Good morning, and welcome to the Keros Therapeutics 2023 American Society of Hematology Annual Meeting update call. At this time, all participants are in listen-only mode. Later, we will conduct a question- and- answer session, and instructions on how to ask a question will follow at that time. As a reminder, this call will be recorded, and the link to the recording will be available on Keros's corporate website. I would now like to introduce your host for today's program, Justin Frantz, Keros's Head of Investor Relations. Mr. Frantz, please go ahead. Thank you, operator. Thank you all for joining us on today's call. As we announced this morning, we are very excited to report clinical updates from our hematology franchise. A press release is available on our website at kerostx.com and is also included as an exhibit in the Form 8-K that we filed with the Securities and Exchange Commission. During this call, we will be making a number of forward-looking statements. Please take a moment to review our disclaimer slide on the webcast, which notes that these forward-looking statements involve risks and uncertainties, many of which are beyond Keros's control. Actual results can materially differ from those expressed or implied by such forward-looking statements, and any such risks can materially and adversely affect our business, financial condition, results of operations, and trading prices of for Keros's Common Stock. For a detailed description of applicable risks and uncertainties, we encourage you to review the Risk Factors section of the company's quarterly report on Form 10-Q, filed with the SEC on November 6, 2023, as well as the company's other documents subsequently filed with or furnished to the SEC. All forward-looking statements made during this call speak only as of today's date. Except to the extent required by law, the company does not undertake any obligation to publicly update its forward-looking statements based on the subsequent events or circumstances. Today, we will discuss select updates from our clinical presentations at the American Society of Hematology, or ASH. Joining me on today's call are Jasbir Seehra, President and CEO of Keros Therapeutics, Simon Cooper, our Chief Medical Officer, Christopher Rovaldi, our Chief Operating Officer, and Keith Regnante, our Chief Financial Officer. After a formal presentation of the data, we will open the call for Q&A. I will now turn the call over to Jasbir Seehra. Thanks, Justin. Keros is developing potentially differentiated product candidates designed to alter TGF-β signaling and target pathways critical for the growth, repair, and maintenance of a number of tissue and organ systems. On today's call, we will provide updates from our hematology franchise and are honored to have the exciting backdrop of ASH to provide updates on our ongoing phase II clinical trials of KER-050, one in myelodysplastic syndromes and one in myelofibrosis. The 5 abstracts that were accepted for presentation at ASH, 3 clinical and 2 preclinical abstracts, are shown here. Having 5 abstracts accepted demonstrates the great work our entire team continues to accomplish. The clinical presentations, which will be the focus of this call, provide an update on our ongoing KER-050 phase 2 clinical trials in MDS and myelofibrosis. Myeloproliferative neoplasms, which include MDS and myelofibrosis, are complex diseases. They are, they are diseases of the bone marrow, but within the bone marrow is an osteo-hematopoietic niche where bone and blood cell precursors interact to regulate hematopoiesis. Within this niche, disruption in these interactions leads to ineffective hematopoiesis and have downstream consequences that lead to poor systemic outcome that include progression to AML, heart failure, bleeding, iron overload, and bone loss. Increasing evidence suggests that imbalanced signaling by TGF-β signaling superfamily members, particularly activin A, is a key driver of this pathogenesis of MDS and myelofibrosis. Activin A is a pro-inflammatory TGF-β ligand that is increased in the bone marrow in these patients and has been shown to impair osteogenesis and hematopoiesis. KER-050, or elritercept, is an activin receptor type II ligand trap designed to treat ineffective hematopoiesis. It has been engineered to bind select TGF-β ligands, including activin A, and restore balanced TGF-β signaling within the osteo-hematopoietic niche. KER-050 has been designed to promote maturation and differentiation across all stages of both erythropoiesis and thrombopoiesis. Importantly, this reflects a differentiated mechanism of action relative to ESAs and luspatercept, both used to treat MDS, which primarily stimulate either early or late-stage erythrocyte precursors, respectively. As we will discuss on this call, KER-050 also demonstrated the potential to increase bone formation, improve iron utilization, and reduce myocardial strain, thereby potentially addressing the cascade of poor outcomes we have just discussed. I will now hand the call over to Chris Rovaldi to walk through MDS. Chris? Thank you, Jas. Dysregulated signaling due to somatic mutations, aging, and inflammation leads to ineffective hematopoiesis in MDS. People living with MDS experience multiple cytopenias, including severe anemia, and have reduced quality of life due to factors such as fatigue and the emotional burden of the disease and treatments. Unmet need remains for treatments that can address the multifaceted pathophysiology leading to ineffective hematopoiesis and the severe consequence of MDS, including progression to acute myeloid leukemia and cardiovascular disease, which is the second leading cause of death in MDS patients. Before we dive into the clinical data, I want to cover the current treatment landscape and the need for novel treatments for patients living with MDS. Current options for symptomatic anemia include red blood cell transfusions, erythropoiesis-stimulating agents, or ESAs, and Reblozyl, an erythroid maturation agent. MDS patients often require transfusions, which provide symptomatic relief. However, repeated transfusions are associated with iron overload and have been shown to be associated with increased risk of AML progression and reduced overall survival. ESAs have long been the first-line standard of care in MDS and have been shown to improve anemia, but benefit is limited in patients with high transfusion burden and high endogenous erythropoietin levels. Reblozyl is approved in first-line lower-risk MDS and in second-line RS-positive patients. In the more severe second-line patients with HTB, only 20% of patients achieve transfusion independence for eight weeks following treatment with Reblozyl. Importantly, in the second-line setting, no improvements in patient-reported outcomes of quality of life were demonstrated with Reblozyl in the phase III trial. Although the field has progressed in developing assets to improve anemia, the current treatment options do not fully address the needs of patients, and the unmet need remains for a treatment that can address the multifaceted pathophysiology of MDS. I will now review the trial design of our ongoing phase II trial in lower-risk MDS. In our phase II trial, we cast a wide net to explore the potential for KER-050 to address ineffective hematopoiesis in lower-risk MDS. As Jas shared earlier, KER-050, with its potent inhibition of activin A, has the potential to ameliorate multiple components of the pathophysiology of MDS, not just anemia. This two-part phase II trial is assessing the safety and efficacy of KER-050 in a broad population of lower-risk MDS patients, including those non-transfused and transfusion-dependent patients, RS positive and non-RS patients, and patients who are ESA-experienced, ESA-naïve, or unlikely to respond to ESAs. We are currently enrolling Part 2 and treating ongoing patients from both Part 1 and Part 2 at the recommended Part 2 dose of 3.75 mg/kg every 4 weeks, with the option to uptitrate to 5 mg/kg based on individual titration rules. Endpoints include hematologic improvement, or HI-E, for 8 weeks per IWG 2006 criteria, and red blood cell transfusion independence for 8 weeks in patients who require greater than or equal to 2 units of red blood cells at baseline. All KER-050 data in lower-risk MDS will be presented as of the September 1, 2023 data cutoff date. At the data cutoff, 79 enrolled patients received at least one dose of KER-050, which we refer to as a safety population. Approximately one quarter of patients have reached their 1-year treatment milestone, and the median duration of treatment was approximately 29 weeks, with 63% ongoing and remaining on treatment. Additionally, hematologic response and markers of hematopoiesis are being presented for the exploratory analysis of the recommended Part 2 dose patients with at least 6 months of KER-050 treatment or who have discontinued. The demographics and baseline characteristics of the 79 patients in the safety population for this update are shown here. These data collectively demonstrate that this trial enrolled a hard-to-treat population with high disease burden. As you well know, 81% of patients were transfusion-dependent, with 56% of these patients having high transfusion burden. The vast majority of patients with a known dysplasia category had multiple lineage dysplasia, and 25% had thrombocytopenia at baseline, a characteristic that is independently associated with poor prognosis. Approximately 25% of patients had received prior ESA treatment, and the median baseline EPO levels were elevated in this trial population. I will now turn the call over to Simon to review the safety and efficacy data. Thanks, Chris. Even with the high disease burden of the enrolled patients, KER-050 has remained generally well-tolerated as of the data cutoff date. The most frequently reported treatment-emerging adverse events occurring in at least 15% of patients were dyspnea, diarrhea, fatigue, nausea, and headache. Most treatment-emerging adverse events were mild to moderate, and among serious adverse events, few were assessed as treatment-related. As previously reported, there were two fatal treatment-emerging adverse events: cardiac failure with myocardial infarction, and both were assessed as not related to treatment. Importantly, no patients progressed to AML while on treatment. I first want to summarize the pharmacodynamic data for KER-050. As Jas and Chris previously noted, KER-050 has the potential to address ineffective hematopoiesis and address multiple facets of the pathophysiology of MDS.... In this slide, you can see that the KER-050 treatment led to sustained and clinically meaningful increases in hemoglobin over 6 months of treatment. At the same time as this hemoglobin increase, increases in soluble transferrin receptor were observed in non-transfused and low transfusion burden patients, indicating an increase in erythropoiesis. Changes in ferritin, a measure of iron overload, were observed in patients dosed at the recommended Part 2 dose, regardless of baseline transfusion burden or erythroid response status. 48% of these patients with high baseline ferritin had decreases to less than 1,000 nanograms per ml, and 2 were able to discontinue iron chelation therapy. These data further support that treatment with KER-050 improved iron utilization among patients with iron overload at baseline and has the potential to ameliorate iron overload in patients with MDS, regardless of baseline transfusion burden. Inhibition of activin A has been shown to increase bone-specific alkaline phosphatase, a marker of osteoblast activity. Here, we report for the first time that KER-050 treatment led to sustained increases in BSAP during the first six months of treatment in MDS patients. These increases were seen regardless of hematologic response, which is suggestive of the direct effect of activin A inhibition. This supports the potential that KER-050 can act on multiple components of the osteohematopoietic niche to support functional hematopoiesis. This anabolic effect on bone has the potential to provide additional benefit to elderly MDS patients who have high rates of osteopenia and osteoporosis. Here we see the hematologic response rates observed in the modified intention-to-treat 24-week population, the mITT 24. That includes 60 recommended Part 2 dose patients with at least 24 weeks of KER-050 treatment or who have discontinued. Response was assessed by 2006 IWG criteria for HI-E or transfusion independence, shown here as TI, depending on the baseline transfusion burden. Overall response reflects either criterion being met. In the first column, we show response rates for the entire mITT 24 population, while the second column shows response rates for the difficult-to-treat high transfusion burden subset. HI-E and TI response rates were generally similar in the two groups, supporting the potential for KER-050 to treat a broad array of patients with MDS, including those with greater transfusion burden and bone marrow dysfunction. As Chris mentioned, this phase II trial enrolled a broad population of lower-risk MDS patients to help inform the design of future clinical trials, including selection of an appropriate patient population. Here we show the mITT 24 response rate, excluding the 9 patients with endogenous EPO levels greater than 500 units per liter, of which 6 were non-RS. EPO levels greater than 500 are a negative predictor of erythropoietic response and have historically been used to guide treatment decisions in lower-risk MDS. Response rates for the subpopulation of mITT 24 patients with a baseline EPO of less than 500 are shown in this table. More than half of these patients experienced a response, and response rates were comparable between RS-positive and non-RS disease in the high transfusion burden group. Here, we review the durability of transfusion independence in the mITT 24 population. On the panel on the left, you can see the rates of transfusion independence over periods from 8 weeks through 24 weeks. The majority of patients who achieved 8 weeks TI within the first 6 months of treatment maintained transfusion independence for at least 24 weeks. The observed rates of transfusion independence for at least 24 weeks, shown here, support the durability of response to treatment with KER-050, and response rates were relatively higher in patients with baseline EPO levels below 500. The durability of transfusion independence can also be seen in the Kaplan-Meier curve here. As of the data cutoff, 11 out of the 18 TI responses were still ongoing, and therefore the median duration of response has not yet been reached. Notably, 61.1% of the responders in this graph had high transfusion burden at baseline. The durability of KER-050 treatment can also be seen as 72% of TI responders had TI durations greater than 24 weeks, and 6 patients who were still ongoing had TI greater than 52 weeks. Health-related quality of life is negatively impacted by MDS, where prolonged transfusion dependence and worsening fatigue have been associated with reduced survival. This trial assessed health-related quality of life using various quality of life assessments, including the FACIT- Fatigue scale, a validated 13-question measure of health-related quality of life in patients with MDS. Patients achieving TI of 8 weeks or longer experienced clinically meaningful improvements in FACIT fatigue scores. We believe the ability to address the patient's fatigue is an important treatment objective for lower-risk MDS. Finally, in patients with lower-risk MDS, cardiovascular disease represents a major cause of death, possibly due to myocardial stress, exacerbated by chronic anemia, inflammation, and iron overload. Activin A has been shown to play a pathophysiologic role in cardiac disease in humans, and targeted inhibition of activin A by a research form of KER-050 led to improvement in cardiac function in preclinical models. NT-proBNP is a biomarker that increases with myocardial stress, and elevated levels have been associated with increased risk for cardiovascular mortality. In a limited dataset, the majority of patients had elevated levels of NT-proBNP at baseline. While elevated NT-proBNP was more common among those with high transfusion burden, the highest baseline levels were observed among two patients with low transfusion burden. Treatment with KER-050 resulted in marked decreases in serum NT-proBNP in patients with an elevated baseline. Decreases in NT-proBNP were observed among both erythroid responders and non-responders, suggesting that KER-050 may ameliorate cardiac strain, both directly, consistent with inhibition of activin A, and indirectly by improving anemia and reducing transfusion burden. In summary, the data presented show that the ongoing phase II clinical trial of KER-050 in low-risk MDS, the majority of patients enrolled had high transfusion burden or multilineage dysplasia, indicating a difficult-to-treat population. As of the cutoff date, KER-050 was generally well-tolerated, with a safety profile consistent to that previously reported for this trial. Importantly, durable responses of transfusion independence were observed in a broad range of patients with low-risk MDS, including those with high transfusion burden, especially when factoring in baseline EPO levels. The data presented demonstrate that patients who achieved transfusion independence showed clinically meaningful improvements in FACIT fatigue scores, indicating potential for KER-050 to improve quality of life in patients with low-risk MDS. Additionally, our observations from the exploratory assessments of additional biomarkers are supportive of the broad profile of KER-050 to potentially treat MDS beyond anemia and have an effect on the pathogenesis and progression of the disease. Collectively, these results support advancing KER-050 into a phase III registration trial in patients with low-risk MDS. I'll now hand the call back to Chris. Thanks, Simon. Myelofibrosis is a myeloproliferative neoplasm that results in abnormal proliferation of megakaryocytes in the bone marrow, which leads to ineffective hematopoiesis, inflammation, and ultimately fibrosis in the bone marrow. People living with myelofibrosis experience enlargement of the spleen and multiple cytopenias, including severe anemia, which results in fatigue and reduced quality of life. Treatment objectives for people living with myelofibrosis include ameliorating the constitutional symptoms, reducing the enlarged spleen, and addressing the cytopenias. Current treatments, including ruxolitinib, provide symptomatic relief and can reduce splenomegaly, but additional treatment options are still needed. We believe KER-050 has potential to address the multifaceted pathophysiology leading to ineffective hematopoiesis and the severe consequences of myelofibrosis. RESTORE is an open-label, two-part, phase II clinical trial evaluating the safety and efficacy of KER-050 in patients with myelofibrosis. Our aim is to understand the safety and efficacy of KER-050 to address ineffective hematopoiesis, either in combination with ruxolitinib or as a monotherapy in patients who have previously been treated with ruxolitinib. Data from the dose escalation Part 1 was used to select the recommended Part 2 dose. The primary endpoints include safety and tolerability. Secondary and exploratory endpoints will evaluate the PK, PD, and efficacy of KER-050, with or without ruxolitinib, in treating anemia, splenomegaly, and constitutional symptoms. The data we will share with you today are provided as of the data cutoff of September 14th, 2023. Safety data are presented for all patients who received at least one dose of KER-050 in Part 1. Evaluations of markers of hematopoiesis over 12 weeks-... along with measurements of spleen volume and symptom scores over 24 weeks, are presented for the lowest 3 dose levels, ranging from 0.75 to 3 mg/kg. Data for dose level 4, the highest dose level in Part 1 of 4.5 mg/kg, are not included due to limited exposure as of the data cutoff. Following the recommendation by the Safety Review Committee, dosing for Part 2 of this trial was initiated a starting dose of 3.75 mg/kg, administered subcutaneously once every 4 weeks, with an opportunity to dose escalate to 5 mg/kg based on individual titration rules in both combination and monotherapy arms, which mirrors the recommended Part 2 dose from our ongoing MDS trial. To date, the patients enrolled in this trial had marked splenomegaly and severe erythropoietic dysfunction. Approximately one quarter of patients enrolled were characterized as high risk, according to the DIPSS risk stratification, and 24% of patients enrolled in the monotherapy arm had triple-negative myelofibrosis. 37% of patients were transfusion-dependent, according to IWG 2013 criteria, with a median transfusion burden of 10 red blood cell units for 12 weeks. The median transfusion burden for non-transfusion dependent patients was 3 units over those 12 weeks. Approximately 70% of patients in the monotherapy and combination arms had splenomegaly, and marked splenomegaly was observed in some patients, even in the combination arm, indicating that ruxolitinib was not providing sufficient control of disease. In the baseline biomarkers graph, you can see that both transfusion-dependent and non-transfusion dependent patients had elevated levels of EPO, underscoring the erythropoietic dysfunction in both groups. Transfusion-dependent patients also had lower levels of soluble transferrin receptor, indicating lower levels of erythropoiesis. I will now let Simon cover the preliminary safety and efficacy data from this trial. Thanks again, Chris. KER-050 was generally well-tolerated in these patients who had significant disease burden and notably complex comorbidities consistent with a frail MF population. Treatment-emergent adverse events were observed in most patients, but treatment-related TEAEs were relatively infrequent. Most treatment-related TEAEs were mild to moderate, with two patients experiencing Grade 3 or higher worsening cytopenias. One dose-limiting event was experienced in Part 1 of RESTORE. A patient in the monotherapy dose level two cohort had an increase in hemoglobin of at least two grams per deciliter, which met protocol criteria for dose reduction at the end of cycle one. There were no adverse events associated with this event, and the maximum observed hemoglobin remained within normal limits. There were three treatment-emergent adverse events leading to death, and all these deaths were deemed unrelated to treatment. Changes in markers of erythropoiesis were assessed in non-transfusion dependent patients to reduce the confounding effect of transfusions. Sustained increases in hemoglobin were observed in these patients over the first 12 weeks of treatment in both monotherapy and combination therapy arms. The bottom figure shows the changes in markers of erythropoiesis averaged over 12 weeks or 8 weeks for soluble transferrin receptor. Given small sample sizes, data were pooled across both monotherapy and combination arms at each dose level. The observed increases in soluble transferrin receptor, reticulocytes, and hemoglobin were generally higher, with increasing dose levels up to the 3 mg/kg, supportive of increases in erythropoiesis. Part 1 of the RESTORE trial enrolled small cohorts of heterogeneous patients. As a reminder, data we are presenting are from the lowest 3 cohorts, with dose levels below the recommended Part 2 dose. The figure on the left shows the maximum mean changes observed in hemoglobin over a 12-week period by patient for non-transfusion dependent patients to minimize the confounding effect of transfusions. Data for patients who received KER-050 monotherapy are shown in green at the top panel, and for those receiving combination therapy in blue on the bottom. Increases in hemoglobin were observed over 12 weeks for most non-transfusion dependent patients in both arms, at dose levels ranging from 0.75 mg/kg to 3 mg/kg. The observed increases in hemoglobin in the monotherapy arm suggest the potential for KER-050 to address anemia due to the underlying myelofibrosis, while increases in hemoglobin in the combination arm indicate the potential for KER-050 to also mitigate ruxolitinib-associated anemia. The figure on the right shows the maximum mean% reduction in transfusion burden over a 12-week period for patients who had received at least 3 units of red blood cells per 12 weeks at baseline. So this includes all the transfusion-dependent patients and some of those who were not classified as transfusion-dependent per IWG 2013 criteria. Reductions in transfusion burden were observed in most patients, and 2 patients in the monotherapy arm achieved transfusion independence, including one with a baseline transfusion burden of 9 units over 12 weeks. In addition, 7 patients in the combination arm, including 5 who are considered transfusion-dependent based on IWG criteria, achieved a reduction in transfusion burden of at least 50%. Notably, these observed reductions in transfusion burden were seen in patients who received up to 15 units of red blood cells per 12 weeks at baseline. Collectively, these data support the potential of KER-050 to improve both anemia due to myelofibrosis and ruxolitinib-associated anemia, even among patients with more severe transfusion burden and greater bone marrow dysfunction. Finally, we're excited to share preliminary data suggesting that KER-050 has potential to address multiple aspects of myelofibrosis, in addition to ameliorating ineffective hematopoiesis. Treatment with KER-050 led to improvements in hematopoiesis, including mean increases in hemoglobin, reductions in transfusion burden, and maintenance or improvements in platelet counts. Seven patients were evaluable for spleen volume reduction as of the data cutoff date. Four patients had a spleen volume reduction at week 24, with a median reduction of 27% and a range from 11%-47%. One monotherapy patient achieved a 38% reduction in spleen volume. Of the 12 patients evaluable for Total Symptom Score, reductions were seen in 8 patients, which is 67% at week 24. In summary, KER-050 was generally well-tolerated in RESTORE Part 1, including patients with high disease burden and complex comorbidities. We believe the RESTORE data presented today support the potential for KER-050 to ameliorate ineffective hematopoiesis and address cytopenias, including anemia and thrombocytopenia due to myelofibrosis and associated with ruxolitinib, based on observed increased markers of erythropoiesis, increased hemoglobin, and decreased transfusion burden. We are also encouraged by the preliminary data showing the potential of KER-050 to provide broader clinical benefit in patients with myelofibrosis, as observed by decreased spleen size and improved symptom score. I will now pass the call back to Jas to summarize the key points from the data shared today. Thank you both, Simon and Chris. The data we shared today continues to demonstrate the potential of KER-050 to address ineffective hematopoiesis in MDS and myelofibrosis. But just as important, today, we have shared that the mechanism of KER-050 targeting activin A can provide benefit beyond just addressing cytopenias. In MF, at the initial three dose levels, we have observed increases in hematopoiesis, including sustained increases in hemoglobin observed over the first 12 weeks of KER-050 treatment and reductions in transfusion burden in both monotherapy and combination arms. We also observed reductions in spleen size and improvements in Total Symptom Score in our initial dose escalation cohorts. Our preliminary data support the potential of KER-050 to address multiple aspects of MF. As we previously announced, we have now initiated the Part 2 dose confirmation cohorts and look forward to future data readouts to confirm the potential of KER-050 in MF. In MDS, the observed increase in bone-specific alkaline phosphatase, a marker of osteoblast activity, demonstrate that KER-050 has the potential to restore a bone marrow microenvironment conducive to functional hematopoiesis. KER-050 treatment also reduced NT-proBNP, a marker of cardiac stress, which is consistent with our preclinical observation across our portfolio of assets, that targeting activin A can improve cardiovascular health. The MDS phase II data demonstrate the potential of KER-050 to treat broad array of patients with MDS, including those with greater transfusion burden and bone marrow dysfunction. The 18 patients in the mITT24 population who achieved transfusion independence had durable benefit, with one-third of those responders already reaching 1 year or more of transfusion independence. Importantly, patients who achieved TI had improvements in the self-reported fatigue scale, FACIT- Fatigue. Based on the data presented today, we believe that collectively, the results support advancing KER-050 into a phase III registration trial in patients with low-risk MDS. We're excited to engage with regulators, which we plan to do in the first half of next year, and look forward to sharing the design of the phase III trial following that feedback. I will now pass the call over to the operator to begin the Q&A. Thank you. We'll now be conducting a question- and- answer session. If you'd like to be placed in the question queue, please press star one on your telephone keypad. In the interest of time, we ask that you please ask one question, then return to the queue. Once again, that's star one to be placed in the question queue, and please ask one question, then return to the queue. Our first question is coming from Joe Catanzaro from Piper Sandler. Your line is now live. Hey, guys. Appreciate you taking the time and my questions here and the update. I guess I'll stick to one question. So, Jas, wondering if you could just speak to the potential read-through on the reductions in NT-proBNP you're seeing here with 050 to 012. You know, how are baseline levels you're seeing in MDS compare to PAH? And then how does the potency and affinity to activin A compare between 050 and 012? Thanks. Thanks, Joe, for that question. So I think the first thing to note is that, what we are seeing in these patients are elevated levels of NT-proBNP that are equivalent to what you see in PAH patients. Secondly, at the dose level that we're at with KER-050 of 3.75 mg/ kg, this is an intermediate dose between the two highest doses in the phase II TROPOS trial of 3 and 4.5 mg/ kg. Therefore, we are at levels of target engagement with KER-050 that will be equivalent to what we would see, at the two higher doses in TROPOS. Seeing the decreases in NT-proBNP from the first dose and then sustained decreases in NT-proBNP, they are consistent with the mechanism and therefore have read-through to 012, and we believe that this will be demonstrated in future trials. Thank you. Next question is coming from Thomas Smith from Leerink Partners. Your line is now live. Hey, guys. Good morning. Thanks for taking the questions, and, congrats on the updates. Just, on the 050 MDS program, I know you're going to take these phase II data to regulators and have those discussions, but was just wondering if you could provide an update on your current thinking with respect to the phase III trial design. And then, more specifically, the durability response and the improvement in the FACIT fatigue scores look pretty striking. So I wonder if you could just comment specifically on how you're thinking about incorporating those findings into that pivotal design to try to capture some of that differentiation. Thanks. Simon? I mean, thanks for the question. I mean, as we are working on what does a phase III trial look like, I think, you know, we've talked about this being potentially a placebo-controlled trial still at this stage, in both patients in the second-line therapy, or could be the second-line therapy. And then in terms of the quality of life, I think, you know, we were all very encouraged to see that data. And we know that, you know, it's exciting to be able to show improvements in FACIT fatigue, something that, you know, we haven't seen before in MDS patients. So including endpoints related to quality of life are obviously at the front of our mind, and it'll be part of those discussions that we have with the regulatory agencies. Thank you. Next question is coming from Tiago Fauth from Wells Fargo. Your line is now live. Hey, thank you so much for taking the call. Congrats on the updates. I just wanted to dig into the non-RS patients and the EPO data cut. Again, once you kind of exclude some of those patients, the data looks a little bit better, and it sounded like some of them were too far gone perhaps to see a clinical benefit. Can you share a little bit more detail on those patients? And do you think that the EPO cutoff is the best way to address that? Thank you. Sure. This is Chris. Yeah, I think as we looked at this data, again, as Jas mentioned, we designed this study to look at a wide swath of patients. And as we're looking at our erythropoietic endpoints, as we were trying to identify criteria that would help us consider enrichment for our registration study. And as you can imagine, looking at endogenous EPO levels gives a lot of clues in terms of their ability to respond to ESAs. And so as we thought through the data with our steering committee members, we excluded those patients that had greater than 500 EPO in that one analysis because they really don't have that ability to respond. Elevated EPO levels are indicative of a poor bone marrow state, historically have been correlated with lack of response to erythropoietic agents. As we look more deeply into those nine subjects, the elevated EPO levels as a median were about 1,300. We had individuals that had EPO levels as great as 4,000 and transfusion burden of greater than 30 units. So as we look through those characteristics, those are patients whose bone marrow are too far gone to be able to respond to an erythropoietic agent like carfilzomib. Thank you. Next question is coming from Tyler Van Buren from TD Cowen. Your line is now live. Hi, thanks. Good morning. So I know MEDALIST is the best comp, but can you put the durability data in context relative to luspatercept? And in which populations do you think your data compares most favorably? Thanks. I think the data that we look at for 050, we reference back to the MEDALIST trial. The durability of effect in the MEDALIST trial was roughly 30 weeks for transfusion independence. As you look through cross-trial comparisons, obviously very difficult to do that based on differences in patients that were enrolled. But we look at transfusion burden, EPO levels, the degree of multilineage dysplasia. The MDS population is the one that most represents the population from our phase II study. Thank you. Next question is coming from Kripa Devarakonda from Truist Securities. Your line is now live. Hey, guys. Thank you so much for taking my question, and congrats on all the progress. I have a question versus around the EPO experience versus naive in your trial. About a fifth of patients are prior ESA exposed, and you're talking about going into second line, which are probably going to be all ESA experienced. What gives you the confidence that prior ESA experience is comparable to patients who have high baseline EPO levels and are transfusion-dependent, basically, the 20% versus the 80% of patients in your current trial? So in the phase II, we had roughly one quarter of patients had prior ESA experience. The patients that were allowed to enroll either were ESA naive, experienced, or unlikely to respond to ESAs. Now, we talked about 80% of our patients that were enrolled had high transfusion burden, characteristic that's representative historically of non-response to ESAs. It's a characteristic that's been well known for decades that ESAs do not perform well in a high transfusion burden setting. And then again, as you look at the EPO levels, greater than a third of our patients had EPO levels greater than 200. And so again, I think the data that we have here represents a difficult to treat population where we have belief in our drug's ability to have that benefit in the ESA-experienced population or those that are unlikely to respond. Thank you. Next question today is coming from Greg Harrison from Bank of America. Your line is now live. Hey, good morning. Congrats on the data, and thanks for taking the question. On the myelofibrosis update, given the monotherapy response that you observed, where would you see KER-050 fitting in within the treatment paradigm? So, I mean, I think, you know, we've seen responses for our elritercept in myelofibrosis in both monotherapy and a combination setting with ruxolitinib. The monotherapy patients are those who'd already been exposed to ruxolitinib, so have already failed. But I think we also have to look at how the treatment paradigm is evolving for the myelofibrosis. It's likely that combination therapy is going to be more common going forward. You know, we have results that suggested that we have a strong acting combination therapy. We will also always be able to demonstrate the efficacy in monotherapy as well. I think the other thing with KER-050, it is mechanism agnostic with respect to other treatments. So it can be combined, whether it is ruxolitinib, whether it's momelotinib, whether it's pacritinib, should they get approved. We think, okay, that this mechanism can augment whatever efficacy you're seeing with those drugs. Again, in the RESTORE study, we're seeing obviously improvements in both the mono and the combination cohorts, which I think is really exciting. And to be able to consider combination therapy where KER-050 is showing those signals of effect also, spleen volume response and the total symptom score. Again, we think it's a really exciting profile of response, even at these low doses that were evaluated in dose escalation. As we move forward with Part 2 of the study, looking at a more robust patient population and longer-term treatment, I think it will be really important to confirming that profile. Thank you. Next question today is coming from Julian Harrison from BTIG. Your line is now live. Hi, good morning. Congrats on the update, and thank you for taking my questions. The FACIT fatigue results look very encouraging. So I guess I'm curious if there's a good mechanistic explanation for why you're seeing benefits here, while fatigue is a leading adverse event for blinatumomab. And then, again, great to see lack of progression to AML. You know, with that in mind, I'm wondering if, you know, that there's a point, maybe sometime next year beyond in the ongoing phase II MDS trial, you know, you would consider that a signal beyond noise if that observation continues? I mean, both from the mechanistic point of view for the improvements in patient fatigue, as you know, are set by activin A, which is something that maybe acts as a stop sign or doesn't. So we know that activin A is involved in inflammatory processes. So we know that in diseases where inflammatory processes are prominent, patients become fatigued. So I think with our elritercept's ability to block and bind that activin A, we're seeing impacts of that across the board, but that, I think, is what's driving those improvements in fatigue. In addition, Julian, in the phase II data that we presented, we see elevated levels of serum ferritin, and we see reductions in those serum ferritin. In patients that have extremely high elevated serum ferritin and are heavily transfused, you can imagine that's partly due to increase in erythropoiesis and utilization alike. However, in the non-transfused patients, we're also seeing these dramatic decreases in serum ferritin. That's consistent with a reduction in inflammation, because serum ferritin is also a acute phase reactant. And therefore, we are getting signals that we're getting inhibition of inflammatory process in these patients. Thank you. Next question is coming from Eun Yang from Jefferies. Your line is now live. Hi. Thank you for taking our question. So what are you hearing from physicians regarding the areas where they would like to see the most improved... I guess to see the most improvements from luspatercept with the next product? And based on Keros's emerging data, where do you think KER-050 is most differentiated from Revlimid, and how would you design Phase III to highlight the differentiation? Thank you. So this is Chris. Yeah, great question. I think as we're looking at the data that we've discussed with our treating physicians and our members of our steering committee, the broad effect of KER-050 in improving hematopoiesis, we think was very well received. Improvements in red blood cell production, hemoglobin, obviously very important, but the effects on improving platelets and thrombopoiesis was also considered very meaningful and really provide an opportunity to look at a broader set of patients in MDS. I think clinically, the durability of effect, especially in this high transfusion burden population, was viewed as very meaningful. Again, we're really excited about the proportion of patients that are reaching 24-week and 1-year transfusion independence milestone. I think that durability is really critical as we think about designing the registration study. Really focusing in on the benefits that we're observing in the high transfusion burden population will be critical, for that to differentiate. Thank you. We've reached the end of our question- and- answer session. I'd like to turn the floor back over to Jas for any further closing comments. I want to thank everyone for joining us on today's call and for your thoughtful questions. We're very excited about the data we presented at the 65th Annual ASH Congress, and we look forward to providing further updates about our pipeline in the future. Thank you. Thank you. That does conclude today's teleconference and webcast. You may disconnect your line at this time, and have a wonderful day. We thank you for your participation today.