This conference call transcript was computer generated and almost certianly contains errors. This transcript is provided for information purposes only.EarningsCall, LLC makes no representation about the accuracy of the aforementioned transcript, and you are cautioned not to place undue reliance on the information provided by the transcript.
spk04: Good afternoon, ladies and gentlemen, and welcome to the 8th Higher Pharma First Quarter 2022 Conference Call. At this time, all participants are in a listen-only mode. Later, we will conduct a question-and-answer session, and instructions will be given at that time. As a reminder, this conference is being recorded for replay purposes. It is now my pleasure to hand the conference call over to Ashley Dunston, ATAR's Director of Investor Relations and Corporate Communications. Ms. Densiton, you may begin.
spk00: Thank you, Operator, and good afternoon, everyone. Thank you for joining us today to discuss ATAR's first quarter 2022 operating results and corporate update. We are joined today by Dr. Sanjay Shukla, our President and CEO, and Ms. Jill Broadfoot, our CFO. On the call, Sanjay will provide an update on our corporate strategy and including our clinical program for Exocetamol and our research and discovery programs in Neuropilin 2, including our preclinical program for ATYR 2810. Jill will review the financial results and our current financial position before handing it back to Sanjay to open up the call for any questions. Before we begin, I would like to remind everyone that except for statements of historical facts, the statements made by management and responses to questions on this conference call are forward-looking statements under the safe harbor provision of the Private Securities Litigation Reform Act of 1995. These statements involve risks and uncertainties that can cause actual results to differ materially from those in such forward-looking statements. Please see the forward-looking statement disclaimer in the company's press release issued this afternoon, as well as the risk factors in the company's SEC filings, and included in our most recent annual report on Form 10-K, subsequently filed quarterly reports on Form 10-Q, and in other SEC filings. Undue reliance should not be placed on forward-looking statements which speak only as of the date they are made as facts and circumstances underlying these forward-looking statements may change. Except as required by law, a tire farmer disclaims any obligation to update these forward-looking statements to reflect future information, events, or circumstances. I will now turn the call over to Sanjay.
spk06: Thank you, Ashley. Good afternoon, everyone, and thank you for joining us for our first quarter 2022 results conference call. We're very pleased with the start of 2022 as we work to develop a new class of medicines from our tRNA synthetase biology platform. Throughout the first quarter, we continue to make important progress with our F-sulfidamide clinical program in pulmonary sarcoidosis, our initial interstitial lung disease, or ILD, indication. With the receipt of FDA orphan drug designation for efsofitamide for sarcoidosis and a positive end of phase two meeting with the FDA, we are on track to initiate a planned registrational study in pulmonary sarcoidosis in the third quarter of this year. As we begin, I will summarize a few highlights since we last spoke in March. We announced that posters for efsofitamide in pulmonary sarcoidosis were accepted for presentation at the American Thoracic Society or ATS International Conference. We received FDA orphan drug designation for efsofetamide for the treatment of systemic sclerosis, or SSC, also known as scleroderma. We presented preclinical data in a poster at the American Association for Cancer Research, or AACR, annual meeting for ATYR2810, or 2810, our lead antineuropilin 2, or NRP2, antibody in cancer. We've had a highly productive first quarter and a good start to the year. The second quarter is shaping up to be a very important period as we prepare to present clinical data from the Phase 1b-2a study of F-sulfenamide in pulmonary sarcoidosis at ATS next week and anticipate the potential publication of a related manuscript. We're focused on operational preparation for upcoming planned registrational study. So the balance of the year may center upon initiating the study in the U.S. and Europe and supporting our partner, Cure and Pharmaceutical, with the anticipated launch of the study in Japan. Let's discuss our clinical program for efsofitamide first. Efsofitamide is a potential first-in-class immunomodulator for fibrotic lung disease. Efsofitamide is a novel FC fusion protein based on naturally occurring splice variant of the lung-enriched tRNA synthetase HARS fragment that downregulates average immune responses in inflammatory disease states. Epsifidamide has been shown preclinically to downregulate inflammatory cytokine and chemokine signaling and reduce inflammation and fibrosis. NRP2 is upregulated on key immune cells, known to play a role in inflammation, and is enriched in inflamed lung tissue. Epsifidamide binds selectively to NRP2 and, therefore, has the potential to normalize the immune system, serving to resolve inflammation and prevent progressive fibrosis. thereby stabilizing lung function and alleviating morbidity and mortality for patients. We're developing F-sulfidamide as a potential treatment for patients with fibrotic lung disease, initially focusing on patients with ILD, a group of rare immune-mediated disorders that can cause progressive fibrosis of the lung. Our initial ILD indication for F-sulfidamide is pulmonary sarcoidosis, which is an inflammatory disease characterized by the formation of granulomas or clumps of immune cells in one or more organs of the body. Sarcoidosis that affects the lungs is commonly called pulmonary sarcoidosis, and the lungs are affected in more than 90% of SARC patients. The formation of these granulomas is driven by persistent aberrant inflammation, which, if left untreated, can lead to irreversible scarring or fibrosis and diminish lung function, which may lead to respiratory failure or the need for a lung transplant. We estimate there are close to 200,000 patients with pulmonary sarcoidosis in the U.S., although estimates do vary. About half of these patients will require some form of systemic therapy, and 30% of all patients will have chronic progressive disease despite available treatments. The current standard of care typically includes treating the inflammation with corticosteroids and other immunosuppressive therapies, which can help manage inflammation and alleviate symptoms such as cough and shortness of breath. However, they have no demonstrated efficacy on disease progression and can result in serious long-term toxicity. Additionally, many patients do not respond to currently available treatments. There's a substantial need for safer, more effective treatments that could reduce or replace the requirement for chronic corticosteroid or other immunosuppressive therapy and prevent disease progression. Because this is an orphan disease and treatment options are limited, We applied for and received FDA orphan drug designation for efsofitamide for the treatment of sarcoidosis. We recently generated a clinical proof of concept for efsofitamide based on the positive results from a Phase 1b-2a study in pulmonary sarcoidosis that we reported in September 2021. The study, which included a forced steroid taper, demonstrated safety, tolerability, and consistent dose response for efsofitamide on key efficacy endpoints. and improvements compared to placebo, including measures of steroid reduction, lung function, sarcoidosis symptom measures, and inflammatory biomarkers. According to medical experts, this is the first randomized placebo-controlled trial of any therapy for pulmonary sarcoidosis that demonstrates effects on physiologic and quality-of-life measures concurrent with steroid reductions. These findings confirm the potential of esophidamide to be a tremendously impactful therapy. We're excited to present additional data from this study in two posters at ATS next week. Some of the clinical findings that we will present for the first time include greater details regarding steroid reduction and improvements in lung function. Notably, we will also present details of the biomarker data for the first time. The hallmark lung granulomas in patients with pulmonary sarcoidosis are comprised of immune cells that secrete pro-inflammatory chemokines and cytokines, and if left untreated, can promote aberrant inflammation both systemically and locally that lead to fibrosis. Standard of care agents such as oral corticosteroids can suppress inflammation, but may come with toxicity, and in some cases can oversuppress the immune system, leading to increased risks. The ability of F-sulfidamide to effectively control inflammatory and sarcoidosis disease biomarkers in a dose-dependent manner over 24 weeks in the context of a corticosteroid taper are very important findings, as they are the first demonstration of F-sulfidamide's anti-inflammatory mechanism in pulmonary sarcoidosis patients. We encourage you to review the posters, which will be available on our website once they are presented. During ATS, we also plan to host a company reception. The event will bring together sarcoidosis medical experts, principal investigators, advocacy organizations, analysts, investors, and members from ATAR's management team, providing an opportunity to learn more about our F-sulfenamide clinical program and the ways in which we can all work together to deliver a potential new treatment to patients in need. A presentation featuring leading sarcoidosis experts, Dr. Daniel Culver, Director of Diffuse Parenchymal Lung Disease at the Cleveland Clinic, and Dr. Robert Boffman, Emeritus Professor of Medicine at the University of Cincinnati, will review results from the Phase 1b-2a study and discuss the outlook for the planned registrational study. In addition to the posters at ATS, we also anticipate the potential publication of a related manuscript with the full results of the study in a major medical journal in the very near future. An additional abstract further exploring the molecular and cellular mechanisms of action of F-sulfidamide in sarcoidosis that was previously accepted for presentation at ATS will instead be submitted for inclusion at another medical conference later this year. As we mentioned, we've been busy preparing for the next stage of F-sulfidamide's clinical development in pulmonary sarcoidosis. We had a positive end of phase two meeting with the FDA that provided productive feedback regarding trial duration, dose evaluation to assess the optimal dose for chronic use, and endpoint prioritization, including discussion around outcome measures that would best support the evaluation of esophitamide's efficacy, including a combination of both objective and subjective clinically meaningful outcomes. Preparations for the study are underway, and we are on track to initiate this study in the third quarter of this year. While our primary focus for efsofitimod is on our planned registrational study in pulmonary sarcoidosis, efsofitimod's mechanism of action, compelling translational and clinical data, and the shared immune pathology in ILD strongly suggest that efsofitimod could have potential to treat other ILD indications as well. One such ILD that carries a high unmet need is an ILD that results from underlying systemic sclerosis, also known as scleroderma. Scleroderma is a chronic progressive autoimmune disease characterized by inflammation and fibrosis of connective tissues throughout the body. More than half of all patients with underlying scleroderma may develop ILD, which is the primary cause of death in these patients. Like sarcoidosis, SSC-ILD results from an uncontrolled persistent immune response, which if left untreated can result in scarring that permanently causes loss of lung function. Also like sarcoidosis, current treatment options are limited. The pathology of SSC-ILD is driven by the same immune cells that are central to sarcoidosis pathology. An NRP2-F-sulfidamide binding partner is upregulated on these cells, particularly on macrophages. Furthermore, efsofetamide has been shown to reduce lung and skin fibrosis in animal models of fibrotic disease, such as scleroderma and IPF, where it matched or outperformed approved known antifibrotic agents, including nintenatib and profenadone. Nintenatib was recently approved for slowing the rate of lung function decline in scleroderma ILD patients. but did not display any effects on the underlying disease or patient quality of life in those clinical trials. We believe our differentiated mechanism of action targeting NRP2 on immune cells has the potential to translate into benefit not only on lung function, but on the underlying disease as well. It's estimated that approximately 100,000 people in the U.S. are affected with scleroderma. We recently obtained FDA orphan drug designation for F-sulfidamide. for the treatment of scleroderma, which validates the antifibrotic effects of eslifidamide observed in those previously mentioned preclinical models of ILD. Now let's take a few minutes to discuss our preclinical programs, including 2810, an anti-NRP2 antibody in development for cancer. NRP2 is a cell surface receptor that plays a key role in lymphatic development and in regulating inflammatory responses. In cancer, NRP2 is upregulated on a variety of solid tumors and is particularly expressed in many aggressive cancers. Increased NRP2 expression is linked to worsened patient outcomes in several cancers, which may include the promotion of drug resistance to certain current therapies, such as chemotherapy or targeted agents, metastasis, tumor recurrence, and overall survival. 2810 is a fully humanized monoclonal antibody that selectively and functionally blocks the interaction between NRP2 and VEGF, one of its primary ligands. VEGF is a validated mediator of tumor survival and growth and correlates with tumor invasiveness and metastasis. Current therapies that directly target classic VEGF-VEGFR signaling do not block Neuropilin 2. Preclinical data suggests that blocking VEGF interaction through NRP2 that ATYR2810 may be an effective novel therapeutic antibody with a differentiated approach that can target aggressive cancers through the inhibition of metastasis and enhanced chemosensitivity. Last month, we presented some important findings at AACR that characterized the effects of 2810 in highly aggressive tumor subtypes. Research showed that highly aggressive cancers and those associated with metastasis including triple negative breast cancer, or TNBC, were responsive to treatment with 2810 in combination with chemotherapy. Importantly, treatment with 2810 alone is able to inhibit metastasis in models of TNBC, consistent with an emerging understanding of NRP2 slash VEGF signaling as a driver of metastasis and therapy resistance. Additional findings provided key insights regarding 2810's ability to impact the lineage plasticity of cancer cells, which contributes to their ability to differentiate into states that are known to play a role in metastasis. Notably, 2810 has been shown to downregulate ZEB1, a central regulator of these processes, in different model systems, including patient-derived organoids and patient-derived xenografts. The poster highlighted work that characterized the gene expression signatures of breast cancer cells that respond to 2810 treatment in combination with chemotherapy, paving the way for bioinformatic analysis that may help with clinical development design. We're in the process of completing the required work for 2810 to support its planned clinical development in oncology, and we expect to initiate a phase one study of 2810 in cancer patients in the second half of this year. I'll now turn it over to our Chief Financial Officer, Jill Broadfoot, to review our financial results.
spk02: Thank you, Sanjay. I'm happy to report that we ended the first quarter 2022 with $98.7 million in cash equivalents and investments. Research and development expenses were $8.9 million for the first quarter of 2022, which consisted primarily of product development and manufacturing costs for ESSO-FIDMOD and our 2810 programs. General and administrative expenses were $3.5 million for the first quarter of 2022. Common shares outstanding were approximately $28.1 million, and fully diluted shares were $29.2 million as of March 31, 2022. As we head towards the planned Registrational Study for ESSO-FIDMOD, we feel confident that with our current cash position of nearly $100 million, a clean balance sheet with no debt, and support from several high-quality, long-term focused investors, we are in a very good position to carry out our upcoming catalyst. Now I'd like to turn the call back over to Sanjay before we open it up to Q&A.
spk06: Thanks, Jill. As Jill mentioned, we feel like we are in a very good position amidst what I'm sure we can all acknowledge is a very challenging environment for biotech. We have an experienced management team in place and have actively been building out the team as our programs progress. We have clinical proof of concept data for a novel therapeutic for sarcoidosis, a rare disease that has limited to no treatments. We believe our clinical execution, which includes investing early in our manufacturing in order to have drug product available to meet timelines, puts us in a leading position to bring a transformative product to the market for this debilitating disease. Additionally, we have preclinical data and strong scientific rationale to expand this program to other ILDs, in addition to other preclinical pipeline candidates that are progressing. And finally, with our tRNA synthetase biology platform and strong intellectual property portfolio surrounding it, we have an opportunity to replicate what we've done with efsofitamide and one tRNA synthetase with some of the other tRNA synthetase gene families. For a company of our stage and size, we're well capitalized coming off an oversubscribed follow-on financing last fall and have been good stewards of our capital. We continue to take a deliberative approach to the programs that we choose to invest in to drive the most meaningful value for the company. We appreciate your interest and continued support. At this time, Jill and I will be happy to take your questions.
spk04: Thank you. At this time, I would like to inform everyone in order to ask a question, press star 1 on your telephone keypad. Again, that is star 1 to ask a question. We have your first question from Hartaj Singh with Oppenheimer. Your line is open.
spk03: Great. Thanks for the questions and the update. I apologize if there's a little bit of background noise. Rosante, looking forward to ATS and the company presentation, not to front run, you know, your presentation, but as you've been gearing up for this, you know, what are some of the aspects of the data that really excite you, especially in terms of sort of the unmet need, you know, out there in pulmonary sarcoidosis? And then any updates in protocol design for the registration on trial, you know, number of patients, has that been updated, you know, number of sites, et cetera, anything you could share there? And then lastly, you know, for HR 2810, how do you see that phase one? Would it be a classic of dose escalation with dose expansion, a basket trial? Would it be in a specific tumor type? Thank you for all the questions.
spk06: Good questions, Artaj. Thank you. I'll start with the easiest one first. You know, the protocol, design, details, sites, duration. I'm just going to ask you to hold off for one week. We have a pretty detailed presentation next week. at ATS with Dr. Culver and Dr. Boffman. We anticipate many of the thought leaders from around the world to be in San Francisco, and everyone is really anxious to get started and see those details. So I'm going to hold off on that as next Monday we're going to be outlining really all those details you want in the protocol design. As I've mentioned before, and we've put this out previously, we had a really important and what I would call a successful end of phase two meeting where we really got clarity around the design of the trial and the doses to proceed forward with, the duration of the trial, the number of patients, and really the most important thing is which of our endpoints should we prioritize. We were in a unique position because we actually hit on all of those endpoints. And I think this goes to your point about what are we excited about? We are really the first potential therapy here that has seen this level of improvement in lung function, symptom scores, controlling biomarkers. In all of those endpoints, we saw really better effects than any of us or the experts would have expected. And we did all of that while reducing steroids. It's something that really hasn't been done before in the field. So I think this really, really positions our therapy to be a transformative therapy. And you're starting to see even the agency start to recognize that with our ODD for scleroderma, another condition where it's a debilitating fibrosing condition. So when we talk about sort of the marketplace opportunity here, we've always been very conservative and said there's a, you know, a multi-billion dollar market opportunity. As we start to generate the data we produce, we clearly are leading therapy and we're set up really well here with this trial. So I'll be able to go through those details next week. With regard to 2810, we are honing in on that clinical strategy. We clearly like 2810 for a number of tumor types. Your question around will it be a basket trial or whether or not we actually will focus in on one tumor type. Stay tuned with that. We can go in either of those two directions. Again, we've seen effects with 2810 in a number of solid tumor environments. It seems to play a really, really nice role in blunting metastasis, and we know that that also comes with the ability to enhance chemotherapy. So we are working now Through that program, I really want to get the sarcoidosis trial launched, and then we'll come back to you around plans. And inevitably, everyone will want to see the protocol designed for 2810 in the future as well.
spk03: Great. Thank you, Sanjay. Thanks for the updates. I'm looking forward to the update on ATS and through the rest of the year.
spk06: Thanks.
spk04: We have your next question from . Your line is open.
spk05: Hi. Thanks for taking my questions, and congrats on the progress. I'm really, really excited that you'll be starting the study or registration study by the third quarter of 2022. That's pretty fast. And so I was just wondering if you could just comment on, you know, some of the things that have the investigators excited about this program. and your plans around clinical execution. How many sites do you have? I think I may overlap with what you just said, but just kind of comment a little bit more on that and how you expect the cadence of that to kind of pick up over time. And then at what point, you know, do you start with Alphard in Europe and even in Japan?
spk06: Great. Thanks for the questions, Agba. So we have been fast, and we've been fortunate not only reading out the data, but quickly having that sort of correspondence with the FDA. And now we're in a position to start, as you said, very quickly here. The timelines between our last data readout and when I expect to initiate this trial is a quick turnaround. In between there, we've obviously had to also discuss things with our partner in Japan, so I'm really proud of the way that we've executed in this quote-unquote downtime between these two trials, the last trial reading out and this next trial starting. We want to start fast with this trial. We have more demand worldwide with at least eight to ten countries very, very interested in participating. I'm going to be having, you know, many discussions next week in San Francisco with those investigators that are traveling. ATS is the preeminent respiratory meeting. And as I said, our event is going to be where we'll be able to outline all of the details that everybody wants to see. We think that's the best moment for us to put everything out where we have the greatest number of eyes on our story. Our clinical execution, you know, I think what people sometimes forget is we were able to execute, enroll, and read out our trial with minimal disruption during COVID. And this was a severe respiratory disease we're talking about. So I have no doubt that our clinical operations team is two standard deviations better than, you know, really anybody out there in industry, because many companies had to abandon trials during COVID. We were in respiratory. We completed a trial. But I think that speaks to also efsofitimab, that the patients, they really continue to come into the clinic and did everything that they needed to do because obviously they were feeling good and the drug was doing something for them. So I think that's what I'm excited about. I'm excited to get more patients in this next trial. And I'm looking forward to next Monday where we can go through all of the details that I'm sure you want.
spk05: Thank you. And then of course the last one here is just about 2010. I know you kind of noted that the study will be starting in the second half of 2022, but you have previously commented on, you know, working through some manufacturing issues, so we're just kind of confirming if, you know, getting the drug product manufactured is a limiting factor here regarding the timeline. And then I know you're still going to work on disclosing the indications, but I was just wondering, you know, the clinicians you've spoken to about the program, how excited are they, and have they been actually talking about maybe even having you explore other combinations beyond chemo?
spk06: Yeah, so for your first question, we invested rather early in sort of the manufacturing development plan, and if you recall, for 2810, we qualified for a bit of a faster track program that Lonza had. We are not in any way rate limited by that. I think it's fortunate that we actually planned ahead. Right now there are a lot of supply issues with a number of CDMOs out there, but our timelines are not going to be affected because we did invest quite early in making sure that this was organized well. So we're looking forward to starting that trial on time. Really, your second question around indications, we have shown data consistently in a number of models here that, again, as an anti-metastatic, as something that basically potentiates chemotherapy, we are seeing that rather consistently. This last data that we presented at AACR, I think, got most of the notice from most of the clinical oncologists that we have something really differentiated. So right now it's really around honing in on which of those neuropillin-enriched tumors we want to move into. We've shown a lot of good data over the last couple of years. This program is built well, has a cogent preclinical program, and now we're basically looking forward to starting the phase one trial, as I mentioned, There are some approaches here to look at basket versus not. I think right now that's what the team is working through, and we'll be coming back to the public with the plans there later this year.
spk05: Thanks, Andre. And then just a follow-up on the last one about potential combinations beyond chemo. I know I'm getting ahead of myself, but just kind of excited again.
spk06: Okay. There is some evidence that we're seeing with different combinations. I think you're sort of probably thinking, probably listening to what's occurring right in our research team meetings, because I think right now it is something where we are looking at different types of combo therapies. As you're aware, combination therapy is something that a lot of companies are looking at. How do they enhance and potentiate existing products? We are continuing to produce more evidence there. And it could very well be something that we incorporate in our next protocol, looking at a combination from a known marketed therapy. So stay tuned. I know you're excited to hear more about that program, but there will be more data coming.
spk05: Thanks, and congrats again on the progress.
spk04: We have your next question from Yael Jan with Lalo and Company. Your line is open.
spk01: Good afternoon and congrats with all the progress and anticipate more next week. Two quick questions here. The first one is for the scleroderma. What's your current thought or maybe the gating factors before you formally committed to a clinical study?
spk06: That's a great question, Yale. I mean, I think right now we are really focused on the sarcoidosis trial and getting that, you know, on track and launched. My point is we had data previously in a scleroderma model. I think following our data release for sarcoidosis, it really validated the compound as potentially being a game changer in ILD. Because we have this data in an animal model, we submitted for that ODD and quickly got an a green light on that. So scleroderma ILD is another very, very serious debilitating condition, high degree of mortality. You'll see us kind of dig in a little bit more as we think about how do we want to position efsofitamod in that program. But right now, I'm really focused on getting sarcoidosis launched. We may continue to do more work in the background to potentially you know, validate efsofitamide in scleroderma. There are some things that we can do from a research and mechanistic point of view. I alluded to the fact that one of our posters we're going to be just holding back as we have, you know, more data to present now. So I think this is another area for us, for the public to start paying attention to because the market opportunity just grows tremendously as you start to move into other interstitial lung diseases, of which, as I point out, there is really no therapy like ours that has shown physiologic and quality-of-life benefit.
spk01: Okay, great. And maybe one more question here. It's actually quite forward-looking at this point, which is in the cancer side, that earlier, a few weeks ago, there's a ODAC meeting talking about that the FDA seems to have greater preference for placebo-controlled study versus a single-arm study. I know it's still early for 2810 at this stage, but does that have any impact on your thoughts going forward in terms of how to think about the future study design and other sort of aspects? And thanks.
spk06: So we're monitoring very closely the comings and goings from the FDA. Sometimes the consistency is something that may not always be there, but from the cancer division, we are paying very close attention to how they're thinking about oncology drug development. We want to be crisp with our execution on the oncology side as well, similar to what we've done on the respiratory side. And I think you're right that we are looking very closely at the design, what's the next-gen type design they want to see. As more and more therapies start to fail as they get into second, third line, and more treatment resistance, we think 2810 is positioned really, really well as a therapy that can aid existing therapies in addressing some of the resistance you start to see there. And then, as I said, as an anti-metastatic therapy, we are well differentiated compared to, as a potential anti-metastatic, we're really well differentiated to some of the other things out there. So, again, stay tuned on that protocol, that design. As we get into the second half of the year, I'll be able to give you more details as we get closer to the launch of 2810's Phase I trial.
spk01: Okay, great. Thanks. And, again, congrats on all the progress.
spk06: Thanks, Gail.
spk04: Again, if you would like to ask a question, press star 1 on your telephone keypad. Again, that is star 1 to ask a question. I'm showing no further questions at this time. I would like to turn the conference back to Mr. Sanjay Shekla, President and CEO, for any closing remarks.
spk06: Well, thanks, everybody, for listening. This was a quick update. Obviously, we're going to have another meaty update in about a week at American Thoracic Society. I'm really looking forward to seeing some of the analysts that are traveling out to that event. Appreciate the questions here, and we will certainly be talking to you in the near future. Thank you for your support.
spk04: Ladies and gentlemen, this concludes today's conference call. Thank you for your participation. You may now disconnect.
Disclaimer