Thank you very much, operator. Thank you everybody for joining us on the operational highlights and financial results for the period ending September 30, 2021. Joining me today are our Chief Medical Officer, Dr. Fred Grossman, and our Interim Chief Financial Officer, Andrew Chaponnel. If we could move to slide four, which is our pipeline slide. We are developing product candidates derived from our mesenchymal stromal cell platform technologies, Remestemcel-L and Rexlemestrocel-L. Remestemcel-L product pipeline focuses on pediatric and adult systemic inflammatory conditions, including pediatric acute graft-versus-host disease, adult GvHD, acute respiratory distress syndrome, and inflammatory bowel disease. Rexlemestrocel-L platform technology is being developed for localized inflammatory conditions, including advanced chronic heart failure and chronic inflammatory low back pain. As you can see on this slide, we have a number of global and regional strategic partners for various of our programs. Slide five. The platform technology has an underlying mechanism of action that is derived from the fact that these cells express on their surface a variety of receptors for inflammatory cytokines. When the cells find themselves in the milieu of inflammation in various tissues, they're able to be activated, and following activation by these inflammatory cytokines, they release various factors that in concert turn off the degree of inflammation mediated by multiple arms of the immune system. Next slide, please. We have a very strong global intellectual property patent estate, which puts us in a leadership position in the mesenchymal stromal space globally, with a patent portfolio of over 1,000 patents, with protection extending through 2040. This provides strong protection around compositions of matter, around manufacturing, and equally as important around every indication that we target. When outside of our core commercial areas, we may consider granting rights to our portfolio to third parties who require access to our patents to commercialize their particular products, and we've already entered into those type of partnerships, which results in royalties on a worldwide basis back to us. Next slide. The manufacturing allows us to scale allogeneic off-the-shelf products with stringent criteria, meeting regulatory body requirements internationally for robust quality assurance, final product lots with batch-to-batch consistency and reproducibility. We have proprietary ownership of media that is animal-free, that allows us to increase our yields and output to commercial scale, and we have the ability, again, with proprietary technologies, to move to 3D bioreactors to further reduce labor, improve manufacturing efficiencies, and ultimately meet the commercial requirements for some of the large volume indications that we're targeting, as well as significantly reduce our cost of goods. Now I'd like to move to the financial results. Andrew Chaponnel, would you please take the next few slides? Thanks, Silviu Itescu. Now turning to slide nine, I'm very pleased to confirm that we have successfully refinanced and expanded our senior debt facility with Oaktree Capital Management. The new $90 million five-year secured loan facility has a three-year interest-only period, after which time 40% of the principal is repayable over two years, with the final loan repayment due no later than November 2026. Cash on hand at the end of the quarter was $116 million. In the quarter, revenues from TEMCELL royalties in Japan were $2.4 million, an increase of 22% on the previous quarter and 90% on the comparative quarter of last year. Net cash operating usage was $19.6 million for the quarter, a reduction of $8.6 million on the comparative quarter. Our loss after tax improved by $1.9 million on the comparative quarter. Now on slide 10, I'll explain further our loss after tax result. Within commercialization revenues, we recognized $2.4 million in royalties from TEMCELL in Japan, a 90% increase on the comparative quarter, and we recognized $1.2 million of milestone revenue after Takeda received approval to manufacture and market Alofisel in Japan for the treatment of complex perianal fistulas in patients with non-active or mildly active luminal Crohn's disease. Within R&D expenditure, we saw a 52% reduction of $10 million, as clinical trial activities for our COVID-ARDS, back pain, and heart failure product candidates reduced given that clinical trial recruitment and data analysis is now complete. For our manufacturing expenditures, we recorded a 37% saving of $4.4 million due to a reduction in process development activities. During the quarter, we continued to build our pre-launch inventory levels of Remestemcel-L to support the long-term commercial supply of GvHD and COVID-ARDS. To date, we have manufactured $26 million worth of Remestemcel-L pre-launch inventory in anticipation of launch. This pre-launch inventory will be recognized on the balance sheet if we receive FDA approval. Within management and administration, there was a 23% saving of $1.8 million as employee compensation costs reduced. For contingent consideration, we saw a $14.8 million reduction in gains recorded compared to the comparative period. This period-on-period reduction was due to a $15.1 million gain being recognized in the comparative period. Now I'd like to hand the call back to Silviu Itescu for the remainder of the presentation. Thanks, Andrew. If we can turn now to slide 12, which focuses on graft versus host disease and our approach to treating it with Remestemcel-L. Acute GvHD is a serious and fatal complication of an allogeneic bone marrow transplant, and it's due to activation of the T cells in the donor graft, recognizing the host as foreign and initiating a severe cytokine storm that ultimately destroys the gut and the liver and is potentially fatal. Slide 13. This is a particular problem in children who have high risk of treatment failure and death because there are no drugs approved for treatment of pediatric GvHD under the age of 12. In these children, of whom there are more than 2,000 that undergo an allogeneic bone marrow transplant in the U.S. alone on an annual basis, if they develop steroid refractory graft-versus-host disease, a condition that occurs in up to 50% of these children, mortality can approach 90% when involving the gut and the liver and is associated with very high levels of inflammation. Slide 14. In three prior trials, one of which was a randomized controlled study, one of which was a salvage therapy in children who had failed all other existing therapies, and the most recent phase III trial, study 001. In all three of those trials, we have observed a very consistent day 28 overall response, as shown in yellow, of between 64%-69% following four weeks of therapy with Remestemcel-L. In addition, treatment of these children across each of these three trials has resulted in survival rates of between 66% and 79%. In contrast, on the left two panels, in two different control groups, one of whom were children within a randomized controlled study of steroid refractory GvHD and the other, the MAGIC cohort, children who are matched historical controls, matched for disease severity and inclusion criteria into our phase III trial. As you can see, the day 28 response using best available therapy is of the order of 38%-43% only, and day 100 survival only of 54%-57%. These data were all presented to the FDA last year. Next slide, please. Slide 15. As you can see here on the left-hand panel is the two-year survival probability of a single-center study published of children treated with steroids for graft-versus-host disease. At six months, steroid-refractory children have, in this particular study, a 49% overall survival, and by 24 months, a dismal 35% survival. In contrast, the slide on the right shows the day 180 six-month survival in children from our phase III trial, 001, 002. As you can see, a 69% six-month survival in those children treated with Remestemcel. These results also were presented to the FDA last year, and we think are very encouraging for the potential use of Remestemcel in children with this severe disease. Let's move to slide 16. The MAGIC algorithm is an algorithm developed by investigators at Mount Sinai Medical Center in New York and has been developed and validated as a biomarker score that predicts outcomes in patients with acute graft-versus-host disease. In particular, the MAP score of at least 0.29, above 0.29, is a validated threshold that identifies those patients at high risk of non-response to treatment and death. In these three figures as shown on this slide from Magenau et al. in Journal Blood, you can see three different cohorts, all of whom validate the same algorithm. What they show is that those patients with a MAP score above 0.29 have mortality rates of the order of up to 90% over a twelve-month period of follow-up. This biomarker score is now used routinely by clinicians who follow their patients with acute GvHD. Next slide, please. Slide 17. In a recent publication in Bone Marrow Transplantation in the last two months, the Mount Sinai investigators performed an analysis comparing 52 children, 27 of whom came from their MAGIC cohort, and 25 of whom came from the phase III trial of Remestemcel-L. An analysis of outcomes by stratification on a MAP score of 0.29 below and above as a risk stratification category. As you can see in the figure on the left, amongst the MAGIC cohort treated with best available therapy, and that includes the recently approved Ruxolitinib, only in those patients with a MAP score above 0.29, only one out of 10 were responders to treatment through day 28. In contrast, eight out of 12 or 67% of Remestemcel-L-treated patients with a high MAP score were responders to Remestemcel-L, and this was a significant difference. When they looked at survival between these two groups, not surprisingly, on the right-hand figure, the children in the MAGIC cohort who had MAP scores above 0.29 had a 90% mortality through six months. In contrast, the Remestemcel-L-treated children with a MAP score above 0.29 had a 64%... had a 64% survival through that same six-month period, and this was significant. This identifies that remestemcel-L treatment specifically provides a survival and a treatment advantage in those children at highest risk for mortality and with highest inflammatory biomarker scores. If we can go now to slide 18, I'd like to give you all an update on where we are on the regulatory pathway towards approval of Remestemcel-L for steroid-refractory GvHD. The data that I've just shown you provide further support for the proposed anti-inflammatory mechanism of action of Remestemcel-L and its immunomodulatory activity in those patients with particularly the highest risk of steroid-refractory GvHD, and evidence that the anti-inflammatory immunomodulatory activity of our cells result in improved survival outcomes. At the upcoming scheduled meeting with the U.S. FDA's Office of Tissue and Advanced Therapies or OTAT, this advice will address the appropriateness of our potency assays related to Remestemcel-L's proposed anti-inflammatory mechanism of action, how it relates to these biomarkers, how our potency assays relate to changes and improvements in our biomarkers, and ultimately in patient outcomes such as response and survival. These discussions could support a resubmission of the current BLA with a six-month review up to a six-month review, with the aim ultimately of achieving approval for Remestemcel-L in the treatment of steroid-refractory GvHD in children. Remembering that there are still no approved therapies in those under the age of 12, who continue to have a high mortality. If we could move now to slide 19. An overview of where Remestemcel-L is being developed now for ARDS, acute respiratory distress syndrome due to COVID-19. This is the number one cause, and continues to be the number one cause of death in those patients who are infected with the COVID-19 virus. We've taken knowledge of the extensive safety database of Remestemcel-L as it's being developed for the inflammatory components of GvHD and adapted both the protocol, the dosing strategy, and accessed and leveraged the fact that the cell's intravenously home to the lungs to address the potential for use of Remestemcel-L in inflammatory lung disease, in particular, in particularly respiratory distress syndrome due to COVID-19. Slide 20 is a very important slide about what has been learned in the last 18 months or so during this pandemic. Essentially, in the bottom left figure, a normal individual with a normal immune system is able to eliminate the virus rapidly, and the viral load goes up and then goes down as the immune system, driven by T cells, eliminates virus. The panel immediately to the right of that shows that in older individuals with defects in their T cells, the virus is not eliminated as rapidly. Viral load is much higher for a lot longer. In response to a higher viral load, the residual immune system attempts ineffectually to eliminate the virus, and that results, particularly in older patients, in a very severe inflammatory process that destroys the lung, but unfortunately is not effective in eliminating the virus. It has been established now that age is probably the most important predictive factor for a bad outcome following COVID-19. While age over 65 is a major risk factor, it is a fairly linear relationship between age and disease severity at all ages. If we now go to slide 21. The clinical experience with Remestemcel-L in COVID-ARDS has been informed based on a pilot study of 11 patients and a more recent phase III study of 222 patients. In the initial 11 patients at Mount Sinai Hospital in New York, 10 out of the 11 were under the age of 65, and in these first 11 patients, we saw that 82% successfully came off ventilators and were discharged from the ICU within a median of 10 days. On that basis, the protocol of two infusions five days apart was implemented into a randomized controlled study, which in the middle of the chaos of the pandemic changed quite significantly during the course of the initial 12-month period and progressively enrolled older patients such that while the median age in the first half was 59, the median age in the second half was 67. We were able to evaluate the outcomes by age, and we have been able to identify that using this particular dosing strategy, those patients under the age of 65 responded very favorably. The slide 22 demonstrates the effect of age on mortality in our study in the control population. As you can see here, whilst older patients had a mortality of 70% through 60 days, and that was significantly higher than younger patients. Nonetheless, younger patients under the age of 65 still had a mortality of 42%, which is extremely high for anybody of that age through 60 days. This is despite the fact that control patients continued to receive maximal standard of care. The only drug that is approved for this group of patients is dexamethasone or steroids. If we can now go to slide 23. In the younger patient population, in the subset analysis, what you can see on the left-hand side is that, in fact, two doses of Remestemcel-L reduced mortality by 46% through 60 days. That was associated on the right with improvement in disease severity score at every time point studied. Slide 24, moreover, shows that in an exploratory subset of patients on dexamethasone as per approved protocols, and this accounted for, I think, about three-quarters of the overall study. You see a significant synergy between Remestemcel-L and dexamethasone. On the left-hand panel now, the mortality rate in the younger patients is reduced from 48% to just 14% through 90 days through three months. On the right-hand side, again, the combination of the two cells plus dexamethasone significantly increased the proportion of patients who improved in red by at least one category of ARDS severity score at every time point measured. This strongly suggests to us that the combination of steroids plus Remestemcel-L is a combination that should be explored in a confirmatory study for this preliminary data set. If we move to slide 25, what is the regulatory pathway to a potential emergency use authorization for COVID-19 ARDS? That's become clear having met with the FDA very recently, and the FDA advised Mesoblast that a single additional study, if positive, could provide a data set in conjunction with the data that I've just shown you, that might be sufficient to support an EUA. The FDA indicated that the potency assays that we are in discussions with respect to GvHD and the whole GvHD BLA can be referenced, but that such a potency assay should be agreed to prior to commencement of this proposed pivotal phase III trial. We plan to move forward with an additional phase III program in COVID-ARDS, with the next step being to obtain agreement with the FDA on the final protocol and supported by our potency assay development. Now let's move forward and talk about Rexlemestrocel-L, some updates on our chronic heart failure program. Slide 27. Cardiovascular disease remains the leading cause of death in the U.S., even in the post-COVID era. Heart failure affects as many as 6.5 million patients in the U.S., and as the population is aging, the prevalence is increasing. It's a disease that has a mortality that is as bad as many cancers and approaches 75% after an initial hospitalization. Patients with heart failure not only develop symptomatic failure and recurrent hospitalizations for shortness of breath, but importantly remain at very high risk of recurrent adverse major cardiac adverse events, including vascular occlusions of heart attacks and strokes. While new therapies have been developed that are keeping patients out of the hospital for symptomatic heart failure, i.e., shortness of breath, these newer therapies have not made a material change or improvement in overall cardiac mortality or major ischemic events, including heart attacks or strokes. That's where the unmet need continues to be, and that's where we believe that Rexlemestrocel-L has an edge over other therapies. If we go to slide 28, this slide talks to the mechanism of action of Rexlemestrocel-L in this disease. It is well established that progressive heart failure is associated with progressive inflammation within the heart as a result of macrophage secretion of inflammatory factors such as interleukin-1, TNF, and interleukin-6. Those same factors that are relevant to disease progression in inflammatory lung disease and in graft-versus-host disease. When Rexlemestrocel-L are placed within the inflamed myocardium, they're activated by these factors, resulting in release of anti-inflammatory and immunomodulatory factors that have ultimately two outcomes. One is they reduce the intracardiac inflammation, protecting heart muscle cells. Secondly, they induce a new vascular endothelial network of blood vessels, which also improves vascular flow and protects cardiac muscle cells against ischemic death. Together, we believe that these are important mechanisms that protect both the heart muscle from intracardiac damage as well as the extracardiac vascular abnormalities that are important in the complications of this disease. Slide 29. The data from the randomized controlled phase III trial of Rexlemestrocel-L in 565 patients with class two and class three heart failure were presented very recently as a late-breaking presentation by Dr. Emerson Perin at the American Heart Association annual scientific sessions. The featured program was building on the foundations of treatment advances in heart failure therapy. Dr. Perin is the medical director of the Texas Heart Institute and clinical professor at Baylor College of Medicine. The data that we're presenting, as I'll show you in a minute, identify this as a landmark study showing a significant relationship in outcomes between the presence of systemic inflammation and treatment effect with Rexlemestrocel-L on cardiovascular mortality, heart attacks, or strokes. Slide 30 provides an overview of the phase III trial itself. It was a 1:1 randomized controlled double-blinded study conducted over 55 sites in North America using 150 million allogeneic cells of Rexlemestrocel-L immunoselected culture expanded cells versus controlled sham procedure in 565 patients. The primary endpoint was reduction in recurrent heart failure-related hospitalizations due to predominantly shortness of breath and volume-related complications. The key secondary endpoints, which were all pre-specified, were reduction in ischemic cardiovascular events such as heart attacks and strokes, reductions in hospitalizations from these events, and reduction in overall cardiac mortality and other non-cardiac mortality. The composite of the pre-specified endpoints was a post hoc that I will show you the data of. Next slide, please. Unfortunately, the primary endpoint of reduction in hospitalizations from symptomatic shortness of breath was not improved by Rexlemestrocel-L over and above the reductions in hospitalizations that one gets with maximal existing and newer standard of care therapies. This symptomatic improvement in neurohormonal symptoms is not an area that apparently Rexlemestrocel-L has a major impact on. However, on slide 32, we see some pretty dramatic effects of Rexlemestrocel-L on top of maximal standard of care. First of all, we see a significantly reduced incidence of heart attacks and strokes. In the overall 537 patient population on the left, you see a 65% reduction in risk with a p-value of 0.001 across the entire patient population. That's equally represented in New York Heart Association class two patients, the middle panel, and New York Heart Association class three patients, the right-hand panel. If we go to the next slide 33. Looking at time to cardiac death, we see a significant impact on cardiac mortality, which is predominantly evident in the class two patients on the left-hand panel, where we see again a 57% reduction in mortality. If you look at the middle panel, that is almost exclusively in those patients with evidence of inflammation, as measured by a positive CRP level above 2 mg/L. You see here that in the CRP positive patients, the hazard ratio is 0.204, indicating an 80% reduction in mortality, p = 0.005. CRP is a well-established biomarker for risk in cardiovascular outcomes. It has been validated across many studies. It is a biomarker that predicts worse outcomes in patients with heart attacks, with atherosclerotic disease, and with heart failure. It's really the end result of cytokines that are inflammatory cytokines made by the macrophages. We believe that circulating CRP in these patients reflects inflammation within the myocardium itself. What this says to us is that we can identify those patients with evidence of inflammation, and that those patients are most susceptible to death, and that these patients are most likely to respond to Rexlemestrocel-L therapy in a beneficial way. If we can move to slide 34 now. When we take into consideration the composite endpoint of major adverse cardiac events defined as either cardiac death or myocardial infarction or stroke, and this is an endpoint that the FDA has used to approve multiple drugs for cardiovascular diseases, particularly those patients being diabetics with high risk for cardiovascular events. When we look at this as an endpoint, and remember that all of the components of this composite endpoint were pre-specified. The composite itself was post hoc. You see on the left-hand side, in 537 treated patients, this endpoint was statistically significant, P = 0.02 with a hazard ratio of 0.67, meaning a 33% reduction in the composite of the three endpoints. I think what's most interesting and exciting is the middle panel, which demonstrates that in the 301 patients who had evidence of inflammation as measured by an elevated CRP at baseline. This is the group that was most likely to benefit from treatment. Here the hazard ratio was 0.55, meaning we reduced the risk of this composite endpoint by 45%. This is the target population that we will be focusing on and is the most likely to be where the benefit is and where the risk is greatest. Let's move to slide 35, because this is the conclusion slide of Dr. Parent's presentation and gives you a sense of where we are going as a company in the heart failure program. In conclusion, the transendocardial delivery of the cells was safe, did not elicit any clinically meaningful immune-related responses despite the fact that these were allogeneic cells. Over a mean follow-up of 30 months, a single injection of Rexlemestrocel-L compared or added on top of maximal standard of care, significantly reduced the incidence of heart attacks or strokes, the incidence of cardiac death, particularly in Class II patients, and the composite of cardiac death or non-fatal MI or non-fatal stroke across all patients. These benefits were most likely to be seen in those patients who had evidence of inflammation. We have a biomarker that can guide our future therapy in this target patient population. With that, I think I'll stop, and we would welcome any questions. Thank you. If you wish to ask a question, please press star one on your telephone and wait for your name to be announced. If you wish to cancel your request, please press star two. If you are using a speaker, please pick up the handset to ask your question. We kindly ask that you please limit yourself to one question during your turn, and if you have a follow-up, you may join the queue again by pressing star one. Your first question comes from Louise Chen with Cantor, p lease go ahead. Hi, team. Congrats on the progress. This is Wayne Ang for Louise. Just one question from us. On the Remestemcel-L, has the FDA indicated how big the additional clinical study needs to be, and what do they expect to see in addition to the potency assays? Thank you. Thank you for that question. As we have said over the past few months, we do not believe we will have to do any further clinical studies with Remestemcel-L for GVHD. The discussions that we are having shortly are all about CMC and potency data. We do not believe we need any further studies. As I've shown you, we had a positive phase III trial. We've demonstrated further studies of evidence of efficacy in high-risk children, and the discussions we're having are solely around potency and manufacturing. Oh, sorry, I mean for the COVID-ARDS. Ah. Sorry for that confusion. Oh, I see. Thank you. No, I'm glad you clarified. Yes. For the COVID-ARDS study, we believe that the target patient population is, as we have defined it, i.e., patients who are younger, under the age of 65, which, and this is obviously a shifting demographic depending on country, state, et cetera. Predominantly the new infections are happening in younger people, predominantly those who continue to be unvaccinated and at risk of ICU and ventilator-related deaths are younger people. It's an appropriate target population. It's where we saw a positive result. It's where we've proposed to the FDA that our pivotal trial would focus on. The size of the study, I think it will be very similar to the study that we've just completed powering. Really let me ask Dr. Grossman to address that, please. Yeah, that's correct. We are currently in discussions and we'll be sharing our protocol with the FDA to have agreement on the step forward. As Silviu just mentioned, it'll probably be very similar in terms of size and scope, focusing on those younger than 64. We also plan to study those older than 65 as well with a different dose because we do believe that those patients could potentially respond to a different dose pattern. Got it. Thank you so much. Your next question comes from Kennen MacKay with RBC Capital Markets, p lease go ahead. Thank you. Hi, good morning. This is Jackie Yan. Thanks for taking our questions. Maybe, you know, just on a recent heart failure data presented at AHA, you know, that subgroup data you presented. Wondering what prompts that subgroup analysis and what's the plan for the potential regulatory path forward? And then have you presented this data set to the FDA yet? Yeah, that's a critical question, and I appreciate you asking it. That is precisely the basis of our active and ongoing discussions with the FDA. The data have been presented, and we are waiting on feedback. We clearly have a view that the high-risk population in this study can be identified and responds most effectively to our therapy. We think that we've identified the highest risk population where there is a benefit on the three-point MACE, which is an FDA approvable endpoint. Got it. Thank you. I just wanna confirm. I heard right. You will meet with the FDA in December to address the potency assay. Once assume it's been resolved for that ARDS trial, you can just go ahead and initiate a phase III without like meeting with the FDA again, right? That's exactly right. We have a discussion with the agency in very short order about potency assay for the product. We expect that they will be comfortable with the data that we're putting in front of them. At that point, the clinical group will move forward with an IND proposal for a pivotal trial. Got it. It's super helpful. Thanks again for all the questions. Thank you. Your next question comes from Tanushree Jain with Bell Potter Securities, p lease go ahead. Hi, Silviu and Dr. Grossman. Andrew, thanks for taking my questions. Really happy with the progress so far. Just one question from me on the recent late-breaker data for the heart failure. Before this data came out, we were kind of focusing on the Class II patients because they were earlier in the disease, you know, with, I guess, better heart muscle, et cetera. I guess the correlation that was presented in terms of high levels of inflammation, that's kind of negated, I guess, this class difference between Class II and Class III in your therapy working. Can you perhaps talk a little bit about how this high levels of inflammation is compensating for the fact that these Class three patients don't have a lot of heart muscle, but this therapy is still able to work? That is a great question, Tanushree. Thank you for that question. Very important question. The high levels of inflammation, as in this particular case, measured by CRP, but not only CRP, right? The other cytokines go along with CRP have a predictive value on both loss of viable heart muscle and also vascular major vascular occlusions, particularly coronary arteries, which are right next to the source of the inflammation within the heart. It is clear from looking at our own data that the Class two patients are at greater risk of or can be helped sooner in terms of reduction in cardiac death because they have more heart muscle left to salvage. While the Class three patients are more advanced in their disease, but they're at a higher risk really of coronary artery disease and death or progression to death following an occlusion in the coronary arteries. The stratification based on severity allows us to look at the spectrum, the continuum really across Class two and Class three patients, using inflammation as a biomarker for treatment effect more broadly speaking. Okay. Does that address the question? Inflammation is at the core of the cardiovascular complications in all of these patients, all of which are major outcomes that will reduce, you know, that'll cause death, that contribute to the high rates of mortality in this population. It is apparent that a single injection into the myocardium of our cells reduces the inflammatory risk both in the muscle, in the heart, as well as the extra cardiac vasculature. It's appropriate to target both in the patient population at risk, which is that patient population with inflammation. You know, you had a slide where you've actually just shown Class two patients with high levels of inflammation. How does Class three patients with high levels of inflammation, how does that group compare to Class two with high levels of inflammation? When we look at the composite of cardiac death or MI or stroke, we see similar directionality in Class II and Class III. The contributions to those three, the three-point MACE within each is slightly different. That contribution of reduction in cardiac mortality is more evident in Class II. The contribution of reduction in myocardial infarction is seen in both groups, but perhaps a greater risk reduction in Class III. Both groups are improved in the composite endpoint using the cells. Therefore, as we move forward, I think we're gonna be looking at the risk factor of inflammation as a predictor overall of treatment effect without having to sub-stratify by class. Right. You will focus on class two and class three both, rather than just class two? I think as we move forward. Because of the inflammation. Yeah. This continues to be, you know, an active discussion with the FDA, so I think it's premature to make definitive statements, but that's the direction based on the data that we're going towards. Yes, we're looking more broadly at the inflammatory population across all patients. Great. Thank you. That brings us to the end of today's call. I'll now hand back to Dr. Itescu for closing remarks. Well, I'd like to say thank you to everybody for joining us today. We're very excited by the progress that we're making as a company in our technology, as we're moving towards our first product for potential approval and launch. We're very pleased to have entered into a strategic financial alliance with Oaktree Capital Management that shores up our existing balance sheet. We look forward to updating you shortly on some other very important key milestones. Thank you.