First Quarter 2005 Financial Results Conference Call Transcript
Moderator: Denis Burger; May 9, 2005, 10:00 a.m. Central Time
Operator: Good morning Ladies and Gentlemen and welcome to the AVI BioPharma 2005 First Quarter conference call.
At this time all participants are in a listen-only mode.
Following management’s prepared remarks we’ll hold a Q&A session. To ask a question at that time please press star followed by 1 on your touchtone phone.
If anyone has difficulty hearing the conference please press star 0 for Operator assistance.
As a reminder this conference is being recorded today, May 9, 2005.
I would now like to turn the conference over to Ms. Jody Cain. Please go ahead ma’am.
Jody Cain: This is Jody Cain with Lippert Heilshorn & Associates. Thank you for participating in today’s call.
Joining me from AVI BioPharma are Denis Burger, Chairman and Chief Executive Officer; Alan Timmins, President and Chief Operating Officer; and Mark Webber, Chief Financial Officer.
This morning AVI BioPharma released its financial results for the first quarter of 2005. If you have not received this news release or you’d like to be added to the company’s distribution list please call Lippert Heilshorn in Los Angeles at 310-691-7100 and speak with (Cheryl) Guertin.
This call is also being broadcast live over the Internet at www.avibio.com and a replay of the call will be available on the company’s Web site for the next two weeks.
Before we begin I’d like to note the comments made by management during this conference call will include forward-looking statements within the meaning of the Federal Securities laws.
These forward-looking statements involve material risks and uncertainties. For a discussion of risk factors I encourage you to review the AVI BioPharma Annual Report on Form 10-K and subsequent reports as filed with the Securities and Exchange Commission.
The content of this conference call contains time sensitive information that is accurate only as the date of the live broadcast, May 9, 2005.
The company undertakes no obligation to revise or update any statements to reflect events or circumstances after the date of this conference call.
With that said, I’d like to turn the call over to Denis Burger.
Denis?
Denis Burger: Thank you Jody and thank you all for joining us. Following my opening comments on today’s call, Mark Webber will summarize our financial results. Alan Timmins will then discuss recent developments and I will conclude the prepared remarks with a review of our milestones.
As we have stated before at AVI we believe that our third generation NeuGene antisense technology has the ability to revolutionize drug development. Based on the highly versatile nature of this technology, we are developing several very promising drug candidates for the treatment of viral diseases, cardiovascular disease, cancer and other life-threatening diseases, some of which have no treatment alternatives.
We designed our third generation antisense technology more than a decade ago to overcome what we believed to be perceived shortcomings with second generation technologies. As you may know several high profile Phase 3 clinical trial failures by other companies based on drugs developed with earlier generations of antisense technologies were reported last year.
Our third generation NeuGene antisense agents have a mechanism of action that is completely distinct from other antisense compounds and avoid the side effects, off-target effects and toxicities that have plagued other antisense chemistries, advantages instability, specificity, potency, delivery and importantly, safety have been demonstrated extensively in animals and confirmed in 11 human clinical trials involving more than 300 patients.
AVI is the only company that we know of today that is clinical studies with third generation antisense drug candidates.
Among the areas where our technology has proven most useful is in developing drug candidates that address RNA viruses. We demonstrated the ability to (unintelligible) candidates expeditiously, in some cases in a matter of days after receiving gene sequencing information.
The implications of this rapid response technology are substantial as NeuGene technology may be used to effectively counter bioterrorism threats, emerging viral diseases and even foreign infectious disease outbreaks such as the recent Marburg virus epidemic in Angola.
Further, unlike vaccines that target the protein coat of a virus, our NeuGene compounds target the genetic core of the virus. The likelihood that a virus can mutate at the genetic sites that we target are extremely low. This means for example that a single influenza drug based on our gene technology could be used through multiple flu seasons without the need for annual reinvention.
We believe that this will prove extremely important as we address upcoming concerns over the reemergence of Avian flu.
We have numerous drug candidates that target multiple indications within our pipeline. Our business strategy is to enhance shareholder value by dedicating internal resources to drug candidates that can be developed relatively quickly and target large market opportunities while seeking collaborations and partnerships with scientists, institutions, government agencies and large pharmaceutical companies to support longer-term opportunities.
During the short time period since our last conference call, we have announced the presentation of favorable data at several - from several NeuGene-based studies at two highly respected scientific conferences and in two peer reviewed journal articles.
Among our collaborators for these studies are the United States Army Medical Research Institute of Infectious Diseases and the Center for Disease Control and prevention. These presentations serve as important scientific validation for our drug development programs and our - a key to our objectives at increasing visibility of our NeuGene technology’s potential within the scientific community.
We believe that heightened awareness of this supportive data could lead to additional collaborations and partnering opportunities.
With those opening remarks, I now ask Mark Webber to review our recent financial performance.
Mark?
Mark Webber: Thanks Denis. Today I’d like to review our 2005 first quarter results and our cash position and reiterate our financial guidance for 2005.
Our revenues for the first quarter of 2005 were approximately $45,000 but compares with revenues of approximately $99,000 reported in the first quarter of 2004.
Operating expenses for the 2005 first quarter were $5.1 million, compared with $7.9 million in the comparable quarter of 2004. The decrease was due to lower research and development expenses, which were $4.1 million for the 2005 first quarter down from $6.6 million reported in the first quarter of 2004.
Approximately $2.4 million of this decrease in research and development was due to lower contracting costs for the production of GMP subunits.
Our net loss for the first quarter of 2005 was $5.5 million or 13 cents per share, which compares to the net loss of $7.5 million or 21 cents per share for the first quarter of 2004.
Reviewing our balance sheet - at March 31, 2005 we reported cash, cash equivalents and short-term securities of $37.2 million, an increase of $17.7 million from December 31, 2004.
This increase is attributed primarily to the completion of a direct equity placement with several institutional investors resulting in net proceeds of $22.3 million, which we announced in January of this year.
This is offset by $4.4 million used in operations and approximately $400,000 used for the purchases of property and equipment and patent related costs.
Additionally, we were informed in 2004 that AVI would be allocated $5 million in government funding for the 2005 fiscal year to work on two viral disease research projects. These funds have yet to be received however are not reflected in our financial statements.
As for our 2005 financial guidance we expect cash burn for the year to be in the range of $25 to $27 million.
With that overview, I would like now to turn the call over to Alan Timmins.
Alan Timmins: Thanks Mark and let me add my welcome to those of you joining us this morning on the call and on the Internet.
As Denis mentioned I’ll discuss some recent presentations and publication of data based on our NeuGene technology.
Two peer reviewed manuscripts reporting favorable data from antiviral collaborative studies appeared in the April issue of the Journal of Virology. The first of these articles called Inhibition of dengue virus serotypes 1 to 4 in (virocell) cultures with mopholino oligomer covered impressive data from a study that demonstrated the ability of several NeuGene drug candidates to effectively inhibit dengue viral replication up to 1 million fold and in some cases reduce the amount of virus in the cells to undetectable levels.
Dengue virus produces a spectrum of illnesses ranging from a non-specific viral syndrome to severe and fatal hemorrhagic disease. Dengue fever and dengue hemorrhagic fever are caused by one of the four closely-related but distinct viral serotypes. Infection with one of these serotypes does not provide cross-protection to the other three.
Viral inhibition reported from this study was specific dose dependent and extended to all four dengue serotypes, which appears critical in developing an effective clinical agent for this disease.
This study was based on our close collaboration with the Centers for Disease Control. We have an active cooperative research and development agreement or CRADA with the CDC for dengue virus drug development.
In the second study called Inhibition of Flavivirus Infections by antisense oligomers specifically suppressing viral translation and RNA replication, an epidemic strain of West Nile virus was treated with specific NeuGene drug candidates. This resulted in up to 1 million fold reduction in viral levels, without any apparent cell toxicity.
One specific NeuGene candidate was identified and inhibited other mosquito born Flaviviruses, which is very important in developing a single clinical drug candidate that could treat potentially most of the viruses, if not all of the viruses, in this group.
Dengue and West Nile virus are both members of the single strand RNA Flavivirus genus, a group of mosquito foreign viruses that cause significant human diseases. This viral family includes Japanese encephalitis, yellow fever, Murray Valley encephalitis and tick-born encephalitis.
No drug therapies are currently available to treat any Flavivirus infections. With approximately 50 to 100 million human cases of dengue virus infection occurring annually and with the disease spreading into the United States, we’re targeting dengue fever and dengue hemorrhagic fever in upcoming internal drug development programs.
West Nile virus outbreaks have caused significant morbidity and mortality in the United States during the past several years. We currently have an ongoing trial for the treatment of patients with acute West Nile virus disease who have serious neurological impairment, known as West Nile virus neuro invasive disease.
Also last month we presented pre-clinical data from our studies of evaluating the effectiveness of our NeuGene antisense drugs, the American Association for Cancer Researches Annual Meeting. Two presentations - the first called c-myc antisense phosphorodiamidate mopholino oligomer inhibits lung metastasis in a (syngeneic) lung tumor model and the second called (WT1), a novel target for antisense mediated prostrate tumor therapy evaluated studies conducted by our scientists in collaboration with Oregon Health and Sciences University.
Findings in the first study indicated that our antisense drug AVI-4126 decreased the formation of lung metastasis in an aggressive lung tumor model. AVI-4126 has been studied in other cancer settings based on its ability to inhibit c-myc over expression, which has been correlated with cancer progression and chemotherapy resistance in several solid tumor models.
In the second study, inhibition of WT1 led to a reduced tumor volume in a prostate cancer model.
We also presented a study entitled Inhibition of XIAP, an antiapoptotic molecular target potentiates radiation induced cell death in cancer. This study evaluates a novel approach of using NeuGene drugs to target the XIAP gene which has been found to protect cancer cells from the effects of radiation, which of course is a common therapy that plays an important role in the management of a majority of cancers.
Earlier in April we announced the release of extensive data from Ebola, influenza, dengue, SARS coronavirus and Bunyavirus studies at the 18th International Conference on Antiviral Research.
Our Senior Vice President of Research and Development, Dr. Patrick Iverson, delivered an oral presentation highlighting experiments performed at the U.S. Army Medical Research Institute of Infectious Disease, also known as USAMRIID, which are part of our ongoing research and bio defense with the chemical and biological defense program of the Office of the Secretary of Defense.
Our studies in collaboration with scientists at USAMRIID have established that our antisense drug candidates are efficacious in protecting and treatment multiple animal species from the lethal challenges from Ebola. These results represent both an exciting alternative to current antiviral drug therapies and a real possibility of treating the currently untreatable Ebola virus.
In a second presentation, Dr. (Benjamin Newman) of the (Scripts) Research Institute presented findings from SARS studies undertaken in collaboration with AVI scientists. Data from these studies demonstrated that our NeuGene antisense drug candidate reduced all three parameters of the SARS viral infection, including cytopathic effect, viral titer and viral spread.
In addition, one antisense candidate was found to be particularly effective at reducing viral titer to undetectable levels, while another that was designed to affect the same target of a related virus reduced viral titer by 10,000 fold in mice.
Additionally, three of our scientific reports were included in a poster presentation. First was drawn from a collaborative study with scientists at the Massachusetts Institute of Technology. In this study NeuGene antisense agents targeted influenza strain H1N1 and exhibited up to a 1000 fold reduction in viral titer in infected cells and further suggested that a single antisense agent could be developed targeting both influenza A and Avian influenza strains.
The second poster encompassed the results of the collaborative study with the CDC facility in Port Collins, Colorado where NeuGene compounds in the study were found to be highly efficacious in cell culture by reducing viral activity up to 1 million fold, and most importantly, inhibiting all four disease serotypes.
The third poster presentation was the result of a collaboration with Dr. (Ramon Flick) and his colleagues at the University of Texas Medical Branch in Galveston and at the Institute Pasteur in Paris. More than 60 members of the (bunya) virus family can cause severe disease in humans and in livestock.
Several members of this viral family as classified in the bioterrorism category. A list as those that are easily disseminated and highly contagious and that can induce a high rate of mortality.
Our NeuGene agents were highly effective at inhibiting transcription as well as translation of these viruses.
As Denis mentioned presenting study data conducted with well-respected researchers at top-level institutions and government agencies and presented a peer review publications and at respected scientific conferences creates additional awareness of the advances in our developing antiviral drug candidates.
Further, these activities create continued validation for our NeuGene technology and support our efforts to develop additional collaborations and partnerships.
Now I’ll turn the call back to Denis for some further remarks.
Denis?
Denis Burger: Thanks Alan. Before opening the call to your questions, I would like to provide an update on clinical programs.
In reviewing progress with our cardiovascular program, we are pursuing two distinct approaches with our NeuGene drug candidate, AVI-4126 to treat restenosis, both of which we believe represent large market opportunities.
First, with our Resten-MP microparticle technology for the systemic delivery of AVI-4126. We plan to initiate a European trial in combination with (bare) metal stents around mid-year to support our ongoing U.S. trial underway at the University of Nebraska Medical Center. Enrollment for this trial should approximate 50 patients.
In pre-clinical studies Resten-MP was as effective in preventing restenosis as either using a drug alluding stent or delivering the drug with a catheter.
We also intend to initiate late this year a 200 patient European late-stage study with Resten-NG delivered on our drug alluding stent platform or DES. If this trial is successful it should lead to CE mark approval. As previously announced, we have developed and assembled the components that we believe will be the next generation of drug alluding stent or DES.
The most important component is Resten-NG, which has advantageous characteristics compared with the drug components in Cypher or taxis DES.
Our drug alluding stent involves a non-polymer loading and allution system for Resten-NG. We believe this is the proper approach to DES considering healthcare issues concerning all polymer-based systems.
We have taken extra time this year to develop this system but again, we believe we could reap medical and economic advantages by commercializing the first polymer free DES in the marketplace.
We see a tremendous opportunity for Resten-MP and Resten-NG in countries like Germany where about one third of the stents placed during balloon angioplasty are drug alluding stents and two thirds are bare metal stents largely based on concerns with cost effectiveness with the polymer-based systems.
Turning to our infectious disease programs, we plan to report pre-clinical results from our HCV program in the second quarter of this year and file an IND application to initiate clinical trials with our NeuGene drug for HCV around mid-year.
HCV is the principal cause of chronic liver disease, the number one cause of liver failure, and the tenth leading cause of death among U.S. adults. As (Alan) mentioned earlier, the market for HCV is sizable with estimates ranging from $10 to $20 billion worldwide.
Also we are moving forward with our Dengue virus program in collaboration with the CDC and we expect this to be the next viral program to move into the clinic – into clinical development following HCV. We have completed clinical preparations to support our 50 patient phase 1B/2 West Nile clinical trial including selection of the sites, study approvals in several western states. West Nile disease is just now emerging in the West as we enter the 2005 mosquito season. Details on this study are found on the CDC Web site.
With our oncology program, we plan to initiate an additional cancer study in the next few months using AVI 4126 in a safety and efficacy trial in bladder cancer. As cancer clinical studies are typically lengthy and costly, we are actively seeking pharmaceutical partners to advance our oncology program into later stage development.
Some of you have asked us about the possibility of developing NeuGene based compounds that address the avian flu. We currently have incorporated avian flu research into our influenza program as avian flu is an RNA virus in the influenza family.
In closing this promised to be an exceptional year for AVI as we gain additional recognition through our collaboration with well-respected institutions and presentations of study data in well-regarded medical journals and at conferences.
Positive results from our pre-clinical and clinical data continue to be corroborated by numerous outside sources. Importantly we are prepared to advance into late stage studies with our lead program with our near term opportunities in cardiovascular and viral diseases and are looking to partner and collaborative opportunities with our longer-term opportunities in cancer, PKD, drug metabolism, among others.
At this point, I’d like to open the call to questions. Operator?
Operator: Yes sir. Ladies and gentlemen, if you wish to register a question for today’s Q&A session, you will need to press star then the number 1 on your telephone keypad. You will hear a prompt to acknowledge your request. If your question has been answered and you wish to withdraw your request, you may do so by pressing star then the number 2.
If you are using a speakerphone, please pick up your handset before entering your question.
Again, we request that if you have pressed star 1 to ask a question before this time, please press star 1 again to ensure that you enter the queue.
One moment please for our first question.
The first response comes from Ren Benjamin with Rodman and Renshaw.
Ren Benjamin: Hi. Good morning everyone and congratulations on your ongoing progress.
Couple of quick questions. Can you talk to us a little bit about AVI 4557, I believe. The last data we saw was actually quite compelling and it was looking at the oral form. What’s going on with that program?
Man: We believe that that program accomplished a couple of things. First, when we delivered the drug either by intravenous or subcutaneous root in a large number of patients, we were able to prove that antisense targeting the liver enzyme could be knocked down and we could measure that reduction with two different test drugs.
So for us, it proved that antisense delivered in two different ways could in a very defined way in known systems be shown to enter the liver, knock down the gene target and produce the desired effect.
The third study that we did showed that we could actually deliver the drug orally. Taken together, our opportunity now and what we’re aggressively pursuing is to partner that program for use with drugs that are currently approved in the marketplace. The gene target was cytochrome P453A4, which is responsible for the metabolism of about half of all approved drugs. Everything from aspirin and caffeine to the cancer drugs and drugs used for pain management.
So the idea is to partner with major pharma and we felt one of the key features in initiating that partnership was the oral data. So it’s now been about six months since we’ve finally analyzed all of the oral data and we’re actively seeking partnerships.
Ren Benjamin: Okay. Great. How about the – if memory serves me correctly there were two phase two trials that were currently ongoing utilizing the microbubble technology. Can you update us a little bit on those two trials? I believe on was in Nebraska. One was in South America. How are those progressing and when might we see some results from those studies?
Man: The first trial is in Nebraska. We’re still enrolling patients. It’s in combination with a drug alluding stent system. And to support that, we had always planned to initiate a second study. We looked at sites in Latin America. We looked at sites in Asia. And finally decided that the most reliable site to do this study would be in Europe and that’s the study we plan to initiate around mi-year this year.
We’ve selected sites. We’ve selected principal investigators. We have a couple of more steps before the trial can begin, which involves the final approval of getting an import license into the countries where we’re doing the study, which allows us to get the export license through the FDA to deliver the drug.
We’re well down that path and we actually expect the study to start somewhere right around mid-year.
Ren Benjamin: And if it starts like you’ve said on time, how do you project enrollment to proceed and can you tell us a little bit about the details of the trial?
Man: Yeah. We’ve spent a lot of time making sure that the sites and investigators we picked were aggressively enrolling patients and patients that were getting bare metal stents because this study where we use the Resten-MP in combination with the bare metal stent.
And we believe that enrollment will be just a few months, certainly less than three months and therefore, will have data in that six to nine month window after enrollment.
Ren Benjamin: Okay. Great. Can you talk to us a little bit about the hepatitis C vaccine – hepatitis C program? You know you mentioned that there’s going to be a publication of pre-clinical results potentially by – well sometime in the second quarter. And then the filing of an IND. What’s the target that you know, you guys have designed the (antisense) against? And what are your thoughts as to how that program will proceed?
Man: This is a key program for us. We’ve been in pre-clinical studies in various models from mice to contrived monkey models for the last three years. So we’ve very carefully put together the scientific evidence to support the targeting of HCV.
We’ve looked at principally three different types of targets. Targets around the initiation of translation of the viral gene, what we’ve referred to as the AUG start site. We’ve looked at the internal ribosomal assembly sites or (Iry) sites. And we’ve looked at sites involved in regulation of replication of the gene.
We’ve eventually zeroed in on the AUG start site and a particular region in that coding frame pre-viral gene. And because of that, we think we’re in a very strong position both with recent patent issue and with the efficacy we’ve seen in comparing these targets.
We’ve finished all of the pre-clinical work including pharm tox and tox in different species including monkeys. So we’re in the final stages of putting the package together for the IND filing.
Our phase – our program involves a small phase 1A and simultaneously a larger phase 1B clinical study. In the phase 1B clinical study, we’re looking at both a subset of patients that are naïve in term of treatment with other drugs and patients that are (riboviren) interferon failures. So there will be two initial study groups.
As I believe we said before, we feel strongly that none of the HCV models are really very accurate and predictive. And that’s what makes developing a drug to HCV such a challenge. So we believe that the phase 1B data that will derive from the study will be the most important indication of how successful the program will be.
The end points are easily measured. They’re viral titers. And what that means is in a 14 day treatment regime you actually have indications of whether or not you’re getting a knock down in the virus titer, which is a surrogate marker of efficacy within the first month.
So we’d expect if we treat people this summer that by the early fall, we’ll have the early clinical data.
Ren Benjamin: Okay. Fair enough. I think – let’s see. One final question is can you talk to us a little bit about the presentations – any future presentations that you may have coming up at scientific conferences?
Man: Let’s see. We have a couple of conferences that are in the fall where we’re really peaking to and of course, the one important one in the cardiovascular program is the interventional conference in Washington, DC in the fall.
There’s also toxin pharmacology conferences in the fall. And we expect that we’ll present an update on our viral program.
And most importantly, we’ve over the last couple of years, we’ve really rounded out our scientific programs with our collaborators and what you’ll see as you’ve seen in the first quarter, you’ll see again in the second quarter and in the second half of this year. Finally the publications in peer reviewed journals from all this work, which is really the formal documentation of the strength of the program.
Thanks Ren.
Ren Benjamin: Perfect. Thank you.
Operator: Our next question comes from Quynh Pham with Delafield Hambrecht.
Quynh Pham: Good morning.
Man: Good morning.
Quynh Pham: Hi. I just have a kind of follow on question about the Nebraska study. So that study was supposed to enroll 50 patients right for the Resin MP?
Man: Yeah. That is correct.
Quynh Pham: And so it’s been ongoing for about a year and a half now? Is that correct?
Man: It’s been ongoing for quite some time. I don’t know if it’s been a year or a year and a half but…
Quynh Pham: What are the issues behind that enrollment and why is it that you expect the use study to enroll in less than three months when this ongoing study is having such a problem with enrollment?
Man: We would expect the European studies to enroll faster simply because they treat more patients. They are centers of excellence within Germany and their throughput of patients is significantly higher than Nebraska’s. We haven’t said that Nebraska is a problem, per se. I think that we would be honest in telling you that we think the enrollment has been slower than they anticipated providing but we are moving down the road with that.
But the German study will enroll patients much faster according to just simple numbers of how many patients they treat. That, of course, to be modified by the occurrence of the holiday that lasts, you know, through August. But other than that, we anticipate that they’ll be very rapid enrollers.
Quynh Pham: All right. And then how are you monitoring the restenosis in the German study?
Man: We look at both six and nine months with angiography and at the end of the study at nine months with intravascular ultrasound.
Quynh Pham: Okay. And then just trying to understand that some of these studies for your antiviral programs, the ones in SARS, Ebola, Dengue virus. These are very kind of very infectious diseases. How does a program like that move forward when you certainly have these animal models. But you know, you can’t necessarily treat them in patients?
Man: Yes. I think that’s a great question. And we’ve tried to explain in the past our overall approach and that is we feel that there’s a great similarity in all of the RNA viruses. All the RNA viruses are single strand RNA. And we’ve felt strongly that if we can be efficacious in some of the different families, we can probably be efficacious against the significant viruses that have large economic markets.
So we fully recognize that some of the unusual viruses that we’re addressing aren’t going to result in drugs going to clinic. But they teach us a great deal in both culture and in animal models about how to deliver the drug. About how to deliver the drug to various organs where the virus proliferates. And what to expect.
Quynh Pham: So it’s more of – in a pre-clinical model, it’s a proof of concept for you?
Man: That is correct.
Quynh Pham: Learning – like a long learning curve.
Man: Many of these we’re not going forward clinically.
Quynh Pham: So it’s mainly the hepatitis C and then perhaps the flu?
Man: Hepatitis C, Dengue if we get the appropriate support from the government and the military because it’s a very important virus to – in certain parts of the world. Influenza, obviously a very important one and a large economic market. Another one that was a large economic market is respiratory (systitial) virus, the main one cause of respiratory disease in children.
Quynh Pham: Are you making a lot of progress in the RSV model because that would be very significant?
Man: It would and we’ve done quite a bit in the RSV model. And influenza and RSV are the two viruses next to come along with major clinical markets.
Quynh Pham: And there’s a model for RSV?
Man: Yes there is.
Quynh Pham: Okay. Do you think you’ll have anything published on that any time soon?
Man: I know that we plan some presentations in that arena. I do not know to this morning whether or not the data is yet significant enough to put into a publication.
Quynh Pham: Okay. And those presentations are coming this year?
Man: Yes.
Quynh Pham: Okay. Well, thank you very much.
Man: Thanks Quynh.
Operator: There are no further questions at this time. Please proceed with your presentation or any closing remarks.
Man: Well I’d just like to thank everyone for participating in the call. It’s been a very short period since our last call, less than three months and we really appreciate your support.
Thanks and good day.
Operator: Ladies and gentlemen, that concludes your conference call for today. Again, that you for participating. You may now disconnect.
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