NASDAQ:INKT MiNK Therapeutics Q1 2023 Earnings Report $7.63 -0.20 (-2.55%) Closing price 04/17/2025 03:58 PM EasternExtended Trading$8.12 +0.50 (+6.49%) As of 04/17/2025 04:48 PM Eastern Extended trading is trading that happens on electronic markets outside of regular trading hours. This is a fair market value extended hours price provided by Polygon.io. Learn more. Earnings HistoryForecast MiNK Therapeutics EPS ResultsActual EPS-$1.70Consensus EPS -$2.40Beat/MissBeat by +$0.70One Year Ago EPSN/AMiNK Therapeutics Revenue ResultsActual RevenueN/AExpected RevenueN/ABeat/MissN/AYoY Revenue GrowthN/AMiNK Therapeutics Announcement DetailsQuarterQ1 2023Date5/11/2023TimeN/AConference Call DateThursday, May 11, 2023Conference Call Time8:30AM ETUpcoming EarningsMiNK Therapeutics' Q1 2025 earnings is scheduled for Tuesday, May 13, 2025, with a conference call scheduled at 8:30 AM ET. Check back for transcripts, audio, and key financial metrics as they become available.Q1 2025 Earnings ReportConference Call ResourcesConference Call AudioConference Call TranscriptPress Release (8-K)Quarterly Report (10-Q)Earnings HistoryCompany ProfilePowered by MiNK Therapeutics Q1 2023 Earnings Call TranscriptProvided by QuartrMay 11, 2023 ShareLink copied to clipboard.There are 9 speakers on the call. Operator00:00:00Ladies and gentlemen, thank you for standing by, and welcome to the Make Therapeutics First Quarter 2023 Financial Results Call. I would now like to turn the call over to Zach Erman, Head of Investor Relations. Please go ahead. Speaker 100:00:16Thank you, operator, and thank you all for joining us today. Today's call is being webcast and will be available on our website for replay. I'd like to remind you that this call will contain forward looking statements, including statements regarding our clinical development, regulatory and commercial plans, well as timelines for data release and partnership opportunities. These statements are subject to risks and uncertainties, and we refer you to our SEC filings for more details on Joining me today on the call are Doctor. Jennifer Buell, President and Chief Executive Officer Doctor. Speaker 100:00:49Mark Van Dyke, Chief Scientific Officer Doctor. Joy Xu, Head of Manufacturing and Christine Klaskin, Principal Financial and Accounting Officer. Now, I'd like to turn the call over to Doctor. Buell to highlight our progress from the quarter. Speaker 200:01:07Thank you very much, Zach. Good morning and thank you for joining our Q1 2023 earnings call. We're very happy to be here with you and to present on an exciting Q1, which actually culminated in a significant presentation at the American Association of Cancer Research Conference or the AACR Conference just a couple of weeks ago. Doctor. Benny Carniero, a medical oncologist and associate professor at Brown University Oncology presented data on our Phase 1 study. Speaker 200:01:41He reported first of its kind clinical benefit of an allogeneic We're off the shelf INKT therapy in patients with solid tumor cancers. Doctor. Carnier Specifically highlighted clinical responses and biomarker responses in patients who have failed all available therapies including anti PD-one therapy. We observed these responses in patients with metastatic gastric cancer, non small cell lung cancer, testicular cancer and long term disease stabilization in a number of other solid tumor cancers. These data underscore what we believe to be The most flexible and impactful cell therapy in development. Speaker 200:02:25MYC remains at the forefront of this technology advancing INKTs in the clinic And we're advancing this not only in the clinic as well as in our manufacturing suite, but also we're advancing A very robust pipeline of novel therapies that Doctor. Marc Sundyce will share with you shortly. So first, I'm going to highlight the clinical data in a bit more detail. At AACR, we reported that our lead product, which AGEN-seven ninety seven, an allogeneic off the shelf product of native non engineered and variant natural killer T cells. HS-seven ninety seven delivered benefit to patients with heavily pretreated solid tumor cancers, 34 patients with metastatic cancer who have exhausted all available treatments, including prior anti PD-one treatment, We're treated with a single dose of agent 797 without administration of toxic lymphodepleting agents And we administered 797 alone or in combination with tambrolizumab or nivolumab. Speaker 200:03:31We reported that AGM-seven ninety seven was well tolerated up to 1,000,000,000 cells dose and promoted clinical benefit in a range of heavily pretreated solid tumor cancers. And in particular, we saw encouraging activity in a patient with metastatic gastric cancer who had no prior response to anti PD-one therapy. And that includes a single treatment with anti PDU on pembrolizumab, the patient received for cycloZab. And after failure on pembrolizumab, the patient received nivolumab in combination with standard of care chemotherapy, again with no response. After being treated with a single dose of AGEN-seven ninety seven in combination with nivolumab, The patient achieved a partial response with a 42% reduction in tumor burden and this continues now beyond 12 months 9 months, sorry, that is our reporting period. Speaker 200:04:27This response is continuing at 9 months. We also saw benefit in other solid tumor cancers, including durable disease stabilization and biomarker responses in patients With non small cell lung cancer who had failed prior NIP1, vesicular cancer, appendiceal cancers and other solid tumors. The safety profile of 797 was found to be tolerable to a 1000000 cells, no evidence of neurotoxicity. No dose limiting toxicities were observed And no severe cytokine release syndrome greater than Grade 3 reported in the trial. And really importantly, We gained insights into the persistence in the homing and the immune modulating activity of INK T cells in patients. Speaker 200:05:10We found that while INK rapidly leave the periphery and enter in home tissues, we see that they're also still persistent and detectable in the periphery for about 8 weeks. This is really quite important because this demonstration shows that these cells actually can be viable and persistent without having to lymphodeplete patients. We also reported important translational findings that highlight INKT's ability to generate and drive immune cells into the tumor For destruction of cancer cells and Mark is going to tell you a bit more about these data in just a moment. Overall, our findings showcase the potential of analazimab off the shelf INK T cell therapy in combination with anti PD-one in cancers resistant to current treatment, including immune therapies. They support the expansion of our solid tumor program into PD-one refractory non small cell lung cancer as well as gastric cancer. Speaker 200:06:10And our trial in gastric The trial will advance through non dilutive grant funded program targeted to start in just a few weeks and is planned to enroll about 40 patients Over 9 centers will be treated under Memorial Sloan Kettering's umbrella and will be treated with a cell therapy in combination with standard of care chemotherapy As well as in combination with a very exciting multifunctional anti CTLA-four antibody, which is advancing in late stage trials. Botanselimab is a lead program from our parent company, Agenus. Now as a refresher, we have previously published preclinical models and data, which demonstrate the potent synergy between INKPs, Anti PD-one and now and fotencilimab, we published this data and presented them previously at AACR. These data reveals that in models preclinical models of metastatic lung disease, The combination of INKT cells, PD-one and vote in silumab resulted in near complete tumor elimination in this model, V16 These data and the safety and clinical benefit that we've observed with 797 in solid tumors to support our next phase of development with this program. We expect to provide additional data update as well as more detail on our clinical programs in the second half of this year. Speaker 200:07:53I will now turn the call over to Doctor. Mark Van Dijk, our Chief Scientific Officer will provide an update on our next generation pipeline, which includes the IND enabling activities of our novel fat CAR INKT cell therapies as well as more detail about the functional attributes of 797 that we believe underscore the observations of clinical benefit Speaker 300:08:22at AACR of clinical benefit in patients with heavily pretreated metastatic cancers. These patients are the ones who inspire our work as we leverage our We are INKT platforms to expand the clinical benefit observed with approved therapies and develop innovations to address areas where current therapies So our technologies, which you'll hear more about at our Annual Shareholder Meeting, includes the ability to generate armored CAR INKTs, Develop INKT Engagers, cell engagers and advanced novel PCR therapies. In addition to our native clinical stage AGEN-seven ninety seven program, Our most advanced preclinical programs include armored allogeneic FabCAR INKT And the next generation ARMOURD BCMA INKT. So our lead program, AGEN-seven ninety seven is designed to clinical benefit observed with improved therapies and our data at AACR is the first glimpse of the possibility of these cells to deliver on these benefits. It's a well known phenomenon that anti PD-one therapies are effective at countering tumor immune suppression. Speaker 300:09:30However, chronic use of these therapies leads to immune exhaustion. So we've previously shown that AGEN-seven ninety seven can improve the antitumor activity of immune cells that are present in the tumor microenvironment. Specifically, we've shown that IK T cells can activate dendritic cells, preferentially kill M2 macrophages And restore killing capacity of exhausted T cells. So in data, as certain from our clinical trial of AGEN-seven ninety seven, we showed AGEN-seven ninety seven induced pro inflammatory cytokine responses, including significant increases in interferon gamma, A hallmark of INKT activation and potentially indicative of tumor INKT activation, which is paramount to tumor control and tumor destruction. Importantly, INK T cells are naturally tissue homing. Speaker 300:10:19So in preclinical data previously presented, we've demonstrated that NKTs could be administered without lymphodepletion. They are rapidly traffic out of the circulation within days of administration and into tissues, including bone marrow, Liver and lung, where they remain in some cases exceeding 35 days. So in our clinical trials, we reported the similar pattern of rapid translocation out of the circulation, while they remain at detectable limits and persist for approximately 8 weeks. In our patient with durable response beyond 9 months, we also Show that ITPs drive clonal T cell expansion in cancers with a high neoantigen burden, immunogenicity really triggering the expansion of these Cancer fighting T cells. While we plan to report more detailed information of YNK teams in the tumor microenvironment at a later update this year, Currently, our data demonstrate the mechanism of INK T cells to enable T cells and NK cells trafficking 2 tumors, reinvigorate partially exhausted TDA T cells and improve effective functions within the tumor microenvironment, is exemplified in these patients with clinical biomarker response after a single dose of AGEN-seven ninety seven. Speaker 300:11:32As we continue to expand the potential of IKTs in solid cancer, we have advanced our next generation IKT programs, including our novel IL-fifteen armored fat CAR NKG MINK215. Cancer associated fibroblasts, Which are targeted with this therapy are key tumor supportive components of the immune suppressive tumor market environment in several cancers, including non small cell lung cancer. This adverse tumor microenvironment can be addressed by our fibroblast targeting or FAP, CAR NKT therapy, which naturally homes to tissues such as the lung. In preclinical models, we reported very exciting data showing the potential of MYC-two fifteen, through stromal remodeling. This is a program we're actually very excited about and Doctor. Speaker 300:12:30Shannon Boy, one of our lead scientists at MYC We'll be presenting new data at the American Society of Gene and Cell Therapy Annual Meeting on May 19. I will now turn the call over to Jim for closing comments. Speaker 200:12:46Thank you, Mark. Well, I get more and more enthusiastic about The data that we're advancing and the technology and the science behind these very powerful cells. And in conclusion, I'm really happy to With you the progress that we've made in advancing this platform and as Mark just mentioned, not only addressing and expanding the benefits from available therapies for patients today about what they will need tomorrow. This process, of course, is made possible by the Incredible advancements of Doctor. Joy Zhao and her team in our CMC group. Speaker 200:13:21Our current process, our manufacturing process is designed to generate for 5,000 doses per year and we are building currently and expect to have a fully known or independent process over the course of this next year. And the development will come without some kind of capital intensive efforts associated with most cell therapy entities. And Joy is with us today to answer any questions. We'll also be showcasing a deep dive into our manufacturing process technologies and advancements at our annual meeting this year. Very importantly and what has been contributing Our high efficiency is our team is small and we've kept it that way and we've made tremendous progress. Speaker 200:14:07Launching the company as an IPO in October of 2021, advancing 3 clinical programs highly efficiently and now identifying tumor types That may allow us to develop AGEN-seven ninety seven on a rapid path to development to expand benefit to patients and Specific set of solid tumor cancer sets us up very well and we're doing this with a team of under 35 people and as Christine will share with you, We've been able to manage our team and our expenses very efficiently and we're looking forward to So being able to financially support the initiatives that I shared with you throughout the course of the year and into well into next year. Christine? Speaker 400:14:53Thank you, Jen. We ended the Q1 of 2023 with a cash balance of $14,900,000 as compared to $19,600,000 at December 31, 2022. Our cash used in operations for the Q1 was $4,400,000 which compares to Speaker 500:15:12$4,200,000 for Speaker 400:15:13the same period in 2022. Net Speaker 500:15:16loss for Speaker 400:15:17the quarter ended March 31 was $5,700,000 or $0.17 per share compared to a net loss for the Q1 of 2022 of $7,800,000 or $0.23 per share. Thank you. And we'll now turn the call back to the operator for questions. Operator00:16:03Our first question comes from the line of Emily Bodnar from H. C. Wainwright. Your line is open. Speaker 500:16:11Hi, good morning and thanks for taking the questions. Is there anything you can share about details for the non small cell lung cancer Expansion study. And then also I believe you previously said that you were going to also do an expansion in testicular cancer. So is that also still the plan? And then at this point, do you think you're just focusing on combination approaches? Speaker 500:16:35Or do you still think there's a role for monotherapy in your view? Maybe just discuss plans for multiple dosing? Thank you. Speaker 200:16:44Emily, thank you very much. So to your first Question on small cell lung cancer and testicular cancer indications in which we have observed some specific benefits And non small cell lung cancer, we are advancing our Phase I into a Phase Ib and we're able to enrich a little bit more Clearly, in lung cancer, the more prevalent tumor non small cell lung cancer and in patients who are refractory, There's really nothing for those patients and very low response rates. We believe that when patients fail anti PD-one therapy, they have a profile where INTPs benefit, as Mark mentioned, just a bit ago and adding on to what's available standard of care is It allows us to take a monotherapy approach to development, just taking standard of care, Patients who are on standard of care when it's not active for those patients adding on to that gives us an opportunity for rapid development. So while we do see a path for INKT alone and we've seen benefit as you can see with the data presented at AACR, we do see benefit With INKT-seven ninety seven specifically without other therapies, both long term disease stabilization and biomarker responses, We see more robust activity and a very clear path to rapid path to registration when we can add on to available therapy and expand the benefits or reinvigorate a patient's immune system and reactivate it to respond to what's We will be doing multiple doses in our study while the cells are persisting for about 8 weeks. Speaker 200:18:28We do plan to dose within and we'll share more about Commonly used therapies at week 6 or 8 that will take advantage of the pharmacology that we're seeing As well as make the treatment burden as light as possible for our patients. And with respect to testicular cancer, that is also a study that will also continue to interrogate signals. With that Indication, it's a bit rarer and so we are just currently enrolling some more patients to deepen our understanding of the biology of patients who fail On prior therapies with testicular cancer, but that's an area that we do see benefit and want to continue to explore that. Operator00:19:29Our next question comes from the line of Jack Allen from Baird. Your line is open. Speaker 600:19:35Great. Thank you so much for taking the questions and congratulations to the team on the progress made throughout the quarter. I wanted to ask on the updates surrounding I think in the press release you outlined that there will be some data presented in late May here. I'd love to hear what we should expect ahead of that data set and any comments you have around, I think there were some ongoing negotiations with DARPA around potential funding for some of these viral disease, I guess, response Programs, I'd love to hear any updates there. Thank you so much. Speaker 200:20:07Thank you so much, Jeff, for your question. I am incredibly excited about an upcoming The pulmonary conference is an international conference of infectious disease and Pulmonary Science, the largest of its kind, is about 30,000 participants. It's in Washington, D. C. This year and our presentation is slated And the presentation is on Sunday 21st, and we'll share a bit more about that data and at the release A bit. Speaker 200:20:47What we see is the opportunity here. Now and very importantly, we had a number of key observations with these Number 1, we could administer these cells. They were at the site in emergency settings when the patients needed them and they were able to be administered Very easily within the standard practice in an emergency room and an ICU setting. So that set us up for Addressing and confirming that these cells are logistically feasible, they could be cryopreserved, they could be administered in the hands of non oncology experts, These are ICU experts and emergency room critical care physicians who don't have as much with cell therapy products and we were able to deliver benefits to some patients and we reported pronounced benefit in our cohort that So survival rates in patients who were elderly, mechanically ventilated, and we saw survival benefits of over 70% alive after a single administration of 797. We also showed that these cells can be dosed in that severe critically ill population, they could be those tolerably to a 1,000,000,000 cells. Speaker 200:22:00And we also show that these data compared so favorably to an in control that had a survival rate of less than 22% and the CDC data, which was really comparable with the in hospital controls at the time of our enrollment. We've also demonstrated that we administer these cells not only tolerably, we saw no cytokine release in the population, But we also showed that these cells could be administered in patients who were so severely sick that they needed supportive Essentially ECMO procedure. This is a procedure that requires Heavy intervention is very difficult. It's recirculating the patient's blood supply and we were able to administer the cells in that setting and see benefit as well. You'll see a deep dive into that data set at the upcoming ATS conference. Speaker 200:22:58You will also hear about some Exceptional cases where we've administered the cells and saw some remarkable benefit in patients who have cleared COVID, But it had secondary infections and that were resistant to all available antibiotic therapy and the cells actually promoted Some really exciting data in that setting. So you'll hear all about the data sets there. In advancing this program, we do believe that the data we're observing is really far too good to turn away from, yet our focus and our prioritization has Really been advancing the cells in solid tumor cancers. While we have our negotiations are with Non dilutive government sponsored sources and clinical trial platforms that allow us to very rapidly And the potential benefit of these cells in patients with acute respiratory distress syndrome secondary to virus This could go beyond COVID-nineteen. Those discussions are very actively underway and we will certainly be making some public announcements About the collaborations in the upcoming near Speaker 600:24:14term. Great. Thank you so much for that And then just one brief follow-up on the CARi and KTs and very much looking forward to that presentation as well at the upcoming ASGCT meeting. I'd love to hear a little bit more though about your development strategy as it relates to the KARA NKTs. Are these assets that you look to bring forward on your own or would you look to partner these assets? Speaker 600:24:34I'd love to Speaker 200:24:41I want to make one last comment that I did make about the sales in ACS and then I'm going We also will report some very important translational data that shows What these cells can do biologically in cancer, we saw that these cells can home to tumors and generate a pro inflammatory Phenotype, which is what we really need in that setting. What we see in infections, particularly in ARDS is that the cells actually induce an anti inflammatory phenotype, which is really powerful And showcases how these cells can modulate immunity based on the disease setting that they're in, which makes them a really remarkable candidate and also underscores the next steps in our platform. On the fatCAR INKT and partnering, partnering is absolutely core to our strategy. As you know, we've been an incredibly aggressive team. Mark and I have worked together with the Agenus Group and we allowed the access to our Remarkably fast and innovative discovery, research and finance the business in parallel. Speaker 200:25:50So through nearly $1,000,000,000 in partnerships, were able to continue to finance our innovative pipeline at Agenus and at MNQ. Mark and his research team have continued that pace of discovery and innovation. And for our ability to get the science into as many hands and out to as many patients as possible, partnering will be necessary for that. That includes local, national U. S. Speaker 200:26:16Based pharma partners who may be seeking They have the capabilities that will allow us to expand more quickly, but also regional partners where we don't yet have the infrastructure You will be hearing more about that also in the near term and our strategy and access To advancing Sacchar INKT very quickly. Suffice it to say though today, we are well positioned to advance Sacchar INKT Through the IND enabling and into the clinic and that's a very high priority for our company. Operator00:27:01Our next question comes from the line of Matthew Phipps from William Blair. Your line is open. Speaker 700:27:09Hi, thanks for taking my question. Jen, I'm wondering if you guys think what could be special about that gastric cancer patient that had such a strong response? They had an MSI Hi, tumor, but I didn't respond to 2 prior rounds of checkpoint inhibitors. Do you think MSI patients in general might be more prone to INKT Selectivity, do they have more CD1D expression or anything like that? Speaker 200:27:36Yes, that's a great question and I'm I'm going to turn it over to Mark just after a couple of words. This is there are a few points that I'd like to have Mark also expand on that we observed, which included The tumor microenvironment modulation that I'll have Mark sort of further expand on, But a very important part of that modulation included increased TCR clonality and diversity. And some of the drivers of that are continuing to be under investigation. But I think what I do see is that MSI high tumors are quite responsive to PD-1s for a period of time and then no longer. And in this case, we saw absolutely no response, not on Pembrolana, not on nivo combo And not until we added the cells. Speaker 200:28:24And there are a couple of features that we presented and Mark will go into that They help us better understand the disease modifying benefit in this particular data set. To the extent that it is Translatable across MSI tumors, we will explore and are actively doing so. Our clinical trial with Doctor. Jitsi Yin will allow us To answer this question as well. Martin, I'll open it to you to say a few words. Speaker 300:28:52Yes. Thanks, Tian. It's an interesting question and we've been, of course, scrutinizing this deeply. And it's the case that in Tumors that actually have an infiltrate of T cells or that are high in tumor mutational burden. There is a T cell response, but clearly with this patient Going through 2 rounds of PD-one directed therapy, this isn't enough to actually either get into the tumors So basically, you actually start doing something. Speaker 300:29:20And what happened after INKT infusion is that somehow that got unlocked and these T cells started to do what they were actually Genominated for is attack the tumor cells. So what we see in preclinical models is that, IK T cells are more resistant To quite a few of the immunosuppressive mechanisms that tumors employ to keep T cells down. And what we see in, for instance, our Fab CAR model, but also in some of our 797 preclinical models is that these tumor suppressive of these immune suppressive mechanisms actually get neutralized Or countered by our NK T cells. You could think about the local TGF beta or actually the cells that secrete TGF beta, CXCL12 that keeps the T cells out, all of those actually and specifically the myeloid component, all of those get translated, transformed into Pro inflammatory, non immune suppressive environment and that actually brings the T cells in and also reinvigorates the T We've also seen that, for instance, supernatant that we get from activated INK T cells is able to rescue partially exhausted T cells. So all of those mechanisms, I think, contribute as a whole, as a package. Speaker 300:30:31It's not a one trick pony To activating the T cells that are there in the gastric cancer patient, but obviously you're not able to do anything. And I think that very well fits What we see in our preclinical models as well and is one of the key features that we think is going to build the platform for IK T cells in solid tumors. Speaker 700:30:51Great. Thanks, Mike. Operator00:30:55Our next question comes from the line of kalpit Patel from B. Riley Securities. Your line is open. Speaker 800:31:03Good morning. This is Andy on for Kelpeth. Thank you for taking our questions. Starting off, what should we anticipate next from AGEN-seven ninety seven in solid tumors? Is there any dose escalation work still remaining? Speaker 200:31:19Andy, thank you. We will continue to interrogate dose, Frequency and optimization. Though I should say to you that I feel based on the pharmacology data that we've generated And the signals of activity that we've identified and the tolerability profile, we feel very close and confident with our dose. But it will be important just to strengthen our data packet for future regulatory interactions to continue to deepen Our scientific exploration of dose and dose frequency. The next phase for us will be multiple doses and that will be happening near immediately. Speaker 800:32:01Great. And then maybe one additional follow-up. With your upcoming presentation on MINK215, Is it fair to say that you're prioritizing this program ahead of 413? And maybe give us a sense of the timelines of when we should anticipate these programs to enter the clinic? Speaker 200:32:19Sure. So I'll answer the second question, which is on 413. I personally Believe and our key opinion leaders have continued to emphasize this point that there is a critical need For an accessible affordable product that targets BCMA that expands the duration, the durability And really eliminates the continued antigenic profile of the BCMA target. What we do see today with autologous products is They work well, high response rates. They're not as durable as they need to be and when patients progress about 2 thirds of them Are still revealing the antigen BCMA. Speaker 200:33:01So I do think that there's a major opportunity to advance an allogeneic off the shelf ARMOR BCMA That shows superior qualities as a next generation therapy for patients. For MYC To do so, given the competitive landscape, we would be an intensive effort and one that we are Deprioritizing to FAP, which is novel, engineered and within our solid tumor strategy. So our BCMA program has continued to advance. We've continued to deliver the manufacturability and scalability and we're interrogating it and getting it ready For a Phase 1 clinical trial and it's really quite close. Yes, this would be something that we have advanced some discussion To really expand our footprint and leverage additional external Non dilutive capabilities to advance this program in this competitive setting. Speaker 200:34:03VASCAR NTP is really, we think, An outstanding product. Our preclinical data continue to get stronger. The profile of the molecule is very compelling. The need is great. And there are a host of solid tumor valve expressing cancers that actually we believe we can bring benefit to. Speaker 200:34:23And for all of those reasons, we've accelerated this novel and differentiated product into the forefront of our And we will be filing an IND in 2024. That will bring us into the clinic very, very quickly. We have a very fast path from IND Filings to First and Human. So those would be tied together really quite quickly towards the middle to second half of twenty twenty four. Operator00:34:59Thank you, ladies and gentlemen. This does conclude today's call. Thank you for your participation. You may now disconnect.Read morePowered by Conference Call Audio Live Call not available Earnings Conference CallMiNK Therapeutics Q1 202300:00 / 00:00Speed:1x1.25x1.5x2x Earnings DocumentsPress Release(8-K)Quarterly report(10-Q) MiNK Therapeutics Earnings HeadlinesEarnings call transcript: Mink Therapeutics Q4 2024 reports reduced net lossMarch 20, 2025 | uk.investing.comMiNK Therapeutics, Inc. (NASDAQ:INKT) Q4 2024 Earnings Call TranscriptMarch 19, 2025 | msn.comNow I look stupid. Real stupid... I thought what happened 25 years ago was a once- in-a-lifetime event… but how wrong I was. Because here we are, a quarter of a century later, almost to the exact day, and it’s happening again. April 20, 2025 | Porter & Company (Ad)MiNK Therapeutics reports Q4 EPS (62c), consensus (50c)March 19, 2025 | markets.businessinsider.comQ4 2024 Mink Therapeutics Inc Earnings CallMarch 19, 2025 | finance.yahoo.comMink Therapeutics rapporteert lager nettoverlies in Q4 2024March 18, 2025 | nl.investing.comSee More MiNK Therapeutics Headlines Get Earnings Announcements in your inboxWant to stay updated on the latest earnings announcements and upcoming reports for companies like MiNK Therapeutics? Sign up for Earnings360's daily newsletter to receive timely earnings updates on MiNK Therapeutics and other key companies, straight to your email. Email Address About MiNK TherapeuticsMiNK Therapeutics (NASDAQ:INKT), a clinical stage biopharmaceutical company, engages in the discovery, development, and commercialization of allogeneic, off-the-shelf, invariant natural killer T (iNKT) cell therapies to treat cancer and other immune-mediated diseases. Its product candidate is AGENT-797, an off-the-shelf, allogeneic for iNKT cell therapy and treatment of various myeloma diseases and solid tumours, which is in Phase 1 clinical trials. The company was formerly known as AgenTus Therapeutics, Inc. The company was incorporated in 2017 and is based in New York, New York. MiNK Therapeutics, Inc. operates as a subsidiary of Agenus Inc.View MiNK Therapeutics ProfileRead more More Earnings Resources from MarketBeat Earnings Tools Today's Earnings Tomorrow's Earnings Next Week's Earnings Upcoming Earnings Calls Earnings Newsletter Earnings Call Transcripts Earnings Beats & Misses Corporate Guidance Earnings Screener Earnings By Country U.S. Earnings Reports Canadian Earnings Reports U.K. Earnings Reports Latest Articles Archer Aviation Unveils NYC Network Ahead of Key Earnings Report3 Reasons to Like the Look of Amazon Ahead of EarningsTesla Stock Eyes Breakout With Earnings on DeckJohnson & Johnson Earnings Were More Good Than Bad—Time to Buy? 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There are 9 speakers on the call. Operator00:00:00Ladies and gentlemen, thank you for standing by, and welcome to the Make Therapeutics First Quarter 2023 Financial Results Call. I would now like to turn the call over to Zach Erman, Head of Investor Relations. Please go ahead. Speaker 100:00:16Thank you, operator, and thank you all for joining us today. Today's call is being webcast and will be available on our website for replay. I'd like to remind you that this call will contain forward looking statements, including statements regarding our clinical development, regulatory and commercial plans, well as timelines for data release and partnership opportunities. These statements are subject to risks and uncertainties, and we refer you to our SEC filings for more details on Joining me today on the call are Doctor. Jennifer Buell, President and Chief Executive Officer Doctor. Speaker 100:00:49Mark Van Dyke, Chief Scientific Officer Doctor. Joy Xu, Head of Manufacturing and Christine Klaskin, Principal Financial and Accounting Officer. Now, I'd like to turn the call over to Doctor. Buell to highlight our progress from the quarter. Speaker 200:01:07Thank you very much, Zach. Good morning and thank you for joining our Q1 2023 earnings call. We're very happy to be here with you and to present on an exciting Q1, which actually culminated in a significant presentation at the American Association of Cancer Research Conference or the AACR Conference just a couple of weeks ago. Doctor. Benny Carniero, a medical oncologist and associate professor at Brown University Oncology presented data on our Phase 1 study. Speaker 200:01:41He reported first of its kind clinical benefit of an allogeneic We're off the shelf INKT therapy in patients with solid tumor cancers. Doctor. Carnier Specifically highlighted clinical responses and biomarker responses in patients who have failed all available therapies including anti PD-one therapy. We observed these responses in patients with metastatic gastric cancer, non small cell lung cancer, testicular cancer and long term disease stabilization in a number of other solid tumor cancers. These data underscore what we believe to be The most flexible and impactful cell therapy in development. Speaker 200:02:25MYC remains at the forefront of this technology advancing INKTs in the clinic And we're advancing this not only in the clinic as well as in our manufacturing suite, but also we're advancing A very robust pipeline of novel therapies that Doctor. Marc Sundyce will share with you shortly. So first, I'm going to highlight the clinical data in a bit more detail. At AACR, we reported that our lead product, which AGEN-seven ninety seven, an allogeneic off the shelf product of native non engineered and variant natural killer T cells. HS-seven ninety seven delivered benefit to patients with heavily pretreated solid tumor cancers, 34 patients with metastatic cancer who have exhausted all available treatments, including prior anti PD-one treatment, We're treated with a single dose of agent 797 without administration of toxic lymphodepleting agents And we administered 797 alone or in combination with tambrolizumab or nivolumab. Speaker 200:03:31We reported that AGM-seven ninety seven was well tolerated up to 1,000,000,000 cells dose and promoted clinical benefit in a range of heavily pretreated solid tumor cancers. And in particular, we saw encouraging activity in a patient with metastatic gastric cancer who had no prior response to anti PD-one therapy. And that includes a single treatment with anti PDU on pembrolizumab, the patient received for cycloZab. And after failure on pembrolizumab, the patient received nivolumab in combination with standard of care chemotherapy, again with no response. After being treated with a single dose of AGEN-seven ninety seven in combination with nivolumab, The patient achieved a partial response with a 42% reduction in tumor burden and this continues now beyond 12 months 9 months, sorry, that is our reporting period. Speaker 200:04:27This response is continuing at 9 months. We also saw benefit in other solid tumor cancers, including durable disease stabilization and biomarker responses in patients With non small cell lung cancer who had failed prior NIP1, vesicular cancer, appendiceal cancers and other solid tumors. The safety profile of 797 was found to be tolerable to a 1000000 cells, no evidence of neurotoxicity. No dose limiting toxicities were observed And no severe cytokine release syndrome greater than Grade 3 reported in the trial. And really importantly, We gained insights into the persistence in the homing and the immune modulating activity of INK T cells in patients. Speaker 200:05:10We found that while INK rapidly leave the periphery and enter in home tissues, we see that they're also still persistent and detectable in the periphery for about 8 weeks. This is really quite important because this demonstration shows that these cells actually can be viable and persistent without having to lymphodeplete patients. We also reported important translational findings that highlight INKT's ability to generate and drive immune cells into the tumor For destruction of cancer cells and Mark is going to tell you a bit more about these data in just a moment. Overall, our findings showcase the potential of analazimab off the shelf INK T cell therapy in combination with anti PD-one in cancers resistant to current treatment, including immune therapies. They support the expansion of our solid tumor program into PD-one refractory non small cell lung cancer as well as gastric cancer. Speaker 200:06:10And our trial in gastric The trial will advance through non dilutive grant funded program targeted to start in just a few weeks and is planned to enroll about 40 patients Over 9 centers will be treated under Memorial Sloan Kettering's umbrella and will be treated with a cell therapy in combination with standard of care chemotherapy As well as in combination with a very exciting multifunctional anti CTLA-four antibody, which is advancing in late stage trials. Botanselimab is a lead program from our parent company, Agenus. Now as a refresher, we have previously published preclinical models and data, which demonstrate the potent synergy between INKPs, Anti PD-one and now and fotencilimab, we published this data and presented them previously at AACR. These data reveals that in models preclinical models of metastatic lung disease, The combination of INKT cells, PD-one and vote in silumab resulted in near complete tumor elimination in this model, V16 These data and the safety and clinical benefit that we've observed with 797 in solid tumors to support our next phase of development with this program. We expect to provide additional data update as well as more detail on our clinical programs in the second half of this year. Speaker 200:07:53I will now turn the call over to Doctor. Mark Van Dijk, our Chief Scientific Officer will provide an update on our next generation pipeline, which includes the IND enabling activities of our novel fat CAR INKT cell therapies as well as more detail about the functional attributes of 797 that we believe underscore the observations of clinical benefit Speaker 300:08:22at AACR of clinical benefit in patients with heavily pretreated metastatic cancers. These patients are the ones who inspire our work as we leverage our We are INKT platforms to expand the clinical benefit observed with approved therapies and develop innovations to address areas where current therapies So our technologies, which you'll hear more about at our Annual Shareholder Meeting, includes the ability to generate armored CAR INKTs, Develop INKT Engagers, cell engagers and advanced novel PCR therapies. In addition to our native clinical stage AGEN-seven ninety seven program, Our most advanced preclinical programs include armored allogeneic FabCAR INKT And the next generation ARMOURD BCMA INKT. So our lead program, AGEN-seven ninety seven is designed to clinical benefit observed with improved therapies and our data at AACR is the first glimpse of the possibility of these cells to deliver on these benefits. It's a well known phenomenon that anti PD-one therapies are effective at countering tumor immune suppression. Speaker 300:09:30However, chronic use of these therapies leads to immune exhaustion. So we've previously shown that AGEN-seven ninety seven can improve the antitumor activity of immune cells that are present in the tumor microenvironment. Specifically, we've shown that IK T cells can activate dendritic cells, preferentially kill M2 macrophages And restore killing capacity of exhausted T cells. So in data, as certain from our clinical trial of AGEN-seven ninety seven, we showed AGEN-seven ninety seven induced pro inflammatory cytokine responses, including significant increases in interferon gamma, A hallmark of INKT activation and potentially indicative of tumor INKT activation, which is paramount to tumor control and tumor destruction. Importantly, INK T cells are naturally tissue homing. Speaker 300:10:19So in preclinical data previously presented, we've demonstrated that NKTs could be administered without lymphodepletion. They are rapidly traffic out of the circulation within days of administration and into tissues, including bone marrow, Liver and lung, where they remain in some cases exceeding 35 days. So in our clinical trials, we reported the similar pattern of rapid translocation out of the circulation, while they remain at detectable limits and persist for approximately 8 weeks. In our patient with durable response beyond 9 months, we also Show that ITPs drive clonal T cell expansion in cancers with a high neoantigen burden, immunogenicity really triggering the expansion of these Cancer fighting T cells. While we plan to report more detailed information of YNK teams in the tumor microenvironment at a later update this year, Currently, our data demonstrate the mechanism of INK T cells to enable T cells and NK cells trafficking 2 tumors, reinvigorate partially exhausted TDA T cells and improve effective functions within the tumor microenvironment, is exemplified in these patients with clinical biomarker response after a single dose of AGEN-seven ninety seven. Speaker 300:11:32As we continue to expand the potential of IKTs in solid cancer, we have advanced our next generation IKT programs, including our novel IL-fifteen armored fat CAR NKG MINK215. Cancer associated fibroblasts, Which are targeted with this therapy are key tumor supportive components of the immune suppressive tumor market environment in several cancers, including non small cell lung cancer. This adverse tumor microenvironment can be addressed by our fibroblast targeting or FAP, CAR NKT therapy, which naturally homes to tissues such as the lung. In preclinical models, we reported very exciting data showing the potential of MYC-two fifteen, through stromal remodeling. This is a program we're actually very excited about and Doctor. Speaker 300:12:30Shannon Boy, one of our lead scientists at MYC We'll be presenting new data at the American Society of Gene and Cell Therapy Annual Meeting on May 19. I will now turn the call over to Jim for closing comments. Speaker 200:12:46Thank you, Mark. Well, I get more and more enthusiastic about The data that we're advancing and the technology and the science behind these very powerful cells. And in conclusion, I'm really happy to With you the progress that we've made in advancing this platform and as Mark just mentioned, not only addressing and expanding the benefits from available therapies for patients today about what they will need tomorrow. This process, of course, is made possible by the Incredible advancements of Doctor. Joy Zhao and her team in our CMC group. Speaker 200:13:21Our current process, our manufacturing process is designed to generate for 5,000 doses per year and we are building currently and expect to have a fully known or independent process over the course of this next year. And the development will come without some kind of capital intensive efforts associated with most cell therapy entities. And Joy is with us today to answer any questions. We'll also be showcasing a deep dive into our manufacturing process technologies and advancements at our annual meeting this year. Very importantly and what has been contributing Our high efficiency is our team is small and we've kept it that way and we've made tremendous progress. Speaker 200:14:07Launching the company as an IPO in October of 2021, advancing 3 clinical programs highly efficiently and now identifying tumor types That may allow us to develop AGEN-seven ninety seven on a rapid path to development to expand benefit to patients and Specific set of solid tumor cancer sets us up very well and we're doing this with a team of under 35 people and as Christine will share with you, We've been able to manage our team and our expenses very efficiently and we're looking forward to So being able to financially support the initiatives that I shared with you throughout the course of the year and into well into next year. Christine? Speaker 400:14:53Thank you, Jen. We ended the Q1 of 2023 with a cash balance of $14,900,000 as compared to $19,600,000 at December 31, 2022. Our cash used in operations for the Q1 was $4,400,000 which compares to Speaker 500:15:12$4,200,000 for Speaker 400:15:13the same period in 2022. Net Speaker 500:15:16loss for Speaker 400:15:17the quarter ended March 31 was $5,700,000 or $0.17 per share compared to a net loss for the Q1 of 2022 of $7,800,000 or $0.23 per share. Thank you. And we'll now turn the call back to the operator for questions. Operator00:16:03Our first question comes from the line of Emily Bodnar from H. C. Wainwright. Your line is open. Speaker 500:16:11Hi, good morning and thanks for taking the questions. Is there anything you can share about details for the non small cell lung cancer Expansion study. And then also I believe you previously said that you were going to also do an expansion in testicular cancer. So is that also still the plan? And then at this point, do you think you're just focusing on combination approaches? Speaker 500:16:35Or do you still think there's a role for monotherapy in your view? Maybe just discuss plans for multiple dosing? Thank you. Speaker 200:16:44Emily, thank you very much. So to your first Question on small cell lung cancer and testicular cancer indications in which we have observed some specific benefits And non small cell lung cancer, we are advancing our Phase I into a Phase Ib and we're able to enrich a little bit more Clearly, in lung cancer, the more prevalent tumor non small cell lung cancer and in patients who are refractory, There's really nothing for those patients and very low response rates. We believe that when patients fail anti PD-one therapy, they have a profile where INTPs benefit, as Mark mentioned, just a bit ago and adding on to what's available standard of care is It allows us to take a monotherapy approach to development, just taking standard of care, Patients who are on standard of care when it's not active for those patients adding on to that gives us an opportunity for rapid development. So while we do see a path for INKT alone and we've seen benefit as you can see with the data presented at AACR, we do see benefit With INKT-seven ninety seven specifically without other therapies, both long term disease stabilization and biomarker responses, We see more robust activity and a very clear path to rapid path to registration when we can add on to available therapy and expand the benefits or reinvigorate a patient's immune system and reactivate it to respond to what's We will be doing multiple doses in our study while the cells are persisting for about 8 weeks. Speaker 200:18:28We do plan to dose within and we'll share more about Commonly used therapies at week 6 or 8 that will take advantage of the pharmacology that we're seeing As well as make the treatment burden as light as possible for our patients. And with respect to testicular cancer, that is also a study that will also continue to interrogate signals. With that Indication, it's a bit rarer and so we are just currently enrolling some more patients to deepen our understanding of the biology of patients who fail On prior therapies with testicular cancer, but that's an area that we do see benefit and want to continue to explore that. Operator00:19:29Our next question comes from the line of Jack Allen from Baird. Your line is open. Speaker 600:19:35Great. Thank you so much for taking the questions and congratulations to the team on the progress made throughout the quarter. I wanted to ask on the updates surrounding I think in the press release you outlined that there will be some data presented in late May here. I'd love to hear what we should expect ahead of that data set and any comments you have around, I think there were some ongoing negotiations with DARPA around potential funding for some of these viral disease, I guess, response Programs, I'd love to hear any updates there. Thank you so much. Speaker 200:20:07Thank you so much, Jeff, for your question. I am incredibly excited about an upcoming The pulmonary conference is an international conference of infectious disease and Pulmonary Science, the largest of its kind, is about 30,000 participants. It's in Washington, D. C. This year and our presentation is slated And the presentation is on Sunday 21st, and we'll share a bit more about that data and at the release A bit. Speaker 200:20:47What we see is the opportunity here. Now and very importantly, we had a number of key observations with these Number 1, we could administer these cells. They were at the site in emergency settings when the patients needed them and they were able to be administered Very easily within the standard practice in an emergency room and an ICU setting. So that set us up for Addressing and confirming that these cells are logistically feasible, they could be cryopreserved, they could be administered in the hands of non oncology experts, These are ICU experts and emergency room critical care physicians who don't have as much with cell therapy products and we were able to deliver benefits to some patients and we reported pronounced benefit in our cohort that So survival rates in patients who were elderly, mechanically ventilated, and we saw survival benefits of over 70% alive after a single administration of 797. We also showed that these cells can be dosed in that severe critically ill population, they could be those tolerably to a 1,000,000,000 cells. Speaker 200:22:00And we also show that these data compared so favorably to an in control that had a survival rate of less than 22% and the CDC data, which was really comparable with the in hospital controls at the time of our enrollment. We've also demonstrated that we administer these cells not only tolerably, we saw no cytokine release in the population, But we also showed that these cells could be administered in patients who were so severely sick that they needed supportive Essentially ECMO procedure. This is a procedure that requires Heavy intervention is very difficult. It's recirculating the patient's blood supply and we were able to administer the cells in that setting and see benefit as well. You'll see a deep dive into that data set at the upcoming ATS conference. Speaker 200:22:58You will also hear about some Exceptional cases where we've administered the cells and saw some remarkable benefit in patients who have cleared COVID, But it had secondary infections and that were resistant to all available antibiotic therapy and the cells actually promoted Some really exciting data in that setting. So you'll hear all about the data sets there. In advancing this program, we do believe that the data we're observing is really far too good to turn away from, yet our focus and our prioritization has Really been advancing the cells in solid tumor cancers. While we have our negotiations are with Non dilutive government sponsored sources and clinical trial platforms that allow us to very rapidly And the potential benefit of these cells in patients with acute respiratory distress syndrome secondary to virus This could go beyond COVID-nineteen. Those discussions are very actively underway and we will certainly be making some public announcements About the collaborations in the upcoming near Speaker 600:24:14term. Great. Thank you so much for that And then just one brief follow-up on the CARi and KTs and very much looking forward to that presentation as well at the upcoming ASGCT meeting. I'd love to hear a little bit more though about your development strategy as it relates to the KARA NKTs. Are these assets that you look to bring forward on your own or would you look to partner these assets? Speaker 600:24:34I'd love to Speaker 200:24:41I want to make one last comment that I did make about the sales in ACS and then I'm going We also will report some very important translational data that shows What these cells can do biologically in cancer, we saw that these cells can home to tumors and generate a pro inflammatory Phenotype, which is what we really need in that setting. What we see in infections, particularly in ARDS is that the cells actually induce an anti inflammatory phenotype, which is really powerful And showcases how these cells can modulate immunity based on the disease setting that they're in, which makes them a really remarkable candidate and also underscores the next steps in our platform. On the fatCAR INKT and partnering, partnering is absolutely core to our strategy. As you know, we've been an incredibly aggressive team. Mark and I have worked together with the Agenus Group and we allowed the access to our Remarkably fast and innovative discovery, research and finance the business in parallel. Speaker 200:25:50So through nearly $1,000,000,000 in partnerships, were able to continue to finance our innovative pipeline at Agenus and at MNQ. Mark and his research team have continued that pace of discovery and innovation. And for our ability to get the science into as many hands and out to as many patients as possible, partnering will be necessary for that. That includes local, national U. S. Speaker 200:26:16Based pharma partners who may be seeking They have the capabilities that will allow us to expand more quickly, but also regional partners where we don't yet have the infrastructure You will be hearing more about that also in the near term and our strategy and access To advancing Sacchar INKT very quickly. Suffice it to say though today, we are well positioned to advance Sacchar INKT Through the IND enabling and into the clinic and that's a very high priority for our company. Operator00:27:01Our next question comes from the line of Matthew Phipps from William Blair. Your line is open. Speaker 700:27:09Hi, thanks for taking my question. Jen, I'm wondering if you guys think what could be special about that gastric cancer patient that had such a strong response? They had an MSI Hi, tumor, but I didn't respond to 2 prior rounds of checkpoint inhibitors. Do you think MSI patients in general might be more prone to INKT Selectivity, do they have more CD1D expression or anything like that? Speaker 200:27:36Yes, that's a great question and I'm I'm going to turn it over to Mark just after a couple of words. This is there are a few points that I'd like to have Mark also expand on that we observed, which included The tumor microenvironment modulation that I'll have Mark sort of further expand on, But a very important part of that modulation included increased TCR clonality and diversity. And some of the drivers of that are continuing to be under investigation. But I think what I do see is that MSI high tumors are quite responsive to PD-1s for a period of time and then no longer. And in this case, we saw absolutely no response, not on Pembrolana, not on nivo combo And not until we added the cells. Speaker 200:28:24And there are a couple of features that we presented and Mark will go into that They help us better understand the disease modifying benefit in this particular data set. To the extent that it is Translatable across MSI tumors, we will explore and are actively doing so. Our clinical trial with Doctor. Jitsi Yin will allow us To answer this question as well. Martin, I'll open it to you to say a few words. Speaker 300:28:52Yes. Thanks, Tian. It's an interesting question and we've been, of course, scrutinizing this deeply. And it's the case that in Tumors that actually have an infiltrate of T cells or that are high in tumor mutational burden. There is a T cell response, but clearly with this patient Going through 2 rounds of PD-one directed therapy, this isn't enough to actually either get into the tumors So basically, you actually start doing something. Speaker 300:29:20And what happened after INKT infusion is that somehow that got unlocked and these T cells started to do what they were actually Genominated for is attack the tumor cells. So what we see in preclinical models is that, IK T cells are more resistant To quite a few of the immunosuppressive mechanisms that tumors employ to keep T cells down. And what we see in, for instance, our Fab CAR model, but also in some of our 797 preclinical models is that these tumor suppressive of these immune suppressive mechanisms actually get neutralized Or countered by our NK T cells. You could think about the local TGF beta or actually the cells that secrete TGF beta, CXCL12 that keeps the T cells out, all of those actually and specifically the myeloid component, all of those get translated, transformed into Pro inflammatory, non immune suppressive environment and that actually brings the T cells in and also reinvigorates the T We've also seen that, for instance, supernatant that we get from activated INK T cells is able to rescue partially exhausted T cells. So all of those mechanisms, I think, contribute as a whole, as a package. Speaker 300:30:31It's not a one trick pony To activating the T cells that are there in the gastric cancer patient, but obviously you're not able to do anything. And I think that very well fits What we see in our preclinical models as well and is one of the key features that we think is going to build the platform for IK T cells in solid tumors. Speaker 700:30:51Great. Thanks, Mike. Operator00:30:55Our next question comes from the line of kalpit Patel from B. Riley Securities. Your line is open. Speaker 800:31:03Good morning. This is Andy on for Kelpeth. Thank you for taking our questions. Starting off, what should we anticipate next from AGEN-seven ninety seven in solid tumors? Is there any dose escalation work still remaining? Speaker 200:31:19Andy, thank you. We will continue to interrogate dose, Frequency and optimization. Though I should say to you that I feel based on the pharmacology data that we've generated And the signals of activity that we've identified and the tolerability profile, we feel very close and confident with our dose. But it will be important just to strengthen our data packet for future regulatory interactions to continue to deepen Our scientific exploration of dose and dose frequency. The next phase for us will be multiple doses and that will be happening near immediately. Speaker 800:32:01Great. And then maybe one additional follow-up. With your upcoming presentation on MINK215, Is it fair to say that you're prioritizing this program ahead of 413? And maybe give us a sense of the timelines of when we should anticipate these programs to enter the clinic? Speaker 200:32:19Sure. So I'll answer the second question, which is on 413. I personally Believe and our key opinion leaders have continued to emphasize this point that there is a critical need For an accessible affordable product that targets BCMA that expands the duration, the durability And really eliminates the continued antigenic profile of the BCMA target. What we do see today with autologous products is They work well, high response rates. They're not as durable as they need to be and when patients progress about 2 thirds of them Are still revealing the antigen BCMA. Speaker 200:33:01So I do think that there's a major opportunity to advance an allogeneic off the shelf ARMOR BCMA That shows superior qualities as a next generation therapy for patients. For MYC To do so, given the competitive landscape, we would be an intensive effort and one that we are Deprioritizing to FAP, which is novel, engineered and within our solid tumor strategy. So our BCMA program has continued to advance. We've continued to deliver the manufacturability and scalability and we're interrogating it and getting it ready For a Phase 1 clinical trial and it's really quite close. Yes, this would be something that we have advanced some discussion To really expand our footprint and leverage additional external Non dilutive capabilities to advance this program in this competitive setting. Speaker 200:34:03VASCAR NTP is really, we think, An outstanding product. Our preclinical data continue to get stronger. The profile of the molecule is very compelling. The need is great. And there are a host of solid tumor valve expressing cancers that actually we believe we can bring benefit to. Speaker 200:34:23And for all of those reasons, we've accelerated this novel and differentiated product into the forefront of our And we will be filing an IND in 2024. That will bring us into the clinic very, very quickly. We have a very fast path from IND Filings to First and Human. So those would be tied together really quite quickly towards the middle to second half of twenty twenty four. Operator00:34:59Thank you, ladies and gentlemen. This does conclude today's call. Thank you for your participation. You may now disconnect.Read morePowered by