Sangamo Therapeutics Inc (SGMO) 2012 Q2 法說會逐字稿

Good afternoon, and welcome to Sangamo BioSciences' teleconference to discuss second quarter 2012 financial results. This call is being recorded.

I will now pass you over to the coordinator of this event, Dr. Elizabeth Wolffe, Senior Director of Corporate Communications.

Thank you, Kate. Good afternoon, and thank you for joining Sangamo's management team on our conference call to discuss the Company's second quarter 2012 financial results. Also present during this call are several members of Sangamo's senior management, including Edward Lanphier, President and Chief Executive Officer; Ward Wolff, Executive Vice President and Chief Financial Officer; and Geoff Nichol, Executive Vice President of Research and Development; Philip Gregory, Vice President of Research and Chief Scientific Officer; and Dale Ando, Vice President of Development and Chief Medical Officer.

Following this introduction Edward will highlight recent activities and significant events from the past quarter. Ward will then briefly review second quarter financial results as well as our financial guidance for 2012. Philip and Geoff will provide an update on our ZFP Therapeutic programs, and, finally, Edward will update you on our goals for the rest of 2012. Following that, we will open up the call for questions.

As we begin, I'd like to remind everyone that the projections and forward-looking statements that we discuss during this conference call are based on the information that we currently have available. This information will likely change over time. By discussing our current perception of the market and future performance of Sangamo with you today we are not undertaking an obligation to provide updates in the future. Actual results may differ substantially from what we discuss today, and no one should assume at a later date that our comments from today are still valid.

We alert you to be aware of risks that are detailed in documents that the Company files with the Securities and Exchange Commission, specifically our quarterly reports on Form 10-Q and our Annual Report on Form 10-K. These documents include important factors that could cause the actual results of the Company's operations to differ materially from those contained in our projections or forward-looking statements.

Now I'd like to turn the call over to Edward.

Thank you, Liz, and thank you all for joining us on our conference call to discuss our second quarter results for 2012 as well as recent events and our plans for the rest of the year.

It has been a busy first half of the year, during which we have made significant progress in advancing our clinical and preclinical programs as well as our business model, and we are pleased to have an opportunity to provide you with more details and the expected timing of clinical milestones on this call.

First, our preclinical pipeline, which includes programs that we are developing for our own account as well as with our partner, Shire, are progressing very well. To remind you, in early February we entered into a strategic alliance with Shire to develop our ZFP Therapeutics as a potential genetic cure for hemophilia and other monogenic diseases. Upon executing the agreement, we announced the selection of hemophilia targets Factors VII, VIII, IX and X. Shire also received an option to name three additional targets.

I'm very pleased to announce today that Shire has selected a fifth target and has committed to support the development of a ZFP Therapeutics for Huntington's disease, a program that we had previously initiated with funding from the CHDI Foundation, a research foundation focused on developing a cure for Huntington's disease. I've asked Philip to provide you with some background on the disease and more details on why we believe our technology can generate a unique approach to the treatment of Huntington's later on the call.

Because our ZFP technology works very specifically and efficiently at the DNA level, it enables us to provide unique therapeutic solutions to diseases where the cause has been traced to a defect in a single gene, so-called monogenic diseases. Huntington's is a well-studied example, as you will hear later. However, there are many monogenic diseases. We are actively working on several other single-gene-based disorders, some of which were highlighted in presentations at the annual American Society for Gene and Cell Therapy meeting in June.

However, up to this point, beyond presentations of data at scientific meetings and publications in peer-reviewed journals, we have not provided a great deal of visibility on these programs. That will change at the end of this year. We plan to host an analyst briefing on December 6th, at which time we will discuss our preclinical monogenic disease programs, our development plans and the timing for IND filings and associated financial projections. The briefing will be webcast, and details regarding the exact timing of the event will follow later this year.

Moving on to our lead clinical program, SB-728, which we are developing as a potential functional cure for HIV, I am pleased to report that our two Phase 2 studies are also progressing on plan. As most of you know, based upon encouraging Phase 1 data, we announced the initiation of two Phase 2 trials during the first quarter of this year. At that time we said that we would update you on the expected timing of clinical data once we had had an opportunity to assess the rate of enrollment. I have asked Geoff to provide you with more details on the trials and anticipated timing of data from those studies later on this call.

However, before I hand the call over to my research and development colleagues to provide more details on our ZFP Therapeutic programs, let me ask Ward to summarize our second quarter 2012 financial results as well as our financial guidance for 2012.

Ward?

Thank you, Edward, and good afternoon, everyone.

As you know, after the close of the market today we released our financial results for the second quarter ended June 30, 2012, and I'm pleased to review the highlights of those results.

Revenues for the second quarter of 2012 were $4.6 million, compared to $1.5 million for the 2011 quarter. Second quarter 2012 revenues were comprised of revenues from the Company's new collaboration and license agreement with Shire to develop ZFP Therapeutics for hemophilia and other monogenic diseases, existing collaboration agreements with Dow AgroSciences and Sigma-Aldrich Corporation, including a $1 million commercial milestone from Sigma, enabling technology agreements, as well as approximately $0.8 million of revenue from research grants.

As we mentioned in today's press release, the increase in collaboration agreement revenues was attributable to the Company's agreement with Shire. As we explained on our first quarter call, we are amortizing the $13 million upfront license fee over the initial six-year research term, resulting in $0.05 million recognized as related revenue in the second quarter. In addition, collaboration agreement revenue included $1.5 million in revenue related to the reimbursement of internal and external program-related costs from Shire during the quarter.

Total operating expenses for the second quarter of 2012 were $10.3 million, compared to $11.8 million for the same period in 2011. Research and development expenses were $7.6 million for the 2012 quarter and $8.1 million for the prior-year quarter. General and administrative expenses were $2.7 million for the second quarter of 2012, compared to $3.7 million for the 2011 quarter. Noncash stock-based compensation expense was $1.2 million for the quarter, equally split between research and development and general and administrative.

For the second quarter of 2012 we reported a consolidated net loss of $5.7 million, or $0.11 per share, compared to a net loss of $10.3 million, or $0.20 per share, for the second quarter of 2011.

Turning to the balance sheet, we ended the second quarter of 2012 at approximately $81 million in cash, cash equivalents and marketable securities. Net cash used in operating activities was $6 million for the quarter and $3.1 million for the year to date.

Our financial guidance for the year remains unchanged from the first quarter call in May. We expect to have cash and investment balances of at least $75 million at the end of 2012, inclusive of the Shire agreement but exclusive of any new funding from a partnership or other sources. We also expect 2012 operating expenses to be in the range of $43 million to $47 million and revenue to be in the $14 million to $18 million range, again, inclusive of the research funding from Shire for internal and external program-related costs -- research program-related costs.

In summary, we are pleased to report that the second quarter results are tracking to our 2012 operating plan. Our therapeutic collaboration with Shire has enhanced our leverage in managing our finances and balance sheet and complements the business model established for our existing partnerships outside of human therapeutics. We are in an excellent financial position to complete our ongoing clinical trials and continue to advance our preclinical pipeline, and we look forward to keeping you updated on our progress.

Thank you, and I will now turn the call back over to Edward.

Thank you, Ward.

Our business model for developing our ZFP technology platform has enabled us to partner not only therapeutic programs, as we have recently demonstrated with Shire, but also nontherapeutic applications of our technology. These nontherapeutic partnerships with Sigma-Aldrich in research reagents and Dow AgroSciences in plant agriculture have brought significant resources into the Company, over $85 million to date.

We are very pleased to announce today the achievement of our first commercial milestone, which, as Ward described, was a result of sales of ZFP products for research applications by Sigma. In addition to the revenues that we have received as a result of this agreement, Sigma's broad distribution of our technology into the hands of scientists all over the world as a result of their impressive and imaginative product development and marketing efforts, have been very useful to us, as it has significantly broadened the appreciation of the power of our ZFP technology, particularly in the pharmaceutical industry.

The amortized upfront payment and ongoing research funding from our strategic alliance with Shire as well as the ongoing revenues from our collaborations with Dow and Sigma enable us to aggressively and expeditiously move our ongoing clinical- and preclinical-stage therapeutic programs to points of significant value inflection while maintaining a very modest burn rate. As you have heard, we have a solid cash position and remain on track to meet our guidance of ending 2012 with at least $75 million in cash.

So, with very strong financial underpinnings, on to our preclinical and clinical development programs. I've asked Philip to update you on the Shire-selected Huntington's disease program and Geoff to update you on our ongoing HIV clinical trials, the expected timing of those data and our plans to provide more details later this year on our preclinical pipeline, particularly our work in rare and monogenic diseases.

Philip?

Thanks, Edward.

Our ZFP technology functions at the DNA level, enabling both control of gene expression, the ability to turn gene expression on or off, and the direct editing of gene sequences, which gives us the ability to correct a mistake within a gene sequence, add or delete a gene. The ZFPs that Sangamo engineers are highly specific, designed to affect the activity or the sequence of an individual gene within the genome. These capabilities mean that our ZFP technology provides an ideal platform to create novel therapeutic solutions to address monogenic diseases. Development of ZFP Therapeutics for monogenic diseases is the major focus for us both in our internal programs and our collaboration with Shire. Our aim is to develop disease-modifying therapies that could provide a genetic cure.

As Edward announced, Shire has selected Huntington's disease as the fifth target in our collaboration. By way of background, Huntington's disease is an inherited, progressive neurologic disease for which there is no treatment or cure. It is a devastating disease that has a very high prevalence for an inherited disorder, affecting approximately 30,000 people in the US, according to the National Institute of Neurological Disorders and Stroke, or NINDS. A similar prevalence of one in 10,000 is believed to occur in the major European countries. The NINDS estimates that at least 150,000 patients beyond its stated 30,000 US symptomatic HD patients, have a 50% risk of developing the disease.

The disease is generally fatal within 10 to 20 years of the initial onset of symptoms. The symptoms commonly become noticeable between the ages of 35 and 44 years, but can start earlier. The most obvious early symptoms are jerky, random and uncontrollable movements, which progress to rigidity and writhing movements called chorea. In fact, you may have heard of the disease as Huntington's chorea. Gradually, as the disease progresses, any action that requires muscle control, such as speaking or eating, is adversely affected. In addition, there's a progressive impairment of cognitive ability and memory.

In 1993, scientists demonstrated that the disease is caused by a specific type of mutation in a single gene called huntingtin, which encodes a protein of the same name. The mutation is very well characterized and is specifically an expansion of a repeated stretch of DNA sequence within the gene. The huntingtin gene normally has somewhere between 18 and 25 copies of this so-called CAG repeat, but individuals with Huntington's disease have many more, generally greater than 40 CAG repeats. The greater the number of repeats, the earlier the disease manifests itself and the faster the progression of symptoms. However, several groups have shown in a variety of mouse models of the disease that reducing the levels of mutant huntingtin can prevent the onset and in some cases reverse the symptoms of Huntington's disease.

So, just to recap, Huntington's disease is a classic example of a monogenic disease that is absolutely correlated with a DNA mutation that takes the same form in all affected individuals. We know from animal studies that affecting the levels of expression of the mutant gene and thus the protein it encodes can have a therapeutic effect. All of this gives us an ideal target for our ZFP technology.

To that end, we have been developing approaches to specifically and selectively repress the expression of the mutant or disease-causing gene. The potential of this selective approach is something that CHDI also recognized, and they have been funding our early research program in Huntington's for the past year or so. The success of this research to date is what caught Shire's attention and prompted them to select Huntington's as their next target in our collaboration.

I look forward to updating you on our progress in this and other programs at our analyst briefing in December, where we plan to present a comprehensive overview of our entire preclinical pipeline. And with that, let me hand you back to Edward.

Thank you, Philip.

We were delighted that Shire has chosen Huntington's disease as the fifth of the seven targets of our collaboration. As with the hemophilia programs, Shire is funding all of our internal and external costs associated with this program through the filing and approval of an investigational new drug application, or IND, or the European equivalent, a CTA. Shire will then be responsible for clinical and commercial development of the product. As Philip mentioned, we are exploring several approaches to this indication and look forward to updating you on our progress later this year.

Now let me turn to our ZFN therapeutic programs in HIV. As many of you will have no doubt heard or seen, the International Aids Conference is going on in Washington, D.C. this week. One of the major areas of discussion in the sessions and in the corridors has been moving beyond the current chronic treatment of the infection to a cure for the disease. Our ZFN CCR5 gene disruption approach in both CD4+ T-cells and in CD34+ hematopoietic stem cells have been front and center in these conversations and in the media as one of the leading strategies for the generation of a functional cure for HIV.

To provide you with more color on our HIV programs and specifically to outline the progress of our Phase 2 trials and the timing for data from these studies, let me turn the call over to Geoff.

Geoff?

Thanks, Edward.

As you all know, our zinc-finger nuclease technology allows us to specifically modify and effectively knock out the CCR5 gene, which encodes a major coreceptor for HIV entry into cells. By doing this, we aim to create T-cells that will be both protected from HIV infection and capable of mounting an effective immune response to HIV, similar to a naturally occurring situation in individuals who carry the CCR5delta32 mutation on both copies of their CCR5 gene. If successful, this ZFN approach would enable a functional cure in these patients such that they could control their HIV without taking antiviral medication.

Our therapeutic product, ZFN-modified autologous CD4 T-cells, is called SB-728-T. Thus far, results from Phase 1 studies of this product have been very encouraging. The data demonstrate a statistically significant relationship between the level of engraftment of ZFN-modified cells in which both copies of the CCR5 gene are disrupted, so-called biallelic modification, and the level of virus in the blood of HIV-infected subjects during a treatment interruption from their antiretroviral medication. This observation is consistent with the hypothesis under which we began this program, and with this clear early signal at the beginning of the year we moved quickly into two Phase 2 studies.

The first trial, Cohort Five SB-728-902, exclusively enrolls HIV-infected subjects that already carry the natural mutation, CCR5delta32, on one of their two copies of the CCR5 gene. These individuals, heterozygotes for CCR5delta32, comprise approximately 5% to 10% of the population of HIV-infected individuals in the US. Compared to individuals with neither allele modified, as they already have one copy of their CCR5 gene disrupted by the natural mutation, treatment with our ZFNs results in roughly a doubling of the numbers of biallelically modified T-cells.

This Phase 2 study follows up on an observation made in an earlier Phase 1 trial in which we measured a reduction in viral load to undetectable levels in a 728-T-treated CCR5delta32 heterozygote individual during a treatment interruption, or TI, of their antiviral medication. That individual, although with undetectable viral load at the end of the TI, was required as part of the protocol to go back onto HAART. Our new Phase 2 trial is structured so that a longer period of TI can be monitored.

Up to 20 HIV-infected CCR5delta32 heterozygotes who are on HAART may be enrolled in the trial. These subjects are treated with 728-T and eight weeks later undergo a treatment interruption where they discontinue their HAART for a period of 16 weeks. If their viral loads decrease to undetectable levels, they may remain off their HAART for as long as this effect persists, enabling us to measure the durability of such a response.

When we began this study we were uncertain as to the availability of subjects for this trial, as, as I've said before, they represent only 5% to 10% of the HIV-infected population in the US. However, to date the challenge of enrollment in this study has been reduced, as many HIV-infected individuals are aware of their CCR5 gene status.

Our second trial, SB-728-1101, which is applicable to the other 90% to 95% of the US HIV-infected population, was initiated later in the first quarter. This Phase 1/2 study employs a lymphopenic preconditioning regimen with a drug called Cytoxan, intended to expand the numbers of biallelically modified cells in subjects post infusion. This preconditioning regimen, which temporarily reduces the number of lymphocytes in the body, results in an increase in the levels of T-cell growth factors, stimulating the remaining immune cells to rapidly expand and divide. So if we infuse 728-T immediately after preconditioning we expect a significant increase in the numbers of engrafted biallelically modified cells, potentially by orders of magnitude.

In this study, just prior to infusion of 728-T, we are pretreating each subject with a dose of Cytoxan. Again, there is a 16-week TI built into the study which begins six weeks after 728-T treatment and can be extended if subjects attain an undetectable viral load. This strategy has been previously used in individuals with HIV in a variety of settings. However, as we are combining this with 728-T treatment and need to explore the dose required for optimum preconditioning, we are carrying out a dose escalation phase of three dose cohorts each, with three subjects per cohort.

Dose escalation studies are frequently designed to include observation periods both between subjects enrolled into the trial and initiation of a new dose cohort, and so they generally take longer than a non-dose escalation trial of a similar size. In this study, we are required to wait for two weeks after the treatment of a subject before we treat the next subject in that cohort. After the treatment of the final subject in a cohort, we need to observe and collect data for four weeks and then present our findings to the data safety monitoring board before advancing to the next dose cohort.

Thus, while enrollment is progressing well in both of our studies, these trials will take time. We therefore expect to present preliminary data from all of the subjects in the first half of 2013 and a complete data set in the second half of 2013. As usual, we expect to present the data at a major medical meeting.

Consistent with that approach, I am pleased to announce today that we have been notified that two abstracts have been accepted for presentation at ICAAC in September. These presentations will focus on important immunological analyses and methods for evaluating the proviral reservoir from our earlier Phase 1 trial.

Moving on to our preclinical programs, our ZFN platform provides a range of powerful gene regulation and gene modification outcomes, including gene disruption, addition and correction, and, importantly, can be designed to target any DNA sequence with singular specificity. Furthermore, in our preclinical hemophilia work, we have demonstrated that we can deliver ZFP Therapeutics systemically. This direct in vivo approach significantly expands our ZFP Therapeutic applications and the diseases for which our technology can provide genetic cures.

In monogenic diseases we can use ZFNs therapeutically to permanently correct that error, as in the case of our hemophilia program, and ZFP transcription factors to control expression of a gene, as in the case of our Huntington's disease program. These are both programs that are part of our collaboration with Shire. Independently, we are also applying this technology in other monogenic diseases, including hemoglobinopathies such as sickle cell anemia and beta-thalassemia, lysosomal storage diseases and gene-based immune disorders.

Finally, as you may recall, I joined Sangamo just about a year ago, and one of my initial tasks was to work with Dale Ando, Philip Gregory and our business team to assess our portfolio of programs and prioritize them from both a technical feasibility and business perspective. We look forward to providing you with the conclusions of our analysis at our analyst briefing in December.

And with that let me turn the call back to you, Edward.

Thanks, Geoff.

As you have heard, our clinical trials in HIV are progressing very well. As such, we expect to present interim and complete data next year. In addition, we have a rich pipeline of preclinical programs, which include internal targets as well as those that are part of our collaboration with Shire. We expect to have much more to say about our preclinical pipeline, specifically regarding preclinical data, milestones and expected timing to IND filings, at our analyst briefing at the end of the year.

Our partnerships in the nontherapeutic applications of our technology also continue to thrive, as can be seen by achievement of -- this past quarter of our first commercial milestone with Sigma.

On the financial side, we are on track to end 2012 with cash and cash equivalents of at least $75 million, which is more than sufficient capital to allow us to achieve our goals of aggressively advancing our clinical and preclinical therapeutic programs. This cash projection does not, however, include any new agreements or partnerships that we may develop beyond the recently announced agreement with Shire.

And, on that point, our business model is to establish additional partnerships to help drive our programs forward through the development process and into the market. Our collaboration with Shire, which is a great example of this strategy, is off to a great start. With funding for the hemophilia and Huntington's programs, we have moved into high gear to advance both our collaborative programs as well as a number of programs that Sangamo is pursuing independently. In addition, the knowledge and experience that we gain as we advance ZFP Therapeutic applications for hemophilia and Huntington's disease can and will be applied to the development of numerous ZFP Therapeutics in other disease areas.

So, as you can see, it's an exciting time at Sangamo. We have a great deal on our plate. We have the balance sheet to support our aggressive objectives, and, perhaps most importantly, we are making significant progress towards our goal of establishing ZFP Therapeutics as a new and highly differentiated class of human pharmaceuticals that can provide the potential for genetic cures for many diseases.

I sincerely look forward to keeping you informed of our progress. In the next few months we will be presenting at the Wedbush Securities Life Sciences Management Access Conference in New York on August 14 and the Stifel Nicolaus Healthcare Conference in Boston on September 6. And, finally, as Geoff mentioned, we will be presenting additional SB-728-T data at ICAAC in early September.

This completes our prepared comments. I would now like to open the call for your questions.

Thank you.

(Operator Instructions)

Our first question comes from the line of Liana Moussatos, with Wedbush Securities. Your line is open.

Thanks for taking my question, and can you repeat the data that's going to be released in the first half of next year? And also you mentioned something about reservoir measurements, Phase 1 data at ICAAC. Can you go through that again, please?

Sure. Let me start, and then Geoff and/or Dale can add to it. I think what we guided to on this call, Liana, as it relates to the Phase 2 trials, is that we would have interim data or expect to have interim data presentations in the first half of next year and a complete data set in the second half of next year. In terms of data that will be presented at ICAAC, I think we said that that would be data from our Phase 1 trials, and as it relates to the specific topics of that, Geoff, I'll turn that over to you.

Yes, I mean, Liana, what we'll be presenting will be in two areas. One is data looking in a deeper way into the immunological status of our patients from the Phase 1 program, and the other is more of a methodological look at using new and very refined techniques for evaluating the status of the proviral reservoir in these patients.

Thank you very much.

Sure. Thanks, Liana.

Our next question comes from the line of Charles Duncan, with JMP Securities. Your line is open.

Hi, guys. Thanks for taking my question, and congrats on the good progress.

Hi, Charles.

Edward, thanks. Heterozygote study, Geoff mentioned that going into it you were a little bit concerned about whether or not patients knew their status, yet he said that the challenge has been pretty much reduced. Can you provide a little bit more color on that? And, secondarily, he also outlined nicely the kind of rate-limiting steps in the second study to enrollment and trial completion. I'm wondering if he could provide that for that particular study, for the heterozygote study.

So, Charles, I'll go a little bit on the first piece, and Geoff and Dale, again, can add or subtract to my comments. And then I think I missed the second part, so maybe we can come back to that. But in terms of the accrual process, as I think I've mentioned several times, when we started this study, given that the estimate of delta32 HIV-infected subjects in the US is in the 5% to 10% range, it was uncertain how difficult or not this trial would be to accrue. And one of the observations that we learned as we initiated this study, it was a sort of surprising number of HIV subjects who did know their CCR5 status, and because of that we did have people showing up at the site saying, "Hey, I'm a delta32." So it ended up being, at least to date, a more efficient process than maybe a worst-case scenario might have anticipated. Geoff or Dale, any other thoughts about that part of the question?

No, I mean, that's pretty much it, Charles. I mean, we thought we could get seriously hung up, with very, very few patients, by the time we looked at our entry criteria and dealt with the CCR5 heterozygote issue requiring us to screen hundreds or thousands of patients in order to get the patients in, and it has not been that bad. Nevertheless, we are making good progress with recruitment on both of the studies. You asked about the second study, and that is very much just a timetable issue. We just are recruiting well, but we simply have to wait between patients and between cohorts, so it's sort of -- it steps forward in a measured fashion.

Yes, that part I understand. I'm sorry for miscommunicating. What I was really asking is if you could outline for the actual conduct of the heterozygote study if there are any rate-limiting steps to the conduct of that as you did nicely for the lymphodepletion study. And then, with regard to that heterozygote study, the knowledge of whether or not a patient is delta -- is a heterozygote, I'm wondering if that has changed your perspective on the percentage of those patients in the population and if that selects for certain patients in terms of socioeconomic status or anything.

On the first question, Charles, no, there are no analogous rate-limiting steps in the heterozygote study like the dose escalation time frames associated with the Cytoxan study. So, no, there are no timing or gating items like that. In terms of learnings about the demographics or so on on delta32 subjects, is there anything that, Dale or Geoff, you'd comment on that?

No, Charles, again, I mean, we are dealing with relatively few sites. They obviously have large catchments in really quite -- in their own geographical areas, and really there's nothing that we can really derive from our data that would speak to the broader epidemiological question you asked.

That's good news. I'll hop back in the queue. Thanks for the added color.

Yes, thanks, Charles.

(Operator Instructions)

Our next question comes from the line of Ted Tenthoff, with Piper Jaffray. Sir, your line is open.

Excellent. Thank you very much for taking the question, and appreciate very much the detail on the revenue side, as we're starting to see progress from Sigma and the details on the Shire deal. One quick question, and I apologize if this is a bit dated, but are you still enrolling cohort five with the -- from the Phase 1 study, and will we get an update on that data, or is the primary focus on the Phase 2 studies now?

Well, I'm -- so we initially, and I'll start here, had four cohorts in that study. The cohort five of that trial, that 902 trial, is this delta32 --

Phase 2.

-- yes, is the delta32 trial.

I got you. Okay. So that's (inaudible). Okay, excellent, that's really helpful. And so that's the data that we will get interim results from both of the Phase 2 in the first half and full data by year end next year. Is that correct?

That's absolutely correct.

Excellent. Thank you very much.

Thanks, Ted.

Thank you. And we have a follow-up question from the line of Charles Duncan, with JMP Securities. Sir, your line is open.

Hi, guys. Thanks for taking the follow-up. Congrats on the Shire program visibility with regard to Huntington's disease. Wondering if you have any additional perspective on when we might see the first IND in that program.

Well, thanks for the question, Charles, and it's a good one. I'll try and repeat what we said on the call. A lot of activity right now, both in terms of the hemophilia target, the Huntington's target, all under the Shire collaboration, also a lot of activity in the monogenic disease space, and Geoff listed several areas that we're pursuing, sickle cell and beta-thalassemia, lysosomal storage diseases and others, for our own account.

And our plan is to roll out in a more comprehensive way instead of just an individual target or an individual program but roll out in a more comprehensive way the data underpinning our platform approach to monogenic diseases, the timing for IND filings, both for the Shire targets as well as our own, and also, and I think very importantly, the financial overview or guidance over the next several years under which we'll be able to execute on that plan, and our goal is to do that in a comprehensive way at the end of the calendar year, and specifically on December 6 at an analyst briefing.

That sounds good. Thanks, Ed.

Sure. Thank you.

Thank you. I'm not showing any further questions at this time. I'd like to turn the call back over to management for closing remarks.

Great. We'd like to thank you for joining us, and we look forward to speaking with you again when we release our third quarter financial information. We'll be available later today if you have any follow-up questions. Thanks very much.

Ladies and gentlemen, thank you for participating in today's conference. This does conclude the program, and you may all disconnect. Everyone have a great day.