Please note this event is being recorded. I would now like to turn the conference over to Courtney Solberg. Please go ahead. Good afternoon, and thank you for joining our call to discuss our updated data in multiple myeloma and our first data in non-Hodgkin's lymphoma from the ongoing Cemsidomide phase I-II trial. These data were presented at the ASH annual meeting earlier today. We will be making forward-looking statements today, and slide two contains our legal disclaimer on this matter. Those presenting on today's call are Andrew Hirsch, our President and CEO, and Len Reyno, our Chief Medical Officer. We will begin with opening remarks and then walk you through new clinical data for Cemsidomide. We will end today's call with a Q&A session with the management team, which will include Kendra Adams, our CFO. I will now turn the call over to Andrew Hirsch for some introductory remarks. Thank you, Courtney, and thank you all for joining our call. Earlier today, we issued a press release highlighting the Cemsidomide data in multiple myeloma and non-Hodgkin's lymphoma presented here at ASH. Cemsidomide is a top priority, and we are committed to ensuring it reaches its full value for patients, physicians, and shareholders. We believe today's data reinforce the potential of the drug to become a best-in-class IKZF1/3 degrader used as a backbone therapy of choice. Before we walk through the Cemsidomide data, I want to recap the incredible progress we've made over the past 12 months and how it positions us as a leading degrader company focused on early bioavailable degraders. We continue to believe that targeted protein degradation is an important therapeutic modality that can improve how diseases are treated today. Our field is at an exciting inflection point with a steady stream of clinical data and collaborations that we believe position several degraders on the path to commercialization. C4T has been driving many of these exciting clinical and collaboration updates shaping the field. In the past 12 months alone, we've made major progress across our portfolio that has resulted in a steady flow of clinical updates and innovative collaborations. We've quickly driven Cemsidomide to important milestones and delivered data that suggests a best-in-class profile that positions it to become the backbone therapy of choice for combination regimens where IKZF1/3 degradation is warranted. In September, we also delivered initial clinical data on CFT1946, the first BRAF V600X degrader to enter clinical trials, demonstrating proof of mechanism and initial signs of proof of concept. We believe degradation of BRAF V600X offers the potential to overcome limitations of inhibitors, which include common resistance mechanisms and toxicities associated with inhibiting wild-type BRAF. And in collaboration with our partner, Beta Pharmaceuticals, we also initiated the first in-human clinical study of CFT8919, a degrader of EGFR L858R, which binds to an allosteric site created by the LR mutation. This provides CFT8919 with two potential advantages. The first is absence of toxicities associated with inhibiting wild-type EGFR. The second enables it to have activity independent of secondary mutations to the orthosteric binding site or other non-classical driver mutations, which reduce the effectiveness of first and third-generation EGFR inhibitors in this patient population. And turning to our discovery engine, we've continued to build our internal pipeline over the past 12 months and forged new collaborations that have further validated our highly productive TORPEDO platform. Strong execution has helped us build momentum and make progress in unlocking value across our portfolio. In each of our programs, there is an opportunity for degraders to offer improvements over the current standards of care. We have strategically selected targets that address diseases in large markets with significant unmet needs. Taken together, our momentum, progress, and opportunity to make a meaningful impact on patients create an exciting path ahead. The data we'll share in a moment supports moving Cemsidomide forward into multiple combination regimens across multiple lines of therapy, and we're currently planning trials that reflect this opportunity. For our earlier stage pipeline, the CFT1946 phase I trial is advancing, with several data readouts planned for 2025, and we are planning for potential ex-China development strategies for CFT8919. Finally, our platform remains one of the most productive in the industry, and we continue to focus on opportunities to extend its potential. This progress across our portfolio positions us in the years ahead to build a fully integrated biotechnology company focused on early bioavailable degraders. We are excited about what's to come for C4T. Now I'll turn it over to Len to walk through today's Cemsidomide data and how it's positioned to become a best-in-class IKZF1/3 degrader. Thank you, Andrew. Notwithstanding the many novel treatment advances in both multiple myeloma and non-Hodgkin's lymphoma, the importance of Ikaros and Aiolos, also known as IKZF1 and IKZF3 respectively, remains central to the disease biology. These targets are transcription factors essential to cancer cell growth for both multiple myeloma and NHL, and regulate the activity of IRF4, another transcription factor that these cancers are dependent on for survival. As a result, both indications have strong dependencies on IKZF1 and IKZF3, and degrading these targets leads to cell death. These proteins are therefore a critical therapeutic target and will continue to play a significant role for both indications. It is also important to remember that neutropenia is an inevitable consequence because IKZF1 and IKZF3 also play a role in early neutrophil maturation. Neutropenia is observed with this class of medicines because of reduced replenishment of neutrophil populations over time, rather than a direct effect on neutrophil viability. Therefore, incorporating a dosing holiday period allows for the natural process of stem cell replenishment of neutrophils to resume. With a potentially best-in-class profile, an effective dosing schedule, and exquisite cell selectivity of the target, Cemsidomide has the potential to become a backbone therapy in multiple myeloma and NHL. First, let me review with you our progress from our ongoing first-in-human phase I trial. Last year, we completed our monotherapy multiple myeloma arm utilizing the 14 days on, 14 days off schedule. The data demonstrated that Cemsidomide is well tolerated with evidence of dose-related anti-myeloma effects as well as immunomodulatory effects. Today, we are excited to present updated dose escalation data from Cemsidomide plus Dexamethasone in relapsed refractory multiple myeloma, as well as the first results of Cemsidomide as a monotherapy in relapsed refractory NHL. Let's begin with the results from our dose escalation trial evaluating Cemsidomide with Dexamethasone in multiple myeloma. Despite new emerging treatments, including CAR-Ts and BCMA-directed therapies, and irrespective of a patient's prior treatment, IKZF1 and 3 degradation remain an important and critical target because of its link to IRF4. This fact is reflected in the clinical treatment paradigms where degraders are used in treatment regimens across all lines. We believe our updated data that we present today positions Cemsidomide to be a degrader of choice for combinations and across various lines of therapy in the multiple myeloma landscape. Today, I will share data from the highlighted green boxes shown on this slide, which includes four dose levels up to and including the 75-microgram dose level. Safety enrollments in backfill cohort size are determined using a Bayesian logistic regression model, or BLRM, which permits maximum flexibility to characterize both safety and early signals of anti-myeloma activity at any given dose level. As a result, each cohort includes an initial group of patients to determine safety in cycle one, and then patients are added to backfill cohorts to increase the sample size at doses of interest. The 100-microgram dose level has just started to enroll, so we will not be sharing data from this cohort today. To date, we have not exceeded the maximum tolerated dose. The next slide describes the demographics of the 47 patients enrolled across the Cemsidomide plus dexamethasone phase I cohort. The median age was 67 years old, with a median of six prior therapies ranging from three to 22. 100% of these patients are triple-class exposed, and 85% of patients are penta-class exposed, thus representing a very heavily pretreated population. Importantly, patients enrolled on this trial have not only received prior lenalidomide, pomalidomide, and anti-CD38 antibodies, but the majority have also received CAR-T or T-cell engager therapy. This reflects the contemporaneous refractory multiple myeloma population and current patient unmet needs. Only 66% of patients enrolled had progressed on or after receiving either CAR-T or T-cell engager, and 70% had progressed from prior BCMA-targeted direct therapy. Cemsidomide plus dexamethasone was well tolerated across the range of doses studied. In this regard, while 47% of patients experienced the class effect of neutropenia, the rate of grade 3 and grade 4 neutropenia is modest at 13% and 26% respectively. This has also been associated with low rates of grade 3 and grade 4 infections of 17% and a febrile neutropenia rate of only 6%. The primary reason for Cemsidomide discontinuation was progressive disease. There were two patients with treatment-emergent adverse events that resulted in discontinuation, and there were no treatment-emergent adverse events leading to dose reduction. Overall, only 33% of patients had treatment-emergent events leading to dose interruption, and taken together, Cemsidomide has a compelling safety profile with modest neutropenic-related events in this multi-refractory patient population. Let's now examine neutropenia, febrile neutropenia, and infection rates at individual dose levels. The data demonstrated that these events were low across all dose levels studied, and importantly, these events were infrequent and did not increase at higher doses. In fact, we only observed one dose-limiting toxicity, which occurred at 62.5 micrograms, where a patient experienced grade 4 neutropenia lasting more than seven days. This patient, however, continued treatment after the event. These infrequent events, especially in a heavily pretreated population, highlight that Cemsidomide is well tolerated at multiple dose levels, which is important as we think about its future development in combinations at doses below the MTD. Now, let's look at the rates of neutropenia, infection, and G-CSF use by cycle. It is noted that the majority of on-target adverse events related to neutropenia occur in the first two cycles. The graph demonstrates the cumulative incidence of these events. Such as, if a patient had neutropenia at cycle one and also neutropenia at cycle two, they will be counted twice. There was only one patient who experienced grade 3 or 4 neutropenia for the first time after completing cycle two, while all other patients experienced neutropenia for the first time in these first two cycles. In total, only 26% of patients received G-CSF across the trial. This limited use of G-CSF, along with low rates of grade 3 or greater neutropenia, infections, and febrile neutropenia, is further evidence of Cemsidomide's compelling safety profile and points to a wide therapeutic index when we consider the anti-myeloma activity across these doses, which I will present shortly. Before we describe the IMWG response seen on the trial, let's examine the pharmacokinetic and pharmacodynamic relationships. The panel on the left of this slide shows the PK profile of Cemsidomide plus dexamethasone, which demonstrates that exposures are dose proportional as measured by plasma PK. The Cemsidomide plasma clearance over the observation period is consistent with a half-life of approximately two days, and this PK profile is also consistent with our monotherapy data set that we shared last December. On the right panel, we display the change in serum free light chains from baseline as a pharmacodynamic outcome in 35 patients who have elevated light chains as part of the disease profile. The waterfall plot shows 40% of patients had a 50% decrease or better in serum free light chains, which is a prerequisite for reaching objective responses per IMWG criteria. It is important to note that some of these patients have other manifestations of the disease, such that a 50% reduction in serum free light chains will not always be associated with an objective response using the IMWG criteria. On this next slide, we describe the population pharmacokinetic relationships. All orally administered drugs, including Cemsidomide, have some degree of inter- and intrapatient variability in plasma exposure resulting from any given dose. Thus, we have conducted a preliminary population pharmacokinetic analysis using the relationship between PAP-PK-derived AUC and reductions in serum-free light chains to better understand exposure response relationships. On the left-hand portion of the slide, you will see the plot of individual plasma exposures. Again, here you see that patients may have a range of exposures, both lower and higher, related to any dose level due to the inter- and intrapatient variability expected with oral drugs. The best-fit EMAC model for exposure is represented with the green curve. These data elements are plotted versus percent change from baseline in serum-free light chains. The maximum decrease in serum-free light chain from baseline occurs at the highest exposure cohort, quartile four, which maps to an estimated Cemsidomide dose of 78 micrograms. The data demonstrates that higher exposures are correlated to greater impact on serum free light chain reductions. We therefore conclude that 75 micrograms is a target dose for plus dexamethasone regimens using the current data set. As we continue to explore higher exposures at those higher dose levels, other higher doses may also be considered. This observation of exposure mapping to response, combined with the fact that we have manageable neutropenia with low rates of neutropenic complications, strongly supports that the drug has a wide therapeutic index as measured by the difference between efficacious exposures and the maximum tolerated dose, which we have currently not exceeded. On this slide, we display the swimmer plot that describes the response and duration at each dose. On the left-hand side, we identified patients with EMD and those who had received the CAR-T or T-cell engager therapy. Again, it is important to remember the majority of patients enrolled in this trial had received prior CAR-T or T-cell engager and are refractory to these therapies, which have been recently added to the standard of care, thus highlighting that this is a uniquely pretreated patient population. The data shown on this slide demonstrates responses across all dose levels, with deepening responses over time in some patients. It should be noted that at the two highest dose levels evaluated to date, 62% of patients are still ongoing. Anti-myeloma activity seen across all dose levels supports Cemsidomide development in combinations and across multiple lines of treatment. On this next slide, we demonstrate objective response rates as defined by IMWG criteria. We have calculated an overall response rate of 26% across all dose levels. At 75 micrograms, we observed a 36% overall response rate with a 45% clinical benefit rate, the latter rate including patients with a minimal response. These responses are clinically important, especially at the highest dose level evaluated to date, considering these patients have progressed after all standard of care regimens. Cemsidomide is often compared to other next-generation degraders in multiple myeloma. In this regard, our Cemsidomide plus dexamethasone data compares very favorably to the available data of Mezigdomide plus dexamethasone, with the caveat that there are limitations in doing cross-trial comparisons, both in terms of patient numbers and differences in the patient populations. Our phase one dose escalation experiences in this uniquely pretreated population have a similar anti-myeloma activity signal to Mezigdomide phase one trial, but our safety profile has fewer neutropenic events, including grade 3 or greater febrile neutropenia and infection. Additionally, we only had 26% of patients receiving G-CSF. Considering Mezigdomide profile, higher rates of neutropenic events were observed in the backdrop of 77% of patients requiring G-CSF. It is important to note that while G-CSF is often used, it's not always successful at mitigating the risk for complications, as manifested by persistent risk of grade 3 and 4 events despite its use. Mezigdomide safety experience in their dose 100 patient expansion cohort at the declared RP2D is similar to its safety experience in their dose escalation trial. Even with more follow-up, the safety profile remained consistent. To conclude, Cemsidomide plus Dexamethasone has a compelling safety profile manifested by only 38% of patients experiencing grade 3 or 4 neutropenia, with no cases resulting in discontinuation, and importantly, we observed low rates of infection and febrile neutropenia coupled with low G-CSF use. These findings are seen in a population where 66% of patients enrolled have received prior CAR-T or T-cell engager. This safety profile, along with the anti-myeloma activity across dose levels, including the particularly compelling activity seen at 75 micrograms, supports the use of Cemsidomide in combinations and across multiple lines of therapy, which may include the following. For Cemsidomide plus dexamethasone regimens, we believe 75 micrograms is the target dose for Cemsidomide, with the potential for higher doses to also be considered. In addition, Cemsidomide in combination with T-cell engagers, utilizing doses lower than 75 micrograms, is supported by the immune activation and anti-myeloma activity from our monotherapy data set that we shared last December. Together, this data sets Cemsidomide apart and positions it to be a potential best-in-class IKZF1 and IKZF3 degrader. With respect to next steps for future clinical development of multiple myeloma, we plan on completing our phase 1 dose escalation and characterizing doses for further development as we have not exceeded an MTD. We are also working on initiating combination trials of Cemsidomide with immune-based therapies and Cemsidomide with dexamethasone plus an anti-CD38 antibody. It's clear Cemsidomide's profile, with a wide therapeutic range, supports its development across multiple lines of multiple myeloma treatment, allowing us to capture a share of the approximately $42 billion market opportunity by 2028. Now let's turn to our monotherapy experience of Cemsidomide in non-Hodgkin's lymphoma. As a reminder, this is a distinct patient population with different prior treatments from those used in multiple myeloma and potentially a different safety profile, in part related to effects of prior treatments on bone marrow function. We recognize that NHL's treatment landscape is highly competitive, especially for B-cell lymphomas. However, it is important to again highlight that IKZF1/3 degraders are currently used across all subtypes, and there remains an unmet need. In this regard, PTCL, a subtype of NHL, has one of the highest unmet needs, as there are no targeted treatment options for non-CD30 positive patients. Given the biology and compelling profile, Cemsidomide has the potential to be considered as part of combination regimens in both B and T-cell lymphomas and as a single agent in refractory PTCL. This slide describes our NHL cohort trial design, where we have enrolled 23 patients as of the data cutoff. This morning, at the ASH annual meeting, we shared data from the dose levels highlighted in the green boxes. As of the data cutoff, we observed two DLTs at 100 micrograms. Unlike a 3 plus 3 design, the two DLTs using the BLRM model does not mean we have exceeded the MTD. By utilizing this model, we've now opened up the 75 microgram dose level to further understand the safety signal in lymphoma. Once this level is available for safety, we will make a data-driven decision on whether or not we will enroll additional patients back at 100 micrograms and/or explore other dose levels. The demographics of the patients enrolled are summarized on this slide. The median age of participating patients is 68 years old. The median prior range of therapies is three, with a range of one to 14, again representing a heavily pretreated population. Notwithstanding that any patient with refractory non-Hodgkin's lymphoma is eligible for the study, 17 patients, or 74% of patients enrolled, have a diagnosis of PTCL, clearly reflecting the unmet need in this population. As it relates to safety, Cemsidmide as a monotherapy is well tolerated in this refractory lymphoma population. It is important to note that Cemsidomide in NHL has a unique safety data set, especially since the drug is used as a monotherapy and due to the pretreatment characteristics of the patient population. The rate of grade 3/4 neutropenia is an expected on-target adverse event associated with IKZF1 and 3 degraders, and importantly, we continue to see low rates of grade 3 and 4 infections as well as febrile neutropenia. The two DLTs at the 100 microgram dose level include grade 4 thrombocytopenia in both patients, and one of these patients also had febrile neutropenia. Across the lymphoma cohort, only 39% of patients received GCSF. The next slide summarizes AEs by dose level for Cemsidomide as a monotherapy. The majority of adverse events occurred at the highest dose level of 100 micrograms. While neutropenia is clearly related to degradation of the target, the true rate of thrombocytopenia will be further explored as we continue to enroll more patients. On this slide, we start to characterize the response rates at each dose level, with a 38% overall response rate demonstrating compelling activity at a range of doses. We enrolled patients of all NHL subtypes, which is depicted on the column of the left-hand side of the slide. As of the data cutoff, at the highest dose level of 100 micrograms, all three patients responded, with two patients achieving a complete metabolic response and one patient achieving a partial metabolic response. Focusing now on PTCL, we summarize the response rates of PR or better by PTCL subtype. Overall, we had a 44% response rate in all PTCL patients across a range of doses, with a 25% complete metabolic response rate as of the data cutoff. The bar graphs on the right demonstrate ORR by PTCL subtype, and notably, we observed an ORR of 100% in the AITL subtype. This data in PTCL thus demonstrates compelling and deep responses in this highly unmet need population. While additional dose finding is ongoing, the compelling monotherapy anti-lymphoma activity and well-tolerated safety profile in PTCL patients demonstrate that Cemsidomide has a wide therapeutic index. Together, the data supports a development path for Cemsidomide as a monotherapy in relapsed refractory patient population, as well as potentially in combination in other settings. Cemsidomide has the potential to capture a share of the expected $30 billion market opportunity in NHL by 2028. As it relates to our next steps in clinical development, we will complete the dose escalation trial and plan to trigger an expansion cohort in PTCL. We also plan for a discussion with regulatory authorities regarding next steps. To conclude, based on the data we shared today across both multiple myeloma and NHL, we believe Cemsidomide has the potential to be a best-in-class IKZF1 and 3 degrader in two distinct indications across multiple therapeutic lines. This is supported by both a well-tolerated and compelling safety profile, as well as compelling anti-myeloma activity and anti-lymphoma activity across a range of dose levels. Taken together, Cemsidomide has a wide therapeutic index and has the potential to become a degrader of choice within the evolving treatment landscape, which has an expected $40 billion market opportunity in multiple myeloma and $30 billion market opportunity in NHL by 2028. We look forward to continuing to progress this trial to get Cemsidomide as quickly as possible to patients and prescribers. Operator, please open the lines for Q&A. Thank you. We will now begin the question and answer session. To ask a question, you may press star then one on your telephone keypad. If you're using a speakerphone, please pick up your handset before pressing the keys. To withdraw your question, please press star then two. At this time, we will pause momentarily to assemble our roster. The first question comes from Gavin Clark-Gartner at Evercore ISI. Hey, guys. Congrats on the data, and thanks for taking the questions. I just wanted to start off with a couple more detailed questions on the swimmer plot for myeloma. For the two patients at the 75 microgram dose, for the two patients with PRs who came off treatment fairly shortly thereafter, maybe you could just elaborate on the one unrelated death and also the reason for the second patient withdrawing consent so quickly? Thanks, Gavin. This is Len Reyno speaking, the Chief Medical Officer. Let's start with the one where the patient came off by choice, because that's an easy one to explain, and it actually reflects the therapeutic efficacy of the drug. So this is a patient who enjoyed a very early PR, and once that PR was established, the patient, in collaboration with their investigator, decided to use that as a bridge to put them onto a program to get them on a CAR-T. So that's what happened in that patient. The second patient is a patient who had an unrelated death in the context of multiple advanced complications of myeloma. Point of fact, notwithstanding how safe this drug is, in general, we're treating a very ill population with multiple competing morbidities, often with other diagnoses in the background. And so they received very little drug, although it was working, and had complications the investigator deemed to be unrelated to drug. That's super helpful. And could you help me square some of the numbers between the safety and efficacy analysis sets? For the 75 dose, though, I think there were 14 patients in the safety and then 11 patients in the efficacy. Was it just a timing difference there? Yeah. So great observation. And yes, it's just a difference of the data cut timing. The data cutoff, I believe, for this study was done on October 11th, and we enrolled these cohorts sequentially. The patients enrolled at 75 were obviously recruited later in the year. The earliest that you can declare a response for these patients is in patients who have light chain predominant disease. Patients with any mixed features of the disease, actually, it can take two to four to six cycles to get a response, and they may not have had their first objective parameters done for efficacy analysis at the data cutoff. We include their safety data, but we don't know their efficacy outcome at the time of the cutoff. Okay. Great. Also super helpful. Taking a step back, why do you believe that doses below 75 micrograms may be optimal for immune-based therapy combinations? And also, as you go up to the 100 microgram dose, might that change your view? Again, great question. So let's separate it two things here. And part of your question relates to data that was actually predominantly shared in the monotherapy experience last December. So if you think about the ways this class of drug works therapeutically, one of the pathways it works is immune enhancement, and one of the ways it works is direct anti-myeloma activity. As it relates to direct anti-myeloma activity, we know that that's actually highest for the class of drugs when given with dexamethasone. So the immune-based activity, first of all, you don't want to inhibit it by giving a high dose of steroids. And so you're going to give it as a monotherapy. And if you go back to the data set shared in December last year, what you'll see at monotherapy is, in fact, that we showed data that at a dose that's below the MTD, and in particular, at a dose that's mapped to 50 micrograms, that you get T-cell effector enhancement at that dose. So you need to break apart how are you using the drug in combos. So if you're using the drug in combos predominantly because you want to emphasize the immune activity portion and the effect on T-cell exhaustion, etc., it's no dexamethasone, and you want to give it at a dose that does not cause significant neutropenia. And we think that our data really to date supports aiming for a dose of 50 micrograms. If, on the other hand, you're using it in a plus dex regimen to get the maximum anti-myeloma effect as it is in this trial, or, for example, as you might if you're combining with a CD38, then there, higher doses matter. You want to push that dose to the highest tolerable, and our data supports that 75 is a very effective dose. And you can certainly make full development decisions for the plus dex at 75. There's no reason to wait making those decisions. There is actual reason for optimism that there might actually still be more to be gained by the higher dose level. We'll find that out over the coming months. Taken together, we have a situation where the profile, the clinical profile, and the data we've generated over the last year and a half in particular really makes the case that you have a degrader that's ready for full development, whether you're using it to maximize the anti-myeloma effect or whether you're using it to maximize the effect on T-cell exhaustion and immune enhancement. Yeah. Then just I'll say, remember, we were specific in saying that those are target doses. Ultimately, we'll run a study, and the answer on what the right dose to use in combination will be determined empirically in that study. But based on, as Len said, the body of data we've generated to date, we think those are target doses. But to your point, that doesn't preclude it being a higher dose if data in a combination study supports it. Okay. Great. That makes sense. And this is my last question. I just wanted to be clear on the next steps on the myeloma side. So you're planning to start up both of those combination studies that you laid out. Is that stage-gated, having a partner? And then when you're engaging on the registrational path, is that also for the combination studies, or is that just for the plus dex option potentially in late lines? And then maybe you could just discuss kind of cost and financing plans for that. Thanks. Yeah. So right as we understood, so right now, we are working on planning those two studies that were outlined. Len's team is busy working on operational plans for those studies, right? So independent of whether we have a partner or not, we believe those are the next steps that we need to take for the program. Yeah. What that looks like, just to be clear, obviously, it's one thing to put on the slide. You'll consider those combinations. We're building detailed protocol synopses, and so we're ready to go to start to be able to plan on how you'd actually operationalize them practically, what dose you'd start with, etc. So that works ongoing. That's been ongoing for a few months, and we'll continue doing that into the new year. As you heard us say before, right, the phase 1/2 study is primarily up in the US, only in the US, and we'd like to do global. So that requires some broader work to do that. And then to the regulatory question, I think, again, that's a broad discussion with regulatory agencies on a path forward for a label that's independent of a partner, but it's a broader discussion, not specifically those two trials we've outlined. And Gavin is attending just on the financing and runway question. So within the existing runway, obviously, we've got runway to continue all of the phase one work for Semzidamide. Full conduct, though, of additional studies, combination studies, etc., that is not assumed within our current runway. All right. Got it. Very helpful. Congrats on the data. Great. Thanks, Gavin. The next question comes from Etzer Darout at BMO Capital Markets. Great. Thanks for taking the question. Congrats on the data. Just a couple of questions. First, can you talk a little bit about the sort of increase in neutropenia as your dose escalate? I thought that looked interesting. Just wondered if it was a factor of small ends, or could there be something else going on there as you kind of get sort of lower neutropenia as you go up in dose, particularly the grade 3 plus neutropenia? Then I have a follow-up question. Yeah. No, it is a great question. And I'm going to start answering the question with a clinical anecdote and then talk about the literature and things that we do and don't understand. So clinical anecdote, when I first joined the company 18 months ago and started talking to investigators about how problematic was neutropenia with our drug, the response was not very. And I said, "Tell me more." And they told me, "Well, it's really in the first couple of cycles," which was interesting, as is seen with this class. And as it turns out, actually, it's been under sort of focused on. But in fact, this is the unique feature of the class of drugs that for both Len and Tom, there is some literature, and we have some references that we can connect you with, where it's been summarized that, in fact, as a class effect, it does appear that more patients are at risk for neutropenia in the first two cycles. So in fact, what we're seeing was also been seen across the class, and it's actually a unique feature of degraders. Now, the obvious question is, why is that? And I'll be clear, I don't really understand the mechanism why it's particularly in the first couple of cycles. Now, of course, that said, at any point during the treatment, and if you look at our dose relationships, you'll see what I have described qualitatively. You see that you get sporadic events of neutropenia at any given cycle, at any given dose, and that remains true for the class of drugs, and it remains true for our drug, Semzidamide. It's important to note that the impact of those late onset, when it occurs sporadically, of course, is much less, because in order to get late onset neutropenia, you have to be benefiting from the drug, so it actually has very little impact, if at all, on the therapeutic index because you're already benefiting, so I think it's an important observation, and it's one area in oncology where the rule that we often think about is that your cycle one toxicity is the baseline level that it only gets worse over time. It's simply not true. It's not true for our drug, and it's actually not true for other publications, so hopefully, that answers your question. No, great. Thank you. And then another question I had, I didn't spend a lot of time on slide 19, but I just was curious around the post-BCMA activity with Semzidamide. I mean, we've seen some data with Navigdomide, right, at least a numerical improvement in patients that were post-BCMA. And could you comment on what you're seeing for Semzidamide in sort of that post-BCMA population, the activity there? Sure. I think it's premature to try to assign a response rate to that population. But what's very clear is those patients are benefiting of the drug as much as, and potentially even more than other patients. So that there's nothing that makes those patients less likely to benefit to Semzidamide. I don't know if that's true for other drugs in the class because we actually have the largest experience of patients in that group, and we have 70% of our patients who've had BCMA. So when other people make comments, at least with commenting related to therapy after BCMA, as an example, those cohorts tend to have a handful of patients. So at least for IKZF1/3 degradation, this is probably the most important data set to benchmark. But I think the important thing is the drug works. The other important thing, these patients are showing up at clinic needing treatment decisions. And there's really no FDA label for that population, but we have the beginning of a signal that would support that this class of drugs and our drug in particular has meaningful benefit here. Yeah. I mean, I would add we do some people. I was going to say some people often ask the question, does this even matter in a world of CAR-T and BCMA? And I think the fact that those patients are showing up for our study proves that it does. Yeah. I want to comment on that further because I think it's super important. When we showed the lines of therapy with the size estimated of the population, that data is collected, obviously, it's always a couple of years behind the onset of standard of care. But I think there's 12,000 patients in the U.S. estimated annually that would be fifth line. If anything, that number of patients is going to go up with time. So the unmet need in patients who've actually seen T-cell directed therapies is going to get bigger, not smaller, because notwithstanding the effectiveness of those drugs, when patients relapse, they're still in actually good shape. They should be considered for other therapeutic modalities as opposed to transitioning to hospice care. So I think the exciting part about our data is we are really characterizing meaningful activity for our Semzidamide in the population of patients that are really beginning to show up and needing treatment decisions and treatment plans from their docs. Great. Thank you. Congrats again on the data. Thanks, Edgar. The next question comes from Brad Canino at Stifel. Thank you. And good to see this profile evolve. Just a two-parter from me because as I look at your exposure data, it supports 75 is right at a developable dose. But with the inter-patient exposure variability you mentioned, how should we think about the ability to get the necessary exposure for all patients at 75 instead of needing to get to 100 or higher for the total population? And I guess on a correlated second question here, if you find it better to move to 100 for exposure and efficacy, how should the emerging safety signal from the NHL study at that dose translate or not translate to myeloma patients? Thank you. Yes. Okay. Great questions, Brad, as always. Let's start with first principles. Obviously, we have an efficacy signal in our data set that's occurring across all the dose levels we've tested with the majority of patients being dosed below 75. So what we're actually saying is that we think we can get more patients at 75 or above into those exposures that, if anything, are going to make this already meaningful response rate higher. To your point, we would happily recommend dosing 100 if it looks safe because I think the other thing that our data set is saying loud and clear is that more is better over the range of the safety that you've seen. You correctly asked the next logical question, and that is, does the lymphoma data actually predict what will likely happen in myeloma? And before I answer that question, I want to remind everybody on the call, why is there a separate lymphoma arm? And so before we ever did the trial, because this is the safety trial, so you could make the case out of the gate that you just put lymphoma and myeloma together. And in fact, regulators and clinicians don't do that. The reason they don't do that is because people recognize that the bone marrow tolerance of lymphoma patients, especially refractory lymphoma patients, is different in part because they've had treatment regimens they've progressed through that are heavily cytotoxic chemotherapy and particularly have been emphasizing alkylator-based regimens. What we know about alkylator-based exposure on bone marrow is it just renders the bone marrow more sensitive in general to any drug that can suppress the bone marrow. In fact, we don't think that the data set as it relates to thrombocytopenia is predictive of what will happen in myeloma. We continue to believe, and as do our clinicians, that in the myeloma population that we are likely to eventually get a dose-limiting toxicity that is rooted on the neutropenia signal. Obviously, the data will be the data, and we will see it. But I don't think there's reason to conflate the safety from the two things, and that's why they're actually separate populations and not lumped together for the purposes of safety determination, not only on the trial, but at the level of the agency. Yeah. Just to add a comment, I think you see the exposure variability, and that's actually something you see with all oral drugs. It's not sort of unique to our drug. It's not unique to degraders. And in fact, the variability that we see is consistent with other agents in the class. So we don't see it as any different. We're putting it all out there with full disclosure because we think it's important. And actually, the data doesn't, as a clinician and as a drug developer, it actually doesn't give me pause. I'm very, very excited about the data. When I saw the PopPK, it actually really confirmed what I wanted to see, which is exposure matters, more is better, and that when we look at the rate of toxicity as it relates to neutropenia, we've seen is obviously there's some, but it's not associated with curtailing dosing. And so I think we're in an incredibly exciting place, ultimately, for patients where we have this potent degrader with a very predictable and very manageable side effect, and we still haven't exceeded the MTD. Very helpful to walk through all that. Thank you so much. The next question comes from Yinfa Xu at Jefferies. Ethan, please go ahead. Do you have us on mute? Can you hear me now? Now we can hear you. Okay. We can hear you. Thank you for taking the question. This is Yifan from Jefferies on behalf of Akash. I have the first question is about durability. I noticed that on the swimmer plot, it seems not too close to reach median DOR, but I'm curious if you could model median DOR across all those levels based on the available data set right now. Second question is about data interpretation. I noticed that there are about more than 30% of patients had data interruption. I'm wondering, most of this happened at what dose level and the possible impact on the durability of response? Thank you. Okay. Those are two great questions, and let's tackle them separately. You could conceivably get to a place where you could model durability response, but you need to make sure that every patient had an opportunity to at least get to a threshold window of a response duration. For example, you might say after every patient on the study has been treated long enough that they could get to six months or one year, etc., you might engage in that kind of work. It would be really premature to do it now because you just don't have enough observations at the doses that we believe are going to be the most efficacious to do that. You could come back to that at a future state. I'll call your attention to that in terms of the durability data we do have. We have a patient with a durable response that's actually 18 months into therapy, actually on both the myeloma arm and the lymphoma arm, both at doses that are not optimal. I think that it remains to be seen what it will be, but I am cautiously optimistic as we get more patients at the more efficacious doses that the issue will take care of itself in terms of being able to estimate it. Your second question, though, is also a really important question. And that is dose interruptions and, in fact, what does happen in practice? Because the pattern that we're seeing actually is interesting because what it reflects is these are patients that have got complicated illnesses, often with comorbid conditions. Things happen, and at some point, the clinicians periodically make decisions to not give the full 14 days as an example or to interrupt for a few days if they sort something out that might be an intercurrent illness, etc. Notwithstanding those interruptions, and that's what's reflected, to be clear. That's part of the variability in the PopPK as to why those numbers are different because that also includes those interruptions. But they're not dose interruptions because the doc thinks that the drug's too toxic for patients. So the doc doesn't interrupt the drug and then dose-reduce them. It's usually, for example, it can be a viral illness. It can be something else that's going on. We don't have good data to break it out at dose levels. Suffice to say, I know qualitatively we've seen it at all dose levels. It's a conversation we often have in our regular data update calls with investigators. But the important observation is the exposure response PopPK incorporates the impact of dose interruption. And the other important concept is the dose interruption does not change prescribing behavior. The doc says, "I'm still comfortable with the dose. I just needed to skip three days this time for whatever reason," so I hope that answers your question. It is a great question. Yeah. Just to be clear, it's treatment emergent. It's not classified as treatment-related. So that's the key distinction there. Yeah. It's patients who, as they go through treatment, they're not dose-interrupting because they think it's related to the drug. They're just saying there's other things going on. It's often in the winter months. I'll tell you what. It's often viral illness, and it depends, so I don't think we can break it out further than that at this time. Thank you. The next question comes from Derek Archila at Wells Fargo. Hey, guys. Congrats on the update, and thanks for taking the questions. We just have a few on the G-CSF usage in the trial. I guess the first one, just wanted to see if you could provide some more color on which dose the GCSF usage was the highest. It actually is not correlating well with dose at all, which is actually part of the excitement, which tells us that our doses are well below the MTD, and so, in fact, I think its peak use occurs in cycle two. If you look at the plot we have on that slide, and that makes sense why the peak use would be in cycle two for two reasons. You now have the information the clinician has in hand what happened in cycle one. And even if they didn't do G-CSF, they now have the kinetics of the neutrophil count, and they think, "Well, maybe this patient is a little bit more sensitive, and I'm going to give them G." But in fact, if that's been previewed that there was going to be a problem, you would expect the G to go up in each subsequent cycle. And that's what does not happen. And in fact, so irrespective of dose or cycle, the G use predominantly is in the first two cycles. And then afterwards, the phrase I use to describe it was sporadic use thereafter, which is driven by individual patient need. And for those patients where it occurs after multiple cycles, you have to put that in the context that they're actually also benefiting from the drug. That's why they're getting multiple cycles. Yep. Understood. And then just second question, just on the comparison to Mezigdomide, I guess, can you provide some clarity on whether or not the protocols for G-CSF usage in both trials is the same? I guess I was just wondering whether or not that's pretty standardized or is it more like a physician discretion? Well, it's both standardized and physician discretion. How can both be true? How can both be true? It's standardized in so the standard consensus is across the field that when you're doing dose finding, i.e., before you've declared a dose level safe in cycle one and for both trial programs, you can't give G because you need to see, and then the regulators want to see they want to see the kinetics of the neutrophil changes with growth factor support. However, once you've declared a dose level safe for both them and us, you can then, if you're adding patients, then you can use G at physician's discretion. And as far as we know, for example, there are 100 patient data set at their RPTD that they declared as one for that purpose, that patients could get G in any cycle at any time per physician's discretion. And that then led to a use of it where 77% of patients got G during their dosing with Mezigdomide. What they didn't share, at least I haven't seen, if anyone's seen it, please, I'd be happy to see it, they didn't break it out then by cycle. They didn't break it out by how many of patients got G in multiple cycles, etc. But what we can say in aggregate is that the G-CSF use is substantially higher using the same rules for prescription as our group. Yeah. And I would say we didn't also, if you look at the numerator in slide 21, right, in their dose escalation. They didn't. They did not break out at all overall G-CSF use. But to Len's point, the rules were the same in the dose escalation portion. The difference is in that phase two expansion. And that's why in the scripted part of the call where I referred to their phase one experience mapped to their higher expansion, that's an important point there is because in that phase one where they didn't break it out with the G-CSF use, that in fact, they have exactly the same rate. I mean, it's remarkable how those slides overlap. And so I have no reason to believe that they used less G in phase I. Flip side is if they did use less in G one, they didn't actually improve their rates with G because it's exactly the same as it was in their phase I experience. So I think it's an interesting data set, but we can only compare the parts that they disclosed that match. Got it. Excellent. Thanks so much for the color and congrats again on the data. Thank you. The next question comes from Terence Flynn at Morgan Stanley. Great. Thanks for taking the question. I was just wondering to add a two-part on the regulatory conversations in myeloma. So just wondering when you'll be able to provide us with an update from those conversations, number one. And then the second piece is I know you mentioned a fifth-line population. Is that the targeted population you think there is a path potentially for accelerated approval, or how would you define the accelerated approval population path? And then the related question there is just remind us what you think the bar for ORR and DOR is in that specific population. Thank you. Yes, and Andrew, I'll take the first part. At this point, we're not prepared to comment on timing of when we would share regulatory guidance. When we have it and we have a sense that there's something to share that's important, we will. But we're not guiding to that right now. I'll let him take the question on the line. Clearly, we think that you could potentially get an approval, potentially even an accelerated approval in late-line multi-refractory. But I think the decision has to be made really carefully because clearly, the value driver for patients first and foremost, but also therefore investors, is in earlier lines of therapy. And we want to make sure that you set the drug up for maximum success. So before committing to a program of pursuing only late-line as the first approval, we remain very interested in the opportunity that may come from enhancing effects in combination, for example, with BCMA BiTEs or in combination with the CD38. And so again, before you commit to an accelerated approval strategy, you also have to commit to a full approval strategy. And you want to make sure that in your zeal to get that accelerated approval thing, you don't actually compromise your ability to maximize value in what would be the full approval program. There's other considerations, obviously, in 2024 and beyond with respect to how you price based on first approval, etc. So we haven't made a final decision there, but we stand by the comment, which I think is super exciting, is that you can place this drug in various combinations and various strategies across the spectrum of myeloma care. The next question comes from Sudan Long, I'm sorry, Logan Nathan at Stephens. And I'm sorry if I mispronounced that. Hi, C4 team. Thank you for this update and opportunity to ask questions. My first one is regarding the combination strategy for CFT7455. Will you still stick with the 14-day on and 14-day off strategy, or could there be a more aggressive approach to reduce that 14-day off, maybe down to seven if you can kind of achieve an anti-tumor response and still optimize on efficacy? Then secondly, just kind of going off of the answer you gave on the last question regarding getting into early lines of therapy with a combination strategy. When you speak with the prescribing physicians, what is their sentiment knowing this class effect within the degrader over the other CAR-T options or what may be currently the standard of care, early line of care? How do they feel about this adverse event profile jumping into early line therapy with administration? We have limited time, and there's a lot to unpack there. Let's say, first of all, we are very happy with the 14-days on, 14-days off schedule. Our being very happy with it and knowing that it's safe and effective does not mean that at some future stage, in particular, you might consider alternatives to it, but not as the core development strategy out of the gate right now. And so that's the first part. The second part, when we talk to our investigators, and one of the things they consistently say is what impresses us the most, and I've been having conversations here at the ASH meeting individually with folks and just revisit with me what it's like to prescribe this drug. And in fact, they consistently say this drug has a predictable neutropenia that's completely manageable and doesn't have a lot of other side effects. And that's manifested in the tables that we showed you. And therefore, they're incredibly enthusiastic because it's both safe and easy to give and think it's a great drug to consider for combination. And they fully support its development. Their goal is they want to bring good drugs and better therapies to patients writ large. But I think the enthusiasm level with both the efficacy and the clear safety signal is really strong. Through conversations at ASH, kind of reiterating that fact. And then lastly, just as Mezigdomide from Bristol kind of is noted as a monotherapy potent IMiD degrader as well. Just as you look at the combination strategy and lining up with what could be presented there as well, that side of things, what is the pros and cons of going versus monotherapy highly potent, maybe dealing with more neutropenia versus maybe going with a combination strategy that lowers that class effect? Yeah. This is Andrew. I just think that the way we use Mezigdomide is really going to be based on the combination agent. I think, as Len mentioned earlier in the call, certainly when you're combining it for its T-cell activation activity, for instance, with a BCMA-targeted BiTE, you don't want Dexamethasone necessarily on board. And so we think that we can achieve the necessary T-cell activation at tolerable doses. And so that's where we think about what's the right combination regimen based on what you're trying to accomplish therapeutically and what doses does that occur at with Mezigdomide. Thank you for all the answers to the questions, and congrats again on the updates here. Great. Thank you. This does conclude the question and answer session. I would like to turn the conference back over to Mr. Hirsch for closing remarks. Great. Thank you. So I just wanted to close by thanking everybody for joining us today. I also want to take the time to thank the patients, their families, caregivers, and all the employees at C4 team for working on our study. It's really gratifying to see the results and the patient impact that we can have. As you can see, we're really excited about the emerging profile of Semzidamide to really be a best-in-class degrader of IKZF1 and IKZF3 across two distinct indications where there are clear unmet needs. And so we look forward to updating you on our progress as we advance the program. Thank you for your attention today, and all of you have a great rest of your weekend.