Good morning, everyone. Welcome to Geron's second quarter 2022 conference call. I am Aron Feingold, Geron's Vice President of Investor Relations and Corporate Communications. I'm joined today by the following members of Geron's management team. Dr. John Scarlett, Chairman and Chief Executive Officer. Olivia Bloom, Executive Vice President of Finance and Chief Financial Officer and Treasurer. Dr. Faye Feller, Executive Vice President and Chief Medical Officer, and Anil Kapur, Executive Vice President of Corporate Strategy and Chief Commercial Officer. Before we begin, please note that during the course of this presentation and question and answer session, we will be making forward-looking statements regarding future events, performance, plans, expectations, and other projections, including those related to the therapeutic potential and potential regulatory approval of imetelstat, anticipated clinical and commercial events and related timelines, the sufficiency of Geron's financial resources, and other statements that are not historical fact. Actual events or results could differ materially. Therefore, I refer you to the discussion under the heading Risk Factors in Geron's quarterly report on Form 10-Q for the quarter ended June 30, 2022, which identifies important factors that could cause actual results to differ materially from those contained in the forward-looking statements. Geron undertakes no duty or obligation to update our forward-looking statements. Now I will turn the call over to CEO, Dr. Scarlett. Chip? Thanks, Aron. Good morning, everyone. Thanks for joining us today. Throughout the year, we've highlighted our vision for Geron, which is to become a leader in the treatment of hematologic malignancies. The strategic pathway to achieving this goal is defined by our expected journey to develop and commercialize imetelstat. Based on the imetelstat phase II data in lower risk MDS and in relapsed and refractory myelofibrosis, we believe imetelstat has a highly differentiated, compelling clinical profile. First, as a telomerase inhibitor, imetelstat has a unique mechanism of action that strikes at the very heart of these malignancies by targeting the malignant stem and progenitor cells that drive both lower risk MDS and JAKi relapsed and refractory MF. Second, the phase II data also provided strong evidence for disease modification. At a molecular level, in both phase II studies, we reported depletion of mutated and cytogenetically abnormal myeloid cells that have been correlated with the direct clinical benefits of imetelstat, providing additional evidence of disease modification. Imetelstat's potential for disease modification not only differentiates it from other currently available therapies, but also directly addresses critical unmet needs in lower-risk MDS and relapsed/refractory MF, which we expect will provide a needed treatment option for patients with these diseases. Third, in both lower-risk MDS and relapsed/refractory MF patients treated with imetelstat, we saw unprecedented durability of clinical effects. For instance, Faye will describe an ASH abstract published today in which we reported approximately one-third of the 38 patients in our phase II lower-risk MDS study, who despite a median pretreatment transfusion burden of six RBC units per eight weeks, experienced one year or more of transfusion independence. Similarly, in our phase II relapsed/refractory MF study, median overall survival for patients improved to almost twice as long as has been reported in medical literature. Based on these attributes of imetelstat and compelling phase II data, we expect potentially highly differentiated clinical profiles from the results of our ongoing imetelstat phase III trials in these indications. We are therefore very excited by the lineup of expected milestones coming soon and over the next 2 years. We expect disclosure of top line results or TLR from our IMerge phase III trial in lower risk MDS in only two months from now in early January 2023. If TLR is positive, we expect great value will be unlocked for both patients and for shareholders. Assuming positive TLR, the next expected key Geron milestones are regulatory submissions for imetelstat and lower risk MDS. As of today, we expect submission of the NDA during the first half of 2023 and of the EU MAA during the second half of 2023. As Faye will discuss in a few minutes, we've been actively preparing for many months for both disclosure of TLR in early January 2023, as well as for these key regulatory submissions later in the year. Similarly, we've also been preparing for potential commercialization of imetelstat and have recently made key hires across the team in order to begin building the foundation for a successful commercial launch for lower risk MDS. Finally, becoming a leader in the treatment of hematologic malignancies requires breadth of effect. Thus, the next significant step is to bring imetelstat to patients who suffer from JAKi-relapsed refractory myelofibrosis. To achieve this, we're working towards having an interim analysis from our IMpactMF phase III trial in patients with this indication in 2024, and then the final analysis in 2025. This study is the first and only phase III myelofibrosis trial with overall survival as the primary endpoint, and thus represents great potential value for patients as well as for our shareholders. Achieving these milestones requires the motivation and expertise of each Geron team member. Their continued dedication and commitment inspire me every day. With that, I'll turn the call over to our Chief Medical Officer, Dr. Faye Feller, for a clinical update. Faye? Thank you, Chip, and good morning to everyone on the call. We at Geron are incredibly excited that the top-line results of the IMerge phase III study in lower-risk MDS are just two months away. The clinical team has been actively preparing for the readout in accordance with industry best practices. The clinical cutoff for the top-line results occurred last month, which, per protocol, is one year following the first dosing of the last patient randomized in the study. We have been continuing database cleaning activities and monitoring visits with our clinical sites in preparation for database lock, which is expected to occur before the end of the year. In early January 2023, we expect to deliver the phase III IMerge top-line results, which will comprise a robust package of data that we believe will highlight the differentiating qualities of imetelstat. We anticipate sharing data on the primary endpoint of eight week transfusion independence, or TI, as well as key secondary endpoints of 24-week TI and hematologic improvement erythroid, or HIE, which is a composite measure of the percentage of patients who experience an increase in hemoglobin and/or a reduction in their transfusion burden. We also plan to provide safety data in order to give a balanced benefit-risk profile of imetelstat in lower-risk MDS. As is typical for a phase III trial, top-line results represent only a portion of the full clinical study readout, and we anticipate to present more comprehensive results at a future medical meeting. We expect the later additional data will include information on molecular indicators of disease modification, such as mutational burden reductions and an effect on cytogenetic abnormalities. The phase III IMerge trial design matches many of the elements of the phase II, including clinical site locations and investigators, patient population and enrollment eligibility criteria, imetelstat dose and schedule, primary and secondary endpoints, and other protocol-specified guidelines. Given such similarities, we believe the phase II results will help inform us on the phase III. As Chip alluded to in his comments this morning, on Sunday, December 11, longer-term follow-up data from the IMerge phase II study will be presented in an oral presentation at ASH this year. The abstract for this upcoming presentation, published this morning, is summarized on slide nine of our Q3 earnings call deck and is currently displayed on the webcast for those watching. The abstract describes the 29% of patients in the IMerge Phase Two study who achieved sustained transfusion independence for greater than 1 year in the setting of a median pretreatment transfusion burden of six units of red blood cells over eight weeks. We believe this to be an unprecedented durability effect in patients with lower-risk MDS post-ESA treatment. These 11 transfusion-dependent patients were treated with imetelstat for a median of approximately 2.4 years, and their median duration of TI was 1.8 years. After a median follow-up of 4.3 years, median progression-free survival was 2.9 years, and median overall survival was 4.8 years. None of these patients progressed to AML. Mutation data was available for the majority of the patients who achieved greater than one year sustained TI, and 89% had any reduction in SF3B1 variant allele frequency or VAF, while 56% achieved greater than or equal to 50% VAF reduction. Reduction in VAF correlated with longer TI duration and shorter time to onset of TI. We believe these data, along with the long-term sustained TI, indicate strong evidence of disease modification. Safety findings for these patients were consistent with the overall population, and the most frequent adverse events were reversible thrombocytopenia and neutropenia. The abstract concludes that the greater than one year periods of transfusion independence observed in these patients represents relief from iron overload and other transfusion-associated complications and a decreased demand on healthcare resources. Furthermore, durable TI, meaningful reduction in mutation burden, and good survival post-ESA suggest imetelstat may have disease-modifying activity. These recent data, as well as the prior publications of IMerge phase II data, reinforce what we believe are key attributes of imetelstat in lower-risk MDS. First, we observe durability of continuous transfusion independence, which we consider differentiating from any treatment currently on the market or being investigated today. Second, broad efficacy was observed across patient subtypes, including RS-positive, RS-negative, high and very high transfusion burden patients. Third, there was strong evidence of disease modification as described previously by Chip that due to imetelstat's unique mechanism of action aims at the very nature of the disease mechanistically, and that has not been previously observed with other treatments for this patient population. Moving on to myelofibrosis. There are two posters being presented at ASH this year for our current MF trials in progress. As many of you know, abstracts for this category describe innovative ongoing clinical trials that have not yet reached their primary endpoint. The first trial in progress abstract describes our pivotal phase III IMpactMF study, which is designed to enroll approximately 320 patients with relapsed/refractory myelofibrosis. IMpactMF is the first and only phase III MF trial with overall survival as the primary endpoint. Approximately 85% of clinical trial sites are open to date, and we remain on track to open all selected clinical sites by the end of this year. Under current planning assumptions, we continue to project the interim analysis for IMpactMF will occur in late 2024. Of course, because these analyses are event-driven and it is uncertain whether actual rates for enrollment and rates for events will reflect current planning assumptions, the results of the interim analysis may be available at a different time than currently expected. The second trial in progress abstract accepted at ASH describes IMproveMF, which is our phase I study designed to evaluate the safety and clinical activity of imetelstat in combination with ruxolitinib in patients with frontline MF. This study design was informed by preclinical data that showed that sequential treatment with ruxolitinib followed by imetelstat had a selective inhibitory effect on malignant MF stem cells while sparing normal hematopoietic stem cells. In this clinical study, we expect to determine the safety profile of combination therapy and explore any potential for disease-modifying activity in a frontline MF disease setting, similar to what was observed with imetelstat treatment in the phase II IMbark trial in a relapsed/refractory MF patient population. Two of the three trial sites for this study are open for patient enrollment. We expect to present preliminary data from this study by the end of 2023. As part of our imetelstat pipeline expansion, we are also exploring use of the drug in other indications and combination regimens. At ASH this year, additional non-clinical data related to acute myeloid leukemia, or AML, will be presented. The abstract for the upcoming oral presentation describes the results from non-clinical in vitro and in vivo experiments with imetelstat using AML cell lines and AML patient samples. Conducted by our collaborators in Australia, Germany, and the U.S., the experiments found that imetelstat promotes the formation of polyunsaturated fatty acid-containing phospholipids, which cause excessive levels of lipid peroxidation and oxidative stress in AML cells, potentially leading to programmed cell death. The abstract concludes that this mechanistic insight could be leveraged to develop an optimized therapeutic strategy using oxidative stress-inducing chemotherapy to sensitize patients to imetelstat and potentially cause significant delay of relapse in AML. Based on these and other non-clinical data in AML, as well as the clinical data we have in lower-risk MDS, we are supporting an investigator-led study called IMpress in relapsed/refractory AML and higher-risk MDS. In that study, imetelstat is being evaluated as a single agent. We continue to expect the first site to be open for the study by the end of this year. Meanwhile, we have another investigator-led study in relapsed/refractory AML named TELOMERE. In this study, we plan to evaluate imetelstat in combination with a hypomethylating agent and in combination with venetoclax. This study has been deferred until we have data from the IMpress single-agent study in relapsed/refractory AML. We expect data from IMpress to help inform the dose and schedule to be used in the two combination dosing regimens that will be evaluated in TELOMERE. The principal investigators for both studies continue to be highly enthusiastic as relapsed/refractory AML remains an extraordinarily difficult malignancy to treat. They believe a new mechanism of action from a drug like imetelstat that directly affects the malignant stem and progenitor cells that drive disease progression could provide an effective treatment option for patients suffering from relapsed/refractory AML. Also, in keeping with our pipeline expansion activities, new non-clinical data with imetelstat in lymphoid malignancies will be published online in Blood. The abstract describes the characterization of telomerase activity and telomere length and results from in vitro experiments of imetelstat on a panel of diffuse large B-cell lymphoma or DLBCL and peripheral T-cell lymphoma or PTCL cell lymphoid malignancies. Finally, I am pleased to report that we are making progress in our next generation telomerase inhibitor program, from which we anticipate generating lead compounds for further characterization and evaluation. We anticipate completion of the current discovery effort in 2023, upon which we plan to potentially advance any lead compounds into the next step of discovery research. If successful, these efforts would permit initiation of IND-enabling non-clinical studies. Overall, I am delighted with the progress of the research and development team, both with regards to advancing critical activities for our lead indications in lower-risk MDS and relapsed/refractory myelofibrosis, as well as our pipeline expansion programs, which aim to understand the broader potential of imetelstat. With that, I will turn the call over to Olivia for a financial update. Olivia. Thanks, Faye, and thanks to everyone on the call for joining us today. Please refer to the press release we issued this morning, which is available on our website for detailed financial results. As of September 30, 2022, we had approximately $195 million in cash and marketable securities. This includes approximately $4 million in proceeds from warrant exercises that we received this quarter. Overall, operating expenses were higher for the three and nine months ended September 30, 2022, compared to the prior period, which reflects increased activity across the company, as well as accounting for the recent settlement agreement related to the class action lawsuit. On the R&D side, the increase in expenses for the three and nine month periods of 2022 compared to the same period in 2021 primarily reflects the net result of increased personnel-related expenses for additional headcount and higher consulting costs related to preparation for top-line results and regulatory submissions in lower-risk MDS, which were partially offset by decreased manufacturing costs due to the timing of imetelstat manufacturing batches. On the G&A side, the increase in expenses for the three- and nine-month periods of 2022 compared to the same period in 2021 primarily reflects increased costs for commercial preparatory activities, higher personnel-related expenses for additional headcount, and an accrual of approximately $7 million for our portion of the settlement for the class action lawsuit, which we expect will be paid in either shares of Geron common stock and/or cash at our election after final approval of the settlement by the court by the end of the first quarter of 2023. We continue to expect non-GAAP total operating expenses of up to $150 million for the full year of 2022. Under current planning assumptions, we expect to have approximately $140 million in cash and marketable securities at the time of the lower-risk MDS top-line results in early 2023. We also expect to have up to $171 million in additional funding available to us in 2023, which is comprised of approximately $121 million from potential exercises of currently outstanding warrants and an additional $50 million from potential debt drawdowns under our current loan agreement upon the achievement of certain milestones and capital requirements. Under current planning assumptions, we project our existing capital resources, plus the projected future proceeds that I just outlined, will be sufficient to fund our estimated levels of operations, which includes stage-gated activities for potential U.S. commercial launch of imetelstat in low-risk MDS until the middle of 2024. With that, I will now turn the call over to Chip for closing remarks. Thanks, Olivia. As I indicated at the start of this call, we're on a journey toward becoming a leader in the treatment of hematologic malignancies. On this journey, we expect to achieve very meaningful milestones, which we believe will not only move the company from clinical development towards commercialization, but also potentially change the treatment landscape for lower risk MDS and relapsed/ refractory MF. Thank you all for your interest in the company and support for our continuing activities. We'll be glad to take your questions. At this time, I would like to remind everyone in order to ask a question, press star, then the number one on your telephone keypad. Again, to ask a question, press star one on your telephone keypad. To withdraw your question, press star one again. We'll pause for a moment to compile the current roster. Your first question comes from Kalpit Patel from B. Riley. Please go ahead. Thanks for taking the question. There was a positive announcement earlier this week from Bristol Myers Squibb regarding the COMMANDS study testing luspatercept in the frontline setting for MDS. I guess you know what implications, if any, does this have on your potential path for imetelstat? I think your trial is enrolling patients who have received luspatercept before. Curious if you see or foresee any shift in how imetelstat may be used in the real world, assuming the phase III is positive. Does it change anything from a regulatory perspective as well? Thank you. Pointed out, the imetelstat IMerge phase III trial does include patients who are previously treated with luspatercept. We expect imetelstat to become part of the standard of care in low risk MDS and to be broadly adopted for the treatment of these patients with very high unmet medical needs. Would also like to remind all of us that we had multiple other patient subtypes that were eligible for this trial, irrespective of their ring sideroblast status. This included heavily transfusion-burdened ESA relapsed and refractory patients and also frontline ESA-ineligible patients, given their high baseline serum EPO levels. As Chip and Faye said in their prepared remarks, we expect imetelstat to be highly differentiated given our distinct mechanism of action that targets and kills the malignant stem and progenitor cells and allows for the ability to modify the disease and achieve continuous and highly durable transfusion independence rates. This data, which is reported in today's ASH abstracts, directly addresses significant unmet medical need in low risk MDS, and we expect it to be very favorably received by the physician community. I also want to remind everyone that from a commercial perspective, the market imetelstat is addressing is highly attractive and approximately three times larger than the patient group indicated under the current luspatercept label, which is limited to RS-positive patients. We expect broad adoption and remain confident that what imetelstat is addressing is truly disease modifying, and we expect broad adoption. I'll just stop here. One question on the IMerge readout that's coming up in January. What level of detail should we expect on some of the secondary endpoints, maybe the one-year TI rate and some of the other endpoints there? I think you should expect the secondary endpoints would include, of course, the 24-week TI, and obviously all of the safety data as well as the primary endpoint. Faye, any other comments? Would add HIE as well. Sure. Okay. We shouldn't see any one year TI rates there on in the phase III readout? Not sure. Okay. All right. Thanks for taking the questions. Your next question comes from Steve Willey from Stifel. Please go ahead. Yeah, good morning. Thanks for taking the question. Hi. I guess maybe just following up on the top-line disclosure in January. I was just curious if we should expect to see any specific efficacy data within certain subgroups of interest. I guess those subgroups would be, you know, those patients who have a very high transfusion burden at baseline, maybe have serum EPO levels of greater than 500. Is that something that you think will be saved for a future presentation, or is that something that we could see in a top-line press release, just kind of giving, given the importance of that from a competitive differentiation perspective? Thanks for your question. I'll take that. Yes, we will have subgroup analysis at the time of TLR. We will provide additional data, of course, at a major medical meeting subsequently. Okay. That's good to know. Maybe just a question on IMproveMF. You know, I guess when you look across the competitive landscape, it kind of seems like there's an effort to combine various agents with rux that actually address some of the anemia that is caused by rux. Just curious, just given, I think in the phase II IMbark study, there was, you know, a bit of an anemia signal from imetelstat. How do you just think about the notion of potentially exacerbating the toxicity that is across the competitive landscape trying to be improved right now? Faye, you wanna comment about that study? Sure. The IMproveMF study is, as you say, our combination study in frontline patients with ruxolitinib and imetelstat, and the primary objective of that study will be to assess the safety profile of the combination therapy, including any potential cytotoxicity disease and cytopenias. That's the main objective. We're not 100% sure what we're gonna see, and that's why it's really a safety study as opposed to primarily an efficacy study. We'll obviously look for efficacy signals. Of course, the paradox here is that we know that we have in the phase II data certainly very strong anemia responses, positive anemia responses. I think, you know, we'll just have to see how it works out. I think the real focus of this is indeed getting a safety look. Okay. Just lastly, I guess on IMpactMF, congrats on getting a lot of the sites opened. How should we think about the manner in which you're gonna be communicating enrollment milestones? Is that something that you will not be providing? Go ahead. I guess I'm just thinking about whether or not we hear as to half of the patients have been enrolled or just various milestones like that. Yeah. Historically, Steve, we've communicated when we hit 50% enrollment. We'll probably do that with this study as well. Of course, I'd wanna remind everybody that because this is an overall survival study and it's really event-driven, the specifics of the enrollment kinetics, while they're certainly linked to that, you can't have events unless people are enrolled. At the same time, we're not on a hard schedule of events where enrollment completely dictates when results come. We still currently expect the interim analysis in 2024. Okay. That's helpful. Thanks for taking the questions. Thanks, Steve. Your next question comes from Gil Blum from Needham & Company. Please go ahead. Hi, everyone, and good morning, and thanks for taking our questions as well. Sure. Maybe a quick one on the oral presentation, the long-term follow-up of IMerge. It kinda struck me that some of the details you provided there looked a lot like what you saw in MDS regarding the reduction of specific clones. Maybe a longer-term thought. Is there any reason to consider maybe an overall survival outcome study in MDS at some point? Thank you. Sorry, just to make sure we understood the question, we were having a little bit of trouble hearing you. Overall survival, obviously I think you were trying to relate the question about overall survival in long-term follow-up of MDS. Did I get that right? Yeah, that's correct. Yeah. The results looked a lot like what you saw in myelofibrosis on a molecular level. Yeah. Faye, you wanna comment on that? Sure. Thanks for confirming. Overall survival in addition to progression-free survival are both secondary endpoints on the myelodysplastic syndrome study IMerge. We will be looking closely at that. Okay. Excellent. As for the combination studies in AML, preliminarily, you're gonna first look at you know, the single agent activity and then add combinations on top of it. How do you see that? Mm-hmm Fitting into kind of the evolving landscape? Initially, the goal of the combination studies in AML is evolving into it being and has been actually always treated with combination therapy and multiple approaches, especially in the frontline setting. As we investigate the safety of the combination therapy in the TELOMERE study, combining with either venetoclax or azacitidine, we'll, in addition to the safety, of course, be looking for any preliminary signal of efficacy. Yeah. There's a clear, you know, a clear need for a novel mechanism of action that works differently than the currently available therapies in AML and especially in relapsed/refractory AML. All right. Thank you for the clarifications, and thanks for taking our questions. Sure. Your next question comes from Joel Beatty from Baird. Please go ahead. Good morning. Thanks for taking the questions. The first one is on the phase III MDS trial. Could you discuss the DSMB reviews that have taken place throughout the study and recently, you know, anything learned about safety there? We have. Thanks for your question. We have an independent data monitoring committee in place for the study who review the unblinded safety data. To date, they have continued to recommend the study proceed. As indicated, they meet on a regular basis. Great. Maybe a question on the. Does that answer your question? Yeah. Terrific. Thank you. A question on the COMMANDS study. You know, whenever we get more data from BMS, could you discuss what data points you'd be curious to look for? I can take that question first, Joel, and obviously, Faye can add on to it. One of the more important things in low-risk MDS, especially for patients who are predominantly anemic, is continuous and highly durable transfusion independence rates. In all our market research from clinical scientific forums and discussions with our advisors, this remains a high unmet medical need, and there is significant dissatisfaction in this market being expressed with agents that have been currently approved and have existed for the armamentarium for physicians to treat this disease. We would look for the quality of data, the durability of TI, in various subgroups, and adoption is dependent on all of those things. I also want to restate one more time, we target the malignant stem and progenitor cells. Imetelstat has the ability to modify the disease, and what we are seeing in our phase II data is highly encouraging in terms of continuous and durable transfusion independence in high transfusion burden patients. The value proposition for imetelstat should be very, very strong. Obviously we would be curious to see what happens in the frontline settings. Faye, anything to add from your side? I would add to that that I'd be interested to see not only anemia improvement and improvement in hemoglobins but the amount of transfusion burden reduction, especially as you mentioned, on a continuous basis in that study. Great. Thank you. Thanks, Joel. Your next question comes from Vernon Bernardino from H.C. Wainwright. Please go ahead. Good morning, everyone, and thanks for taking my question. Thanks also for the update on the phase III IMpactMF trial. Looks like that's making very good progress. I'm curious about the IMproveMF phase I trial in frontline myelofibrosis. I think if I remember correctly, the study's being conducted in three sites. Just wondering how enrollment is progressing in that study. Also, you know, Faye, you mentioned the presentation of IMproveMF part one or some of the data at ASH. Just wondering as far as the optimization of dose in part one of the study with ruxolitinib what are your expectations as to how long those patients would be on ruxolitinib? In the phase II part, what if our patients are not able to tolerate at least 4 weeks of ruxolitinib, how that study may be conducted and completed? Thank you. Sure. Thanks for your question. I'll start with the first one first, regarding the enrollment. You are correct that we have planned for three sites to be open. Currently, two of those are open. As this is a dose escalation study, you know, we are proceeding with enrollment as expected at the various dose levels. The next question was regarding ruxolitinib and how long we anticipate patients to stay on ruxolitinib, and I think that is one of the questions that the trial will answer and intends to answer of how long a combination therapy could be tolerated and whether there are options for a single agent treatment as well. Okay. Just to follow up then. Yep. What kind of preliminary data might we expect in 2023 from IMproveMF? We anticipate preliminary safety data most. Yeah. I think it's mostly related to safety. Obviously, if we see interesting efficacy signals, we'll probably talk about that. This is an early phase study, so we can do that, but we'll have to see how it works out. It's an open question of whether the two drugs will be able to be combined and we have great hope. Obviously, where does the dose go? It's a dose-finding study, as Faye just said. That's a critical element of it as we escalate dose. Thank you for taking my question. Yeah. I'm very interested in the frontline possibilities of imetelstat in MF. Thank you. Thanks, Vernon. There are no further questions at this time. I will turn the call back over to Aron Feingold for closing remarks. Thanks so much, everyone, for joining us today and for your questions. We really appreciate you taking the time to dial in and participate. Be well, everyone. Thank you. This concludes this conference call. You may now disconnect.