. So we announced it at the end of Q1 and put it into the public domain, and we're hoping to potentially present updated data at a scientific meeting in the future. We haven't given guidance around that, but I think that's, you know, in a science first company, that's something we'd like to do. So what did we see? Well, you know, maybe taking a half step back, you know, how did we get to this study and what is the study? So we originally ran a phase I/II study- Right ... in a number of different tumor types. And, you know, candidly, in the third line or, you know, two previous lines, colorectal cancer, we saw some really encouraging signals. We saw a PFS benefit, we saw an OS benefit, small numbers of patients. But when you see that kind of benefit, the logical thing is to move it into a randomized setting, and that's exactly what we did. So we kicked off a randomized... Moved it upline, so instead of being essentially in the third line setting, we moved it up to a first line setting. IO works better earlier, we wanted to take advantage of that. And also those patients are, you know, in great need. This is a huge unmet medical need. I think, you know, colorectal cancer is, I think, the second leading, you know, cancer killer in the U.S., and, you know, it's also, a big unmet need globally, you know, over 50,000 cancer deaths a year in the U.S. So huge unmet need... with poor, you know, really, not much innovation that we've seen in this space, so patience in me. So we started this study, and it's a really exciting design. We have first-line patients who, when they get diagnosed, they typically receive, a standard oxaliplatin-based chemotherapy, so 5-FU plus Bev plus oxaliplatin. And then, unfortunately, those patients aren't able to tolerate the oxaliplatin, you know, after about four or five months. They roll off that because of peripheral neuropathy- Mm-hmm. They continue with 5-FU plus Bev maintenance therapy. So the design is all patients in our trial get that oxaliplatin, 5-FU plus Bev plus oxaliplatin, and then they, when they roll off, they'll either receive 5-FU plus Bev plus GRANITE vaccine regimen or versus 5-FU plus Bev. It's a very, very nice design. And it's randomized. So that's, that's our design. Our vaccine does, so ChAd plus we also include checkpoints. In this case, we have Atezo given monthly, as well as two shots of low-dose subcu ipi. That's the vaccine regimen. So what did we see? So you know, something. We published our data from the phase I/II, and what we saw was, you know, we drove T cell responses, right? So we were able to make de novo T cells, good check. Those T cells traffic to the tumor, check. They proliferated, check, and then they killed, and then we saw clinical benefit. Right. In our trial, it's preliminary, so it's still early, but what we saw was super encouraging, for at least me. On the PFS side, we saw, in the overall population, we saw a PFS benefit, hazard ratio of 0.82. Encouraging, but there was a lot of censoring. Mm-hmm. So not as many events at that preliminary time point. So what did we do? We tried to take a look at that, at our patient population to see, is there a subset that was potentially early progressors, a high risk, as some would say, to get an early look into what maybe the Q3 data would look like? And we were able to do that. There's a subset, basically, that we were able to identify by looking at mean variant allele frequency, and it's a standard method that's been published a number of times, basically having a cutoff about 2%, splits the population quite nicely to about two halves. Mm-hmm. When we looked at those early progressors, the high-risk group, vaccine versus control, we saw a really profound hazard ratio of 0.52. Exciting. It's early, but it's exciting, and I think that that's one of the reasons why we wanted to put that data out there, because we think this is a space that a lot of people are watching and excited about. It's a new modality, clearly. And we want to get that data out into people's hands and then continue to provide upcoming data cuts when most appropriate. So we've given guidance around Q3 for mature PFS, and that'll be. That's a nice point in time because the median PFS in this population is around 11 months. We should be right in, right at Q3. It'll be a nice point in time. And then, mid-2025, we should be at OS. Median OS is around 24 months or so in this patient population. So, really encouraging data on the PFS front. And I'm looking forward to the data coming this fall. Nice. Yeah. Yeah. Maybe we can take a step back- Sure. talk more about the initial study design, looking at ctDNA Yeah. and sort of what happened there. Yeah. You know, I think now the focus is on PFS- Yeah Q3 and what led to that decision. Yeah. So it's a great question. So I think, I think we're still big believers in ctDNA. Mm-hmm. And I think ctDNA is still a biomarker that the field is getting excited about. Right. There's, you know, lots of posters clearly at ASCO. You're, you guys are very sophisticated on this. You know, I often point to the Immunocore data, where, you know, ctDNA was a great biomarker, which then, you know, overall survival demonstrated a profound benefit. Obviously, drug was approved. We're big believers in ctDNA. I think the trouble we ran into was we didn't-- we were-- in some ways, we did not have a wealth of ctDNA data- Right ... in this patient population. So we had to take educated guesses, and that's, you know, that's the world we live in as biotech. We have to make bets and guesses based on incomplete information. And so we did that. And the bet, the guess that we had to make was we weren't sure of the ctDNA kinetic. You know, especially in this patient population, kind of post-chemo. Mm-hmm. We were looking at it, and we defined the endpoint basically as a single point in time. You know, did you have a reduction of 30% of ctDNA at this point in time? What turned out to be the case is that it seems to be that there's a delayed effect with chemo. Remember, all these patients, and this is part of the trial design, are gonna be getting chemo in the induction phase. Right. You know? And so there seems to be a bit of a delayed effect of that chemo, where we saw a reduction in both the control as well as in the test arms, post-chemo. And that reduction of 30% basically did not show a difference on ctDNA response across both arms. And so that's the way we defined that endpoint was problematic. Mm-hmm. Now, I don't think it impacts our belief in ctDNA. I think we're still big believers in ctDNA, and we absolutely see, you know, trends looking at ctDNA over time- Right as still very, very important. I think it's not a fault of the ctDNA. I think it's a fault of the definition of our endpoint. And so, you know, going forward, I think you're still gonna hear us talking a lot about ctDNA because we're believers in it, and I think the field believes that that's a really important biomarker for, you know, cancer immunotherapy in general. I think what we're gonna be focusing on for at least the trial going forward is clinical endpoints, so PFS as well as OS. Right. But we're still gonna be learning a lot from ctDNA. But, you know, I would reiterate, I think it was a problem with the endpoint definition, not with and really based on the fact that we had limited experience with how ctDNA would play out in this particular patient population, kinetics, et cetera. Got it. Yeah. From the dataset, you saw a 0.2 hazard ratio. Mm-hmm. This is based on this, Cox PH model. Yeah. So is this a standard practice in oncology? Yeah In measuring hazard ratio? And then, you know, how does that differ from, like, other ways to measure hazard ratio? Great question. The Part A2 was overall population. Remember, there was... when we looked at it, a small subset, we saw a dramatically improved hazard ratio. We'll see how it pans out in the fall. The statistical approach we applied, you know, it is a common approach. We actually used a variant of it, which again is common approach. Mm-hmm ... and piecewise. And, you know, going back to the design, right? Both control and test arms actually have the same induction chemo, right? And at the end of that oxaliplatin-based induction chemo, that's when you have the two different treatments, 5-FU plus Bev plus GRANITE versus 5-FU plus Bev. Right. So the statistical approach we applied, as laid out, pre-specified in the statistical analysis plan, the SAP, was this piecewise approach, where we didn't wait, events basically occur in the induction phase- Right - because they're the same. Yeah. And so, you know, to... Again, it was pre-specified, and it's a, it's a, I guess, well-accepted standard approach. Got it. We'll of course be at the end of our study, we anticipate, well, in the future, what we anticipate doing is going and approaching the FDA with an end of phase II meeting and having discussions about, you know, our specific proposals around a statistical analysis plan. Mm-hmm for phase III. And so these are discussions we're excited to have, obviously, with data in hand, and hopefully, you know, it's the data we expect, based on what we've already seen, just in a more mature form, that we'll take to the agency and have that discussion about, you know, the plan for phase III. Right. It'll be a big year. Yeah, certainly. Yeah. So you mentioned, many of the patients were censored in the- Yeah the data you presented earlier this year. Could you walk us through, you know, why that was the case? And, you know, what do you expect from more mature data with this level of censoring? Yeah. Yeah. So, as I mentioned, the data we presented at the end of Q1, in the overall population, I think it was around 60%, so of the, of the patients were censored, so not, not mature, preliminary data. And, you know, we wanted to get... You know, even in the preliminary state, we wanted, based on what we were seeing and the encouraging signals, we wanted to put this data out there. Right. There's clearly a subset. Again, I think we used high risk as part of our presentation at the end of Q1, but you can also think about this as early progressors. There's a patient population that basically has events sooner, right? Some patients progress earlier, some patients progress slower. And those patients that progress sooner, quicker, high risk, we were able to see more events, and in that analysis, I think there was only 40% censoring, and that's the patient population we saw 0.52 hazard ratio. So looking forward, what do we expect? I think the median PFS at that point in time was around 6 months or so. Mm-hmm. The median PFS for the overall population is expected to be around 11 months. So that's exactly where we'll be at in Q3. We'll have a much more mature overall population, and we may even look at subpopulations again, but I think the overall population is probably gonna be, to me, you know, what I'm interested in. Got it. Yeah... And so like, let's say we get to Q3, you have this data in hand. Mm-hmm. You know, what would be the next steps for the study, you know, on the forward? Yeah, data look great. Let's play that scenario. Right. So data look great. We're in a world where we're gonna engage, be engaging. First off, to see, you know, an improvement in PFS in this patient population, let's just - that would be amazing, right? Right. In a first-line metastatic CRC, we, we've been in a world where we haven't seen innovation, we haven't seen new therapies, and we haven't seen much benefit for these patients. So, you know, we're, we're always patient first and patient focused. So I think, we would all, I think, you know, it would be a surreal moment for all of us to see kind of us helping patients, in this population. So in that world, what's next? Well, we would go to the FDA and have an end of phase II meeting, where we talk about that phase III, because that's what we would be driving towards, right? Positive randomized phase II data. You know, now you're ramping it up because, again, this is a small... You know, this is still only 100 patients, randomized 1:1. So then we'll be moving towards a you know randomized phase III that we can take to registration. So end of phase II meeting, we'll inform the design, we'll have discussions with the FDA, we'll align on some aspects of that trial, and then we'll be moving forward with that. We'll also have in 2025 you know OS data, which we think will be another important data point to share. Again, PFS, we think is a great proxy, an approvable endpoint we know in many different tumor types, but we're all gonna be also interested in overall survival- Right ... of course. Then we'll push forward with the phase III. I think it's also important that, you know, this is a cold tumor. Something that is constantly on our mind is, you know, success in a cold tumor by driving to neoantigen T cells in a tumor that really doesn't have those T cells in the tumor, therefore, checkpoints don't work. Mm-hmm. Where else do you go? And what other indications does this open up? And I think this, this opens up a wealth of opportunities for, you know, patients in need. You can start to think about, you know, warmer tumors or even hot tumors, right? Mm-hmm. You know, ovarian cancer, breast cancer, lung cancer, melanoma is clearly hot. These are all different opportunities that gastric, etc., that GRANITE could work in if we're seeing success in a cold tumor like MSS CRC. Even not only in the metastatic setting, but also in the adjuvant, maybe even neoadjuvant. There will be a lot of work being done within Gritstone to understand: where else are we gonna go? What are those priorities beyond colorectal- Right ... that we would be interested in? Now, I don't want to diminish the huge opportunity, from an unmet medical need, as well as a commercial opportunity for colorectal. I think it's massive and with limited competition. Mm-hmm. But I think we would also be thinking about what's next, what other tumor types would we potentially be interested in, and how do we prioritize those? So those would be, I would say, in the wake of success in Q3, that would be a great dialogue for us to have about what's next, Matt, what's next, Gritstone. Great. Yeah. Thank you. So maybe we should pivot the conversation now to talk about the infectious disease- Yeah ...pipeline, and you know, what updates do you have from the company from there? Yeah, so I think, you know, we obviously started off as an oncology company, but we saw great application of our vaccines, not beyond oncology, right? Right. In infectious disease. And, as I think about it, we have kind of within infectious disease, we kinda have two different big buckets. We have the prophylactic infectious disease vaccines- Mm-hmm ... and we also have therapeutic infectious disease vaccines. And that's kind of a, maybe a, a newer concept in the ID world. So maybe I'll take prophylactic first. So when I think about prophylactic, these are, you know, this is like SARS-CoV-2, our next generation SARS-CoV-2 vaccines. Right. So at the highest level, you know, we're big believers in T cell immunity. Clearly, we talk about that a lot with the cancer immunotherapy side. And we see this opportunity to engage both arms of the immune system, your B and T cell side, with the ID vaccine. So we generate these chimeric payloads for next generation SARS-CoV-2, think spike plus T cell target. Again, both arms of the immune system. And we took a number of products into the clinic, and, you know, I was happy to see a number of partners came on board, so I worked closely on all these relationships and deals to see a number of partners that have come around the table, whether it's Gates- Mm-hmm ... whether it's CEPI, BARDA, etc., NIH, who have worked with us to take these next generation SARS-CoV-2 vaccines into the clinic, and what we saw was really cool. We saw, you know, I think, profound, durable, immune responses, something that I think is in contrast to some of the waning immune responses you see with first-generation mRNA products. Right. So that was exciting. That was based on, you know, some of the studies that Gritstone funded, as well as some of these externally funded studies. I think the largest data set is really from our South Africa CEPI study. And those were in... It's a very cool design. And we've presented some of this data at a number of the meetings, formerly called ECCMID, ESCMID now, I believe. And that led to us working with BARDA, putting a BARDA contract in place. We've hit some hiccups with the BARDA study, so we haven't yet commenced that study. Mm-hmm. But we're working through some of the GMP manufacturing issues, and we hope to, you know, provide an update on timing in the future on that. But that would be a, I think, tremendous for our infectious disease portfolio, because that would be a head-to-head 5,000, you know, Gritstone vaccine, next-generation Gritstone vaccine versus 5,000 approved product- Mm-hmm superiority study. So that's, you know, one aspect of our infectious disease portfolio. We have, obviously, a relationship with Gilead around HIV cure, so I think of this as an HIV therapeutic- Right infectious disease vaccine. T-cell's really important in HIV, so that program, that's theirs. We let them comment on that, but that's still going. And then we have a number of earlier infectious disease assets and programs that we're working on that we'll be disclosing more and more details in the upcoming months. Nothing yet to break today, Omari, but you know, we're excited about you know, the applic... You know, again, going back to those capabilities, we have these vectors, we have this antigen identification technology, which EDGE, which you can deploy, not only in cancer, but also infectious diseases for T-cell targets. We have a lot of experience putting these different cassettes together, whether it's B-cell targets and T-cell targets, and deploying either one vector, like samRNA, for prophylactic ID- Mm-hmm -or whether it's both vectors for other, infectious disease therapeutic applications. So there's a lot there, and I think I remain very bullish on our infectious disease portfolio and where we can take it. I think we've largely been leveraging external dollars- Right for infectious disease, and you know, it's work I'm intimately involved with, and I'm happy to say that there's still a lot of opportunities for that, with partners, et cetera, on the infectious disease front. Got it. Maybe you can expand on that and tell us what a potential partnership could look like? Mm-hmm in the infectious disease. Yeah. So I think there's maybe, maybe a couple different buckets, right? There's, call it, there's governments. Mm-hmm. So, you know, we've had success securing BARDA contract as one, and I think there's other opportunities with government, both U.S. and ex-U.S., so governments. There's what I would call non-government organizations. CEPI, I think, is one, you know, the Gates Foundation. There's other organizations that are non-government. And then there's, you know, let's call it your typical, you know, your biopharma partnerships. Right. So those three buckets, maybe I'll describe in the waning seconds. So governments, I think there's becoming more and more interest, you know, from US and next-generation vaccines. There's also a lot of interest around, you know, some of the flu strains that is prevalent right now. So I think there's opportunities to push the platform forward with governments. On the NGOs, there's a lot of pathogens around the globe where there's interest, and I won't go into detail about where those dialogues are, but I think there's a wealth of opportunities. On the biopharma side, you know, I think we're seeing, you know, there still is interest in infectious disease assets, and those deals can take a number of different forms. There is an opportunity to partner narrowly, like our HIV deal on a single, you know, indication. Our platforms are deployed for HIV cure or pathogen X or pathogen Y. Or you can imagine a broader type of strategic collaboration, where it's multiple pathogens, and there's been deals like that in the past with CureVac, et cetera, where there's a, you know, even CSL, Arcturus, we have a friend in the audience today, where there can be multiple pathogens, and then there's broader relationships where, you know, you're partnering all of infectious diseases, and that would allow us, frankly, to focus solely on oncology. So I think these are all different deal types that, you know, can't go into details here, but things we think about. Right. And maybe briefly, as we wrap up, can you tell us about the cash position, cash burn rate, and where you view potential sources of capital? Yeah, yeah, of course. So, our last reported cash was around $53 million. And then we brought in $32.5 million as part of a round a couple months ago. Mm-hmm. So there's lots of opportunities. I think there's always equity markets. Of course, that's, you know, it's a public company. That's one of the avenues for capital. There's partnerships, right? There's opportunity to bring dollars in potential funding of programs, which would be earmarked dollars, but those are often very interesting to companies like us. CEPI is a good example where we've been successful bringing dollars in to push a program forward. There's partnering, which could bring funding for programs, but also non-dilutive dollars to fund the company. Right. And then there's, you know, what I would call a whole bucket of alternative financing type of deals. You're seeing a lot of these. You know, there's things like royalty monetization, you know, fixed milestone type of deals, which are, I think, quite in vogue right now. Those are all dialogues that we're frankly having right now, and again, nothing to break here today, but, hopefully some news in the future on it. Great. Yeah, sounds good. Thank you, Matt, for telling us all about Gritstone. Thanks, Omari. Thanks for the invite, and really appreciate having the opportunity to talk today.