Fate Therapeutics, Inc. (NASDAQ:FATE)
Q4 2013 Earnings Conference Call
March 17, 2014 5:00 PM ET
Scott Wolchko – Chief Financial Officer and Chief Operating Officer
Christian Weyer – President and Chief Executive Officer
Pratik Multani – Chief Medical Officer
Peter Flynn – Senior Vice President-Early Program Development
Simos Simeonidis – Cowen & Co. LLC
Dilip Joseph – Wedbush Securities, Inc.
Welcome to Fate Therapeutics Fourth Quarter 2013 Financial Results Conference Call. At this time, all participants on a listen-only mode. This call is being webcast live on the Investors and Media section of Fate’s website at fatetherapeutics.com. This call is a property of Fate Therapeutics and recordings, production or transmission of this call without the express written permission is strictly prohibited. As a reminder today’s call is being recorded.
I would now like to introduce Scott Wolchko, Chief Financial and Chief Operating Officer of Fate Therapeutics.
Thank you. Good afternoon and thanks everyone for joining us for the Fate Therapeutics fourth quarter 2013 Earnings Call. At 4:00 PM Eastern Time today we issued a press release with our fourth quarter and full-year 2013 financial results, which can be found on the Investors and Media section of our website under press releases.
In addition, our 2013 10-K was filed shortly thereafter and could be found on the Investors and Media section of our website under financial information.
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 provisions 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 on the company’s earnings press release issued after the close of market today, as well as the risk factors in a company’s SEC filings, including our 10-K for the year ended December 31, 2013, that was filed with the SEC today.
Undue reliance should not be placed on forward-looking statements, which speak only as of the date they are made, as the facts and circumstances underlying these forward-looking statements may change. Except it is required by law, Fate Therapeutics disclaims any obligation to update these forward-looking statements to reflect future information, events or circumstances.
Joining me on the call today are Dr. Christian Weyer, President and Chief Executive Officer of Fate Therapeutics, Dr. Pratik Multani, Chief Medical Officer and Dr. Peter Flynn, Senior Vice President of Early Program Development.
I will first review our financial results for the fourth quarter of 2013, then Christian, Pratik and Pete will provide corporate and development program updates. After that, we are happy to take any questions that you might have.
So, turning our attention to the financial results for the fourth quarter of 2013. In October 2013, we completed our Initial Public Offering, establishing a strong financial foundation to advance our therapeutic platforms and programs and to pursue our long-term goal of bringing novel stem cell therapeutics the patients in need.
In the IPO we have raised net proceeds of $40.5 million, and all our previously issued convertible preferred stock and convertible promissory notes converted into common stock. At the end of the fourth quarter of 2013, our cash and cash equivalents were $54 million, our debt outstanding was $1.8 million, and we had approximately 20.4 million shares outstanding.
For the three months ended December 31, 2013, Fate Therapeutics reported a net loss of $5.7 million as compared to a net loss of $4.2 million for the fourth quarter of 2012. The company did not generate any revenues in the fourth quarter of 2013, compared to approximately $600,000 for the fourth quarter of 2012.
Research and development expenses for the fourth quarter of 2013 was $3 million, compared to $3.4 million for the fourth quarter of 2012. This decrease in the fourth quarter of 2013, compared to the fourth quarter of 2012 was primarily due to the timing of clinical and regulatory related start-up costs, incurred in the fourth quarter of 2012 in connection with the initial launch in December 2012 of our Phase II clinical trial of PROHEMA.
General and administrative expenses for the fourth quarter of 2013 were $1.9 million, compared to approximately $1.3 million for the fourth quarter of 2012. This increase was primarily driven by an increase in employee compensation, including salaries, benefits and stock-based compensation expense and to incremental legal accounting and insurance expenses, primarily to support public company operations.
Total operating expenses for the fourth quarter of 2013 were $4.9 million, compared to $4.7 million for the fourth quarter of 2012. After adjusting for stock-based compensation expense of approximately $400,000, total operating expenses for the fourth quarter of 2013 were $4.5 million. Based on our cash and cash equivalents at the end of the fourth quarter of 2013, which were $54 million. We believe we have sufficient cash resources to provide operating runway until late 2015.
I will now turn the call over to Christian to discuss our execution against key development milestones and our outlook for development programs.
Thank you, Scott and good afternoon everyone. Ever since the founding of Fate Therapeutics in 2007, it has been our mission and passion to pioneer novel therapeutic intervention strategies that harness the funds of stem cells. Today, this steady focus and commitment has resulted in a therapeutic pipeline, that has curative or transformative potential across a range of rare life-threatening diseases, including certain hematologic malignancies, rather than the storage disorders and muscular dystrophy.
Throughout 2013, we successfully executed against key development milestones and a vast of our clinical and preclinical therapeutic programs, tell us important value of production points. This strong momentum has continued in to 2014.
First and foremost, we announced last week a patient enrollment has commenced in our Phase 2 PUMA study of PROHEMA in adult patients with hematologic malignancies. Results from a planned interim analysis are expected in the second half of 2014.
In addition, in the first quarter of 2014, we engaged the FDA and dialog concerning the evaluation of PROHEMA in pediatric patients. We expect to initiate clinical trials in pediatric patients with hematologic malignancies and with certain lysosomal storage disorders later this year.
We also announced earlier in this month, promising additional data from our previously completed Phase 1b study of PROHEMA. Researchers from Harvard Medical School reported improved survival and immunological properties of T cells in patients receiving PROHEMA. Consistent with our findings, we reported low rates of viral reactivation in PROHEMA patients from our Phase 1b study.
We advanced our Wnt7a protein therapeutics program for muscle regeneration into IND-enabling activities, initiated production cell line development and remain on track for initial clinical evaluation of this novel mechanism in 2015.
Finally, we published additional scientific papers describing our proprietary, induced pluripotent stem cell platform and begin exploring therapeutic applications using this technology.
Let me briefly elaborate on some of these important areas of progress, before turning the call over to Pratik and Pete for a more detailed update on our therapeutic programs. That said, last week, we did announce commencement of patient enrollment in our Phase 2 PUMA study of PROHEMA. This key milestone marks the successful implementation of its change to the manufacturing process to further optimize the expected clinical potency and efficacy of PROHEMA.
As you might recall, in preclinical studies, PROHEMA manufactured using the company’s new NRM formulation exhibited more than two-fold improvement in HSC engraftment as compared to the standard cell processing media that we have previously used in the clinical development of PROHEMA.
We were diligently in close contact with FDA and clinical investigators to implement this manufacturing change in a timely manner. We are obviously very excited about the potential impact on patient outcomes and with the trial already approved for conduct at ten leading U.S. transplant centers, we are in fact to meet our previously communicated milestones.
Additionally, we remain on track to amend our existing IND in the second quarter of 2014 to commence clinical development in pediatric patients with hematologic malignancies. We believe this positions us well to pursue a broad indication for PROHEMA as the first product opportunity from our HSC modulation platform.
Moving beyond hematologic malignancies, we believe there is significant potential for PROHEMA franchise expansion in rare genetic disorders. There are considerable clinical precedent for the use of allogeneic HSC transplantation as a definitive one-time corrective therapeutic intervention in over 50 rare genetic disorders.
And since PROHEMA is derived from normal healthy donor HSCs it has the inherent potential to correct genetic defects across a wide range of rare genetic disorders, but they are caused by defective genes including enzymes, hemoglobin or other essential proteins.
In the first quarter of this year, we made significant progress for the initiation of a clinical study of PROHEMA and lysosomal storage disorders, including Hurler syndrome, Krabbe disease and certain leukodystrophies, all of which are characterized by progressive neurocognitive deterioration that cannot be addressed with enzyme replacement therapy.
We’re excited about the potential of PROHEMA in this diverse patient population for which the promise of allogeneic transplant has yet to be fully to be realized. Over the past several months, we generated compelling preclinical data demonstrating that the ex vivo modulation of HSCs improves their homing and engraftment, not only to the bone marrow, but also to the CNS, resulting in a several-fold increase in donor derived expression of missing enzymes within the brain.
These preclinical findings coupled with a potential to improve engraftment outcomes and the overall risk benefit of HSC transplantation provides compelling rationale for the clinical investigation of PROHEMA in patients with LSDs. We also continued with advanced IND-enabling activities for our Wnt7a protein therapeutics program.
Wnt7a, as a natural promoter of muscle satellite stem cells and muscle regeneration, and we have rationally designed proprietary Wnt7a protein analogs that are amenable to scale, manufacturing and therapeutic development. We believe its mechanism has therapeutic potential across a range of muscle disorders, including multiple forms of muscular dystrophy, which is the focus of our initial program development. Based on our encouraging preclinical results to date, we have now expanded the preclinical assessment of our proprietary Wnt7a protein analogs beyond muscular dystrophy to include other areas of muscular damage.
Finally, we continue to be very enthusiastic about the therapeutic promise of iPSC technology. This Noble Prize-winning technology continues to emerge and mature, and is now beginning to move in to initial clinical trials. Fate is well positioned as the leader in the development of iPSC derived therapeutic, as we will further elaborate on later on in the call.
But first, let me turn the call over to Pratik to discuss our PROHEMA clinical program in greater detail.
Thank you, Christian. As Christian mentioned, we’ve recently announced patient enrollment has commenced in our Phase 2 PUMA Study. A randomized controlled Phase 2 multicenter clinical trial in adult patients undergoing double umbilical cord blood transplant for hematologic malignancies.
PUMA stands for PROHEMA in UMbilical cord blood transplant in Adults. This trial was intended to enroll 60 patients. Eligible patients will be randomized at a ratio of 2:1 with approximately 40 patients in the PROHEMA arm, receiving PROHEMA, plus an unmanipulated cord blood unit in approximately 20 patients in a control arm receiving two unmanipulated cord blood units.
Based upon physician’s choice, patients will be treated with one of two conditioning regiments and intend myeloablative regimen or a reduced intensity regimen. Randomization will be stratified by conditioning regimens. The primary-end point uses a categorical analysis. Specifically, the cumulative incidence of neutrophil engraftment or patients in the PROHEMA arm who engraft prior to the median day of neutrophil engraftment in the control arm. The trial was designed to demonstrate with statistical significance that 70% of the PROHEMA arm patients achieve neutrophil engraftment before the median controlled day, and we have 80% power to detect this effect with a one sided P value, less than 0.05.
Safety reviews by the data monitoring committee for the PUMA study are planned after the first six and 12 patients respectively, have been treated with PROHEMA and are valuable for engraftment end points. The results of these reviews will be shared with our site R&Ds and the FDA, and we expect to provide an update on our PROHEMA program in the second half of 2014, following the completion of these initial reviews.
Now let me take a step back and discuss what we are looking for in this study, and how we would define success. As I stated, the primary endpoint is based upon a categorical analysis, a median time to neutrophil engraftment. It is important to point out that this parameter is only one way to look at patient outcomes.
given that it focuses only on the midpoint of the entire distribution of engraftment times across the steady population. We will also be analyzing data from the tail of the engraftment curve. The tail of that curve is highly, clinically relevant and that it captures patients with delayed or failed engraftment who have the highest risk of early mortality.
So, we were also deemed a steady success, and PROHEMA had a meaningful impact here, by either reducing the incident of graft failure or by bringing in the tail of the curve, reducing the number of patients with late engraftment. and of course, we will be analyzing early mortality rates in the first three or four months post-transplant, as well as key parameters contributing to treatment-related mortality such as viral and bacterial infections, graft-versus-host disease and delayed immune reconstitution.
A sizable reduction in anyone of these parameters will be highly clinically meaningful, provides strong rationale and guidance for Phase 3 development. Now as we stated, we’ll be conducting early interim reviews of the data after the first six and 12 patients are treated with PROHEMA and have the engraftment data available.
The analysis is primarily for safety review by the Data Monitoring Committee told us it’s a pre-specified unacceptable rates of either graft failure or early mortality. But since in the context of transplant, safety and efficacy are two sides of the same coin, we will be analyzing other endpoints as well, including the engraftment times, serious infection in graft-versus-host disease rates.
At these initial interim reviews, this study will not have statistical power around the primary or secondary endpoints. nevertheless, the data may provide the important sites to guide future development; if for instance, we were to see evidence of a profound treatment effect. We would explore the potential for more accelerated development plan and seek early input from the FDA, as to how the current trial could be modified, or otherwise leveraged to support pivotal development.
We are also pleased to report progress towards initiation of a clinical study of PROHEMA in pediatric patients. based on our communications with clinical investigators, we have developed a clinical protocol, which we have submitted to FDA.
We planned to file an IND amendment in the second quarter and initiate patient enrollment in the third quarter of 2014. our objective with this study is to develop sufficient pediatric data to supplement our adult Phase 2 experience and potentially, allow a single Phase 3 study, encompassing both adult and pediatric population with the hematologic malignancies.
We’ve also been working for leading pediatric transplant centers on the design of an initial clinical protocol for patients with a range of lysosomal storage disorders, or LSDs. Based on recent interactions with FDA; we planned to file an IND in mid-2014 and to initiate a clinical study in the second half of 2014. In addition to standard assessments related to safety and engraftment, we planned to follow patients longer-term for development outcomes related to the CNS manifestations of their respective enzyme deficiencies.
Importantly, the study is expected to be open-label, allowing us to evaluate patient outcomes on a rolling basis to give us a flexibility to act quickly on compelling data and expedite regulatory interactions. and finally, we may have the opportunity to leverage the efficacy and safety data, we are generating in the hematologic malignancy program to expedite development in LSDs, especially we’re seeing compelling results in our initial experience.
Before I turn the call over to Pete, let me briefly expand on our recent announcement concerning the ex vivo modulation of T cells. collaborators from Harvard Medical School analyzed samples from our previously completed Phase 1b study, PROHEMA, and we reported that ex vivo modulation improved the survival and immunological properties of T cells, including skewing of the T cell population towards naïve CD8+ T cells.
They concluded that this observation may translate into clinically relevant effects on immune memory on, both pathogen and tumor-specific immunity. In fact, consistent with these reported immunomodulatory affects, lower rates of viral reactivation were observed in patients from the PROHEMA cohort in our Phase 1b study.
We are excited by these findings, because as with hematopoietic stem cells, T cells are actively used in current transplantation therapy. for example, donor provided T cell infusions are already used after allogeneic transplantation to treat disease relapse.
In addition, cultured or modified T cells are also under clinical investigation to treat viral infections and certain T cell malignancies. We believe our promising findings concerning the ex vivo modulation of T cells, not only represent a possible additional favorable product attribute of PROHEMA, but may also point to the future potential of our ex vivo modulation platform as a means to optimize T cell-based cellular therapeutics.
Now I will turn the call over to Pete.
Thanks, Pratik. I will be providing an update on the Wnt7a muscle generation program and then some background on our induced pluripotent stem cell technology. As Christian mentioned, our satellite stem cell modulation platform uses analogs the naturally-occurring protein Wnt7a to target the adult stem cell population of muscle and drive tissue regeneration.
We are enthusiastic about the potential of this preclinical program for the following reasons: satellite cells or the regenerative stem cells with muscle, they become activated, revised and reconstitute muscle in response to damage or exercise. Wnt7a is a natural driver of stem cell expansion in muscle and as for receptor that is seem to be predominantly expressed in muscle tissue.
We have established preclinical proof-of-concept in a rodent model of muscular dystrophy, the MDX mouse, with a proprietary Wnt7a protein analogs. Here with significant increase in the number of satellite stem cells and reduced tissue inflammation and damage, we also observed the significant increase in muscle strength of just a single intramuscular administration of protein.
Wnt proteins comprise a major family of signaling molecules that drive development within the embryo and tissue growth and repair in the adult. We believe we are the first group to engineer and analog of Wnt protein that is amenable to scale production and pharmaceutical development, while retaining the specific activity of the protein. We believe there is tremendous therapeutic opportunity here, beyond our first example of Wnt7a.
As we highlighted in our last corporate update call, we have selected two IND candidates for further development. In the first quarter of 2014, we initiated production cell line development and we are currently finalizing our cGMP contract manufacturing plans and outsourcing activities to enable initial clinical assessment of a Wnt7a protein analog in 2015.
Additionally, based on our encouraging findings in the MDX mouse model, we have expanded our preclinical pharmacology assessments to include additional dose regimen studies in both wild-type and MDX model assistance and initiated studies in other non-dystrophy models of muscle trauma and damage.
Importantly, while our human proof-of-concept remains to be established in clinical studies, we have recently published data demonstrating the Wnt7a drives significant hypertrophic effects in culture human muscle cells, including muscle cells derived from the patients with various forms of muscular dystrophy. These in vitro findings provide support for the conservation of the Wnt7a-mediated signaling mechanism and that these proteins have potential to [indiscernible] muscle regenerative activity in patients with muscular dystrophy.
To obtain large quantities of muscle cells from dystrophy patients all these experiments, we have applied our proprietary induced pluripotent stem cells, or iPSC technology platform. We saw skin cells from patients with Duchenne and Becker muscular dystrophy and used our cellular reprogramming technology to derive iPSCs. We then differentiated these iPSCs into muscle cells, which we then treated with our Wnt7a protein analogs.
These experiments demonstrate potential of iPSC technology, which has the ability to take a differentiated somatic cell, such as a skin cell or a blood cell and reprogram it at the molecular and cellular level, back to a state similar to that of an embryonic stem cell.
iPSCs can be expanded and definitely in culture and have the capacity to be differentiated into any cell type in the body, therefore allowing the generation of large quantifies with any human cell type for many genetic background.
One important application of this technology includes the modeling of genetic disease as exemplified by the aforementioned in vitro testing of our muscular dystrophy therapeutic candidates.
Further, the clinical potential of iPSC technology for deriving regenerative cell therapeutics is now being realized. The first clinical trials of iPSC derived cells now underway. The most advanced trial involved the programming of the patient skin cells and differentiating them into retinal cells, an autologous treatment in muscular degeneration.
Supported by the company’s scientific standards who are renowned leaders in the field of iPSC technology, scientists at Fate laboratories have been working for the last five years on approaches to industrialize iPSC technology and further enable therapeutic use.
We have published these findings along the way and we are now actively exploring the therapeutic application of iPSCs in the two areas of our biological expertise on hematopoietic cells and muscle cells. We will continue to provide updates on our progress as we move forward with this platform.
I will now turn the call over to Christian for some additional comments prior to Q&A.
Thank you, Pete. As I believe it’s evidenced from the progress with our programs, we are highly focused on execution again our stated factors. Now I would like to take this opportunity to acknowledge our dedicated employees, who have exhibited tremendous commitment to advancing our mission.
I would also like to welcome Dr. Rob Epstein to our Board of Directors; his appointment was announced separately this morning. Rob’s extensive experience and expertise in health economics and chemical research will be invaluable to Fate as the clinically advanced and expand our novel therapeutic and intervention strategies to harness the promise of stem cells.
And with that, I would like to turn the call over to the operator for any questions.
(Operator Instructions). Our first question comes from Simos Simeonidis with Cowen and Company. Your line is open.
Simos Simeonidis – Cowen & Co. LLC
Hi, thank you for taking the question. I just want to ask you about the internal look on PUMA. you said that, it can’t be mostly FT enhancement [ph], but you’ll be able to bring some efficacy, potentially efficacy in fact. And I’m just wondering, given that, only you are going to have 12 patients on the PROHEMA and more importantly I guess, there is only going to be about half of that, five or six or seven on the control arm and given that as you said, you are going to base – the hurdle that you are going to have on the control arm, given this bundle of patient, how meaningful of an efficacy conclusion can you get from that?
Yes Simos, this is Christian speaking. Thank you for your question. As Pratik pointed out, the trial is powered for time to engraftment based on sixty patients and we remain on track to generate full data of that study in mid-2015. That being said, it is, we believe that is possible that there’s meaningful insights to be gleaned, based on the first 12 PROHEMA patients. Although remind you that the initial Phase 1b experience we have published in latter last fall, actually was based on results from 12 patients, so we – we’ll not be able to draw definitive conclusions from this result. We believe that there is a potential for important, really insights that would allow us to inform our further development of potentially regulatory interactions. Anything to add?
I guess I would just highlight two points. one is, as you’ve already – as I’ve stated during the – earlier in the call, engraftment represents both the safety and efficacy evaluation. and so that’s why we would be looking it on – in both terms. That said, as you’ve already highlighted, there will be relatively few number of patients in the context of the entire planned study size. and so I think the expectation is that, we may be able to see trends. they may or may not materialize by that point, but if we do see trends and it provides us with the opportunity, especially if they are significant trends to act quickly and see if we can capitalize on that really working.
Simos Simeonidis – Cowen & Co. LLC
No. Would you say if that didn’t make sense, just Pratik, when you talked during your prepared remarks that you are not just – again, I think correctly looking just at the median. but you are also going to look at the tails of the curve. That makes the numbers have been smaller, but if you – you’re spreading the number of patients the control arm over a couple of areas in the curve. again, it makes it difficult to see something, unless again, is it something very meaningful. So, thanks for the clarification. The other question I had is on the patient – on the pediatric patient trial, PROHEMA and then on the LSD trial. Can you give us a rough, I think how big of these trials would be and whether they would be U.S. only, interestingly in Europe, can you talk about that?
I would just say that we are planning to conduct a study primarily U.S., but we are in active discussions with FDA around the trial design of study size, what would be appropriate, what would be feasible. So, I can’t comment more specifically, on that at this point.
Simos Simeonidis – Cowen & Co. LLC
Okay. And then finally on Wnt7a, you’ve mentioned two potential molecules, are they different analogs, are they – are you just still trying to figure out which one of my reads the best ones put on the clinic. Can you say anything about these two molecules?
Sure. Absolutely, let me take the first statement and turn it to Pete, I think what’s important to recognize here is that, as we said in our prepared remarks, there is potential for this Wnt7a mechanism across a right range of muscle-related disorders, including muscular dystrophies, as well as non-muscular dystrophy related disorders. So we have elected to take two of those analogs into IND-enabling activities, they are structurally distinct and Pete can comment on that. but we have also clarified that we’ve planned to take one of those into clinical assessment in 2015.
Yes, Simos. I’ll just add to that by saying yes, those two forms that both have been taken into cell line development, which is the best part of the manufacturing process. The reason for taking Q4 is that both – both showing good efficacy in the model systems that we’ve outlined. They do show slightly differing production capabilities, but that we won’t see that all the way through until we get to the next sets – stage of the scale up. and so we really wanted to have the evaluation of scale of the both forms.
Having both forms through that stage also potentially saves time going forward. if we want – want to better take a second generation or multiple generations forward. To clarify, it is our initial intention to take one form through the full cGMP manufacture, the first clinical development, not two forms. but we want to say these two forms have slightly different characteristics and production, at least some ways along the way.
Simos Simeonidis – Cowen & Co. LLC
So I guess that you’re still trying to figure out the best molecule to put in the clinic and it’s not that it’s one of the two forms has is kind of a – is a better target for example, dystrophies or another muscle disorder, it’s more of the best clinical molecule to put forward, correct?
Well, I mean I think that we have a pretty good idea on actual activity within the model systems, I said the only sort of the decision process, which is a near-term to decision process is just that scalability to sort of – obviously, we’re the first people to develop a Wnt-based protein therapeutic. and so we want to take the strongest candidate forward into production. There are some other differences in the molecular characteristics, which may allow want to be better to develop in one therapeutic setting them one in another, but I think it will be best if we update that along the way.
Simos Simeonidis – Cowen & Co. LLC
Sounds great. thank you very much for taking the questions.
(Operator Instructions) The next question comes from David Nierengarten with Wedbush. Your line is open.
Dilip Joseph – Wedbush Securities, Inc.
Hi, it’s Dilip Joseph, sitting in for David. Just had a question related to the current formulation of PROHEMA and whether or not need to be improved, or enhanced in any way for the lysosomal storage disorder trial?
Yes, absolutely, a good question, and thanks for the question. Now we have optimized the manufacturing process on multiple levels, being the temperature, the duration of the modulation process, the concentration of the modulator. and most recently, as we said in our prepared remarks, the media in which the formulation – the moderation actually occurs. and so with that, we are not planning an additional optimization of the PROHEMA program, as we are trying it within hematologic malignancy and into rare genetic disorders.
The only change that we would need to make is, just a smaller volume of PROHEMA in the pediatric setting, not just in LSDs, but also hematologic malignancies. but that’s a sort of a physical manipulation as opposed to any change in how we modulate the network stem cells.
Dilip Joseph – Wedbush Securities, Inc.
So in pediatric patients, whether or not is the hematologic malignancy or LSD setting, a sustained formulation?
Yes. that’s our intent.
Dilip Joseph – Wedbush Securities, Inc.
Thank you. I will turn it back to management for closing remarks.
Well, thank you and thank you for your participation in today’s call. We look very much forward to updating you again, very soon.
Ladies and gentlemen, thank you for participating in today’s presentation. You may all disconnect. Have a great day.
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