Compugen Ltd. (NASDAQ:CGEN)
Q3 2016 Earnings Conference Call
November 16, 2016 10:00 AM ET
Martin Gerstel - Chairman
Anat Cohen-Dayag - President & CEO
Ari Krashin - CFO
John Hunter - VP, Antibody R&D and Site Head, Compugen USA Incorporated.
Mike King - JMP Securities
Ted Tenthoff - Piper Jaffray
Thomas Yip - FBR
Vernon Bernardino - FBR
Good morning and thank you for joining us today. With us today from Compugen are, Martin Gerstel, Compugen's Chairman of the Board; Dr. Anat Cohen-Dayag, President and CEO; Mr. Ari Krashin, CFO; and Dr. John Hunter, Vice President, Antibody R&D and Site Head, Compugen USA Incorporated.
Before we begin, I would like to read the following regarding forward-looking statements. During the course of this conference call, the Company may make projections or other forward-looking statements regarding future events or future business outlook, including statements relating to the potential of the CGEN-15029 program for the development of new cancer immunotherapy treatments for solid tumors, including the potential for drug combination with current immune checkpoint blockers, and the potential of COM701 as a new cancer immunotherapy treatment, anticipated progress on Compugen's pipeline program as well as commercialization efforts.
We wish to caution you that such statements reflect only the Company's current expectations and that actual events or results may differ materially. You are kindly referred to the risk factors and cautionary language contained in the documents that the Company filed with Securities and Exchange Commission, including the Company's annual report on Form 20-F, filed March 7, 2016. The Company undertakes no obligation to update any projections or forward-looking statements in the future.
I will now turn the call over to Dr. Anat Cohen-Dayag. Please go ahead.
On behalf of all of us at Compugen, welcome to our third quarter 2016 conference call and thank you for joining with us today. As we announced in our third quarter financial results press release last week, this quarterly conference call was postponed until today so that we would be able to include the discussion of the very exciting new results for our CGEN-15029 program and its clinical lead antibody COM701. These results were presented by the Company in a late breaking session at the Annual Meeting of the Society for Immunotherapy of Cancer (SITC), last Friday.
Therefore, after my brief introductory remarks, John Hunter, the Site Head of our South San Francisco operation will view key data he presented at this leading Immuno-Oncology Conference. In doing so, John will be referring to a PowerPoint slide presentation which is available on our website. If possible, I encourage you to view this presentation during the call in order to be able to better follow the remark.
Following John's prepared remarks, we will move to a Q&A session where Martin and Ari will be able together with John and myself to answer questions about either today's presentation or our quarterly financial results published last week. The call will end with closing remarks by Martin. Since John is participating from our facilities in South San Francisco, we hope that the difference in locations will not create any communication problem.
In his prepared remarks today as was the case at the Citi Conference last week, John will focus solely on one of the programs in our immuno-oncology pipeline. However, we also announced last week that the Company will hold a R&D Day in New York City on December 7th, which will be webcasted. At this upcoming R&D Day, we will provide an overview of our additional activities in immuno-oncology that can now be publically disclosed.
Moreover, as a follow-up to the CGEN-15029 program data that has now been disclosed, we will provide at the R&D Day detailed information outlining for COM701, the clinical antibody CGEN-15029, the path forward to IND filing and to the clinic, so you can fully appreciate the stage and the status of the program. In addition, our R&D Day will include a presentation of Professor Drew Pardoll, the Chairman of our SAB and a world leader in the field of immuno-oncology.
We therefore believe that both today's call and the upcoming R&D Day should be very helpful in appreciating what we have accomplished in our primary field of focus for the past few years and its potential medical and commercial implication. As will be more fully described by John in his prepared remarks, we believe that the CGEN-15029 program data that was presented for the first time at Citi shows that this checkpoint named PVRIG has a clear role in tumor immunology and the disimpact of CGEN-15029 cannot be ignored as part of the industry's efforts to generate novel treatment solution.
While competition is fierce in the field of T-cell based checkpoints with many other immune checkpoint programs in development and in most cases with each addressed by multiple pharma and biotech companies, our novel immune checkpoint in general and specifically CGEN-15029 also what we believe are clear opportunities for the development of first-in-class drugs. In addition, the data from the knockout mice and certain other data we generated for CGEN-15029 as will be presented by John, our unique compared with other immune checkpoints in the field suggesting both monotherapy as well as combination therapy opportunities for COM701 our clinical antibody for this program.
It is important for our shareholders to note that prior to last Friday, we presented to the public and to the industry only the CGEN name of the program, some initial validation data point, our discovery of its binding partner and the selection of a lead antibody. Now, however, with the substantial data we generated and the advancement of the program protected by our IT strategy, we feel comfortable providing much more specific identifying and supportive data for the target and its lead antibody. We believe that disclosing this information at this stage should not jeopardize the programs competitive edge or its potential value.
The benefit on the other hand is that disclosing the name of the target, its pathway and data on a lead antibody may allow the industry to better evaluate the assets we have generated while we continue to develop the program. While there is fierce competition in the field of immuno-oncology, our immune checkpoints directly inhibiting T-cell function. There are numerous cancers such as pancreatic cancer, prostate cancer, and others in which immune T-cells are not able to infiltrate the tumor or do infiltrate, but are highly suppressed. These cancers are considered non-responsive to cancer immunotherapy treatment including current immune checkpoint inhibitors.
It is believed that in some cases the inability of the immune T-cells to infiltrate this tumor or to be activated in the tumor microenvironment resulting part from the suppressive myeloid cell population in the tumor microenvironment. As we recently disclosed, the second portion of our immuno-oncology target pipeline consists of programs based on targets expressed on myeloid cells identified within the tumor microenvironment. Our myeloid target candidates are predicted to induce immunosuppression where the blocking antibody against them is predicted to enable the T-cells to attack the cancer.
Within this segment so far IO pipeline which will be further discussed at our upcoming R&D Day, we are focusing our activities on target candidates potentially addressing various immunosuppressive mechanism within the tumor microenvironment. We believe that this approach will substantially exemplify the weakness and enhance the breadth and the overall potential of our pipeline in generating novel cancer immunotherapy treatment, particularly when taking into consideration the need for combination therapies.
Again I want to encourage you to join the live webcast of our R&D Day which will be held on the morning of December 7th, East Coast time. Information regarding how to participate can be found on our website.
And now, I'll turn the call over to John. John?
Thanks, Anat. Today, I'll be giving in a few of our lead therapeutic program CGEN-15029, including details on its discovery, functional data for COM701, our lead antibody targeting CGEN-15029, and supporting in vivo data for mouse study showing the utility of targeting CGEN-15029 in the tumor setting. All of this demonstrates the promising potential of COM701 as a first-in-class drug opportunity for cancer Immunotherapy. As previously mentioned, most of the results I will be showing were first disclosed last week, at the Annual Meeting for the Society for Immunotherapy of Cancer.
Since I know that our audience today has varying degrees of scientific knowledge in this field, I will attempt to describe the key points on each of the slides with a minimum of scientific jargon. This will not in some cases captured all of the information presented last week and for those of you who want more of the science, I encourage you to join us for our R&D Day in December, where we will go into much greater detail on the program.
I would like to refer to the slides on our webcast starting with Slide number 3. Six years ago, the first clinical data on ipilimumab commercially knows as Yervoy was published, demonstrating unprecedented responses in late stage melanoma patients. Since then, there has been a slew of new data, not only justifying the original excitement around and immune checkpoint inhibition, but also demonstrating the broader patient populations can be addressed by targeting additional immune checkpoints, and by using checkpoint inhibitors together in combination.
However, even with these advances, the majority of patients don’t derive long-term benefit from current therapeutics; and there is still a substantial unmet medical need. The approach the Compugen has taken to address this unmet need and to generate a competitive edge in this field is to identify novel immune checkpoints that have pronounced suppressive role in the tumor microenvironment and to develop first-in-class drugs against those differentiated checkpoints.
Moving on to Slide 4, identification of novel checkpoint is complicated by the fact that the similarity of protein sequences between known checkpoints in quite low. Therefore, while this approach of sequence similarity has been commonly used for the identification of additional members of proteins with any given family, it can't generally be used as immune to identify new immune checkpoints. To overcome this hurdle of low sequence similarity, we employed a genome level approach to identifying new immune checkpoints.
Applying our predictive discovery approach, Compugen's team developed powerful algorithm to identify other genes with similar genomic structural features as those seen with known immune checkpoints. And PVRIG, which we previously referred to as CGEN-15029 was among the multiple novel genes that fit our search criteria, while the PVRIG protein sequence itself could be found in public data bases, we were the first to identify a cancer relevant function for it when we computationally predicted that it should serve as a new immune checkpoint protein inhibiting immune system activity.
I’ll move onto expression data in Slide number 5, in addition to the gene structure similarity, we saw that our discovery platform demonstrated an expression pattern of PVRIG that fit that of other receptor-like immune checkpoints. Expression of PVRIG is restricted to lymphocyte populations primarily NK and T-cells with higher expression in tumors relative to normal tissue as is the case with PD-1. Follow-up studies on the expression of the protein have confirmed the patterns we observed with RNA.
Now moving to Slide number 6, to test the function of PVRIG which we predicted should inhibit the immune system, we assess the effective high PVRIG expression on activation of T-cells with no cells were incubated with non-immune cell lines. PVRIG in this system had a profound suppressive effect on T-cell activation, providing further evidence that PVRIG is an inhibitory checkpoint molecule.
Moving to Slide 7, having established PVRIG inhibitory activity, we then went onto successfully identify its binding partner, a protein expressed on myeloid and tumor cells known as PVRL2. Identification of PVRL2 is the binding partner, provided biologic insight into PVRIG as it placed within a known immune checkpoint axis that has recently gained acute industry interest in the IO field. PVRL2 is known to serve as a ligand for the T-cell co-stimulatory molecules known as DNM1 and has been reported to bind to co-inhibitory molecule TIGIT albeit with a very low affinity.
The placement of PVRIG in that TIGIT signaling axis who is important in cancer has been low validated pre-clinically strongly suggested that PVRIG functions as part of this immuno-oncology axis and further increased our confidence that PVRIG is an important shut point that can't be ignored when designing new ways to attack immunosuppression in the tumor microenvironment or TME.
Moving to Slide 8, based on the observed function and expression of PVRIG, together with its association to the TIGIT signaling pathway, we set off to develop therapeutic antibodies against the target. The ultimate clinical candidate COM701 with selected based on its extremely high affinity binding to PVRIG, together with its ability to completely block binding of PVRIG to PVRL2 and as you will see in the next slide to enhance T-cell activation in multiple assay systems. We feel all of these attributes are critical to generate not only a first-in-class therapeutic but also a best-in-class therapeutic.
Moving to Slide 9, to test the T-cell activation capacity of our blocking antibodies in a cancer relevant system, we used tumor infiltrating lymphocytes also known as TILs for myeloma patients which were then cultured with targeT-cell line expressing myeloma antigens. As per our predictions treatment in this assay system with COM701, reverse the inhibitory activity of PVRIG resulting in increased TIL activation as manifested by secretion of interferon gamma, a key immunostimulatory cytokines, which is commonly used for measuring activation of anti-tumor T-cell responses. This suggested that tumor specific CDA cells are inhibited by PVRIG and that COM701, our clinical candidate antibody releases this inhibition.
Moving on to Slide 10, given the placement of PVRIG in the TIGIT signaling axis, the obvious question was whether this combination of PVRIG and TIGIT blockade can further increase T-cell activation. As we see in this pathway, shown in the schematic of the top left, you can see that PVR and PVRL2 can both bind the co-stimulatory molecule DNM1, although each seems to bind and signal through a separate inhibitory pathway. In blocking TIGIT alone shown on the top left, you can disrupt its inhibitory activity and also enable greater PVR binding to DNM for stimulatory signaling that leave the PVRL2, PVRIG inhibitory pathway intact.
Conversely, in blocking PVRIG alone shown on the top right, you disrupt its inhibitory activity and leave PVRL2 free to bind and stimulate DNM1 signaling though with the TIGIT inhibitory pathway still intact. Based on this model, combination treatment at the bottom of the slide should remove both inhibitory signals and allow maximum T-cell stimulation in a setting where all of these components are present.
In moving to Slide 11, we see that looking at COM701 plus anti-TIGIT antibody effects in the TIL assay system, the results matched our predictions as interferon gamma secretion was increased beyond what we were able to achieve by blockade of PVRIG or TIGIT alone. More recently, we have expanded this observation to other assay systems involving CDA T-cell activation.
Moving to Slide 12, while the in vitro results were highly encouraging, we wanted to assess the effects of PVRIG blockade more directly in animal tumor models. Since our lead antibodies are not mouse cross-reactive as is the case with many other immune checkpoint inhibitors now in the clinic, we generated surrogate antibodies against the mouse ortholog with PVRIG and screened for antibodies with properties similar to that of COM701. The most potent antibody against mouse PVRIG AB-407 was then tested in mouse tumor models commonly used in checkpoint inhibition studies.
When testing the surrogate antibody in the model presented on Slide 12, we did not see efficacy of AB-407 as a monotherapy. However, when combined with a PD-L1 blocking antibody, under conditions in which anti-PD-L1 by itself had no effect on tumor growth, we saw a clear tumor growth inhibition as shown in the graph on the top left, an increased survival of the combination treated mice as shown in the graph on the top right. This piece of data although in line with our expectations was very encouraging, as it indicated that PVRIG potentially adds to the inhibition exerted by PD1 on the immune system, and that blocking PVRIG may be required in order to release this overall inhibition in a more effective manner in patients.
This effect was not specific to one animal model, as we also see similar tumor growth effects with the same combination in a melanoma tumor model. We are now expanding our in vivo studies to look at additional tumor models in combinations in parallel with the COM701 development activities. We also generated genetically modified mice that lack PVRIG expression called knockout mice to further characterize PVRIG in vivo. Recently, our collaborators and Professor Drew Pardoll's lab at Johns Hopkins University began testing tumor growth in those mice.
Last week, we received exciting data from those studies shown in Slide 13, demonstrating the growth of MC38 colorectal tumors is reduced in the knockout mice relative to the wild-type mice. This binding would suggest the COM701 in the right settings has the potential to work as monotherapy as well as in combination with other checkpoint inhibitors. As we would have anticipated from the in vivo combination studies, knockout mice treated with the anti-PD-L1 antibody demonstrated greater tumor growth inhibition than wild-type mice under the same treatment conditions.
Taking together moving to Slide 14, our results demonstrate the significant potential utility of targeting PVRIG for cancer immunotherapy. Our lead molecule COM701 is currently advancing towards clinical trials, offering the potential for both mono and combination first-in-class therapeutic opportunities.
And now, Martin, Anat, Ari and I will be pleased to answer your any questions you may have.
Thank you. Ladies and gentlemen, at this time, we'll begin the question-and-answer session. [Operator Instructions] The first question is from Mike King of JMP Securities. Please go ahead.
I just wanted to ask the question about -- just help me to understand the model, John, I am just trying to understand, if PVRIG is also -- are the T-cells that you are looking at also co-expressing PD-1? And if so, is there any either crosstalk or competitive action of PD-1 versus PVRIG when you do those experiments? Are they completely devoid of PD-1?
The T-cells that we are using do express PD-1 as well as TIGIT, so all of the relevant checkpoint inhibitors are present in the model system. We're starting to look at combination to see what the effects of co-inhibition with PD-1 and PVRIG are, but based on some recent data presented by Genentech where Ira Mellman has been showing that PD-1 when activated results in dephosphorylation of those CD28 by dNM. We do think that there is a tie end between the two pathways that we are further exploring right now.
Okay. So, we don’t know certain what the temporal relationship is between PD-1 engagement either by an inhibitory antibody or the ligand by PD-L1 versus?
No, we are kind of working through that now multiple assay systems.
Just another follow-up question, so then when you go to the animal experiments, I guess the working assumption or working hypothesis is that the tumors that are implanted at [Indiscernible] all of full compliments of checkpoints. Is that a fair statement?
Yes, in the early models that we have looked at, we do see all the relevant players present in the tumor microenvironment, which you would expect given the combination data that we generated in those models.
Right. Okay. And finally, the cartoon where you showed blockhead of PVRIG, TIGIT, or both, those are theoretical or do you actually -- have you actually done those in kind of what biology? Thank you.
Well, I mean the combination data that we showed in the presentation with the increased activation using dual blockhead would tend to validate that model. I do want to point out that’s a very simplified model.
There is a lot of other players obviously that have to be accounted for, but at least in the assay system that we've set up to look at that the results do replicate our model.
The next question is from Ted Tenthoff of Piper Jaffray. Please go ahead.
I guess my question is looking forward a little bit with respect to [Indiscernible] the clinic. Obviously, we'll do sort of all kind of studies, monotherapy, but those studies to sort of tease up where you would do potential expansion still or do you have from the animal work and the preclinical work kind of some hypothesis in terms of where these interactions may best be applied either as monotherapy for combination?
Yes, I think we are going to use a combination of those datasets. We are doing a number of combinations studies in mice to try to get a better sense of what combinations we want to use and possibly what patient population we want to address. We are also doing a number of translation on medicine studies to look at expression of all of the relevant components within the given tumor, but that work is very early. So, we're not at a stage at where we know what indications we want to focus on. But ultimately, if you look at the history of other checkpoint inhibitors, it's really been in the clinic that people have generated the data they need to know what patient populations they want to do to expansion studies in.
That makes sense. And then just I might have missed this, but the IND on track next year then or what's the call?
Hi, Ted. Just before I am answering that I'd like just to add that in the planning for Phase 1 study, we would like to make sure that we keep our options open and that we target both for a PD-1 treated the patients and also those that do not respond to PD-1. Just in terms of a guidance to IND, with the data that we discussed today at the R&D Day that we are planning on December 7th, we plan to discuss in detail the path for COM701 to IND and to the clinic and will give much more details from this. So, I defer the question to the R&D Day.
Understood that makes a lot of sense. Thanks and I am looking forward to seeing at R&D Day in our conference.
The next question is from Thomas Yip of FBR. Please go ahead.
One question I have is regarding PVRL2, it was identified as a binding partner for PVRIG. What do you think about the potential of binding to PVRL2 alone? And as far as you know, are there other checkpoint targets that are related to PVRL2 as well? Thank you.
We decided in looking at it. I assume the question is whether we would consider targeting PVRL2.
Yes. Sorry, and if there're other existing shape on targets that also associated with PVRL2?
Yes, so we did consider PVRL2 as a legitimate target because it has an activating role when it binds to dNM. We felt that that would counteract what we were trying to accomplish. So, we really feel that targeting PVRIG is a much better way to go because you're very selectively inhibiting that negative signal and allowing the free PVRL2 to bind to and activate through dNM. With regards to other molecules that PVRL2 binds to, as I mentioned in the presentation, it has been reported to bind to TIGIT, although in the literature and in the studies, we've done in house we see that as a very affinity interaction that we're not sure whether it's theologically relevant, but again really one of the key activities for PVRL2 is to send the second stimulatory signal to T-cells through dNM for activation.
Okay, got it, I guess I've one follow-up. So in upcoming on the following, we reasonable to assume that it will include the mechanism of how COM701 the antibody binds to PVRIG and also effects as we discussed PVRL2 and other associated ligand as well?
Yes, the mechanism of action that we have for COM701 is that, it does bind to PVRIG and it completely disrupts the PVRL2 interaction. And studies that we've run which strongly suggest that to get the inhibitory signals through PVRIG, it does require binding to PVRL2. So, it's really just a blocking mechanism of action, and we are looking at effects of blocking that on downstream signaling from PVRIG.
The next question is from Steven Bayer [ph]. Please go ahead.
Hi, this question is more general. Could you give some details about timeframes or the range of timeframes that it takes to move some of the programs forward, and I guess the steps involved, I mean on your mechanism of action, validating in vivo, finding a binding partner et cetera. You know the bare deals over three years old, are there -- I mean I guess apparently given of this 15029 is moving along know. There is obviously a range of timeframes, but sort about the any particular steps that are slower than others, any information that we can maybe gauge what expectations going forward are for other programs or do you learn anything from what you are doing now that might speed up other programs?
Yes, there are couple of variables here, I would say that from the stage of lead selection to IND to Phase 1, Phase 2; in general, I would say that industry standards are relevant to everyone and of course also to Compugen. But I think the pre-lead selection there are different variables that would either shorten or extend the timelines, and it depends on the following.
In general and I think that you know it by now, I am saying it and I relate it to almost every quarterly call, the fact that we are working on proteins that we discovered a drug target that do not have a lot of information in the public domain doesn’t have a lot of years of literature around them, is generating a situation for Compugen that we need to make sure that we have the understanding that other have on their known targets when we are moving ahead with the therapeutic program.
This may vary as to what's the nature of the target. There are targets that we can get this information faster as compared to other targets. And it is really has to do, not with the potential of the target to become a good drug target for the development of therapeutics, but really about the mechanism affection how complicated this is, how new it is, do we have the systems, other industry standards, how much we think we can trust one or two systems or need to expand to 10 or 20 different systems. And this all has to be taken into consideration, both for our internal program.
And also it applies you mentioned the two buyer programs without getting into details with respect to the bio programs that we cannot share, you know by now that’s one of them we already got through different preclinical milestones, and that the consol move to buy for this specific program that is more advanced. And there is another program that is less advanced and takes more time. So, it's really by the nature of the target and the amount of work that has to be on it. And this is the variable, and this is the variable within Compugen internally for each of our program and also with respect to Compugen as compared to the rest of the industry.
The next question is from Vernon Bernardino of FBR. Please go ahead.
Thanks for taking my question and congrats on the reveal of the targets and the candidate. I am just wondering if you could describe a little bit about the efforts and what activities have you already done as far as intellectual property of protection?
Yes, it’s a very sensitive question that I'll give you an answer that is broader than what you are asking because I think this is something that’s interest different shareholders. In general, we do not give any specific information about filings that we do. This is something that has to do with the competition and how we protect our IP, as you could probably see in the public domain, there are patents of Compugen and we always take care not to connect between the CGEN name and this specific target that is mentioned in the pattern, this is now for us, the first time that we have done that with PVRIG and CGEN-15029.
And again, as I was mentioning while we feel comfortable with the IP strategy that we are applying, and with the different filings that we have done throughout the years, it is better for us to make sure that we control when is the right timing for us to speak and when is the right timing for us to connect to the CGEN name to the target. And in general, we preferred to avoid an unnecessary competition and risk that we may put our patterns to. So, in general, the short answer is that we are hearing at out of information on this for a reason.
No, I understand, thanks Anat. I was just wondering confirm, but you have already started the application process?
Yes, of course. We already have prior filings on this, yes.
The next question is a follow-up from Mike King. Please go ahead. Mike, are you with us?
John, I was just wondering if you could clarify for me some terminology because I know there is a paper from Colorado Group in February describing the interaction of PVRIG in the ligand. So, could you just sort of translate for us, if we see these turn up in other publications of CD226, CD112 and CD112R?
Sure, yes, like many other areas of the literature, there is a lot of different names for some of the same molecules. So, CD112 is just a CD designation for PVRL2, and when the Colorado Group realized that PVRIG bound what they renamed it CD112R. The original designation in the data base when we found, it was PVRIG which is why we stuck with that. DNM1 is also known as CD226.
Yes, and then with regards to the findings in the Colorado paper, they actually matched quite well with a lot of the research we have been doing here. So, in terms of looking at effects on T-cell activations, they were more focused on CD-4 cell activation because of our focus on tumor biology, we really have been focusing on CD-8 activation. But we did see some of the same effects that they have reported in the paper.
There are no further questions at this time. Before I ask Martin Gerstel to go ahead with some closing statements, I would like to remind participants that a replay of this call is scheduled to begin in two hours for a period of 72 hours. In the U.S., please call 1-888-295-2634. In Israel, please call 03-925-5921. Internationally, please 972-3925-5921. Martin Gerstel would you like to make concluding statement?
Yes, thank you very much. Pioneering a paradigm shift in the underlying methodology used to create new products in a well established and already very profitable industry is never an easy task, and it becomes much more difficult when the underlying science required for the intended paradigm shift is not yet known. As was the case when Compugen began its efforts at using in silico science based predictive biology to discover novel drug targets.
Today even though all of our programs and product candidates are still at very early stages, the compelling data discussed today for one of our novel checkpoint based immuno-oncology programs clearly demonstrate that in silico predictive science-based methodologies can in fact identify very promising novel drug targets, an important unmet need in the industry and something that few industry leaders would have believed possible prior to our demonstrated success.
In closing today's call, I want to thank all of you for participating and for your interest in our company, and a very special thank you to our long-term shareholders who’ve provided us support and encouragement through the years, as we developed the unique and broadly applicable capabilities that have allowed us to now reach this critical point. And it is just the beginning, thank you very much.
Thank you, this concludes the Compugen Limited third quarter 2016 financial results conference call. Thank you for your participation you may go ahead and disconnect.
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