Thank you for standing by, and welcome to Celldex's phase II PN Data Call. Currently, all participants 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 one on your telephone. To remove yourself from the queue, you may press star one one again. I would now like to hand the call over to Sarah Cavanaugh with Celldex. Please go ahead. Thank you. Good afternoon, and thank you for joining us to discuss the results from our phase II barzolvolimab study in prurigo nodularis, or PN. Joining in the call today are Anthony Marucci, Co-founder, President, and Chief Executive Officer, Dr. Tibor Keler, Co-founder, Executive Vice President, and Chief Scientific Officer, Dr. Diane Young, Senior Vice President and Chief Medical Officer, and Teri Lawver, Senior Vice President and Chief Commercial Officer. Please note the slides for today's call are available on the investor relations section of the website. Before we begin our discussion, I'd like to direct your attention to slide two with respect to information regarding the forward-looking statements that today's speakers will be making. Please be advised that a question-and-answer period will be held later in this call. I'd now like to turn the call over to Anthony on slide three. Thank you, Sarah, good afternoon, everyone. Thank you for joining us. Today, we are reporting barzo's results from our fourth indication, a phase II study in prurigo nodularis, or PN. PN is a chronic itch-driven skin condition with a highly symptomatic patient population. At Celldex, we're leading important science in the exploration of mast cell biology with the goal of delivering life-changing therapies for patients with allergic, inflammatory, and autoimmune diseases. We have repeatedly demonstrated barzol's ability to profoundly deplete mast cells in best-in-disease data observed in three indications to date: chronic spontaneous urticaria, symptomatic dermographism, and cold urticaria. All of these showed unequivocal phase II data and progressed quickly to phase III development. Our interest in understanding if mast cell depletion can provide clinical relief for patients with serious diseases and data from our phase I proof-of-concept study in PN supported the initiation of the phase II study. We are disappointed to share that the trial did not meet the primary or secondary endpoints. Results from this study clearly showed profound systemic depletion of mast cells, as evidenced by the reduction in serum tryptase. Unlike our intravenous phase I study, this phase II subQ study did not result in improvements in itch or skin lesions for patients, indicating that mast cells may not be the key pathogenic driver of symptoms in PN. Because of this outcome, we are discontinuing the phase II trial in PN and will direct our resources to the remainder of our present and future portfolio. We remain focused on driving mast cell category creation and delivering on barzolvolimab's promise for patients, particularly in our three ongoing phase III urticaria studies, which we expect to share top-line data in the September-October timeframe. Before I turn the call over to Diane to walk you through the data, I'd like to extend our gratitude to all the patients, investigators, and site staff around the world who participated in this trial and supported the advancement of mast cell science. Diane will walk you through the results we have to date, and at the end of the call tonight, we will answer as many questions as we can. As a reminder, this is a top-line analysis with additional work still to be done. I will now hand the call over to Diane. Thank you, Anthony. Before we review the data, let's spend a little time discussing this difficult-to-treat indication. Prurigo nodularis is a chronic inflammatory disease. Patients are often covered with hard, itchy skin lesions. The intense itching causes scratching to the point of bleeding and pain, and the scratching, in turn, can cause more skin lesions, perpetuating the disease cycle. PN is further complicated because it is often associated with a range of systemic comorbidities, including chronic kidney disease, metabolic disorders, HIV and tuberculosis infections, hepatic disorders, and autoimmune diseases. Patients with PN have also been shown to have increased rates of multiple cardiovascular comorbidities, including heart failure. Not surprisingly, given the relentless itching, patients frequently also exhibit psychiatric comorbidities such as depression, anxiety, and obsessive-compulsive disorder, further complicating management. While there has been progress in this space with the introduction of recently approved biologic therapies for prurigo nodularis, there is still a significant unmet need. As we explored the science of chronic itch, it became increasingly clear that investigating a mast cell-depleting agent was warranted in prurigo nodularis. Evidence indicated that mast cell interaction with sensory neurons is involved in the amplification of chronic itch and neural inflammation and could play an important role in the scratch-itch cycle. Additionally, studies have shown that mast cell numbers are increased in PN lesions. We conducted a small 23 patient phase I-B study with intravenous barzolvolimab and saw positive results across both itch reduction and nodule resolution at the highest dose tested, and that merited additional exploration in a robust phase II study. Turning to slide four, I will first walk you through the phase II study design. This was a randomized, double-blind, placebo-controlled, parallel group study that evaluated the efficacy and safety profile of two dose levels of barzolvolimab administered subcutaneously compared to placebo in patients with moderate to severe PN who had inadequate response to prescription topical medications or for whom topical medications were medically inadvisable. 140 participants from six countries and 48 sites were randomly assigned on a one-to-one-to-one ratio to receive placebo or barzolvolimab injections of either 150 mg or 300 mg every four weeks after an initial loading dose of 450 mg during a 24-week treatment phase. Participants then entered a follow-up phase with no treatment for an additional 16 weeks through week 40, with an option to enter an open label extension. The primary objective of this study was to evaluate the clinical effect of barzolvolimab compared to placebo on itch response, as measured by the proportion of participants with greater than four-point improvement in the worst itch numeric rating scale at 12 weeks. Key secondary objectives include itch response compared to placebo at different time points, the assessment of skin lesions as measured by the investigator global assessment, and safety. The primary analysis was conducted after all patients had completed the 24-week placebo-controlled treatment period. On slide five, you will see a table of baseline characteristics for this highly symptomatic patient population. Demographics and baseline disease characteristics were generally well-balanced across treatment groups and consistent with other clinical studies in PN. As expected in this indication, patients on study tended to be older and had highly symptomatic, moderate to severe disease. The next slide six, shows the results for the primary endpoint, the percentage of patients who had greater than four-point improvement in their worst itch numeric rating scale. The worst itch numeric rating scale is a single item patient-reported questionnaire that measures itch intensity over the previous 24 hours. The scale ranges from zero, indicating no itch, to 10, indicating worst itch imaginable. Patients in this trial at baseline had a mean worst itch numeric score of greater than eight. As you can see here, patients treated with barzolvolimab did not have differentiated responses compared to placebo across either dose or at any of the time points. Similarly, on slide seven, we show key secondary endpoints, including the Investigator's Global Assessment for Chronic Nodular Prurigo - Stage, which is a five-point clinical scale that dermatologists use to measure the severity of prurigo nodularis. It evaluates the number and appearance of palpable skin nodules to gauge disease severity. There is also a secondary endpoint that looks at both worst itch and Investigator's Global Assessment combined. Across these endpoints, barzolvolimab did not demonstrate differentiation compared to placebo. Based on these outcomes, we are in the process of discontinuing the phase II study in prurigo nodularis. We just received these data, we have more work to do to understand the discrepancy between our phase I-B and phase II studies in this indication. While the patient characteristics across the two studies were similar, the phase II study certainly included a much larger sample size. The route of drug administration was also different, from IV in the phase I-B to subQ in the phase II. IV administration is associated with more rapid and higher drug concentrations relative to subQ. We can't rule out that these differences may have contributed to the difference in outcome. However, both studies achieved profound decreases in circulating tryptase. We have biopsy samples that may give us better insight. We will analyze the biopsies from this study in the coming months as we believe this information will increase our learnings. Our current assessment of the available data suggests that mast cells may not be a key pathogenic driver of symptoms with prurigo nodularis. At this time, we are not planning to move forward with further development in PN. If new data or new science changes our thinking, we are open to exploring this question in the future if it makes sense. For now, we are focusing on indications of higher priority. While we are disappointed that this study did not confirm the promising signal we saw in our phase I-B study, we are really pleased with these new data that further support the favorable safety profile we have observed to date with barzolvolimab. The 450 mg loading dose, followed by the 300 mg Q4W dosing regimen, achieved the highest subcutaneous exposure studied to date. Slide eight provides a summary of the top-line safety data. Overall, barzolvolimab was well tolerated. We are very pleased with the safety profile demonstrated in this phase II study, which remains entirely consistent with our prior studies. At these dose levels, and in an older patient population with high comorbidity burden. As noted on the slide, there was a single serious adverse event reported by an investigator as treatment-related and described as aseptic meningitis. We strongly disagree with the investigator's assessment, and our conclusion was also supported by the independent data monitoring committee. The clinical symptomatology does not support the investigator's assessment. There were no typical clinical signs suggestive of this diagnosis, such as headache, neck pain, or fever. This 65-year-old female patient had a primary complaint of chest pain and weakness, which began three weeks after completing her barzolvolimab treatment. She had an extensive workup over a four-week period, which ruled out cardiac, pulmonary, and GI causes, and subsequently, neurologic diagnoses were considered. Her cerebrospinal fluid showed mild lymphocytic infiltration with normal protein and glucose, which is not typical with meningitis. Steroids, antiviral therapy, and antibiotics were administered, and the patient made a full recovery. We believe the time course, lack of symptoms, and spinal fluid findings suggest this is more consistent with neuroinflammation related to a viral infection and is not related to study drug. 11 patients, including two patients on placebo, discontinued treatment due to an adverse event, five considered related to treatment and six considered unrelated. Urticaria, related, and worsening prurigo, unrelated, occurred in two patients each. The other events occurred in single patients and were in line with what has been seen in prior studies, with one exception. One death, cardiac failure, which was assessed as not related to treatment by the investigator sponsor and the data monitoring committee, was reported on study. This was in a 73-year-old man with multiple concomitant cardiac risk factors at baseline, including diabetes, hypertension, obesity, coronary artery disease, heart failure, COPD, and low baseline oxygen saturation. As a reminder, the PN population is an older population with high comorbidity burden, and as such, it is not uncommon to see serious adverse events that are not related to treatment. When we look across the totality of the safety data in the study, we see a safety profile that is very much consistent with our other studies. Looking to the bottom of the table, the most frequently reported adverse events observed in more than 10% of participants in any treatment group were hair color changes and nasopharyngitis, all of which were Grade 1 and Grade 2. Overall, we are encouraged by the consistent safety profile we have seen with barzolvolimab in this trial, where we explored the loading dose and four-week dosing regimens. These data give us continued confidence in the overall safety profile and particularly in the ongoing phase III studies in CSU, ColdU, and symptomatic dermographism, which also include the loading dose. I will now hand the call back to Anthony, who will wrap things up. Anthony? Thank you, Diane. Turning to slide nine. While we are disappointed that the study did not confirm the promising signal that we observed in the phase I-B, we are proud of our progress and continued execution. As leaders in mast cell biology, we are committed to delivering life-changing therapy to patients in need. The learnings from this study are important for the future of the Celldex pipeline across not only barzolvolimab, but also CDX-622 and additional candidates in development. The new data presented today continue to build barzolvolimab's highly differentiated profile. While expected, it was reassuring to see that the loading dose combined with four-week dosing demonstrated a favorable safety profile consistent with our prior studies and drove rapid declines in tryptase, which positions us well for our ongoing phase III studies. In closing, barzolvolimab has significant potential to become a transformational medicine for patients, we are focused on driving mast cell category creation and delivering on barzolvolimab's promise, executing on ongoing trials, and continuing to explore diseases of high unmet need where barzolvolimab could play a role. We look forward to sharing additional important information about barzolvolimab in the coming months. We expect we will be in a position to report data in both the EMBARQ CSU phase III studies in the September/October timeframe. As previously shared, we anticipate a readout of the phase II data in AD late fourth quarter. In addition, we look forward to sharing more about our broad life cycle development plans for barzol later this year as well. We appreciate your support and look forward to answering your questions tonight. As a reminder, these are top-line results, and we are still reviewing the data. We will do our best to answer your questions, but may need to follow up at some point. Operator? Thank you. As a reminder, to ask a question, you will need to press star one one on your telephone. To remove yourself from the queue, you may press star one one again. We ask that you please limit yourself to one question and one follow-up to allow everyone the opportunity to participate. Please stand by while we compile the Q&A roster. Our first question comes from the line of Thomas Smith of Leerink Partners. Your line is open, Thomas. Hey guys, good afternoon. Thanks for the updates here, thanks for taking our questions. Just first on safety, just wondering if you could provide a little more color on the clinical course for the aseptic meningitis case. Was there any neutropenia observed with this patient? Were there any other confounding factors? It sounds like the patient made a complete recovery, which is good, any other findings you can add from the data monitoring committee review for this patient? Sure. Diane? Yeah. As I said, we don't agree with the investigator on the diagnosis of a causality. As I described, the patient did not have any symptoms consistent with that diagnosis. They did have an extensive workup, as I outlined in the description, ruled out many different other causes. We think that the clinical picture of the chest pain, which really went on for weeks, as well as the modest increased cells in the CSF, really indicates some sort of neuroinflammatory process, most likely due to a virus. They did not have any neutropenia. The patient had absolutely no neutropenia throughout the course. As a follow-up, can you just comment directly, were there any hypersensitivity or anaphylaxis events observed in this study? Then just maybe as a last question, could you just remind us from the phase III CSU program, the timing and outcome of your latest data safety monitoring board committee and any potential read-throughs from this PN study to the CSU program? Thanks so much. In terms of hypersensitivity, there were no cases of anaphylaxis in the study. There were two patients who discontinued treatment for urticaria. One was Grade 3, one was Grade 2. They responded to medications. In terms of the phase III CSU, we're having regular meetings with the data safety monitoring committee. There's nothing particularly there. We do not believe that there is a read-through from these results today to that. Those studies are really supported by very robust phase II studies, both in CSU and in PN. I would say that from the standpoint of this study, so we have no concerns about efficacy. We feel, if anything, that this study, the safety profile really looks great, even with using the higher dose. We feel that that reads through well to all of our indications. Super helpful. Thank you, guys. Appreciate the update. Thank you. Our next question comes from the line of Yaron Werber of TD Cowen. Your line is open, Yaron. Also, the question on, in terms of some of the read-throughs, maybe to atopic dermatitis. I know obviously each condition is very distant from the other, but maybe just remind us the biological support for running the AD study. Secondly, just on the CSU study, can you give us maybe a little bit of a sense on the DSMB side, what are they looking for in terms of? We get a lot of questions as to what are elements that DSMB is looking for that would drive potentially changing the study in any way. I know you obviously enrolled extremely quickly and six months ahead of schedule. Thank you. In terms of the DSMB, there's really nothing particular. They have a charter. They review all the safety in a blinded fashion on an ongoing basis and advise us on things that we need to do with the study, there is nothing particular. We also have the adjudication committee. Yeah. The adjudication committee. All that's in place, Yaron, and it's been pretty consistent since we started the program in phase I, nothing's changed. To your first question, Yaron, regarding the read-through to atopic dermatitis and/or rationale there. Certainly, those indications share some of the components of the pruritic disease, and that was the basis for some of our rationale to move into atopic dermatitis after we had the phase I-B data in PN. However, they are different patient populations. Mast cells are known to contribute to other parts of the inflammatory process in atopic dermatitis, and we certainly plan on completing the atopic dermatitis study and look forward to the readouts and the learnings from that study, as we do appreciate that it's a different indication despite that they do share components of the role of mast cells in driving the pruritic itch part. Yaron, do you have another question? No, that's perfect. Thank you. Okay. Thank you. Our next question comes from the line of Iris Gao of Guggenheim. Please go ahead, Iris. Yeah. Hi, everyone. Thanks for taking my question. Mine would also be on safety. I wonder if you can give more colors on the frequency of neutropenia and skin hypopigmentation from this study, specifically in the 150 mg group. Also how soon was onset and stuff like that. Thank you. As I said, we're very pleased with the safety data in this study. We had a low incidence of neutropenia, it was below the 10% threshold that we are showing in the table. All the neutropenia were Grade 1 and Grade 2. There was no association with infection. There was one discontinuation for neutropenia, which was Grade 2. As far as the hypopigmentation, there were two cases, one on placebo and one on drug. Yeah, thank you. Is there any more color on the onset of the skin hypopigmentation? Like, do you know how long it took for them to show up? The skin hypopigmentation occurred, for the barzolvolimab patient, occurred at about the six-month time point. Thank you very much. Appreciate it. Yep. Thank you. Our next question comes from the line of Kristen Kluska of Cantor. Your line is open, Kristen. Hi, everyone. Thanks for taking the questions. First, I wanted to ask if any of the patients presented with comorbidities where you were able, in a non-direct measurement way, able to see any effects. Second, recognizing you're still digesting this data, I'm wondering if you're thinking about any thesis where this could be a potential candidate to further look at with a bispecific in the future, especially considering there is a Type 2 inflammation component to PN. I can answer. We're going to look at questions like comorbidities and do we have any anecdotal evidence in the study as we do in all our programs. It's a little difficult because in the inclusion/exclusion criteria, you tend to want people that are fairly well controlled for their other comorbidities. We will look and I will let Tibor answer the question about bispecific. Sure. Certainly, we look at all the learnings that we get from our studies with barzolvolimab as helping us understand the role of mast cells and how that affects our pipeline development. Kristen, we obviously consider the option, the possibilities of bispecifics in the future. That's something that as we dig through this data deeper, once we have all of that data in-house, we will look into very carefully. Yeah. Kristen, we're also looking at biopsies that we've taken on study. We'll be analyzing those and comparing them to the phase I-B biopsies since that was IV and this was subQ, see what we can learn from that analysis as well. There's a lot of stuff we still need to do. I mean, we just got these data in a few days ago. Certainly as we learn more, we'll communicate that out to everybody. Thank you. Our next question comes from the line of Sam Slutsky of LifeSci Capital. Your line is open, Sam. Hi, this is Oliver McCammon on for Sam Slutsky. Thanks for taking my questions. First one for me is just as you think about mast cell biology post the urticaria, PN, and EoE randomized readouts, how are you thinking about indication expansion going forward and generally the speed of indication expansion for barzolvolimab and CDX-622? Then I have one follow-up as well. Yeah. We'll discuss more about where we're going in 2027 with barzo later on this year. There are several indications that we're looking at, we would imagine starting those studies up sometime in the first half of 2026 or early second half of 2026. Certainly, as we go through our criteria, it hasn't changed. We look at unmet need, we look at epidemiology, we look at the markets, we look at the ability to do studies and the probabilities of that. That hasn't changed. I think as we look through and as we learn more, we'll have more information to share with you. I think that we go through a pretty rigorous process. Certainly, also we try to learn. We know mast cells are implicated. What we're learning is that, especially in EoE and in now PN, on the subQ formulations, that does not meet our hurdle rates, it certainly doesn't have a big impact. We're looking to learn, we're looking to go back and take those learnings and move forward into new indications. We'll update you on where we're going later on this year on that. Got it. Thank you. Curious on why the aseptic meningitis patient received the lumbar puncture, basically trying to get a sense of maybe whether/why they were worked up for this. Thanks. As I said, the workup was Went on over many weeks. There were several hospitalizations for workup. They really had tests to rule out every possible cardiac, pulmonary, and gastrointestinal disease. In addition to the chest pain, the patient complained of some weakness and had some decreased reflexes. After doing all these other tests, they said, "Well, we should look at possible neurologic causes." That was what caused them to do the lumbar puncture as part of a big neurologic workup. Got it. Thank you again. Does that answer your question? Mm-hmm. That does. Thank you. Thank you. Our next question comes from the line of Derek Archila of Wells Fargo. Your line is open, Derek. Hi, this is Simona for Derek. Thank you for taking our questions. Just one from us today. How should we think about the relevance of serum tryptase as a biomarker moving forward? Are you able to share the magnitude of tryptase reduction achieved and whether maximal mast cell depletion was maintained through week- 12? Sure. I'll take that question. We believe serum tryptase has been a phenomenal biomarker to correlate with the clinical benefits of ORALSOL throughout the program and has correlated very well with what we've seen in terms of tissue depletion of mast cells. Currently, this does not change our view on tryptase. While we haven't given the exact numbers, we certainly see profound depletion with the majority of patients getting below detectable levels, which are maintained throughout the treatment period. Very, very profound impact on serum tryptase levels, which we believe converts to very good depletion of tissue mast cells. As Anthony mentioned, we do have some biopsies from the lesions of these patients, and we hope to gain some greater insight what's happening in these tissues. We'll certainly report that once we have those data. Thank you. Do you have a timeline on when you'll have that data or any possible upcoming medical meetings? No. We're still going through everything. As soon as we get it, we'll share it. Thank you. Thank you. Our next question comes from the line of Judah Frommer of Morgan Stanley. Your line is open, Judah. Yeah. Hi guys. Thanks for taking the question. I'm just curious if you have any updated thoughts, I know it's early, but just on drivers of the non-histaminergic itch here, I think beyond the well-validated cytokines from dupilumab and nemolizumab. Then just specifically, any thoughts on MRGPRX2 ligands and the role they might play given the update here. Thanks. Steve, where you want to take a shot at that? Yeah. I don't think we have thought about this quite a bit. As they mentioned, we received these data, which were surprising to us just a couple of days ago. We're still grappling with the differences between our phase I-B output and this study, which certainly raises questions about the role of mast cells in this indication. Yeah, it's not something we've really thought about to address your question about what other mechanisms can be at play and what the role of X2-mediated activation of mast cells might be. Perhaps after we do additional analyses, Judah, no, there's going to be analyses on a bunch of stuff and as we learn more, we'll be more than happy to share. We think this is important for the science going forward and for patients, anything that we can learn and share, we'll do so. Thanks. Thank you. Our next question comes from the line of Alex Thompson of Stifel. Please go ahead, Alex. Hi, this is Patrick Till for Alex. One quick question on the phase III CSU top line. I guess what exactly will be included? Are we only expecting to get the week 12 primary outcome, or will we get that full 24-week data set? You'll get 24-week randomized safety data with a 12-week primary endpoint. Again, it'll be top line, and we will save the full data set for a medical meeting. Thank you. You got it. Thank you. Our next question comes from the line of Andy Chen of Wolfe Research. Your line is open, Andy. Hi, this is Jason taking it for Andy. I just wanted to ask about drug exposure compared between phase I and phase II, since phase I was IV. We just wanted to ask in terms of the dosage for PN in phase II, did that change or was there anything accounted for when you guys went into dosages for phase II? Steve? Well, certainly, subQ delivery is going to give different kinetics of exposure than intravenous administration. While we get very good sustained exposure with our subQ regimens, you don't get that rapid high concentration exposure. Whether or not this could have contributed to the differences between our outcomes in the phase I-B or phase II is unknown. It's not something we can rule out at this time. Perhaps we'll learn a little bit more from the biopsy samples. Overall, as I mentioned before, we had very good tryptase reductions. We believe we have very strong mast cell depletion in the tissues, and our conclusion currently is that mast cells are not a driver in this disease based on the data we have. I see. Thank you. Thank you. Our next question comes from the line of Richard Law of Goldman Sachs. Your line is open, Richard. Hi, everyone. This is Tawani Uzam for Rich. Thanks for taking our questions. Could you share any thoughts as to why, based on the encouraging phase I-B data that we saw and the alternative lack of effect that we saw in phase II though, could the formulation change from intravenous to subQ have had any effect, and could it have any read-through ongoing trials are using the subcutaneous formulation? You are coming in and out. I'm sorry to make you repeat the question. Could you repeat it? Sorry about that. No problem at all. Yeah. I was asking if you could share any thoughts as to why, based on the encouraging phase I-B data with the IV formulation and then the alternative lack of effect to subQ, could that change in the formulation have had any effect, and could it have any read-through to other trials using the subcutaneous? Sure. The only change in formulation is really the concentration of the drug. I don't think formulation per se was in effect. The route of administration, as we've discussed, is something that we're still trying to understand. There certainly is precedent for some treatments where intravenous induction is optimal for effect. Whether that's a situation here or not, we don't know. We believe that with our subQ formulation, we are impacting the mast cells the way we expect to and certainly has led to dramatic effects in our clinical outcomes in a number of other indications. We still have some work to do with the biopsy samples here to demonstrate that, but we're quite pleased with our subQ formulation. Okay. Got it. Thank you. Just a follow-up, if I may. Is there any read-through, in your view, from these studies, as well as EoE, PN, to CDX-622, and could that drug work when Barzo didn't in these indications? We're again, still learning from these studies. If we don't believe that mast cells are a key driver, it's definitely not a high priority indication, where 622 is also working at least through the mast cell depletion as part of its mechanism of action. We be focused where there is clearly a role for mast cells, but that also includes other drivers in the case of 622, that being TSLP. Yeah, if we are finding out with Barzo that mast cells are not playing a critical role, that diminishes the potential for 622 in those same indications. Understood. Thank you. You're welcome. Thank you. I would now like to turn the conference back to Anthony Marucci for closing remarks. Sir? Thank you. Everyone, thank you for joining us tonight. We know this was short notice, and we appreciate all the time, the questions tonight. We look forward to coming back in a couple of months, September, October timeframe, to discuss our CSU readout. In the meantime, if there are any questions moving forward, don't hesitate to give us a call. Have a great night. This concludes today's conference call. Thank you for participating. You may now disconnect.