Thank you for standing by. Welcome to the Nkarta conference call to review preliminary clinical data for NKX101 and NKX019. At this time, all participants are in a listen-only mode. Please be advised that this call is being recorded at the company's request. I would now like to turn the call over to the company. Thank you, operator, and good morning, everyone. I'm Greg Mann, Senior Vice President, Public Affairs and Investor Relations at Nkarta. Thank you for joining our call this morning. Earlier today, Nkarta issued a press release announcing clinical data on two programs, NKX101 and NKX019. This press release, today's webcast, and corresponding slides are available on our website. We're looking forward to discussing these two sets of preliminary results as we advance toward making engineered CAR NK cell therapy a reality for cancer patients. On the call today from Nkarta are Paul Hastings, President and Chief Executive Officer, Dr. Kanya Rajangam, Chief Medical Officer, and Dr. Nadir Mahmood, Chief Financial and Business Officer. Dr. James Trager, Chief Scientific Officer, and Dr. David Shook, Senior Medical Director, will join for the Q&A portion of the call. We're also honored to have investigators from the NKX101 and NKX019 clinical programs participating. On today's call, we'll be making certain forward-looking statements, including statements regarding the future clinical development, regulatory pathway, and potential of our product candidates. These forward-looking statements are based on current information, assumptions, and expectations that are subject to change and involve a number of risks and uncertainties that may cause actual results to differ materially from those contained in the forward-looking statements. Interim data from clinical trials are subject to the risk that one or more of the clinical outcomes may materially change as patient enrollment continues and more data on existing patients become available. The clinical trial program is ongoing, and the final results may be materially different from those reflected in any interim data we report. These and other risks and uncertainties are described in our periodic filings with the SEC, such as our 10-K and our subsequent filings. You are cautioned not to place undue reliance on our forward-looking statements, and the company disclaims any obligation to update such statements. With that, I'd like to turn the call over to Paul Hastings. Good morning, everyone, and welcome to the call. Earlier today, we announced exciting news for our two co-lead clinical development programs, NKX101 in patients with relapsed and refractory acute myeloid leukemia and higher risk myelodysplastic syndromes, and NKX019 in patients with relapsed and refractory B-cell malignancies. We promised an update on NKX101 in the first half of this year and on NKX019 in this full year. Since both programs recently declared themselves simultaneously, we're here today to deliver on that promise earlier than expected with an update on both. The two Nkarta programs are cryopreserved. They're allogeneic and fully off-the-shelf cell therapy candidates that offer the opportunity to address and overcome the logistical and manufacturing challenges of the approved autologous CAR T products. Both programs are providing evidence of a beneficial safety profile without the types of potentially life-threatening adverse events such as neurotoxicity, cytokine release syndrome, and graft-versus-host disease that are commonly associated with a rapid and prolonged expansion that comes with T-cell therapy. Both programs are showing early indications of highly promising antitumor activity. In the AML trial, we saw deep responses at every dose level and complete responses with normal marrow and blood count recovery, as well as MRD negativity after treatment with NKX101. In AML patients, MRD negativity is associated with increased durability of response. In the non-Hodgkin lymphoma trial, we saw response rates that compare favorably to the remarkable anticancer activity of CAR T therapy with the additional benefit of the very favorable safety profile I mentioned earlier. Now, before we dive into the clinical data, I'd like to briefly review the Nkarta platform used to generate NKX101 and NKX019. Natural killer cells are a critical component of the innate immune system, and we start with real natural killer cells isolated from peripheral blood of healthy donors. We use a proprietary stimulatory cell line to expand active and potent NK cells. We engineer the cells with a proprietary membrane-bound IL-15 to enhance their persistence and serial killing activity and add an engineered chimeric antigen receptor to enhance the innate ability of NK cells to recognize and kill tumor cells. NKX101 and NKX019 are designed to be off-the-shelf therapies that can be manufactured at scale, cryopreserved, and administered at the immediate time and place that a heavily burdened cancer patient needs it. Given their emerging safety profile, we believe that Nkarta's product candidates could have the potential to be administered in outpatient and community medical settings. We have a robust and efficient manufacturing platform that we expect can deliver a reasonable cost of manufacturing at commercial scale in the range of about $2,000 per dose. We're extremely proud of the Nkarta platform and its end-to-end capabilities for generating novel NK cell therapy candidates. We believe the consistency of the activity and the safety we're seeing in the two clinical trial datasets reported today is important validation of the platform and its potential going forward. We're very encouraged by the data from the two Nkarta programs to date. The emerging safety profile of both NKX101 and NKX019 is potentially game-changing and speaks to the remarkable potential of NK cell therapy. There were no reports of dose-limiting toxicity, no cytokine release syndrome, no graft versus host disease, and no neurotoxicity of any grade. Maximum tolerated doses have not been reached, and dose escalation for both programs has recently advanced to the yet higher individual dose level of 1.5 billion cells per dose administered on day zero, seven, and 14. For NKX101, three out of five patients with relapsed refractory AML achieved a complete response with full hematologic recovery in the three-dose regimen of three doses of 1 billion or 1.5 billion cells each. Notably, two of these three complete responses had the additional advantage of MRD negativity, suggesting a deep response to our cells. Tumor responses and blast reduction were observed at every dose level, and blast reduction was seen in patients with higher and with lower baseline blast counts. As many of you know, complete responses are not all the same in AML. Lowering the patient's blast count is one component, and restoring blood cell counts above a certain level is another. Both criteria must be met in order to have a full or true CR. This is the type of complete response that patients achieved after treatment with NKX101 monotherapy. We saw full complete responses with neutrophil and platelet recovery and MRD negativity at a rate not seen with the current standard of care and other experimental therapies. MRD negativity is associated with increased durability and response. These results may be a first in AML with cell therapy, and we're confident that NKX101 is best in class for cell therapy in AML at this stage. For NKX019, five out of six patients with non-Hodgkin lymphoma responded, and three out of six patients achieved a complete response after receiving a single cycle of three doses of 1 billion cells per dose, the highest NKX019 dose studied to date. Complete responses were observed in multiple histologies, including aggressive diffuse large B-cell lymphoma. NKX019, while still in dose escalation, already reflects a CR rate rivaling CD19 CAR-T programs, only with a safety profile that could catapult cell therapy into the outpatient setting once and for all. Responses were seen at both dose levels, and patients are now being enrolled in a higher 1.5 billion cells x3 dose regimen with the potential to show further rapid, deep, and durable responses. Now, we expect to give an update on both programs by the end of this year, which should include the 1.5 billion cell dose cohorts for each candidate. We recognize the preliminary nature of these data sets and the standard caveats of clinical science apply here. These are small numbers from open-label studies distributed across different doses, dosing regimens, and histology. We're still early in the game, and time is needed for more follow-up from more patients to mature. But as early data goes, we have reason to be optimistic. We're seeing response rates that compare favorably to current standards of care. As you'll hear from Kanya in a moment, we'll be focusing specifically on the highest dose level studies in our trials to date in the three-dose regimen and the complete response rates in those dose cohorts. We will also be discussing response and safety data from the whole trial as well. Now, before jumping into the data, I'd like to introduce Dr. Rotta and Dr. Dickinson, who have generously agreed to share their perspectives on the treatment landscape for AML and NHL and the unmet need faced by patients with these diseases. At the conclusion of our prepared remarks this morning, both researchers will join us for the question and answer discussion. Dr. Marcello Rotta, MD, is from the Colorado Blood Cancer Institute, which is part of the Sarah Cannon Cancer Institute at Presbyterian St. Luke's Medical Center, where he serves as co-director of the Leukemia Service. Colorado Blood Cancer Institute is the 15th-largest blood and marrow transplant program in the nation, having performed over 5,000 transplants in the last 30 years. Dr. Michael Dickinson is from the Peter MacCallum Cancer Center and Royal Melbourne Hospital in Melbourne, Victoria, Australia, which is the largest hematology service in all of Australia. There, he is lead of the Aggressive Lymphoma Disease Group in Clinical Hematology. He specializes as a principal investigator in phase I and phase II clinical trials of new anti-cancer drugs with a current focus on aggressive lymphomas and novel immunotherapies. Now I'll turn it over to Dr. Rotta and Kanya to provide an update on NKX101. Then we'll move to NKX019 with a review from Dr. Dickinson on NHL, and then Kanya will present those data. Dr. Rotta? Acute myeloid leukemia, or AML, is a rapidly progressing cancer of immature blood cells called blasts in the bone marrow. It can arise from cumulative genetic mutation as well as after myelodysplastic syndrome or treatment for other cancers. Treatment for AML includes multiple rounds of intensive cytotoxic chemotherapy in patients that are fit enough to receive such treatment. Unfortunately, while many patients initially respond to intensive chemotherapy, most patients will eventually relapse. Tolerability of therapy is also important, as some patients are unable to tolerate the intensity of traditional AML chemotherapy, such as older patients or those who are more medically frail. Among those who are not fit to receive intensive therapy, very few achieve remission, and relapse is virtually inevitable. If AML does not respond to treatment or comes back after previously responding, it may become especially difficult to treat, and even low numbers of blasts may quickly overrun bone marrow and blood and create a life-threatening situation. Patients with relapsed refractory AML have limited treatment options and very poor outcomes. Based on recent publications, about 12%-18% of patients with relapsed refractory AML achieve remission after multiple combinations of salvage chemotherapy. About half of patients have targetable genetic mutations that can be treated with approved targeted agents, but still the response rates are unacceptably low. This translates to poor survival with a median overall survival of less than six months, and only about one in eight patients surviving to five years. Hematopoietic stem cell transplant is often the only opportunity for patients with relapsed refractory AML to achieve long-term remission. A response to salvage therapy is critical to improve responses. Those patients who achieve complete response or CR before transplant will enjoy far better survival with pre-transplant minimal residual disease negativity associated with further improved outcomes. In summary, relapsed refractory AML is an historically hard to treat disease, and given the lack of an effective treatment, people with AML are faced with few options. Thank you. Now let me pass the call back to Kanya. Good morning. I'm happy to be speaking with you all today to share these exciting early results from our programs. We begin with NKX101, our NKG2D CAR-NK. We are evaluating the potential of NKX101 in the treatment of patients with relapsed refractory AML or higher risk MDS. This phase I study enrolled a high-risk population with grim prognosis as just reviewed by Dr. Rotta. For protocol, all patients must have received at least one prior therapy to be eligible, and they must also have received a targeted therapy if they had disease with FLT3, IDH1 or two mutations. Key objectives include the standard safety and tolerability as well as efficacy and PK. NKX101 was evaluated using two different dosing regimens following standard fludarabine cyclophosphamide lymphodepletion, either the three-dose regimen where cells were given on days zero, seven, and 14, or a two-dose regimen where the cells were given on days zero and seven. Based on the data I will be reviewing, our plan is to move forward with the three-dose regimen. Efficacy assessments occurred on day 28 using standard consensus criteria. Patients could receive up to five treatment cycles based on efficacy and safety. Moving now to the next slide. This is a review of all patients who came onto the study. To date, we've enrolled 21 patients on this trial. The vast majority, 17 of them, had a diagnosis of AML at study entry. The trial patients were about 13 months out from diagnosis median, and in that timeframe had received a median of three prior lines of therapy. This means that within a year, they had rapidly cycled through three lines of currently approved and available therapy before enrolling on our trial. All 17 patients with AML had received prior venetoclax, and most patients had neutropenia and impaired bone marrow function at study entry. Turning now to slide nine. NKX101 was well tolerated across both regimens and all dose levels to date. We are encouraged by the safety profile. We observed no DLT and are currently enrolling into the 1.5 billion cell cohort using the three-dose regimen. The most common higher grade toxicities, regardless of relationship to NKX101, were myelosuppression and infection. This is consistent with use of lymphodepletion in a relapsed refractory AML MDS patient population. In terms of adverse events of interest for a cell therapy, two patients experienced grade two infusion reactions after receiving NKX101, both transient and easily managed. Of note, as may be expected for an NK-based cell therapy, there were no CAR T-like toxicities of any grade, regardless of dose level or regimen. No CRS, no ICANS or neurotoxicity. Finally, important for an allogeneic product, again, consistent with NK cell biology, no GvHD without the need for gene editing to avoid such toxicity. Moving on to efficacy on slide 10. This table summarizes responses from all 21 patients enrolled on trial. It contains considerable information, so let me highlight several points. First, reading left to right, patients with AML are summarized in the first column and the patients with MDS in the third column. We saw blast reduction across dose levels in AML, and we did not see responses in the four patients with MDS. Now let's focus on AML. From top to bottom, there were more responses noted with the three-dose regimen in the top few rows compared to the two-dose regimen in the bottom few rows. Lastly, looking at just the three-dose regimen in AML, I draw your attention to the green box, which highlights the CR rate in patients who received the three-dose regimen. As we went higher in doses, three out of five patients at the highest dose level achieved a CR, two of which were MRD negative. In summary, we observed a dose response both with increasing the number of cells per dose and increasing the number of doses per cycle in patients with AML. In the next slide, we will focus on AML and the three-dose regimen. This table summarizes all patients with AML on trial who received the three-dose regimen, their baseline blast levels, what responses they've achieved. Here in green, we highlight both the increased rate and depth of response at the higher dose levels compared to the lower dose levels in red and blue below. In the spaghetti plot on the right, we see that responses were noted across a variety of baseline blast burdens. Regardless of disease burden, most patients had blasts that went down with treatment. Seeing the blast reductions in MLFS at the lower and mid doses is important. Of note, MLFS responses mean the blast went below 5%, same as CR, but the blood counts did not recover. This gives us confidence that NKX101 could have an impact for patients with higher blasts as we continue to enroll the 1.5 billion cell x3 dose level on trial. Moving on now to the swim lane plot on slide 12. In the green box you can see again the five patients who received the highest dose levels of NKX101 in the three-dose regimen, of whom three of five achieved a full CR, two of which went MRD negative. I draw your attention to patient one, who achieved an MRD negative CR after NKX101, received a consolidating transplant, and is currently approximately six months of continuing remissions from study entry or five months durability of response. We are planning a third cycle for patient two, whose MRD positive CR to try and further deepen their response. Below the green box are the responses for the other AML patients on study, the lower dose levels and the two-dose regimen. Notably, we saw meaningful blast reductions even in the low dose levels. Looking at patient six, they achieved a morphologic leukemia-free state, or MLFS, and was eligible for a transplant, and had a durable eight-month remission post-study entry with the consolidating transplant. On the next slide, we present case study of patient one from the swim lane plot. This patient is in molecular remission following treatment with NKX101. The patient is a 68-year-old male with AML with an IDH1 mutation, whose disease was refractory to four prior lines of therapy, including two of the most active agents for their disease, VENETOCLAX AND IVOSIDENIB, an IDH1 inhibitor. At study entry, he presented with 8% blasts by morphology and 25% deletion of chromosome 22 as measured by FISH. At the end of one cycle of 1 billion x3 doses of NKX101, a CR was noted, which was MRD negative by FISH, along with a normal cellular marrow, normal cytogenetics, and normal flow. NKX101 was well-tolerated, with grade three events being largely CYTOPENIAS, which recovered by the end of cycle one. This patient then underwent consolidative transplant and continues to be in CR six months after study entry. The graph on the right is PK from the same patient. It indicates detection of NKX101 transgenes after every dose in the peripheral blood on days zero, seven, and 14, potentially giving the NK cells three opportunities for anti-leukemia activity. Consistent with the allogeneic profile of the product, the cells cleared from the peripheral blood by day 20. In summary, NKX101 was well-tolerated with high preliminary activity in this heavily pretreated AML patient population. There were no DLT or cases of CRS, GVHD, or neurotoxicity. With monotherapy NKX101 after lymphodepletion, three of five patients achieved a CR at the highest dose levels in the three-dose regimen, two of which were MRD negative. Responses and blast reduction were observed across dose levels, including a dose response and a deepening of response. In terms of next steps for the NKX101 program, we intend to continue dosing patients with AML at 1.5 billion cells per dose in the three-dose regimen. If data continues to hold, we believe that there is a potential for approval in patients with relapsed refractory AML using data from a single arm expansion cohort. We are also looking at the potential to move to earlier lines of therapy in combination with other standard of care agents. We plan to announce additional data from our 1.5 billion cells per dose cohort, per dose times three cohort later in the year. This concludes my remarks on NKX101. As Paul mentioned, Nkarta is extremely fortunate to have two programs declare preliminary proof of concept at the same time. Turning now to NKX019, it's my pleasure to introduce Dr. Michael Dickinson, a lead investigator for NKX019 at the Peter MacCallum Cancer Centre in Melbourne, Australia. Michael will review the current treatment landscape and unmet needs for patients with relapsed refractory non-Hodgkin lymphoma. Thank you, Kanya. Non-Hodgkin lymphomas are cancers derived from B cells, include aggressive and indolent forms, and all express the B-cell antigens such as CD19 and CD20. The most common type of non-Hodgkin lymphoma is aggressive diffuse large B-cell lymphoma, which has an especially poor prognosis. Other forms of non-Hodgkin lymphoma, such as follicular lymphoma, may undergo transformation to diffuse large B-cell lymphoma. Initial treatment for non-Hodgkin lymphoma includes multiple rounds of intensive chemotherapy for those who can tolerate it, and response to chemotherapy is critical. About 40% of patients with diffuse large B-cell lymphoma are refractory to first-line therapy or relapse after initially responding, and prognosis of patients with relapsed refractory diffuse large B-cell lymphoma is poor. CD19 is a well-validated target employed by the approved autologous CAR T-cell therapies for diffuse large B-cell lymphoma, as well as other challenging lymphomas including follicular lymphoma and mantle cell lymphoma. While these therapies have altered the treatment landscape and offer a treatment option for some patients with relapse lymphoma, both safety and acceptability limit more widespread use. Complete responses between 32%-50% have been reported for large B-cell lymphoma with these approved therapies, but toxicities are common, with more than 25% of patients requiring ICU admission. Between 60% and 80% of patients experience some form of CAR T-type toxicity, including cytokine release syndrome or neurotoxicity. There are also logistical challenges, which result in a limited number of specialized sites being able to treat patients with potentially curative therapy. Further, in the pivotal studies leading to approval, up to a third of patients who underwent apheresis to bespoke manufacturing of their autologous CAR T therapy did not receive the cells, either due to manufacturing challenges or the necessary delay between apheresis and product delivery. Patients not eligible for cell therapies and treated with other salvage treatments have a poor prognosis, with a median overall survival of about six months. Therefore, across various types of non-Hodgkin lymphoma, there is a critical need for safe and effective therapies which can be delivered rapidly to patients. Thank you, and now let me pass the call back to Kanya. Thank you, Dr. Dickinson. NKX019 is in fact a CD19-targeting CAR NK cell therapy candidate. We are excited about NKX019, which has a CD19 CAR engineered onto the backbone of an NK cell designed for potency and persistence. The preliminary data that we are reporting today give us confidence in the potential of NKX019 as a next wave of therapies, rivaling the antitumor activity, but without the safety and logistical issues of CAR Ts, as outlined by Michael. In our phase I trial, we evaluated a high-risk, high-need patient population. The trial enrolled an all-comers B-cell malignancy cohort, where patients must have received at least two prior therapies. Patients were required to be CAR T naive in this initial dose-finding phase of the trial to avoid confounding either the safety or efficacy results. We plan to evaluate CAR T-treated patients in an expansion cohort later this year. Key objectives and study design are similar to the NKX101 study that I reviewed earlier: safety, efficacy, TK. There are two key differences that I will highlight. First, we only evaluated the three-dose regimen in this trial. Next, by leveraging the wealth of experience in CD19-targeted agents, we were able to start at a higher dose of NKX019 at 300 million cells per dose. Efficacy was based on standard disease-specific criteria on day 28, with the potential to go up to five treatment cycles, including consolidation, post CR in patients with lymphoma. To date, we've enrolled 13 patients on this trial. These 13 patients mirror real-world CAR T patients, heavily pretreated, median of four prior lines of therapy and a poor prognosis. This international study enrolled 10 patients from Australia and the remaining from U.S. centers. 10 of the 13 patients had lymphoma at study entry, and notably, five of these 10 had aggressive large B-cell lymphoma, four of which were diffuse large B-cell lymphoma and the remaining one, a grade 3 B follicular lymphoma. Consistent with NKX101, NKX019 too had an excellent safety profile and was well-tolerated to date. We will highlight one more time that no CAR T-like issues were observed. Myelosuppression that generally recovered as effects of lymphodepletion wore off was the most common higher grade toxicity, regardless of relationship, as summarized in the table. Slide 20 summarizes the responses observed in all 13 patients enrolled to date, and let me orient you to the results. First, looking at the top rows, that includes the lymphoma patients and the bottom row, the three adult ALL patients. Responses were observed in all the lymphoma histologies treated, large B-cell, mantle cell, follicular, and marginal zone lymphoma in one or both dose levels. The three patients with adult ALL shown in the bottom row did not have a response. Next, looking at the lower and higher doses across columns from left to right, we observed a decrease and increase in response rate, such that in our highest 1 billion cell dose level to date on the right, five out of six patients responded, including three out of six CRs. On slide 21, we take a closer look at all patients with lymphoma on our trial to date. In the table, we see again that responses were observed across all histologies. Looking at baseline disease, we see these patients had extensive disease involvement, including nodal and multiple extra-nodal sites. All CRs shown here are ongoing. In the higher 1 billion cell dose cohort, we treated two patients with diffuse large B-cell lymphoma, an aggressive lymphoma subtype. One achieved a CR and the other, a stable disease with tumor reduction, including of their bone marrow disease. The second patient continues on trial, and we hope to see a deepening of response. The dose response that we highlighted in the earlier slide is apparent here as well when comparing the 300 million cell dose in blue to the 1 billion cell dose in green. Further, leveraging the well-tolerated safety profile, a consolidation cycle is available for patients to achieve CRs after any cycle of NKX019, as is outpatient administration. This is currently allowed after the first cycle, and as part of an upcoming amendment, we plan to allow outpatient administration in all cycles. Moving now to the swim lane plot. The rapidity of responses following initiation of therapy is highlighted visually here. Most of our patients to date have achieved best response after one NKX019 treatment cycle. We also see what may be an early indicator of durability for patient seven in the 300 million cell dose in the x3 group. At six-month follow-up from trial entry, this patient remains in remission. Similarly, in the 1 billion cell x3 dose level, we have a patient with DLBCL who's currently in remission at three-month follow-up. Next, we move to slide 23 and our case studies of patient 1 and patient seven from the swim lane. Both patients achieved a rapid CR after receiving a single cycle of NKX019. 300 million cell dose level on the left and 1 billion on the right. The patient on the left is a 74-year-old woman who entered the study with extensive high-risk follicular lymphoma, which had relapsed after two prior lines of therapy. As shown on the scans, she achieved a rapid CR with one cycle of NKX019. She experienced no grade three or higher AEs and continues to remain in CR six months after NKX019. The patient on the right is a 53-year-old male with extensive diffuse large B-cell lymphoma who also relapsed after two rounds of RITUXIMAB-based chemotherapy, and they too achieved a CR after one cycle of NKX019. NKX019 treatment was well-tolerated, with some CYTOPENIA that were reported. PK plots are included for both patients, showing detection of NKX019 transgene in the peripheral blood after the cells were administered. In summary, NKX019 shows compelling preliminary efficacy and safety in patients with NHL. Consistent with the biology of NK cells, there were no reports of CRS, GvHD, or neurotoxicity of any grade at any dose level to date. NKX019 monotherapy after lymphodepletion showed activity generally after a single cycle in patients with extensive disease across different histologies. five of six patients with lymphoma responded, including three who achieved a CR after a single cycle of NKX019 at the highest dose level. CRs were observed across histologies. Early signs and durability are noted in a patient with relapsed follicular lymphoma, currently six months out from study entry and in remission. We are excited about next steps for the NKX019 program. These include the potential to achieve even deeper and higher response rates in the higher 1.5 billion cells x2 dose finding cohort, which is currently open. After we complete the NKX019 dose finding cohort, we plan to open a separate large lymphoma expansion cohort to independently evaluate activity in both CAR T naive patients and patients who were previously treated with CD19 CAR T-cell therapy. We also plan combination studies as we move forward with continued development of NKX019. We look forward to our next data update in the second half of 2022. This concludes our remarks on the clinical data from these two Nkarta programs. I'd like to thank Dr. Rotta and Dr. Dickinson for their presentations this morning and their contributions, along with our other investigators and their respective institutions, to our ongoing clinical trials of both these programs. I also wish to thank the patients and their caregivers who enrolled onto our trials. I'll now hand the call over to Nadir Mahmood, Nkarta's Chief Financial and Business Officer, for wrap up on next steps and future milestones. Nadir? Thanks, Kanya. We are excited to move both NKX101 and NKX019 forward in clinical development over the next couple of years. After completing the dose finding phase for NKX101, we plan to open a monotherapy expansion arm as well as look at potential combinations. As we move into pivotal trials, we believe that this program has the potential to be an expedited program, and we are evaluating potential fast track, RMAT, or breakthrough therapy designations. We have also previously talked about the potentially broad applicability of NKX101 across multiple tumor types, including solid tumors, and we will be advancing the program for the treatment of liver-directed cancers. For NKX019, as Kanya mentioned earlier, we've been conducting the dose finding study in CAR T naive patients. As we advance this program into dose expansion, we will do so in both CAR T naive patients and in patients with prior CAR T treatment. We will also look at investigating NKX019 in a combination study. As with NKX101, we believe that there is a potential for an expedited pathway for NKX019. Now we will stop and look forward to hearing your questions. Operator, if you would please review the instructions for the Q&A section. Certainly. At this time, if you would like to ask a question, please press star one on your touchtone phone. We will take our first question from Yaron Werber with Cowen. Please go ahead. Great. Hope you can hear me, and congrats on the data, really on both datasets. Really nice to see. I have a couple of questions. Maybe the first one. I noticed in here there is PK curves for the first cycle. Do you have it for patients, or I think it's after the first dose, do you have it after the second dose or maybe the third dose? Secondly, at this point, how many patients actually have gone through a second cycle at this point with either drug, if any? Yeah. Thanks, Yaron. PK is early, but Kanya will tell you what we have so far. We want to report what we have out of the sense of transparency, but it's still early days. Kanya? Yes. Thanks, Paul. Yaron, we have the PK plots we've showed there is from the first cycle. We continue to collect PK for all patients as they continue their cycles. In our next update, we hope to have more of that information. The second cycle. Do you manage for everybody to get a second cycle, even if they've already had a CR and even an MRD? Or I assume that's optional or is it not optional? You wanna talk about consolidation? Yeah. The patients can get a second cycle as long as they have some residual disease in general. The best way to look at which patients got the second cycle is obviously on the swim lane plot of both the trials. As long as there was still some residual blast, like MRD positive disease in AML, they can get another cycle to try and deepen it further. Once they achieve CR MRD negativity in the AML trial, they stop. In the lymphoma trial, they can continue to get additional cycles, and once they achieve a CR, they can get one more cycle of consolidation, and then they stop. Okay, got it. Maybe finally, for consolidation in lymphoma, I assume you need to wait after they get a full cycle, look at response, and then to do consolidation, they got to go through full lymphodepletion and everything is normal. Correct. Correct. Important to note that all the CRs in the lymphoma trial were first cycle responders. Maybe finally, do you think or is there any evidence so far that you might get deepening of responses over time? Thank you so much. Yeah. In both of our trials, we know of at least one patient who's deepened their response with additional cycles. It's obviously early days and small numbers, and there are a few more patients who are continuing on, and we hope to continue to see that trend. Great. Thanks again. Thank you. Thanks, Yaron. Once again, as a reminder, to ask a question today, that is star one on your touchtone phone. We'll take our next question from Stephen Willey with Stifel. Please go ahead, your line is open. Yeah, good morning. Maybe just to follow up on the last line of questioning. I guess in the case study that you showed for the one-on-one receiving patient, you know, it looks like with additional retreatment that both Cmax and AUC is maybe declining a little bit with each successive dose. Have you tried to characterize what that rate of immune-mediated clearance looks like? And has there been any thought of providing subsequent doses from a different lot of donor-derived cells to try to slow that down? Kanya? Yeah. We are looking at the host immune cell recovery in our trial as well, but I can tell you from literature that with the lymphodepleting regimen that we use, there's about a two-three-week window when the host immune system recovers, and it's our expectation that our allogeneic product gets cleared naturally after that timeframe. Yes, in the peripheral blood, what we are detecting there does appear to go lower in this particular patient with each of the three doses. We have not so far mixed lots. We continue to, as far as possible, give one lot to a patient. As we get more of that data, we'll have to see if that is even needed. Okay. I guess I know that you had recently escalated the intensity of lymphodepletion within the AML study itself. Should we assume that the patients receiving the higher cell counts, the 1 billion and the 1.5 billion, have received more aggressive lymphodepletion? No, we haven't done that yet. That will be in the next cohort, which is the 1.5 x 3 cohort. That's in AML, they'll start to see that lymphodepletion, flu/cy increased dose of cy. Okay. Is the plan to still keep the intensity of lymphodepletion as is in the CD19 program? Kanya? Steve, we are looking at increasing the LD in the CD19 program as well in an upcoming amendment. But you know, we are quite pleased with the data that we are seeing already, and we will always make our decisions based on in a data-driven way. Okay. Then maybe just lastly, was there any attempt to try to evaluate the expression of NKG2D ligands on patient AML blasts prior to treatment? I'm just curious if there was, what that characterization told you in terms of just the number of different ligands that were present and on what percentage of blasts they were expressed. See, we do those analyses. We don't have those results yet. You know, hopefully in our next update, we'll have some of those correlative data as well. All right. Thanks for taking the questions, guys. Really good update. Thanks, Stephen. We'll take our next question from Salim Syed with Mizuho. Mizuho, please go ahead. Great. Congrats on the data, guys. Just a few from me if we can. So firstly, just looking at the NKX101 data, was there anything in particular about the patient baseline characteristics regarding the patients who were on the two-dose cycle versus the three-dose cycle at the high dose? 'Cause I always thought in theory you should have seen, you know, response with the two-dose given its earlier post the lymphodepletion. I'll just start there. Yeah. Salim, let me just say that what we saw consistently across all doses was that the three-dose regimen outperformed the two-dose regimen, so that's why we selected that one going forward. It dose-to-dose was consistent, and that's why we made our decision to go forward with the three-dose regimen. there wasn't any difference in blast counts? Were they higher for the three patients who had the two dose? First of all, Salim, it's small numbers and we, you know, we can't conclude from this that the two-dose regimen does not work at all. But clearly we are seeing trends with the three-dose, so that's what we're taking forward. Some of the patients who came on the two-dose regimen did have slightly higher blasts, but it's early days still, and we continue to enroll in the three-dose regimen as well. Was it intentional not to do a 2.25 billion x2 dose in that two-dose cycle, two doses per cycle? Was there intention? Oh, was there intention? Yeah, 'cause like, you know, it's always to mimic the three, the total cell count, right? So if you're doing 1.5 × 3, it's 4.5 billion cells, but there wasn't a 4.5 billion cell for the two doses per cycle. Yeah, we won't be going into a two-dose regimen. We've now made the decision to move forward with a three-dose regimen. Okay. Just on the comment you made, Kanya, regarding approval on a single-arm expansion cohort, could you just remind us what sort of dialogue you've had with the FDA around that? What sort of safety database do you think you'll need for that approval cohort, i.e., like how large, and what sort of endpoint you'd be looking at for approvability? Thank you. Salim, it's too early, as you know, for us to be talking about the size of our potential pivotal trial. We intend to engage with the FDA later this year, early next year, as we continue to get data. Our focus now is to identify a go-forward dose, go into the expansion and accrue more data, and we will absolutely be talking to the FDA at the right time with those results. Okay. Sounds good. Thanks so much. Congrats again. Thanks, Salim. We'll take our next question from Dane Leone with Raymond James. Please go ahead. Your line is open. All right. Thank you for taking the questions and congratulations on the data today. Just maybe a couple of easy ones from me. Firstly, is there any analysis at this point that you could point to of a potential difference across the clinical response for patients that received haplo-matched or not haplo-matched manufactured product? And then, if you could maybe touch on the patients in the AML cohort and whether they... You know, it seems like the patient, the case study, that patient would've been transplant ineligible. Clearly, I don't think received a transplant, but in terms of some of the other patients that did respond in the high-dose cohort, could you maybe opine whether any of those patients had a prior transplant? And then maybe I'll ask a follow-up. Thank you. Yes. There were a few questions there. Maybe I'll start with the last one because I remember that the best. In our AML study, patient four who achieved CRMRD minus was previous transplant, and then they relapsed, and then they achieved the response that they did. I'm sorry, I'm back. Haplo versus no haplo. Haplo. We do have. Yes, we are trying to start with both haplo and off-the-shelf patients. What I'll tell you is that based on the results, we are taking forward the off-the-shelf only. That should give you confidence in what we are seeing. We hope to have that sort of granularity in a medical conference presentation coming up later this year. Okay. Sorry, I missed that. Is it a follow-up, Dane? Yeah, sorry, I missed that first part. In terms of the high-dose cohort for 101, were any of those patients prior transplants? Yeah. Patient 4. Okay. That was a CRMRD negative patient? That is a CRMRD negative patient. Okay. All right. Now in terms of the process going forward or the clinical process and the feedback that you're getting right now from your PIs, is there any additional prior treatment experience that your PIs would like to see in the AML setting, as you may be working more sites globally? Is there a thought to start maybe including patients that have had more transplant experience into the clinical studies to understand that profile a little bit different than, you know, the transplant-ineligible patient population? Kind of the same question on the NHL side. You know, how many patients, if any, has had prior CD20 bispecific exposure in the study? It didn't seem like many, but if there were. You know, looking to not only look at patients that had prior CAR T in the NHL setting, but also patients that did have some more of the newer experimental therapies, like the bispecific class. Thank you. Great. Those were two large mouthfuls, Dane. Dr. Rotta had the patient, the first patient you asked about, and then Dr. Dickinson can comment on the NHL trial. Dr. Rotta. If I understood correctly, the question was whether there is a different approach or a feeling whether the patient was relapsed after a previous transplant or not. The trial in the initial phase allow for, and also still for a patient that receive an allo transplant before, but we also enroll patient that were relapse refractory without having a previous transplant. I cannot say that from the data that we have, that there is a specific activity whether the patient was relapsed after a previous regimen, non-transplant or transplant. I think probably the answer to the question is a little bit is yet to come. We don't know exactly what is going to be the right sequence there. Yeah. He also asked about the prior treatment in AML, the patients, what prior treatments they had, Dr. Rotta. Yeah, the patients on this that we enroll on this trial received a very disparate treatment. Received multiple line of treatment, including multiple round of chemo combination. A couple of treatment came from failed previous clinical trial with a combination agent including almost virtually all patients were included in a trial with venetoclax-based combination, and a handful had an allogeneic transplant before. These were all. The substantial thing is that all these patients had very disparate way of treatment, but they all were heavily treated. Yep. All of them had seen venetoclax, every patient in the trial so far? Yeah. Yes. Thank you, Dr. Rotta. Dr. Dickinson, would you like to comment on the NHL? Were there prior CD20 bispecific patients on the trial? The follicular lymphoma patients who are listed here, several of those patients were mine and had bispecific antibodies as the immediate prior therapy and have then gone on to respond. In fact, you know, it's tempting with the follicular lymphomas to think of them as being more indolent, but at least two of the patients in my hands were very aggressive and highly refractory lymphomas, high burden disease. One patient who had a very well-known bispecific antibody as the immediate prior therapy and had been refractory to CHOP chemotherapy, then platinum-based chemotherapy, and had progressed after an initial response on a bispecific antibody before going in to this trial and then responding to the NK cell product. To me, clinically, that was a very striking response in the context of very refractory follicular lymphoma. Yes, the study definitely included patients who've been exposed to the bispecifics. It’s difficult without summarized data to comment on all of the prior therapies across the entire patient cohort, but I can only speak to my experience with those cases. Yeah. Dr. Dickinson, can you talk about how the prior bispecific could correlate with any kind of T-cell response in CAR T therapy? Well, I mean, I can talk in general terms across the space. But most of the data with the bispecifics, as you know, we've got pivotal studies in follicular lymphoma and we're coming close to seeing data in large cell lymphoma, which shows remission rates that, you know, are similar to CAR T-cell products. I think, you know, we'll understand that a lot better over the next 6 to 12 months. What we don't really know is whether patients who are exposed to bispecifics after having not responded to CAR T-cell products are going to respond as well. Whether the mechanisms of resistance to bispecifics are the same as the mechanisms of resistance from CAR T-cells. Intuitively, you would think they're likely to be very similar just by the mechanism of action of T-cell activation. We saw, you know, sparse data with non-Hodgkin lymphoma in that regard in their recent publication from the Regeneron that suggests that some patients have responded to bispecific after CAR T failure. I still think there's good reason to believe that the mechanisms of resistance are gonna overlap between CAR T-cell and bispecifics. These clinical responses that we saw in this trial with these Flu/Cy and impaired patients were just simply very interesting at this point in time. Great. Thanks. Dane, did you get your questions answered? Yeah, that was awesome. Thank you very much. Great. We'll take our next question from Emily Bodnar with H.C. Wainwright. Please go ahead. Your line is open. Hi. Thanks for taking the questions and congrats on the great data. I was curious for NKX101, did any of the other AML patients who responded have any genomic alterations of note beside the patient with the IDH1 mutation? And is 1.5 billion cells per dose the highest that you plan to evaluate before deciding which dose to take forward, or do you think you would dose escalate beyond that? Thank you. Let me just start with where we might go next. When you dose escalate and you have the kind of preliminary efficacy with the dramatic lack of toxicity, you tend to wanna go higher. We'll make those assessments as we go forward. Some of that may have to do with manufacturing constraints on concentrations and vials and things of that nature. Right now, we think the 1.5 x 3 is a really great dose to go to and one that's probably gonna yield some results that we're hoping are similar or better than where we're at now with the 1 billion. Do you wanna talk about the other questions she asked, Kanya? Yeah. We are still getting the data about the baseline genetic mutations. Okay, thank you. Thanks, Emily. We'll take our next question from Matt Biegler with Oppenheimer. Please go ahead. Your line is open. Hey, guys. Thanks for giving us something to be hopeful for. This is really, really great news. I wanted to have a follow-up question for Dr. Rotta on his view of the definition of a clinical benefit in AML. Obviously, you know, remission rate is very important for it, but is it more so about successfully bridging to transplant? And what do you need for a cell therapy to get patients there? Meaning, can you transplant a morphological leukemia-free MLFS, morphological leukemia-free state? I think we did see one instance of that. But you know, kinda what are the risks involved with that and kind of what is the entire calculus that goes on in terms of getting somebody to transplant? For you as a physician, when you're looking at new therapies, is bridging to transplant the first metric that you look at, or is it remission rate? Or just any details on that would be great. Thanks. Dr. Rotta. Yes, this is a great question. Consider just a couple of general consideration. As you know well, if you're dealing with a transplant-eligible patient, somebody fit, once you have a patient that are beyond standard risk, and virtually all the patients we are discussing today, which are relapsed refractory, none of these patients will have a meaningfully long remission, as far as we know, short of an allogeneic stem cell transplant. It's true that we look at these therapies as bridging in this type of patient. That said, also patients that are not fit for transplant will always ultimately benefit from a meaningful reduction of their disease burden. As far as the clinical benefit and the success of the bridging to take patient to allo transplant, of course, what we always try to achieve is the minimal amount of disease burden possible or no disease burden, evaluable by minimal residual disease. Of course, the optimal bridging would be a treatment like has occurred in two of our patients here, on this trial that achieve a minimal residual disease negative, and where they, you know, we are planning toward they receive an allogeneic transplant. As far as clinical benefit, we still consider that if a patient goes into a morphologically leukemia-free status, we, on a case-by-case, you know, discussion will move these folks to transplant, clearly indicating that, for example, still a blast burden above 5% will identify a high-risk transplant, where the clinical benefit of the allo transplant may become questionable. Also the fitness of the patient, the age of the patient will become a critical part of the decision. I don't know if I answered your question there. Yeah. Thank you. Maybe a follow-up. Maybe a quick follow-up is, would you consider using NK cells as kind of a consolidation treatment post-induction to drive a deeper remission, a deeper MRD remission? Because we know that MRD status pre-transplant correlates to outcomes post-transplant. I'm just interested in your thoughts there. Absolutely. Consider that in the ALL, that is already a mentality that we have because in ALL we have a chance to more uniformly get MRD data. If I can and I have a patient with AML that still remain MRD positive, I will try to make him negative before taking him to an allo, and currently I would use cell therapy like CAR T-cells. In AML, unfortunately, we don't have the luck to have MRD more consistently because the disease is much more heterogeneous. It is true that if in the future we will get a more, you know, uniform way to assess MRD in all AML, if we have a non-toxic option of cell therapy to, you know, after, you know, inducing the patient, being able to really, take them to an MRD negative status with the cell therapy, we would do that before considering an allograft. Before we move on, I just would like to say that while we're very excited about bridging the transplant for the AML patients and the physicians who treat them, we're also going to be developing this as a standalone and hopefully see earlier lines of therapy in combination as we move forward. We're gonna do both, and however this drug works, we're gonna be thrilled if it does. It's starting to show signs of it now. Yeah. I just wanted to comment that despite the fact that we have been just discussing about transplant, patients that we enrolled on this trial were not necessarily transplant candidates. This is an option also in the large patient population that will not eventually go for transplant. Yeah, that makes sense. Thanks. Thanks so much. Thanks, Matt. As a reminder, that's star one for your questions. We'll take our next question from Sami Corwin with William Blair. Please go ahead. Morning, guys. Thanks for taking my question. Congrats on the data. I was just curious if you could provide some additional color on how you're thinking about combining both the AML program and the CD19 program with other therapies. Based on the AML data so far, how are you thinking about advancing NKX101 to solid tumors and thinking about that trial design? Thanks. Yeah, let me just say that both programs will move forward in single agent expansions and potential combination expansions. It's our goal to look at combination with standard of care as one potential expansion, and that single agent activity that we're seeing directs us to continue to expand as a single agent looking for that opportunity to accelerate any kind of approvability. Do you wanna talk, Ka, about any of those issues? I don't know that we go into the specifics. Okay. We will be going to earlier lines with respect to standard of care in AML and lymphoma. We are quite pleased with the data we've seen with just monotherapy to date. That'll put us in a good place to move our programs forward. I think your other question was on solid tumor. Plans for solid tumors, yeah. with this data set, we will, you know, it helps leverage the kind of dose we wanna start with solid tumor, especially with this nice clean safety profile. Absolutely, we will be looking at all of this data as we design our solid tumor trial. Perfect. Operator, I think that was the last question. Great. Then we'll turn the call back over to Paul Hastings for any closing remarks. Great. Thanks everybody for joining us, and sorry we've gone a little bit over our allocated time. We don't like to do that, but we really appreciate the questions. We're real excited to move forward and to continue to develop both NKX101 as well as NKX019, and we thank you for your time today. Thank you, and this does conclude today's program. Thank you for your participation. You may disconnect at any time.