Ladies and gentlemen, thank you for standing by, and welcome to the Aclaris Therapeutics Presents Positive Preliminary Top-Line Data for ATI-450-RA201. At this time, all participant lines are in a listen-only mode. After the speaker's presentation, there will be a question and answer session. To ask a question during the session, you will need to press star one on your telephone. Please be advised that today's conference is being recorded. If you require any further assistance, please press star zero. I'll now hand the conference over to your speaker today, Kamil Ali-Jackson, Chief Legal Officer. Thank you. Please go ahead, ma'am. Thank you, Shannon. I'm Kamil Ali-Jackson, Chief Legal Officer for Aclaris. Please note that earlier today, Aclaris issued its press release announcing positive preliminary top-line results from its Phase IIA clinical trial to investigate the safety, tolerability, pharmacokinetics, and pharmacodynamics of ATI-450, its investigational oral MK2 inhibitor, in subjects with moderate to severe rheumatoid arthritis. For those of you who have not yet seen it, you will find a link posted under the Press Releases page of the Investors section of our website at www.aclaristx.com. Joining me today for the call are Dr. Neal Walker, President and Chief Executive Officer; Dr. David Gordon, our Chief Medical Officer; Dr. Joe Monahan, our Chief Scientific Officer; Frank Ruffo, our Chief Financial Officer; and Walter Smith, our Scientific and Business Development Consultant. Before we begin our prepared remarks, I would like to remind you that various statements we make during this call about the company's future results of operations and financial position, business strategy and plans and objectives for Aclaris' future operations are considered forward-looking statements within the meaning of the federal securities laws. Our forward-looking statements are based upon current expectations that involve risks, changes in circumstances, assumptions and uncertainties that could cause actual results to differ materially from those reflected in such statements. These risks are described in the Risk Factors section of Aclaris' Form 10-K for the year ended December 31st, 2019, Form 10-Q for the quarter ended September 30th, 2020, and other filings Aclaris makes with the SEC from time to time. These documents are available under the SEC Filings page of the Investors section of Aclaris' website at www.aclaristx.com. All the information we provide in this conference call is provided as of today, and we undertake no obligation to update any forward-looking statements we may make on this call on account of new information, future events, or otherwise. Please be advised that today's call is being recorded and webcast. A link to the webcast can be accessed on the Events page of the Investors section of our website. I'll now turn the call over to Dr. Neal Walker, President and CEO of Aclaris. Neal? Thank you, Kamil. Good morning, everyone. We are pleased to present our positive results from two studies, RA201, where we studied ATI-450 in patients with moderate to severe rheumatoid arthritis, and PKPD-102, where we studied 80 mg and 120 mg BID in healthy volunteers. Needless to say, we are thrilled with the outcomes. Turning to slide three, as a reminder, Aclaris is a biotechnology company focused on developing small molecule therapeutics for immuno-inflammatory diseases. There are three important aspects to help us drive important breakthroughs in the therapeutic options for inflammatory diseases. First, the people. We have world-class expertise in developing kinase-targeted medicines. Second is our platform. We have a proprietary drug discovery platform in our KINect platform. Third is our pipeline. We have an innovative pipeline that has platform potential within each of our drug candidates. Slide four. Here's our team. We have former senior leaders from both Pfizer and GSK with decades of experience successfully developing a number of therapeutics in the immunology and inflammation space. As you can see, our current team is composed of many of the former founders of Confluence Life Sciences, which we acquired in 2017. Turning to slide five. Our strategic focus and the underpinnings of the company lie in our ability to leverage our kinome target discovery to address the unmet needs that continue to exist in the immunoinflammatory space. Our fully integrated discovery team identifies key targets, utilizes our custom kinase assays to test our molecules, and within our labs in St. Louis, validates the drug candidates prior to moving to IND and clinical development. ATI-450, our MK2 inhibitor, is yet another example of an internally developed asset utilizing our KINect platform. Turning to slide six. As a reminder, ATI-450 is an oral small molecule that inhibits TNF-alpha, IL-1, and IL-6. There are numerous indications that are driven by the cytokines that are targeted by ATI-450, some of which are listed on this slide. These are obviously large markets with global sales in the aggregate of $77 billion, and despite great advancements over the last several years, there are still large unmet needs in these indications. We began our program with ATI-450 looking at diseases driven predominantly by TNF-alpha and IL-1, which is why we initially focused on proof-of-concept studies in both rheumatoid arthritis and CAPS. With that, I will hand it off to Joe to describe the evolution of the MK2 program. Joe? Thanks, Neal. P38 kinase held much promise as the central kinase in a signal transduction pathway required for the production of key inflammatory cytokines such as TNF-alpha, IL-1, IL-6, and IL-8. Despite major efforts across multiple drug companies, inhibitors of P38 kinase have not advanced through clinical development and onto the market. The two key issues encountered with P38 drug candidates as a class were modest transient efficacy and safety concerns. Three of the leading mechanistic hypotheses for the poor efficacy and lack of durable effect or tachyphylaxis with P38 inhibitors are as follows. The inability to dose escalate to maximal efficacy across the dosing interval, presumably due to safety concerns. Secondly, P38 inhibitors induced P38-induced pathway reprogramming in RA patients, resulting in P38-independent production of pro-inflammatory cytokines and apparent tachyphylaxis. Third, P38 inhibitor-induced downregulation of anti-inflammatory cytokines such as IL-10, an effect that could counteract the inhibition of pro-inflammatory cytokines resulting in lower efficacy. The finding that the P38 substrate and downstream kinase MK-2 selectively drives the pro-inflammatory axis of the P38 pathway while bypassing the negative feedback in anti-inflammatory axis, make it an exciting target and led to many pharma companies targeting MK-2 in the early 2000s. To date, no ATP-competitive MK-2 inhibitor has advanced to clinical development due to poor target drugg ability. We have overcome the MK-2 drugg ability hurdle by targeting a unique pocket created upon P38/MK-2 complex formation and designing a drug that selectively binds to that pocket, resulting in the development of ATI-450, our current P38/MK-2 complex inhibitor lead. Along with a modest efficacy and inability to dose to levels that inhibit cytokine production across the dosing interval, transient inhibition of systemic inflammation marker CRP was observed universally with P38 inhibitors in phase II RA studies. Three examples of this transient inhibition of CRP are shown on slide eight. P38 inhibitor-dependent CRP inhibition was observed for the first two to three weeks of dosing, but levels rose with continued dosing to baseline levels by weeks four to eight. The key differentiators for an MK-2 pathway inhibitor relative to P38 inhibitors would be a drug that is, one, safe to dose to levels that demonstrate high levels of inhibition of key cytokines across the dosing interval. Two, demonstrates durable effect on inflammation markers over 12 weeks of dosing. These were the goals of the phase II study that David is going to describe now. Thanks, Joe. I'm very pleased to present the data from our ATI-450 program today. As a reminder, on slide nine, we've been running studies in RA, CAPS, COVID-19, and a high-dose phase I study. Today, we'll be focused on the RA study and the new phase I data. Slide 11 is a summary of the RA201 study design. RA201 was designed to discharge some of the risks associated with the P38 pathway and to investigate if coming down the pathway to inhibit MK2 was the solution. Specifically, we wanted to see if a 450 dose shown to cause marked cytokine inhibition of phase I was well-tolerated. Secondly, we wanted to see if it had durable activity. We plan to assess activity based on the ability to reduce hs-CRP by more than 25% from baseline at all time points over 12 weeks. We hope to see a signal on clinical efficacy assessments. We recruited patients with moderate to severe RA, with at least four swollen and four tender joints. They had to have a CRP greater than or equal to five. They needed to have existence of synovitis on MRI. All of that had to be present despite stable dosing of methotrexate. We randomized 3:1. We were hoping to get at least 15 subjects through week 12. We'll be presenting the endpoint shown on the bottom of this page, with the exception of the MRI and PK data, which is not yet complete and will be part of a future manuscript. Slide 12 summarizes the key demographics. We recruited a population with a baseline mean DAS28 CRP of 5.77 and 5.71 in the placebo and 450 arms, respectively. Since we were interested in exploring CRP reduction, it made sense to recruit patients with elevated levels of entry, but in recruiting patients with long disease duration and elevated CRP despite methotrexate and other available drugs, we may have recruited a group of patients who are perhaps more difficult to treat or relatively refractory. 19 subjects were recruited. We had one dropout in each group, and I'll discuss the reasons for that later. Slide 13 is the first efficacy slide. You can see that in the active arm, there is a rapid reduction in the mean DAS28, and that continues to decline out to day 84. The placebo group did not show a consistent change and was worse than baseline at week 12. The mean drop at day 84 is 2.0 in the active arm, and the median drop was 2.1. I think that puts us firmly in the range of responses you would want to see for an active drug in RA. Slide 14, I'm showing the median percent reduction in swollen joint count. The picture is very similar to what I showed on the DAS28. It shows a rapid reduction and continued improvement to day 84. Again, the placebo patients did not have a good response. Slide 15 shows the median percent reduction in tender joint count. Again, we see a rapid reduction and continued improvement to day 84. Consistent with other endpoints, placebo did not appear to have a marked effect. Slide 16 shows the patient and physician VAS scores. You can see that there is an improvement in the patient scores at the top of this slide. For the physician assessment of activity at the bottom, you can see there is a marked improvement, which is maintained over the full 12 weeks of the study. Slide 17 shows the ACR 20, 50, and 70 scores. There was a rapid increase in the proportion of ATI-450 patients meeting ACR 20 criteria at day 28, and by day 84, that proportion had increased to 60%. By day 84, 33% of 450 subjects had hit the ACR 50, and 20% met the ACR 70 criteria. No patients in the placebo group hit these endpoints. With 60%, 33%, and 20% of patients hitting the ACR 20, 50, and 70, it looks like ATI-450 is delivering efficacy that you would hope to see in an active and effective drug. Slide 18 shows the responder analysis for the DAS28 scores. A DAS28 less than 2.6 represents remission, and that was achieved in 20% of 450 subjects. A DAS28 of less than or equal to 3.2 represents low disease activity, and 40% of 450 subjects achieved that. No placebo patients met this endpoint. Like the ACR scores, I think this responder rate compares well to efficacy shown by other active drugs. Slide 19 shows the median percent change in hsCRP. As a reminder, our hope was that we would reduce the CRP by at least 25%, and that's shown here by the dotted line, and that would represent a marked deviation from what was shown in the P38 inhibitors. You can see on this slide that the ATI-450 arm reduced the median CRP by at least 40% at all study visits, and placebo did not show a sustained reduction. This profile supports the sustained efficacy that I showed on previous slides. Moving to Slide 20, we have cytokine data to support the clinical responses, and I'll pass the mic to Joe to take us through that, beginning on this slide. Thanks, Dave. One of the hypotheses to explain the lack of durable efficacy with P38 inhibitors as a class in RA studies is that dosing RA patients with P38 inhibitors over 12 weeks results in signal pathway reprogramming and inhibitor-induced P38 pathway-independent cytokine production with time. This analysis was designed to ask the question: Will administration of ATI-450 for 12 weeks in RA patients result in a sustained inhibition of pro-inflammatory cytokines? Blood was analyzed from RA patients on day one of dosing and day 84 of dosing following ex vivo stimulation with LPS and evaluated for the ability of ATI-450 to inhibit TNF-alpha and IL-1 beta compared with placebo. Focusing on the third and fourth bars in each group, the data clearly demonstrates that ATI-450 almost completely inhibits TNF-alpha on the left on day one, and that inhibition is maintained through day 84. Similarly on the right, ATI-450 inhibition of IL-1 beta is comparable on day one and day 84. This analysis provides evidence that inhibitor-dependent pathway reprogramming is not observed with the MK2 inhibitor ATI-450 over 12 weeks of dosing, and a durable inhibition of inflammatory cytokines is observed consistent with the durable reduction of CRP that David talked about. On Slide 21, we turn to look at the impact of ATI-450 on endogenous cytokine levels in plasma from these RA patients across the 12-week dosing period. Three pro-inflammatory cytokines from the 13-plex analyzed are shown on this slide, TNF-alpha, IL-6, and IL-8, along with the chemokine MIP-1 beta. The data are expressed as mean percent change relative to pre-dose levels for drug-treated patients. Samples were evaluated at trough drug levels after four, eight, and 12 weeks of dosing, as well as peak levels four hours after the final dose on day 84. The horizontal line describes analyte levels in plasma from normal subjects. TNF-alpha concentrations are significantly reduced after four weeks of dosing, and this reduction is maintained through the 12 weeks and approaches levels of the cytokine present in healthy volunteers. Similarly, IL-6, IL-8, and MIP-1 beta levels are reduced at week four, and this reduction is maintained through the 12 weeks of the study. This analysis provides additional supportive evidence consistent with the data presented thus far, demonstrating durable anti-inflammatory activity of ATI-450 in RA. I'll pass back to David to Slide 22 to describe the safety. Thanks, Joe. Here on 22 are the adverse events that were reported in the study. The drug was generally well-tolerated, and we had no serious adverse events or any severe events either. This slide shows the adverse events that were reported by at least one subject. We had no reports of dizziness in the study. I'll leave that there to let you read that while I tell you about the withdrawals that we had during the study. One subject in the ATI-450 group had a CPK elevation that was associated with palpitations at the study visit. As a result of that combination, the investigator elected to hold drug and refer to a cardiologist. The cardiologist completed a thorough evaluation of the subject and excluded an acute cardiac event. We could have reentered the subject to the study, but he'd been off drug for over one week by the time of the assessment, so we elected not to. One subject in the placebo group required a steroid injection for a musculoskeletal event. Since that was a prohibited medication, we withdrew that subject. As you can imagine, we're very pleased with the results of 201. We believe that this study supports our belief in the potential for 450 to treat immunoinflammatory diseases. I'd like to shift gears now, beginning on slide 24. Given that ATI-450 was well-tolerated at 50 mg BID, we decided to conduct an additional MAD study exploring doses higher than 50 mg BID. As a reminder, Study 101 demonstrated that 450 was well-tolerated with good kinetics up to 50 mg BID. We also established that 50 mg BID achieved trough drug levels above the IC80 for TNF-alpha, IL-1, and IL-8, and above the IC50 for at least part of the dosing interval for IL-6. In the 102 study, we replicated the MAD component of 101 with doses of 80 mg BID and 120 mg BID. The cohorts had eight active and two placebo patients each, which were the same size as Study 101. Slide 25, presents the PK profile of both studies combined. We see nice dose proportionality between 10 mg and 80 mg BID, but not much increased exposure as we move to 120 mg BID. The half-life of 450 in all treatment arms was between nine and 14 hours, suggesting that 450 has potential to be a once-daily drug. The cytokine data from this study is very interesting, and I'd like to pass back to Joe to lead you through that. Thanks, Dave. Going to slide 26. The data on the next three slides summarize the pharmacodynamic marker analysis from the combination of all the MAD cohorts from both the 101 and 102 studies, evaluating ATI-450 at five different doses from 10 mg to 120 mg BID, along with placebo in volunteer subjects over seven days. Blood from these subjects was collected at the indicated times, ex vivo stimulated with LPS, and analyzed for key biomarkers. The data on the left shows level of target biomarker phospho-HSP27 and the inflammatory cytokine TNF-alpha following seven days of dosing at peak drug levels, four hours post-dose, and trough levels 12 hours post-dose, relative to the day one pre-dose. A near complete inhibition of both markers is observed at day seven, four hours post-dose, and the inhibition is maintained across the 12-hour dosing interval. The dose dependency of ATI-450 at four hours post-dose is shown on the right. The 50 mg dose used in the RA study is the third to last bar. An incremental increase in biomarker inhibition is observed with the two higher doses of 80 mg and 120 mg evaluated in the MAD 102 study. On slide 27, the inflammatory cytokines IL-1 beta and IL-8 were analyzed. A comparable dose-dependent and sustained inhibition was observed across the dosing interval on day seven, with incremental increased inhibition in the highest dose groups. Finally, on slide 28, IL-6 demonstrates the same pattern with sustained inhibition across the dosing interval observed with the highest dose groups. Taken together, these data demonstrate the potential of doses higher than the 50 mg dose used in the current RA study to treat patients with autoimmune and chronic inflammatory diseases. P38 is known to modulate the anti-inflammatory cytokine IL-10, thereby potentially limiting inhibitor anti-inflammatory efficacy. Shown on slide 29, we evaluated the impact of ATI-450 in IL-10 production. Analysis of the blood taken from subjects in the 80 mg and 120 mg phase I MAD cohorts on day seven, four hours after the final dose was carried out following ex vivo LPS stimulation to evaluate the impact of ATI-450 and IL-10 levels relative to the pro-inflammatory cytokines TNF-alpha and IL-1 beta. In contrast to the near complete inhibition of TNF-alpha and IL-1 beta, the middle and right set of bars, IL-10 on the left is only inhibited approximately 30% at these high doses. These data suggest that, one, ATI-450 strongly favors inhibition of pro-inflammatory cytokines relative to anti-inflammatory cytokines, in contrast to what has been hypothesized for P38 inhibitors. Two, selectivity for the pro-inflammatory cytokine inhibition is maintained with ATI-450 at these high doses and corresponding exposures. Finally, on slide 30, we ask the question: How effectively does ATI-450 inhibit cytokines induced by a different ex vivo stimuli, potentially more relevant to autoimmune disease? For this analysis, we utilized IL-1 beta stimulation in parallel with the LPS stimulation, as IL-1 beta is a cytokine that has demonstrated involvement in chronic inflammatory diseases such as RA. The data presented is a comparison of ATI-450's efficacy for inhibiting three key cytokines, TNF-alpha, IL-6, and IL-8 following ex vivo stimulation with either LPS or IL-1 beta of blood from subjects dosed for seven days with 80 mg or 120 mg of drug BID. Compared with the pre-dose in placebo, similar high levels of inhibition are observed with TNF-alpha on the left-hand panel with both stimuli. Interestingly, comparable or potentially greater ATI-450 inhibitory efficacy is observed for IL-6 in the center and IL-8 on the right following IL-1 beta stimulation compared with LPS stimulation. These data provide confidence that inflammatory cytokine regulation by ATI-450 is not stimulus-dependent, and that this inhibitor may have broad applicability across inflammatory diseases. Dave will now describe safety in this study. Thanks, Joe. Slide 31 reports the adverse events in the 102 study. The safety of doses up to 120 mg appear to be good with no dose-limiting toxicity. We saw no serious adverse events or labs that were of concern in this study. There are more patients with dizziness in the 120 mg group, and that was generally a lightheadedness that has coded to dizziness. It was mild and didn't stop any day-to-day activities. In all six subjects in the 120 mg cohort, the dizziness resolved while still taking drug. If this is a true drug effect, it's something that we could warn patients about as a transient early event. As I mentioned earlier, we didn't see any dizziness or lightheadedness reported in the RA study. The headaches all happened in the first two days of dosing and were not seen after that. In conclusion, on slide 32, I think we've achieved what we set out to deliver. The ATI-450 delivered durable efficacy as defined by DAS28 reduction, the joint scores, and the ACR responses, which improved early and continued to improve over time. Our original aim to reduce CRP by at least 25% from baseline was exceeded. The disease activity scores that were achieved, the ACR 20, 50, 70 of 60%, 33%, and 20% represent important improvements in RA with a magnitude of response that you would hope to see. The additional phase I data allows us to explore higher doses in the next stage of development. We firmly believe that we've delivered the data to provide confidence to move into the next stage of development of ATI-450. We've already started our phase IIB plans, and we're moving forward with this program. I'll now pass back to Neal for concluding comments. Thank you, Dave, and thank everyone for joining us today. There are a lot of reasons to be excited about ATI-450. First, it's a new mechanism, and we're first in class. Second, it's an oral that targets cytokines traditionally targeted by biologics. Third, because we hit more than one key cytokine, we have the potential for a synergistic effect. Fourth, there's potential for daily dosing, given the half-life that we've already demonstrated across all of our studies. Fifth, this is an opportunity to have a pipeline in a product. There are numerous indications that one can go after when you look at the targets that we're suppressing. Lastly, what we have demonstrated thus far is what we believe to be a favorable safety profile. As such, we believe we have an important new therapeutic for the treatment of not only RA, but a wide variety of diseases that are driven by TNF, IL-1, and IL-6. We are very excited to move ATI-450 to the next stages of development. I would really like to thank our team in both St. Louis and Wayne for all of the hard work, particularly during these challenging times. At this point, I'll pass it off to Shannon, who can poll for questions. Thank you. As a reminder, to ask a question, you will need to press star one on your telephone. To withdraw your question, please press the pound key. Please stand by while we compile the Q&A roster. Our first question comes from Louise Chen with Cantor Fitzgerald. Your line is open. Hi. Congratulations, and thanks for taking my questions here. I had a few. First question I had for you is what type of efficacy and safety do you think you might see in the higher doses, the 80 and 120, and as you extend over 12 weeks of treatment? Second question I had is, in addition to this once-a-day dosing, what other potential competitive advantages do you see? For example, can it be used in combination? Are there any read-throughs to any of your other studies that are happening and ongoing? The last question I had is, if your drug is approved, where would it fit into the treatment paradigm with biologics and JAKs that are already approved? Thank you. Okay. Thanks, Louise. Appreciate the question. In terms of the positioning and the fit, there's still a lot of room within rheumatoid arthritis. There's obviously been a lot of great advancements in the space, and we see opportunities given the profile, the relative efficacy, and safety that we've already demonstrated to look at not only potentially monotherapy or earlier treatment of disease, but also combo treatment, particularly given the safety profile. I think it's pretty well known that polypharmacy is the rule in this indication, and we haven't even begun to tease out those patients who rotate off of TNF-alphas. It used to be that patients would go from one TNF-alpha to the next, and there's a lot of cycling or churn in this disorder. Certainly, patients end up being on multiple medications. I think we've seen with the launch of RINVOQ that there's actually been a lot of switching from the TNFs into JAK inhibitors, in particular because of the oral dosing. I think, the oral dosing is a big advantage, the ability to potentially do QD. The relative safety profile and also looking at the ability to hit multiple cytokines. Often when you look at some of the biologics, they target one particular cytokine, and we're obviously hitting three of them quite potently. We believe that there is a synergistic effect there. In terms of your first question on the efficacy and safety, higher doses and extending the time period. That's exactly why we want to include the PK/PD information in this deck. We certainly believe that the safety profile and the incremental suppression of cytokine supports going higher. We've got a lot of headroom. In this study, we looked at 50 mg BID, and we clearly demonstrated that we can go up to 120 mg BID. In terms of your question about longer treatment, obviously, if you look at the graphs, the curves keep going down. We're assuming that there'll be continued improvement over time. That remains to be seen. We have to do the work. Certainly all the trends look like that would be the case, and we're excited to proceed to the next levels in those studies. Thank you. Thank you. Our next question comes from Tim Lugo with William Blair. Your line is open. Thanks for taking the question. Congratulations on the data. Really impressive work. With tachyphylaxis, obviously, normally the issue in this pathway, it seems like we're seeing a deepening of responses in almost all the clinical measures. Can you maybe just discuss the length of the next Phase IIB and how you'll explore beyond 12 weeks? For the next study, I know you're figuring out as we speak, can you just briefly talk about doses? It looks like 80 mg BID is nice and clean and some additional cytokine suppression. Incrementally, I'm not sure the cytokine suppression data at 120 mg looks to be significant over 80 mg, it does seem like you have this dizziness signal. Can you just maybe talk about those? Sure. Taking that last question first. Just as a reminder, we saw no dizziness at all in the 12-week- Okay RA study. Certainly it was in the phase I unit. Not sure what to make of that since it is quite transient and didn't interfere with any activities. It didn't interrupt dosing. Again, in a more real-world study, we didn't see it at all. I'm not particularly worried about that in the least. I think from my perspective, the RA study trumps what we saw in the phase I unit. In terms of the deepening of responses at 12 weeks. As we continue our program, and we're in that process of getting the design of this study all wrapped up, and it's certainly going to be 12 weeks, and we'll also look at open label extension portions of it. That's not been totally decided, but I think it would behoove us to continue to press the duration of treatment here. We look forward to rolling out a comprehensive Phase IIB program in the near term. This will be, I think, a traditional multi-arm study where we're looking at a few different doses and potentially also exploring the QD dosing aspect. Okay. Maybe briefly, can I just hear your updated thoughts around business development? I assume there's going to be a number of larger companies also intrigued by the data. Can you just remind us what an ideal partner would look like for developing this asset? If you want to just push it through Phase IIB, where you could build even more value given the strength of today's data. Yeah. As you can imagine, we don't typically comment on BD. I think, looking at the breadth of indications that one can go after with this molecule, given the fact that we potently inhibit TNF, IL-1, and IL-6, I do think that exploring different partnerships is an option on the table. But at the moment, we're continuing to operate with moving the Phase IIB forward. Great. Thank you for the questions, and congratulations again. Thank you. If you wish to ask a question at this time, please press star then one or you touch on telephone. Our next question comes from Thomas Smith with SVB Leerink. Hey, guys. Good morning. Thanks for taking our questions, and congrats on the data. First, I guess a couple of questions on the RA data set. I understand you're still in the process of analyzing the data, but can you comment at all, I guess, even qualitatively on some of the imaging data you've collected? Then, on the one ATI-450 patient withdrawal, can you just comment, did this patient have any history of palpitations, or was the patient on any background meds, or were there any other notable confounding factors with this particular patient? Sure. We don't have the MRI data yet, so I can't comment on that. As a reminder, that was predominantly used as a screen-in tool. Because we wanted to make sure that the patients who were screened in actually had active disease. That encompassed both inflammation of the synovium, but also pretty good joint erosion. As Dave mentioned earlier in our presentation, these were pretty hard-to-treat patients. You can imagine the joints were pretty advanced. We look forward to presenting that in a future publication. Regarding the other patient, I'll hand that off to Dave to just describe that patient and that withdrawal. Yeah. Thanks. That patient, I think he was 61. He did have some elevated lipids coming into the study, but was otherwise pretty fit and well. He did have the palpitations and the elevated CPK that led to the cardiologist referral. He had a thorough workup by the cardiologist, as I said, discharged from having any cardiac event. Just to maybe additionally reassuring was that when we assessed the CK-MB portion of the CPK elevation, it confirmed that the elevation of the CPK was not coming from the myocardium. It was musculoskeletal. I think he was slightly elevated at baseline when he came in, he didn't go more than between three and four times baseline. When you speak to rheumatologists in the area, they'll describe that as being a very typical finding that you look at in these patients. There wasn't any cardiac event here. Got it. Okay. Yeah, appreciate the additional color. I guess also in the initial SAD MAD study, you noted a decrease in absolute neutrophil count. Can you comment on patient neutrophil levels in this study? Yeah. I looked at the neutrophils in all the individual patients. There is a little bit of a trend in a decrease in neutrophils as you'd expect. I think it's in keeping with the pharmacodynamic effect of the drug. No one became neutropenic in the study. No one dropped to levels of neutrophils that would have been of any clinical concern. Okay, great. Well, thanks for the additional color and congrats again on the data, guys. Thank you. I'm currently showing no further questions at this time. I'd like to turn the call back over to Neal Walker for closing remarks. Well, thanks everybody for joining us. Obviously, as I mentioned before, the team is thrilled. I want to again thank our team, the patients, the investigators who participated in this trial, particularly during a pandemic. It wasn't easy. We were able to get this study done right on schedule, and we really appreciate everybody's patience with us and look forward to next steps. Thank you. Ladies and gentlemen, this concludes today's conference call. Thank you for participating. You may now disconnect.