Sangamo Therapeutics Inc (SGMO) 2015 Q2 法說會逐字稿

Good afternoon, and welcome to the Sangamo BioSciences teleconference to discuss second quarter 2015 financial results. This call is being recorded. I will now pass you over to the coordinator of this event, Dr. Elizabeth Wolffe, Vice President of Corporate Communications.

Thank you, Nicole. Good afternoon, and thank you for joining Sangamo's Management team on our conference call to discuss the Company's second quarter 2015 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; Geoff Nichol, Executive Vice President of Research and Development; and Dale Ando, Vice President of Therapeutic Development and Chief Medical Officer.

Following this introduction, Edward will highlight recent activities and the significant events from the past quarter. Ward will then briefly review second quarter 2015 results, as well as our financial guidance for the rest of 2015; and Geoff will provide an update on our ZFP therapeutic program. Finally, Edward will update you on our goals for 2015 and beyond. 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 upon 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 the 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 for our conference call to discuss our 2015 second quarter financial results, recent events and accomplishments, and our plans for the development of our ZFP therapeutic pipeline.

While not particularly visible to investors, the last couple of months saw a number of important developments in our pipeline that position us well to execute on our clinical development plans for both our ex vivo programs in HIV, beta-thalassemia and sickle cell disease, and our in vivo programs in hemophilia, lysosomal storage disorders, and Huntington's disease.

On the more visible end of the spectrum, this year we once again had a significant presence at the annual meeting of the American society for Gene & Cell Therapy, or ASGCT, with 18 presentations by Sangamo scientists or collaborators.

One presentation describing efficient, targeted integration of genes into the genomes of hematopoietic stem cells, an alternative to the use of randomly integrating viruses such as lentiviruses, and therefore a significant advance for the development of future ex vivo ZFP therapeutics, was selected for the Presidential Symposium.

A second ASGCT featured presentation, selected as a Clinical Trials Spotlight, covered our work on the effect of SB-728-T treatment on reducing the size of the HIV reservoir, a unique feature of our immunological therapy and a critical element in our goal of achieving a functional cure for HIV/AIDS.

We also presented important proof-of-concept data for our LSD programs, and I've asked Geoff Nichol to provide more detail later in the call.

Dale Ando, our Chief Medical Officer, also provided an update on subjects enrolled in our SB-728-1101 clinical trial. As Dale reported, 2 out of 3 subjects enrolled in cohort 3 of our 1101 study demonstrated control of circulating viral loads at low levels -- that is, under 1,000 copies of the virus -- during a prolonged and continuing treatment interruption, or TI, from their antiretroviral medication.

Speaking of our 1101 study, I am pleased to announce that we plan to update on this trial at this year's Interscience Conference on Antimicrobial Agents and Chemotherapy, or ICAAC, in early September. Later this year, we also expect to have initial data from our Phase 2 clinical trial of SB-728-T, the 1401 trial, which features multiple dosing using mRNA delivery.

And just for completeness, our collaborators, Dr. Carl June and Dr. Pablo Tebas at the University of Pennsylvania, have opened an investigator-sponsored Phase 2 clinical trial that uses our CCR5 ZFN mRNA delivery strategy.

In addition, our Phase 1 clinical trial of the same CCR5 ZFN approach in stem cells, the SB-728 mRNA HPSC study, is actively recruiting subjects. This trial is supported in part by a grant from the California Institute for Regenerative Medicine, or CIRM, and is being run in collaboration with Dr. John Zaia at City of Hope, partnering with a number of clinical sites throughout the country. There appears to be significant patient interest in this study and I look forward to updating you on the progress on future calls.

Earlier in the second quarter we announced our decision with Biogen to accelerate the consolidation of our programs in beta-thalassemia and sickle cell disease. As you may recall, our strategy is to increase the expression of therapeutic fetal globin as a potential curative therapy for both indications.

Our initial approach was to knock out the gene encoding BCL11A, a key regulator of the switch from fetal to adult globin expression. The plan, when we first established our collaboration with Biogen, was to take this approach forward for beta-thalassemia and to develop a second-generation approach for the sickle cell program, based on the science that was emerging at the time around a different element of BCL11A control, a DNA sequence known as the enhancer.

From the beginning of our collaboration with Biogen, the ultimate goal was to eventually consolidate both programs around the enhancer approach. As it transpired, that decision was able to be accelerated based upon the speed with which we generated both the clinical leads and preclinical data supporting the preferred enhancer approach.

The data from these studies demonstrated that there were clear advantages to the enhancer knockout, and a decision by the Biogen/Sangamo joint steering committee was made to develop the enhancer approach for both indications at this earlier stage in the programs, despite the fact that we had an open IND to take our BCL11A knockout approach forward for the treatment of beta-thalassemia. I've asked Geoff to provide more -- some brief background on advantages of the enhancer approach later in the call.

So, once again, it was a very busy, if not particularly noisy, second quarter. Before we go into more detail on our ZFP therapeutic programs and our plans for the rest of 2015 and beyond, let me hand the call over to Ward for an update on our second quarter 2015 financial results as well as our financial guidance for 2015.

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, 2015, and I am pleased to review the highlights of those results with you now.

Revenues in the second quarter of 2015 were $8.4 million, compared to $10.4 million for the same period in 2014. Second quarter 2015 revenues comprised revenue from Sangamo's collaboration agreements with Shire and Biogen, enabling technology agreements, and $600,000 of revenue from research grants.

The decrease in revenues compared to the year-ago quarter was primarily due to a decrease in revenues from the Company's collaboration with Shire, partially offset by an increase in revenues from our collaboration with Biogen.

The decrease in revenues from Shire reflects the timing of manufacturing expenses and natural tapering of research activities as we prepare to file the IND application for the Factor IX program later this year.

Sangamo recognized $3.9 million of revenues related to research services performed under the collaboration agreement with Shire, and $1.7 million of revenues related to research services provided -- performed under the collaboration agreement with Biogen.

In addition, pursuant to the agreements entered into with Shire in January 2012 and Biogen in January 2014, Sangamo received upfront payments of $13 million and $20 million respectively. These payments are being recognized as revenue on a straight-line amortization basis over the initial 6-year research term for Shire, and approximately 40 months for Biogen. The Company recognized $0.5 million of the Shire upfront payment and $1.5 million of the Biogen upfront payment as revenue for the second quarter of 2015.

Total operating expenses for the second quarter of 2015 were $20.6 million, compared to $17.4 million for the same period in 2014.

Research and development expenses were $15.6 million in the second quarter of 2015, compared to $13.5 million for the second quarter of 2014. The increase was primarily due to increases in personnel-related expenses, including stock-based compensation, largely due to increases in head count in our technical operations group, which manages and supports manufacturing operations.

General and administrative expenses were $5 million in the second quarter of 2015, compared to $4 million for the same period in 2014. The increase was primarily due to increases in personnel-related expenses, including stock-based compensation, as well as increases in legal and professional services.

Non-cash stock-based compensation expense was $2.9 million for the quarter, with $1.7 million in research and development and approximately $1.2 million in general and administrative.

For the second quarter of 2015, the Company reported a consolidated net loss of $12.1 million, or $0.17 per share, compared to a net loss of $7 million, or $0.10 per share, for the second quarter of 2014.

Turning to the balance sheet, Sangamo ended the second quarter of 2015 with $218.6 million in cash, cash equivalents, short-term investments and interest receivable. Our net cash used in operating activities was $8 million for the second quarter ended June 30, 2015, resulting in $10.4 million net cash used in operating activities for the year to date.

Regarding our financial guidance for 2015, we reiterate our guidance from our first quarter earnings call. We expect to end the year with at least $180 million in cash, inclusive of research funding from Biogen and research funding and milestones from Shire, but exclusive of any new funding from a collaboration, partnership, equity financings, or other sources.

With regard to operating expenses and revenues, we expect operating expenses in the range of $100 million to $110 million and revenues in the range of $60 million to $70 million for the full year 2015.

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

Thanks, Ward. As you've heard, we ended the second quarter with approximately $219 million, a total cash burn of $8 million for the first half of the year.

We believe this balance sheet strength enables us to aggressively advance our preclinical pipeline with the goal of filing three new [INDs] (technical difficulty) [year] and an additional six by the end of 2016, as well as completing our HIV studies in T-cells and making significant progress on our HIV stem cell program. We have a lot going on in the next 18 months, and more than sufficient capital to see it through.

I've asked Geoff to provide more detail on the recent proof-of-concept data from our in vivo protein replacement LSD programs, how our programs differ from gene therapy approaches that are based on the use of AAV viral vectors, and why we believe our strategy has the potential to be more effective as a long-lasting, curative therapy.

And while this phase of our activities may not be particularly visible, we are aggressively advancing these programs into the clinic and, in so doing, will demonstrate the differential technical (technical difficulty) [advantages] of our in vivo protein replacement program.

Thanks, Edward, and good afternoon to everyone. Our in vivo protein replacement platform, or IVPRP, is an efficient, leverageable, and potentially curative approach to diseases that are currently treated using enzyme replacement therapies, or ERT.

Our platform is designed to add a corrective therapeutic replacement gene into a so-called safe harbor site in the genome. This strategy has several advantages over conventional gene therapy approaches, particularly in terms of the potential durability of the effect.

We've developed the IVPRP with significant funding from Shire for the hemophilia A and B programs, and have leveraged the same strategy for our own programs in LSDs. We've named the first two LSD targets -- Hunter and Hurler syndromes -- but also have active research programs in several other LSDs.

The IVPRP enables us to treat a monogenic disease such as hemophilia or a lysosomal storage disease by targeting a single address in the genome of a patient's liver as a so-called safe harbor site, into which we can add a replacement therapeutic gene.

This allows the patient to produce their own source of therapeutic protein to replace the defective enzyme that gives rise to their symptoms. The approach gives us the flexibility to develop ZFP therapeutics to essentially any disease currently being treated using protein replacement therapies, using a single set of ZFNs.

We chose the albumin gene as our safe harbor, as it has all the properties that we desire. First, it's very highly expressed, being the most abundant protein found in the serum. Adults produce about 80 grams of albumin per week, which is about 9 pounds of albumin per year.

Second, it's safe to co-opt the very small percentage of its expression needed to produce therapeutic quantities of a replacement protein. And third, it's highly tissue-specific, as albumin is only made in the liver.

The concept is, therefore, very simple. By delivering ZFNs designed to specifically target the albumin gene, along with the DNA sequence that encodes the therapeutic protein that we wish to express, we can place the expression of this protein under the control of the powerful albumin promoter in the liver.

Very importantly, we have shown that this approach is agnostic to the protein payload encoded by the therapeutic DNA sequence. So, with this same set of ZFNs, we can insert and express genes from human Factor IX for hemophilia B; Factor VIII for hemophilia A; and replacement enzymes for the LSDs Hunter, Hurler, Gaucher, and potentially many others.

As Edward mentioned, we presented important preclinical data from our LSD programs at the ASGCT meeting in May. In mouse models of the disease we demonstrated that the IVPRP approach can be used to express functionally active proteins that are defective in Hunter and Hurler disease, and these enzymes can reduce the levels of disease-related biomarkers.

We measured the enzymes that were expressed by the replacement genes in the liver, in the blood, and in other tissues such as the spleen, using a variety of techniques including an enzymatic assay which demonstrated that the proteins were functionally active.

Most importantly, in animal models of disease for both Hunter and Hurler syndrome, we demonstrated significant therapeutic benefit. In tissues and in the urine of treated animals, we observed decreased levels of glycosaminoglycans, or GAGs -- the toxic products that accumulate in tissues and produce the symptoms of these diseases.

Additional studies in these animal models are ongoing to further evaluate durability and dosing. However, the important point is that we are obtaining robust levels of expression of these therapeutic proteins from the liver, the protein produced is enzymatically active, and the proteins are being secreted into the circulation and taken up from there into other tissues, where they are having the desired therapeutic effect.

This strategy is designed to provide a single treatment with a long-lasting and, depending on the indication, curative effect. By making a permanent change in the patient's liver cells, we enable the expression of stable levels of the replacement enzyme, not just for the lifetime of the modified cells and their progeny, but also in the event of liver growth and hepatocyte turnover.

This is where our technology is materially differentiated from traditional gene therapy approaches that are being developed to replace a variety of ERTs including LSDs and hemophilia.

Traditional approaches deliver an AAV vector encoding a replacement gene. AAV doesn't integrate as DNA into the genome, which makes it a very safe vector for gene therapy uses. However, because this vector's DNA is maintained independently in the cell's nucleus, when that cell divides, the AAV vector is distributed between the daughter cells and can eventually be diluted out of the system.

This is far less of a concern in tissues that have little or no turnover, such as the brain; but in the liver it could be of concern. This is a particularly important point when you consider that, in order to most effectively prevent damage due to these diseases, the ultimate target population for these treatments will be small children whose livers are not just turning over and replacing cells, but are also actively growing.

To intervene in the very young and achieve a lifelong therapeutic effect from a single administration, demands stability of enzyme expression over the lifetime of the patient. It is precisely this ability to drive a targeted, permanent change at the genomic DNA level that is enabled by our ZFN-driven, in-vivo protein replacement strategy.

Thus, by harnessing a tiny fraction of the liver's powerful albumin promoter and synthesis and secretion pathways, we expect to be able to produce substantial and sustainable levels of therapeutic enzymes for virtually any enzyme replacement therapy.

As Edward noted, we're on track to file IND applications for the Factor IX program and for our programs in Hunter and Hurler syndromes late this year.

Additionally, we're working on other LSDs, including Gaucher disease, and our plan is to file an IND application for this indication, and for an additional LSD in 2016. I sincerely look forward to updating you as we begin preparations to open these clinical trials.

I also wanted to briefly explain the rationale behind our decision with Biogen to consolidate our strategy in the hemoglobinopathies. As Edward described, our first strategy to increase the expression of fetal global was to knock out the gene for the transcription factor BCL11A, which regulates the switch from fetal to adult globin expression in hematopoietic stem cells.

We had previously presented data at the annual meeting of the American Society of Hematology, or ASH, in 2013, to demonstrate that we could achieve this at clinical scale in hematopoietic stem cells; and as Edward mentioned, at the time that we established our agreement with Biogen we were well on our way to our IND filing with that approach for beta-thalassemia.

At that time, we also began work on a second-generation strategy to knock out the enhancer of BCL11A, as it appeared to provide certain advantages for treating the hemoglobinopathies.

In short, the enhancer was identified by genome-wide association studies as a regulatory DNA sequence in the genome that is essential for expression of BCL11A, but that is erythroid-specific, meaning that it is functional only in cells destined to become red blood cells, or RBCs.

This meant that disrupting the sequence in HSCs would make the outcome more precise, and only affect BCL11A expression in those cells destined to become RBCs, and not in HSCs that are destined to become other lineages, such as B-cells.

We also made extremely rapid progress in developing therapeutic lead ZFNs for the enhancer target. When tested, both ZFN-mediated approaches were found to be equally target-specific and efficient, and resulted in similar increases in fetal globin production at clinical scale.

However, the enhancer approach was found to have certain advantages including, as I mentioned, its specificity for red cells, making it preferable as a potentially curative strategy for the hemoglobinopathies. Thus, we determined that the beta-thalassemia program should use BCL11A enhancer approach just like the sickle cell disease program.

Difficult as this choice was, as it results in some delay in the initiation of our beta-thalassemia clinical program, we and our partner Biogen agreed that these decisions have to be made with the patient's best interests in mind, and we believe that the enhancer approach will be a better product that will best serve patients with either disease.

Needless to say, consolidation of these approaches for both indications will ultimately make their development simpler, and our goal is file an IND application for beta-thalassemia in the first half of 2016 and, with Biogen, to file an IND for sickle cell disease in the second half. I look forward to updating you when we prepare to begin our clinical trials.

And with that, I'll turn the call back over to Edward.

Thanks, Geoff. So, as you've heard, there's an awful lot going on at Sangamo. We are focused on filing INDs for hemophilia B, Hunter and Hurler syndrome in the next several months, and an additional six INDs in hemophilia A, beta-thalassemia, sickle cell disease, Huntington's disease, and an additional two LSD indications -- a very busy and important year and a half ahead.

I also want to update you on some internal organizational developments that have occurred this quarter.

On the R&D front, we have promoted Dr. Michael Holmes from Vice President of Genome Editing Research to Vice President of Research. Mike has been with the Company for 14-plus years, and among his many accomplishments has most recently been leading our in vivo (technical difficulty) [programs].

In addition, Curt Herberts, who has been with Sangamo for nearly 5 years and has played an important role in our -- in the business development group (technical difficulty) Senior Director of Corporate Development and Strategy, has been promoted to Vice President of Corporate Development.

Congratulations, Mike and Curt -- very well deserved.

As is probably clear, we have a very busy second half of the year ahead of us, and we look forward to keeping you informed of our progress.

In the immediate future we will be making corporate presentations at the Wedbush Securities Life Sciences Management Access Conference on August 11, and the Morgan Stanley Global Healthcare Conference on September 18, both of which will be webcast and available on the Sangamo website.

As far as scientific updates are concerned, as I mentioned earlier, additional updates from our 1101s trial will also be provided at this year's ICAAC meeting. This concludes our prepared comments. I would now like to open up the call for your questions.

(Operator Instructions). Cory Kasimov, JPMorgan.

This is Whitney, on for Cory. Thanks for taking the questions. First one -- and I'm not sure how much you can say here, but just wondering if the Shire/Baxalta hubbub has changed how you're thinking about your partnership, or timelines, or if there's just anything notable there.

Well, it's only been a couple of days, right? And unclear what's going on. But no, I think the answer is, it hasn't changed anything.

Got it. And then, just given the mechanism of action of your approach in beta-thal and sickle cell, just wondering if there are patients who may be better candidates for gene editing versus gene therapy if, like, they have higher baseline levels of fetal hemoglobin or anything like that?

Yes. Good question. Geoff and Dale, do you want to discuss that?

Yes. I'll actually pass it over to Dale.

Yes. I think we're using the BCL gene to [upregulate] hemoglobin F, so we're very keen about looking at patients that may have a good response to hydroxyurea, or slightly better hemoglobin F levels. But other than that, there's no clear genetic element that would favor patients for the gene editing.

Yes. What we do know -- it's Geoff here. What we do know is that, if for whatever reason you have a genetic background that favors the production of hemoglobin F, then you tend to have reduced symptoms, certainly of beta-thal and potentially also for sickle cell.

Now, whether that helps in terms of adding to the effect of switching off the enhancer to BCL11A, I think, remains to be seen. And certainly, we would anticipate that switching off that enhancer is at the very, very top end of the naturally-occurring genetic changes that promote hemoglobin F, that occur in very, very, very, very rare individuals who basically have a BCL11A knockout already in their genetic makeup.

So, anything that we can do will be significantly out of range compared with the genetic background of the patient. But an interaction is always possible; but that will depend on clinical trials.

Got it. Thanks.

Charles Duncan, Piper Jaffray.

Hi. It's Roy in for Charles. Thanks for taking my question. I think previously you guys were going to do the beta-thal Phase 1 and Biogen was going to do the sickle cell. Is that still the organization that's planned, or is one company going to take both?

Yes, I think that's the -- largely the guidance. Sangamo's going to take the lead on the Phase 1/2 trial on beta-thal. And I don't think we've given formal guidance on sickle, but I think it's likely that Biogen will have a much greater role in that, if not fully taking the lead on that.

Okay. Great. And then, a little bit surprising about the data for the enhancer knockout, looks a little better than the BCL11 gene knockout, based on globin ratios. Do you think that's noise across the experiments, or is there something about the general health of the cells, and is that -- ?

Can you repeat the front end of that question again?

Yes. The data on the enhancer knockout -- the gene knockout, looks a little better for the enhancer knockout, based on the globin ratio.

Right. Yes. I think we would argue that they're essentially equivalent in terms of fetal activation. But Geoff, do you want to -- I mean, I think we'd argue that they're essentially equivalent.

Yes. I mean, I think, given what you typically see in these experiments, with some allowance for variation and so on, we would come down with an equivalence statement -- small differences probably are not telling us a large amount, given all of those factors.

Right. Okay. That makes sense. And then, on your first LSD programs, do you think you're going to go into patients that (inaudible) diagnosed by genotype? Is that a feasible approach (inaudible) or is it going to be someone that's manifested a clinical phenotype? Thanks.

Genotype.

Dale or Geoff, do you want to discuss the initial sort of accrual criteria for those studies?

Yes. We'll basically use genotyping to select out the patients. And basically, the phenotype of these patients is very difficult to differentiate between Hunters and Hurlers except for the most severe forms of Hurlers. So, we'll need to sequence the genes.

Okay. Thank you.

I hope that answers your question. If you're asking, are we going to treat people who've only just been diagnosed early in life by genotyping, rather than treating people who are already suffering from the disease, basically I believe we are biasing towards people who are already suffering from the actual phenotypic manifestations of the disease. But obviously they'll be confirmed -- the actual nature of the disease will be confirmed by genotyping.

Okay. That's helpful. Thank you.

(Operator Instructions). Chris Howerton, Jefferies.

Thanks for taking the questions. I just -- Geoff, I didn't quite catch you -- did you say that based upon the presentations at ASGCT you still had dosing to work out for IVPRP? I just wasn't quite sure exactly what you said regarding dosing.

On which program?

It's toward the IVPRP as it relates to the LSD programs.

Yes. Well, Geoff, go ahead. I mean, I think we've presented data on both the dose escalation as well as in the disease models. So, I don't know, Geoff, maybe you have a better sense of what the question's aiming at.

Yes. I mean, I -- look, just to be clear, we have great data from the models that we have already published on. We're feeling good about the dose range and the dose-related effects that we're seeing.

We continue with, given that the IND is going to happen, targeting the year end. We continue to complete IND-related studies. But we're feeling good about the data that we've already put out there in terms of being indicative of what we're likely to see in the final studies that are ongoing now.

Okay. All right. That's helpful. And I guess, previously, for the beta-thalassemia trial design, you'd talked about getting around 10 patients that would be transfusion-dependent. Are your expectations in line with that, or is there any reason to think that that might change in future?

In terms of total patients on the Phase 1/Phase 2 study?

Yes.

Yes. I think that that's the general number that we're guiding to. Geoff or Dale, is there any update on that?

No, I think that's absolutely clear. It's -- the Phase 1 design that we talked about earlier, you could understand, but it's probably not going to be a whole lot different just because we're affecting the enhancer. The underlying pharmacodynamics, we expect to be essentially the same and have demonstrated that in animal models.

Sure. Okay. And then just one last quick question -- in regards to targeting the enhancer, BCL11A, you kind of highlighted the advantage of it being erythroid-specific. Are there any other advantages that you'd like to -- you can speak to, or anything else that might be pertinent in terms of efficacy or safety?

I think the principal -- the material advantage that the enhancer brings is really the erythroid specificity. And I think that's the critical piece. As more work's done and as we prepare to present and publish that work, we'll have an opportunity to give a more thorough picture.

But I think having the knockout and fetal activation -- but the knockout of BCL11A expression just in red blood cells, in the erythroid lineage, is really the material change in the rationale for the approach. I don't -- is there anything else to add, Geoff?

Yes. Look, I mean, what we know is that it's erythroid-specific. That's the most important thing. And that's certainly what we have clearly demonstrated in our studies. We have also demonstrated that it appears to be just as active and just as effective in promoting fetal expression as the total knockout.

And so, it's with an abundance of caution that, clearly, if it's erythroid -- if there's an erythroid-nonspecific effect, there are a lot of other cell types that are around. But certainly, we know that there is an effect of BCL11A knockout on B-cells. That's well-known.

And that -- while that didn't -- that was an issue that we understood with the knockout, given the fact that we're expecting some mixed chimerism that was not in itself a problem -- neither to us, nor to Biogen, nor to the Agency -- but there are a lot of other cell types.

And so, it just seems to make a lot of sense to avoid any possible future effects becoming manifest due to that, even though we've -- not really seeing any in the initial studies.

So, that's the sort of underlying approach, as well as the opportunity at this stage, given that we had really moved so fast on the enhancer, to essentially consolidate the programs at an earlier point than perhaps we had initially anticipated, just for good drug development housekeeping.

Sure. Okay. All right. Well, thanks for taking the questions.

Charles Duncan, Piper Jaffray.

Thanks for taking the followup. Just a very quick question on the -- actually, the [Penn IST] -- I realize it's not your study, but do you know if they're planning to present anything at ICAAC, and do you have any ideas when we might see some data from that study?

I don't know on either question.

Okay. Thanks.

Thank you. I'm showing no further questions at this time. I'd like to hand the call back over to Management for any 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 for any followup questions. Thank you.

Ladies and gentlemen, thank you for participating in today's conference. That does conclude today's program. You may all disconnect. Have a great day, everyone.