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Epizyme, Inc. (NASDAQ:EPZM)

Q3 2013 Earnings Call

October 22, 2013 4:30 PM ET

Executives

Stephanie Ascher – IR

Jason Rhodes – President and CEO

Eric Hedrick – Chief Medical Officer

Bob Copeland – EVP and Chief Scientific Officer

Analysts

Jonathan Eckard – Citi

Simos Simeonidis – Cowen and Company

Howard Laing – Leerink Swann

Mike King – JMP Securities

Greg Wade – Wedbush Securities

Simos Simeonidi – Cowen and Company

Operator

Good afternoon and welcome to Epizyme’s Third Quarter 2013 Conference Call. At this time, all participants are in a listen-only mode. There will be a question-and-answer session at the end. Please be advised that this call is being recorded at Epizyme’s request.

I would now like to turn the call over to Epizyme’s team. Please proceed.

Stephanie Ascher

Good afternoon. This is Stephanie Ascher with Stern Investor Relations. And welcome to Epizyme’s third quarter 2013 conference call. The news release with our third quarter financial results and company update became available at 4 PM today. And can be found on our website at epizyme.com. You can listen to a live webcast including a set of slides or a replay of today’s call by going to the Investor Center section of the website.

The agenda for today’s call is, Jason Rhodes, Epizyme’s President and CFO will discuss highlights of the third quarter and other recent updates; Eric Hedrick, Epizyme’s CMO will provide an update on the company’s clinical progress and plans; Robert Copeland, Epizyme’s EVP and CSO will discuss the company’s R&D efforts including expansion indication plans for 2014. Jason Rhodes will review the company’s financial position and collaborations. He will then make closing remarks and open the call for Q&A.

Before we begin, I would like to remind you that today’s discussion will include statements about the company’s future expectations, plans and prospects that constitute forward-looking statements for purposes of the Safe Harbor provision under the Private Securities Litigation Reform Act of 1995. Actual results may differ materially from those indicated by these forward-looking statements as a result of various important factors including those discussed in the risk factor section of our 10-Q filed with the SEC on August 1, 2013.

In addition, any forward-looking statements represent our views only as of today and should not be relied upon as representing our views as of any subsequent date. While we may elect to update these forward-looking statements at some point in the future, we specifically disclaim any obligation to do so even if our views change.

Now, I’ll turn the call over to Epizyme’s President and CFO, Jason Rhodes.

Jason Rhodes

Thanks Stephanie. Good afternoon everyone and thank you for joining us today. Robert Gould, our CEO won’t be on the call today because he had surgery this morning to repair the mitral valve in his heart. Robert had originally planned to share this news with you on this call with his surgery scheduled for tomorrow. However, yesterday morning his surgeon moved the surgery to today because of a change in the surgeon’s schedule. This change had nothing to do with Robert’s health. So you have me here to share this news with you instead.

The very good news is that I’m able to tell you that the surgery was successfully completed this morning. He is doing well and while we promised to his family that we won’t bother him over the next few weeks. He will be available to us by phone and email while he is recovering at home. We are looking forward to having him back here at Epizyme very soon. In the meantime, the Epizyme leadership team including myself, Bob Copeland and Eric Hedrick will continue to lead the organization.

2013 has been an enormously important year so far for Epizyme as we translate the science of epigenetics into innovative personalized therapeutics for patients with genetically defined cancer. A year ago, Epizyme was a private company initiating its first dose escalation study. Today we are a public company with two ongoing clinical programs, EPZ-5676, a DOT1L inhibitor for the treatment of acute leukemias with the rearrangements of the MLL gene referred to as MLL-r and EPZ-6438 and EZH2 inhibitor for the treatment of non-Hodgkin lymphoma patients with oncogenic point mutations in EZH2. To our knowledge, these are the first and only histone methyltransferase where HMT inhibitors to enter human clinical development.

On today’s call, we will provide an update on our clinical and research progress this year and highlight an important clinical expansion that we are currently planning for 2014.

For 5676, we anticipate completion of the dose escalation stage of the Phase 1 study this year. There had been no dose-limiting toxicities to-date and we are highly encouraged by the tolerability thus far and believe this represents a significant step forward for this first in class epigenetic therapeutic program as well as for the entire field of histone methyltransferase inhibitors. This quarter we will share top-line data from the dose escalation stage and plan to initiate an expansion cohort that will only enroll MLL-r patients.

The expansion cohort will provide an initial assessment of therapeutic effect of 5676 in this population. For 6438, Epizyme along with our partner Eisai initiated a Phase 1, 2 clinical trial in June of 2013. The Phase 1 dose escalation study is ongoing and while we are early in the study no dose-limiting toxicities have been observed to-date. We plan to initiate the Phase 2 part of the study in 2014 in which only non-Hodgkin lymphoma patients with point mutations in EZH2 will be enrolled.

Similar to the expansion stage of the 5676 study, this will provide an initial assessment of therapeutic effect in EZH2 mutated non-Hodgkin lymphoma patients. Also in 2014, we currently plan to broaden the clinical programs for both 5676 and 6438 in genetically defined cancers beyond the primary indications. For 5676, this includes AML with the partial tandem duplication in the MLL gene referred to as MLL-PTD. For 6438 this includes synovial sarcoma and other INI1-deficient tumors. These potential additional indications are based on insights generated by Epizyme using our proprietary product platform as we continue to rigorously elucidate the oncogenic roles played by histone methyltransferases in the setting of specific identifiable genetic alternations.

Intellectual property is an important part of our product platform and all of our therapeutic candidates have been discovered within Epizyme. In August, we received a Notice of Allowance for the first composition of matter claims for 5676. Once issued, this patent will expire on 2032. This follows the issuance in April of this year of our first composition of matter claims for 6438 which will also expire on 2032. The combination of these patents coupled with the focused and potentially rapid clinical development strategy that we are pursuing is expected to enable long commercial patent lines for our therapeutic programs.

With that introduction, let me turn the call over to Eric Hedrick, our Chief Medical Officer, he will provide additional information on our clinical programs and plans. Eric?

Eric Hedrick

Thanks, Jason. Our general clinical development strategy as compared each therapeutic program with the companion diagnostic that allows us to identify those patients with the genetically defined cancers who may benefit from treatment. First in clinical development and ultimately if the development programs are successful and achieve regulatory approval in clinical use. This strategy allows initial assessment of the therapeutic effect as earlier as possible in clinical development in the patients with the specific genetically defined cancer that we seek to treat.

Turning to our DOT1L Inhibitor, EPZ-5676, the clinical development program is focused on acute leukemia patients with MLL rearrangement. These patients haven’t particularly poor prognosis with the current standard of care treatment. We estimate that an annual incidence of acute leukemia with MML rearrangement to be approximately 4,900 patients per year in the major markets.

As Jason mentioned, we’re on track to complete the plan dose escalation stage of the Phase 1 study of 5676 in advanced hematologic malignancies this quarter and plan to disclose top-line data from the stage of the study including safety, pharmacokinetic and pharmacodynamic data at that time.

We also will outline the expansion stage of the study which will be restricted to patients with the MML rearrangement and will serve as our preliminary assessment of efficacy. We currently have six sites actively participating in this clinical program and expect to have as many as 12 sites in the U.S. and Europe for the expansion stage in 2014. We are developing a companion diagnostic for this program with Abbott and expect to have the investigational use only version of the diagnostic available for the expansion stage. In August, 5676 was granted Orphan Drug Designation by the FDA.

Looking ahead to 2014, we plan to initiate a Phase 1 study in pediatric MLL rearranged patients based on the findings from the dose escalation phase of the ongoing adult study. We are also planning study 5676 in MLL patients with the MLL-PTD genetic alteration.

As Bob will describe later on the call, MLL-PTD is another genetically defined subtype of AML that appears preclinically to be depended upon DOT1L. We estimated that AML with the MLL-PTD occurs with an annual incidence of 2,300 patients in the major markets and has a similarly poor prognosis to acute leukemia with MLL rearrangement.

Our second clinical program EPZ-6438 is directing towards patients with non-Hodgkin lymphoma bearing point mutations in EZH2. These mutations occur approximately one quarter of patients with non-Hodgkin lymphoma of germinal-center origin such as germinal-center diffuse large B-cell lymphoma and follicular lymphoma. To our knowledge, 6438 is the only molecule in clinical development focused on this subset of non-Hodgkin lymphoma.

With our collaborator Eisai, we initiated the Phase 1 dose escalation study of 6438 in June 2013. This is an (old comer) study that will include a number of different types of cancer including non-Hodgkin lymphoma. Dose escalation is ongoing and proceeding has planned with no dose-limiting toxicities have been observed to-date. The study is currently being conducted at two sites in Europe and we are actively identifying additional sites in Europe and the United States in anticipation of Phase 2 initiation in 2014. The Phase 2 part of the study will enroll only non-Hodgkin lymphoma patients with EZH2 mutation. We’re actively working with our partner Roche on the development of a companion diagnostic for this program.

As Bob will detail in a few minutes, EZH2 is now being implicated in a range of cancers beyond non-Hodgkin lymphoma. Notably, INI1-deficient cancers such as synovial sarcoma and malignant rhabdoid tumors, with our partner Eisai, we plan to initiate clinical studies in these indications following the completion of those escalation in 2014. 2014 will be an important year for Epizyme, the entire field and most importantly for patients as we advance our clinical programs into multiple proof-of-concept studies. Now, I’ll pass the call over to our Chief Scientific Officer, Bob Copeland for an overview of our product platform and expansion indication opportunities.

Bob Copeland

Thanks Eric. At Epizyme, we continue to focus our therapeutic R&D efforts on a class of enzymes called histone methyltransferase or HMTs. And we collectively refer to these as the (HMT1). Within the 96 member HMT, we’re actively pursuing 20 HMTs prioritized based on a clear oncogenic hypothesis matched to a patient population with a clinical need. This approach is exemplified by our two clinical programs EPZ-5676 and EPZ-6438. Each of which is directed to a genetically defined cancer as a primary indication that has been described by Eric.

In addition, we also continue to use our product platform to identify and rigorously evaluate new therapeutic opportunities for genetically defined cancers for each of these programs. Eric highlighted two of these, MLL-PTD for 5676 and synovial sarcoma and other INI1-deficient cancers for 6438.

The MLL gene is a common target of multiple chromosomal alterations in acute leukemias and we’re previously demonstrated that DOT1L Inhibitor selectively kills leukemia cells bearing the spectrum of the MLL-fusion proteins that characterize MLL-r leukemia. Another chromosomal alteration affecting the MLL gene is a recombination event that result in a duplication of a portion of the MLL gene. The result in protein is referred to as MLL partial tandem duplication or MLL-PTD. MLL-PTD appears to be a driver of leukemia in an estimated 5% to 7% of AML patients.

Until now, there was no biological hypothesis to suggest that DOT1L played a significant role in this disease. However, studies by Epizyme scientists have demonstrated that the MLL-PTD cell line notice EOL-1 is selectively killed by DOT1L inhibitors in a dose depended manner both in cell culture and (indeed both) xenograft studies. MLL-PTD therefore represents an additional genetically defined cancer and a compelling clinical opportunity for our DOT1L inhibitor 5676.

INI1-Deficient cancers present additional potential clinical opportunities for EZH2 inhibitors. INI1 is a critical component of the chromatin modifier known as the SWI/SNF complex. EZH2 and the action of the SWI/SNF complex have opposing effects on gene transcription. Thus loss or deficiency of INI1 result in cancer cells becoming dependent on EZH2. As we have demonstrated INI1 deficient cancer cells are selectively killed by EZH2 inhibitors such as 6438.

Malignant rhabdoid tumor or MRT is a pediatric solid tumor with a very poor prognosis and is one example of an INI1 deficient cancer with a high unmet clinical need. As published in our PNAS paper in April of this year, EZH2 inhibition selectively kills MRT cancer cells in vitro and cause a sustain tumor regression in vivo in preclinical models.

In addition to MRT, a number of soft tissues sarcomas are known to have high rates of INI1 defects. These include epithelioid sarcomas, atypical chordomas, synovial sarcomas and certain chondrosarcomas.

As presented yesterday at the AACR-NCI-EORTC International Conference on Molecular Targets and Cancer Therapeutics, Epizyme scientist have demonstrated that (cell line) representing INI1-deficient soft tissue sarcomas are selectively sensitive to EZH2 inhibition similar to what we previously published for MRT and for non-Hodgkin lymphoma with point mutations in EZH2. We are continuing these studies now and plan to pursue development of an EZH2 inhibitor in INI1-deficient tumors once we have sufficient dose and safety data in adult patients from our ongoing clinical study with 6438.

This is an example of the potential to treat solid tumors with EZH2 inhibitors and also of the detailed mechanistic work that we undertake in selecting HMT targets for active therapeutic research and development.

We look forward to continuing to publish novel findings about other therapeutic opportunities for 5676 and 6438 as well as opportunities within the broader HMT.

I will now turn the call back over to Jason to discuss Epizyme’s financials, business strategy and upcoming milestones.

Jason Rhodes

Thanks very much Bob. Epizyme continues to be in a strong and secure financial position to pursue our pipeline of personalized therapeutics for patients with genetically defined cancers as we build a leading biopharmaceutical company.

Our financial results were included in this afternoon’s press release and will also be available with additional detail in our 10-Q. Among the financial information that we are providing, the key numbers that we focus on and used to guide and manage the business at this time are our cash position and R&D spend.

In terms of our cash position, we ended the third quarter with $140 million in cash, in cash equivalents versus $149 million at the end of the second quarter of this year. In addition to managing our operating expenses closely, in June, we earned a $6 million milestone payment from our EZH2 collaboration with Eisai that was received in July.

Turning to GAAP revenue, we reported revenue for the third quarter of 2013 of $8.4 million and revenue for the first nine months of 2013 of $32.2 million. Research and development expenses were $14.6 million for the third quarter of 2013 compared to $9.3 million for the third quarter of 2012. This increase was largely due to spending on clinical studies as well as the expansion of our product platform and pipeline.

We expect our full year net cash used in operating activities to be approximately $60 million and we currently plan to end 2013 with a cash position of $115 million or more.

Our therapeutic collaborations with Celgene, Eisai and GSK were carefully constructed to contribute to our strategy of building a leading biopharma company. In our Celgene collaboration for the DOT1L inhibitor program, we retained 100% of United States rights and are currently working together on joint global development.

In our Eisai collaboration for the EZH2 inhibitor program, we have the right to opt into a 50:50 co-development, co-commercialization and profit arrangement in the United States and are currently working jointly with Eisai on global clinical development. Beyond these valuable product rights to the third quarter of 2013, we have received more than $133 million in non-equity funding from our therapeutic collaborations and expect those collaborations to continue to be important sources of non-equity funding for us. Potential future milestones include $25 million for the achievement of proof-of-concept in the 5676 clinical program and $10 million for the Phase 2 initiation in the 6438 clinical program.

As we shared with you today, Epizyme is continuing to execute on our strategy of developing personalized therapeutics for the treatment of patients with genetically defined cancers. We are excited by the progress we have made over the past five years entering an entirely new therapeutic target class building a productive product platform with a significant intellectual property and advancing two first in class therapeutic programs into clinical development.

We look forward to sharing top-line data from the 5676 dose escalation study with you before the end of the year and to initiating the expansion cohort that will enroll only patients with MLL-r.

Looking ahead 2014 will be an important year for Epizyme and the entire field as we plan to have multiple proof-of-concept studies ongoing, each directed to patients with an identifiable genetically defined cancer.

We will now open the call up for questions and answers. Operator?

Question-and-Answer Session

Operator

Thank you. We will now begin the question-and-answer session. (Operator Instructions) Our first question comes from the line of Jonathan Eckard of Citi. Your line is now open.

Jonathan Eckard – Citi

Thank you, guys. And please wish Rob well hopefully, he heals quickly.

Jason Rhodes

Thanks very much Jonathan.

Jonathan Eckard – Citi

Okay. The first question I had was on the Phase 1 for 5676 and then I will follow-up regarding some of the additional indication as you mentioned today for that program. For the dose ranging trial, is the plans for this trial is currently to find a maximum tolerated dose or is the goal primarily to get to a range, it’s a solid buffer above the peak HMT activity for the drug? And what type of – what type of information is going to be disclosed when you release data late this quarter?

Eric Hedrick

Hi, Jonathan. Thanks for the question. This is Eric. Yes, so the sort of data that you mentioned really will be the focus of the data disclosure later in mid-year. As you are probably aware of it that plan dose escalation phase is really designed to detect an MTD, if an MTD has been – to be found. But there is a number of other parameters safety pharmacokinetic and pharmacodynamic parameters that will allow us and inform the dosing for the stage of the study where restricted down that well rearrange patients and that sort of data that will be commenting on by the end of the year.

Jonathan Eckard – Citi

Great. And then for the expanded indication for 5676 of the MLL, PTD, are these patients sort of also identified VSI genetics and therefore fairly easy to identify with basic screening. And I guess the same for the EZH2 program. Beyond the MRT, which is about pretty much all the patients have this – SWI/SNF rearrangement. How do you detect that in some of the other solid tumors that were mentioned on the slides?

Eric Hedrick

Yes. So maybe I will comment on MLL-PTD first so that is an abnormality that’s not detectable on the routine cytogenetics, it’s detectable by PCR phase methods. Those tests are not part of routine clinical practice, they are part of sort of academic practice at some centers. And so diagnostically that program will be different than the MLL rearrangement program that will require PCR based diagnostic to identify those patients.

In the INI1-deficent tumors there are a couple of different diagnostic aspects at play. The scenario with malignant rhabdoid tumor for instance is one where that disease is basically defined by in absence of INI1 and that is the chemical test is part of the routine diagnosis for that disease. This situation with synovial sarcoma for example is a little bit different. And so that is INI1-deficient by virtue of a specific chromosomal translocation between chromosome X and chromosome 18 that is present in all cases of synovial sarcoma. So that would be more aligned with through the MLL rearrangement situation where that is a disease that would be diagnosed on routine cytogenetics. The program is very – in terms of the diagnostic aspects.

Jonathan Eckard – Citi

All right.

Eric Hedrick

But they are identifiable. Yes, I’m sorry.

Jonathan Eckard – Citi

That’s great. Thank you very much for the question – answer, I’m sorry.

Jason Rhodes

And Jonathan consistent, this is Jason, consistent with our approach the other diagnostics all of these patient groups can be identified using existing diagnostic technologies. And so as we partner with Abbott for MLL-r and partner with Roche for 6438, we would enter into similar partnership to develop diagnostics that are from a diagnostic development point of view, these are all very straightforward.

Jonathan Eckard – Citi

Okay, great. Thank you so much.

Jason Rhodes

Thank you.

Eric Hedrick

Thanks.

Operator

Our next question comes from Simos Simeonidis of Cowen and Company. Your line is now open.

Simos Simeonidis – Cowen and Company

Yes, hi. Thank you for taking the question. And please allow me to send my best wishes for full recovery to Robert and his family, hope to get him back as quickly as possible. I know you can’t really talk about the data you have so far in 5676. But can you give us a rough idea maybe in terms of numbers of patients you recruited or potentially the ratio of MLL mutated versus non-mutated patients?

Eric Hedrick

Hi, Simos. Thanks. Thanks for the question. This is Eric. So there is nothing I can say on the call today specifically to those questions, I can say that the date of disclosure will include the description of the different type of patients that we have enrolled to-date. But there is no real detail that I can put on that right now.

Simos Simeonidis – Cowen and Company

But maybe let me try this, you have been able to at least enroll more patients with mutations and this we cannot pass the hypothesis for the drug?

Eric Hedrick

Yes. So again the current stage of the study is open to patients with advanced hematologic malignancy. And again, the composition of the particular disease and so genetic status of those patients will include as part of the top-line data disclosure.

Simos Simeonidis – Cowen and Company

Okay. And would that we – sorry, go ahead Jason.

Jason Rhodes

Okay. We appreciate the interest in the question and obviously look forward to sharing that information with you all at once when we provide the update on the dose escalation data later this quarter.

Simos Simeonidis – Cowen and Company

And have you submitted these data for ASH?

Eric Hedrick

Yes. The data disclosure will not be connected to ASH or any other conference. We have submitted a number of abstracts to the ASH meeting not on the clinical data and at the time those are disclosed publicly, we will let folks know about which have been accepted.

Jason Rhodes

All right. So the timing of the top-line data disclosure will be a function of when we are finishing that cohort and then going into the expansion cohort and that would be independent of any comp.

Simos Simeonidis – Cowen and Company

I see. Okay. That’s great. Thank you for taking the questions.

Eric Hedrick

Thank you.

Operator

Our next question comes from Howard Laing of Leerink Swann. Your line is now open.

Howard Laing – Leerink Swann

Well, great. Thanks very much. Maybe just a question that was asked earlier, how do you, if you don’t try to keep the – how do you decide when to stop?

Jason Rhodes

Yes.

Eric Hedrick

Hi, Howard. It’s Eric. Thanks for the question. So again, the first stage of the study is technically designed to establish MTD, as MTD can be established, but short of MTD the data that will factor into decisions around dose for the expansion phase of the study will be primarily based on pharmacokinetics, pharmacodynamics and safety.

Howard Laing – Leerink Swann

Okay. And question on MLL-PTD, based on the preclinical data, do you expect DOT1L inhibitor to be as effective as in the case of MLL-r patients which is already – seems really impressive.

Bob Copeland

Hi, Howard. This is Bob Copeland. It’s always challenging to make clinical predictions from preclinical data. What I can say is that the preclinical data which I presented yesterday at AACR indicates that both in cell culture and in xenograft models MLL-PTD is sensitive to DOT1L inhibition in the same type of potency range is what we see for various MLL rearrange leukemias.

Howard Laing – Leerink Swann

Okay. Thank you very much.

Jason Rhodes

Thanks.

Operator

Thank you. (Operator Instructions) Our next question comes from Mike King of JMP Securities. Your line is now open.

Mike King – JMP Securities

Thanks for taking the question. And congrats on the progress also to Jason any news true to the rumor that Robert actually tried to outperform, had to be dissuaded from performing the surgery himself?

Jason Rhodes

Yes. The real trick was getting the conference call materials out of his hand as he went into the operating room.

Mike King – JMP Securities

Okay.

Jason Rhodes

If you are at least.

Mike King – JMP Securities

Well, I would I think well my best to him for a speedy recovery. A lot of my questions have been answered. I just wanted to get clarity on malignant rhabdoid, your goals for 2014 seem to prioritize synovial sarcoma and the related sarcoma’s, when exactly should we expect patients to be enrolled for malignant rhabdoid for 6438?

Eric Hedrick

Hi, Mike. It’s Eric. So it’s not possible right now to comment on the specific timing for those programs. But what is sort of within our goals here for the program is, once a dose is established from dose escalation or sufficient dose information from that study to go on to these proof-of-concept type studies that we would pursue these in parallel as much as that’s possible. So we really see EZH2 mutated non-Hodgkin lymphoma patients synovial sarcoma, malignant rhabdoid tumors sort of independent and parallel proof-of-concept opportunities.

And it’s really all sort of gated on establishing or understanding more about dosing safety from the dose escalation study.

Mike King – JMP Securities

Okay. And then just for 5676 with regard to data, Eric you mentioned part of the objective for the Phase 1 dose escalation is for PK PD, so I assume you will be showing data on – how much impact the drugs had on methylation?

Eric Hedrick

Sure. That’s an important piece of the data. We are (clocking) in that stage of the study and that will be included in what we share.

Mike King – JMP Securities

Okay. Thanks very much.

Eric Hedrick

Sure.

Jason Rhodes

Thank you.

Operator

Our next question comes from Greg Wade of Wedbush Securities. Your line is now open.

Greg Wade – Wedbush Securities

Hi, good afternoon and thanks for taking my questions as well my best to Robert. First up, Eric, can you tell us what dose cohort you are working away through in the dose escalation study on 5676. And then Bob perhaps, want to make sure, if you learned of any new HMT target prevalence’s in various malignancies over the last several months and whether any of this knowledge has helped you to reprioritize or elevate in priority as you work on the 20 HMTs that you are targeting? Thanks.

Eric Hedrick

Hi, Greg. It’s Eric. Yes. Regarding your first question, again on the call today we really not disclosing specific information about current dosing cohort. What we will disclose though by the end of the year is, doses we have evaluated number of cohorts, number of patients. But again, not a lead part of this sort of top-line data disclosure.

Greg Wade – Wedbush Securities

Thanks.

Bob Copeland

And in terms of the HMT, we are continuously evaluating data from various cancer genome data bases as well as a variety of other methods for exploring dependencies of cancer cells on HMTs and we have been very gratified with those studies. We have a robust pipeline of preclinical programs and we look forward to sharing more information about specific programs as they mature.

Jason Rhodes

And Greg, this is Jason. The way we think about the businesses, there are four drivers, they are the value creation. They are the primary indications for the two clinical programs. They are then the expansion indications, we’ve just spend some time talking about today in which Bob presented yesterday at the ACR meeting. Then there is the GSK targets which are the next most advanced targets. Those are all progressing and we hope to share more information on those in the not too distant future. And then there are additionally as Bob is describing at the other high priority HMT targets that we are very actively working on.

As you know from our PNAS publication around EZH2, the conventional wisdom about the role of many of these HMTs and cancer is often incorrect. And so, our inclination is to pursue a very deep understanding of the role, this oncogenic HMTs in order to prioritizing for a drug discovery activities and then to announce those programs and share that data, once they are relatively advanced in preclinical research given the proprietary nature of many the insights that we have. And so we recognized the means that we’re not always able to give you new information on in every time we speak but it is a very important part of our strategy and an important growth driver for the business.

Greg Wade – Wedbush Securities

Thanks Jason.

Operator

Thank you. Our next question is a follow up from Simos Simeonidi of Cowen and Company. Your line is now open.

Simos Simeonidi – Cowen and Company

Yes. I was just going to ask you whether you have an idea when we might see the day from the first cohort – from the dose escalation of 6438?

Jason Rhodes

We’ll provide that sometime next year when that study is complete. It began enrolling in June of this year and so while was going well. It’s not far enough for long for us to make a specific timing prediction in order to provide guidance, yes, but we will.

Simos Simeonidi – Cowen and Company

Okay. Thank you.

Operator

Thank you. And at this time, I’m not showing any further questions. So I’d like to turn the call back to management for any closing comments.

Jason Rhodes

So thanks very much everyone for participating and listening to today’s call. We appreciate your interest in Epizyme and your well wishes to Robert. He is doing very well. And thank you for taking the time to join us on the call today. Thanks very much.

Operator

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

Jason Rhodes

Thank you.

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