Epizyme's Management Presents at Morgan Stanley Global Healthcare Conference (Transcript)

Sep.11.13 | About: Epizyme (EPZM)

Epizyme, Inc. (NASDAQ:EPZM)

Morgan Stanley Global Healthcare Conference Call

September 11, 2013; 08:00 a.m. ET


Jason Rhodes - President & Chief Financial Officer


Sara Slifka - Morgan Stanley - Morgan Stanley


So I think its appropriate for us to start off in remembering some of the victims of 9/11 with a moment of silence. So please join me for a moment of silence. Thank you.

And I wanted to welcome you all this morning.

Sara Slifka - Morgan Stanley

Okay, I guess we’ll go ahead and get started. So welcome to day three. I’m Sara Slifka - Morgan Stanley, one of the biotech analysts at Morgan Stanley and I am up here with Jason Rhodes, President and CFO of Epizyme, welcome.

Just before we get started the disclosures, the personal holdings disclosures, Morgan Stanley disclosures are on the Morgan Stanley website.

So with that to start, since Epizyme is relatively new to the public world, can you just give us a brief overview of the company and its view and recent developments.

Jason Rhodes

Sure. Thanks Sara. Its great to be here and to have the opportunity to talk to everyone about Epizyme. Epizyme is a clinical stagy biopharmaceutical company. We are developing personalized therapeutics for patients with genetically defined cancers and we are specifically applying that strategy to a class of Epigenetic enzymes called Histone Methyltransferases.

The HMTs are a very large target class. There are 96 members as we’ve defined it and within that 96-member target class, we’ve actually prioritized 20 targets based on very clear oncogenic hypothesis. We then developed those drugs and as rapidly as possible in clinical development.

We actually focused clinical development specifically on those patients with the genetically defined cancers and in order to do that, we developed companion diagnostics and we are doing that through partnerships with Abbott and Roche.

For example, our lead program is for a genetically defined subtype of acute leukemia called MLL-r or Mixed Lineage Leukemia. That product or compound is called 5676 and our second program that is also in the clinic currently and is called 6438 is targeting a genetically defined subtype of non-Hodgkin lymphoma that’s caused by point mutation in an HMT called EZH2.

Sara Slifka - Morgan Stanley

Okay, great. So maybe to start, interest in personalized medicine for oncology has really grown over the past few years. Can you talk about how your technology is different from others out there?

Jason Rhodes

Sure. So obviously increasingly we are identifying and understanding the specific role that genetic alternations play in driving very specific cancers and so there’s some very good recent examples of that. Probably everyone here is familiar with Xalkori and the Zelboraf for example.

GSK just this year had a B-Raf inhibitor and also a MEK inhibitor approved that had a similar kind of a focus. So this idea of pointing targeted therapeutics to specific patients with genetically defined cancers is an approach that’s relatively new, but that’s becoming I think very well understood.

As I mentioned during the introduction, we are specifically applying that product strategy, which we think is very powerful, in a number of ways to this type of genetic target class, and so our particular expertise at Epizyme is in the definition and understanding of this target class, the oncogenic role that these genetically altered HMTs can play in cancer and what we’ve done over the past 5.5 years is built a propriety product platform that allows us to first understand the biology around these targets and then interrogate and experiment, which is much easier said than done; to identify novel chemistry and then ultimately as we have now in two programs, to move them into clinical development.

And so that overall product strategy I think is something that is increasingly understood in the oncology space and we are doing it in a very unique way and we certainly think we are in a leadership role as applying it for this particular epigenetic target class.

Sara Slifka - Morgan Stanley

Okay. So maybe we can move on to talk about 5676. You’re in a Phase I trial. Can you update us on where you are on enrolment and when we expect to see data in that trial?

Jason Rhodes

Sure. So 5676 again is an inhibitor of an HMT called DOT1L. Due to a translocation, DOT1L becomes oncogenic and it drives the up regulation, in the expression of a set of leukemogenic genes and so it’s a very clear oncogenic driver for that subset of patients, and they represent about 10% of all leukemia. So that initial population is about 5,000 patients per year in terms of the annual incidence.

We entered a Phase I dose escalation stage in late 2012 and that study is ongoing and really importantly, that Phase I study has two stages. It has a dose escalation, which for practical purposes you can think of it as being an all-comers within acute leukemias and so it doesn’t require the inclusion of the patients with the specific genetic alteration of these MLL-r patients, but in fact may and as of our IPO, which also was in may we disclosed that we had seen one MLL-r patient and had actually selectively seen a biological response in that one patient, whereas we did not see a biological response in the non MLL-r patients in the study.

So in terms of the specific status, we have six sites that are currently enrolling. The dose escalation is continuing. We are on track to disclose top line results in the dose escalation study this year and also to initiate a second portion of that Phase I study, which we’re calling an expansion cohort. The expansion cohort will exclusively enroll MLL-r patients and so we expect to initiate that cohort also later this year.

Sara Slifka - Morgan Stanley

So you’ve got up to one patient that you had a response and I think there was a 90% reduction in that, but therapy ended 10 days later because of CNS progression. So was there not enough drug onboard to adequately penetrate the CNS. Is it getting through the blood-brain barrier, what’s happening there?

Jason Rhodes

Sure. So firstly just to step back briefly, so the study design for the dose escalation is really intended to assess safety PK and PD. It’s really not by any means an efficacy study. That said, we do allow for the inclusion of the MLL-r patients and in this case we saw a patient with ALL, so you see MLL-r patients as both ALL and AML patients.

In ALL patients, so stepping back actually just a little bit, MLL-r is seen in both adult and pediatric patients in both AML and ALL patients and the adult patient group is by far the largest population and most of the adult patients are AML patients. So in some ways this was a fairly rare patient.

Among ALL patients it’s not unusual, but its also not very common to have CNS involved. So its roughly 10% of the ALL patient and so what that translates to is about 3% of the adult patients that we may see could have CNS progression, so it represents a relatively small group.

To our knowledge, our drug doesn’t penetrate into the CNS. The typical treatment for patients with CNS progression, which again is seen, but its not fairly common in this group, is the administration of intrathecal methotrexate and so we saw this ALL, MLL-r patient in our second dose cohorts as relatively early in the dose escalation study.

It was very interesting for us to see a reduction in the methyl mark that led to a reduction in blast count, as well as an elimination of a number of clinical symptoms such as the leukemic fevers.

For example, that patient however was a very late stage patient. They did have CNS progression and they went off our drug in order to receive treatment specifically for that. So we think there are very interesting patients in terms of the biological response and the PK/PD relationship that we did see, but they were fairly early in the dose escalation study at the same time.

Question-and-Answer Session

Sara Slifka - Morgan Stanley

Are there any audience questions?

Looking at the data that you’ve released so far, we know from what you put out at the IPO that you’ve gotten for this 24/m2 level and you started to see that one response. Is that the dose level at which based on your pre-clinical was work you saw, you started to see responses and then seperately, what was your DLC in animals?

Jason Rhodes

Sure. So based on our pre-clinical work and obviously everyone in this room understands the translation of pre-clinical data, especially on PK/PD is useful but limited. But based on the pre-clinical data that we had, we expect that the 24/m2 would be sub therapeutic and so what we saw in this patient was a reduction in the methyl mark, but it was a relatively small reduction in the methyl mark relative to what we would have expected would be necessary to have a therapeutic effect. So in that sense, seeing a biological response, but not a true broad clinical response is probably consistent in that observation.

Sara Slifka - Morgan Stanley

Just a high level question. Linearly thinking about the way your drugs work and its reduction in methyl mark, do you think its kind of a gradient of a response, meaning if you get kind of 70% reduction, that’s going to show a more than a 50% reduction or do you think there’s a threshold level where if you get it done not that your going to see the same response level.

Jason Rhodes

Yes. So in our observation it’s more of a threshold step. So what we’re doing by affecting these methyl marks is really affecting gene expression, which ultimately affects phenotype and so what we see is that there is some minimal or threshold level with an addition pre-clinically necessary in order to change the gene expression and ultimately see the change in phenotype, and so while we’re able to observe that in cell lines and also in animal models.

In this case the cell lines are cells that have the respective genetic alteration and the animal models in some ways are really in vivo petri dishes for the cell lines. This really is a tremendous continuity from human genetics into these cell lines and then into the animal models and so that PK/PD data is very useful pre-clinically, and as we head into the clinic, we’re obviously – or now that we’re in the clinic, we’re obviously collecting that data and consider it to be very useful.

Over time what becomes really most relevant and interesting to us is the relationship between PK and then biological response and so the PK/PD data is very important and we’re collecting it and analyzing it, but again, over time the biological responses that we expect to see and hope to see in human patients will really kind of overwhelm the PD data we think.

Sara Slifka - Morgan Stanley

Okay, great. And then just taking a step back there, 5676 you mentioned in your introductory comments that inhibit DOT1L, which is a normal enzyme. But in your pre-clinical work it looks like only the MLL-r rearranged cells are being affected. So why are you not affecting normal cells and then what is the detailed role of DOT1L in normal cells.

Jason Rhodes

Yes, so many of these HMTs play a critical role in embryonic development, make controllable pathways and (inaudible) genes and so for that reason they are typically at least for those that we prioritized embryonically we’re going to knock out.

However in a mature organism they play very different and often much less important roles and so they are relatively quite, biologically immature organisms, unless they are mis-regulated and so what we see as a result of the translocation in MLL-r is that DOT1L is recruited to a location within the genome where it shouldn’t be and as a result of that, if it’s a methyl mark that typically would not be one and in that very specific context, that methyl mark up regulates the leukemogenic pathway.

As a result of that, those cells with that translocation are evicted to the DOT1L methyl mark and so what we see and we published this. That were presented at ash and published it in blood for example earlier this spring is that we very selectively kill stock proliferation in those cells with the translocation and essentially have no effect in those cells that don’t have the translocation and so it’s a very selective and sensitive cell killing of the trans-located cells.

Sara Slifka - Morgan Stanley

Okay, great. So you mentioned during Phase I you’re going to dose escalate and then your going to move into a Phase II expansion cohort. What are you looking to see the response like in that Phase II expansion cohort and warrant movement forward on that?

Jason Rhodes

Sure. So in the case of 5676 we actually consider the expansion cohort to be part of Phase I, just in terms of the sort of technical trial design. In the case of 6438, our other program we did in conjunction with Phase I or Phase II. That aside, the purpose of the expansion cohort, because it is part of the Phase I, fundamentally remains to assess safety PK and PD, although in this case entirely any MLL-r patient.

That said, our expectation and certainly its something that we’re seeking, is to have an initial assessment of therapeutic effect in that population and so in addition to the safety PK and PD, we hope to see that as well.

Sara Slifka - Morgan Stanley

Okay, and then what do you expect the pathway to look like beyond the Phase I expansion? The prognosis of these patients is pretty broad. Do you expect that you’re going to need a single-arm trial or controlled trial? What do you see is the overall path?

Jason Rhodes

Yes, that’s right. So the prognosis is very poor. For adult AML patients with MLL-r, the five-year survival is about 5% to 24% and that’s despite very intensive treatment with standard of care, tumor therapeutics and there’s a similarly poor prognosis for the pediatric patients. So there’s a very high unmet need in that population.

The specific path forward will really be defined by what we see in the expansion cohort and then potentially in the next study and fundamentally there’ll be a question of the nature of the responses that we see and their durability. There certainly are good precedent cases for being able to move ahead very rapidly in focused clinical trials if you have a durable response in a very well defined patient population and so that’s our intended task, our ability to pursue it though will be determined by the actual data that we generate.

Sara Slifka - Morgan Stanley

Okay, any questions?

Okay, in practice MLL-r patients are already identified, using cytogenetics or FISH. Why is there a need to develop a companion diagnostic?

Jason Rhodes

Yes, that’s a good question and that’s when we though we’ll have a doubt. So MLL-r is a well-understood genetic alteration. Patients are already identified as you said, using either cytogenetics or FISH, and the patients that we’re treating initially in the Phase I are actually relapsed or proactive. So they come to us with that diagnosis; we then confirm it.

That said, and so it’s a very well understood patient group by physicians, which is also very attractive. It’s a first indication for us to pursue.

That said, the current FDA guidelines around companion diagnostics are very clear, that you have to have a true IVD that accompanies the drug, a targeted drug like personalized therapeutics if your are going to include the genetic alteration in the indication and so the prudent thing for us to do in order to avoid in any way potentially putting our registration timing at risk, is to begin the development of the true IVD.

We are doing that with Abbott. Abbott today actually provides the FISH reagent that’s already used in a clinical setting, so it’s not the development of the new diagnostic. Its really taking an existing reagent and turning it into an IVD from a regulatory point of view. So our baseline plan is to develop that diagnostic in order not to have any regulatory risks as we progress with the program and have more discussions with the FDA, we can see that, even that could change.

Sara Slifka - Morgan Stanley

Okay. And then if I remember correctly, 5676 is administered via a continuous infusion. Is there any way going forward to make this more convenient?

Jason Rhodes

Yes. So there are a couple of elements to that. So today the standard induction therapy for acute leukemia patients is via continuous IV and so providing 5676 in that clinical form is consistent with the existing standard of care, both for adults and for pediatric patients. It’s really hard to see moving away from that.

5676 itself is essentially not as orally bioavailable, and so we wouldn’t switch that molecule over. We think that as a continuous IV, its very commercially viable, so it’s the drug that we plan to take to market.

That said, for a program like this, where there is much promise and it’s obviously very important to us. We have other earlier stage chemistry efforts ongoing, that conceivably we could have a normal few in the future. Again, that said, we really believe the CID formulation is very viable clinically.

Sara Slifka - Morgan Stanley

Okay, great. And are there other indications that you’re going to potentially look at going forward with 5676?

Jason Rhodes

There are, yes, it’s a good question. So when you think about what drives the business, the primary indications for both of the lead programs are the big drivers today. That said, for both 5676 and for 6438, they are what we refer to internally these as expansion indications that we do plan to pursue.

An example of that with 5676 is another acute leukemia called MLL-PTD. One of our collaborators, Scott Armstrong at the Sloan-Kettering presented data this past March actually on MLL-PTD. So it’s a different genetic alteration than the translocation we see with MLL-r, PTD is Partial Tandem Duplication.

The data that Scott presented showed that MLL-PTD sell lines were similarly sensitive to DOT1L inhibition, and so while we haven’t discussed specific plans around that program, we will in the future and do intend to pursue that indication and its an important indication, both clinically, but also from a commercial point of view and that MLL-PTD is about 50% to 80%, the size of the MLL population and its an incremental population. So it represents a pretty significant expansion and the potential patients that we could treat with this drug.

Sara Slifka - Morgan Stanley

Okay, great. But there are no questions on 5676, so I’m going to move to 6438. So you started a Phase I and you started your plan to move it forward into a Phase II, I believe next year in view of the factor NHL. Looking at that Phase I, are there any other cancers that potentially could show a strong response and if that does occur, would you consider moving other cancers forward next year into a Phase II.

Jason Rhodes

Yes, so as for the PTD examples for 5676, there are other cancers that we’ve already identified, in which EZH2 plays an oncogenic role and so one of them is a really awful pediatric cancer called malignant rhabdoid tumors or MRT and we published on that in PNAS in the spring.

And so in that case there is actually a deletion of another regulatory protein. As a result of that deletion, EZH2 is mis-regulated. So it’s a different genetic alternation than what we’ve seen in non-Hodgkin lymphoma patients, but we see very similar results pre-clinically and that we treat these cells, we selectively kill those with the specific deletion and we go into animal models at the right dose, and it’s a tolerable dose.

We are actually able to completely eliminate the tumor and that tumor elimination, that response to sustain even once we remove the drug for a real extended period. So we do plan to go into MRT in the future and there are other solid tumors that actually represent significantly larger populations than MRT that we’ll also pursue.

I think part of your question is might we see things from the Phase I and so the Phase I is structured as more of an all-comers study. It may include certainly non-Hodgkin lymphoma patients and increasingly those with the point mutation.

And so if we saw any notion of biological response in patients that did not have the point mutation, we certainly want to understand that and if they represent it, what we though were really clear populations with a good mechanistic understating for why EZH2, in addition was having a specimen (ph) that I expected we would, by our demand to the clinical program.

Sara Slifka - Morgan Stanley

Okay, can you follow up on MRT? Do you have any sense of the timing of when that potentially could enter the clinic and what are the rate of any effects to get that going.

Jason Rhodes

Yes, so we haven’t disclosed timing on that yet. That’s a pediatric population and as with MLL-r with its pediatric population, we intend to move into them fairly rapidly. But you do want to have some basic safety and PK/PD data in adults before you do that. So the early dose escalation data at a minimum is really necessary before we move into the pediatric studies.

Sara Slifka - Morgan Stanley

Okay, and what’s your dose on the intoxiticies for 6438 in animals?

Jason Rhodes

Yes, for the 6438 and this is also true for 5676. There essentially weren’t doses on the intoxiticies. What we saw with 5676 was some change in a retro differentiation in some red blood cell count reduction, but it was reversible, it wasn’t significant.

Similarly with 6438 and EZH2 inhibition, we saw some changes in lymphoid tissue, which is kind of mechanistically consistent, but no true dose from any toxicity. So again, in adult differentiated cells and organisms certainly is seen in the context of the pre-clinical study that is conducted to-date, that you can inhibit these in a fairly safe way.

Sara Slifka - Morgan Stanley

Okay, great. And then you have an agreement with Eisai. Maybe you can describe that for people who aren’t familiar with that. What are your thoughts as to whether you’re going to opt into U.S. right. You do have the U.S. right to 5676 and maybe it makes sense to do so and then if you do decide to opt in, what are the timelines to when you have to do that.

Jason Rhodes

Sure, yes. So with both – and the 5676 is partnering with Celgene x-U.S. We have 100% of the U.S. rate and are in active global joint development program with Celgene today.

Eisai is similar on its 6438. In that case the base line agreement with Eisai is that they have worldwide rights, but we didn’t outlet since the program. For them it’s a very active joint program. We have really an equal say in strategy and the conduct of clinical operations.

From the financial point of view, the way that that partnership is structured, Eisai pays for 100% of global R&D, despite our very active involvement. So it’s very attractive in that sense for us, effectively until the initiation of the registration study.

And so our strategy there was to effectively shift the clinical development risk and financial risk during that time on to Eisai, to remain very actively involved in the program, and then given that we focus on genetically defined patients relatively early to if not truly know in the absolute sense, but certainly have a very good understanding of whether we believe the drug can be successful well before we have to opt in.

And so in that sense generally speaking, our approach will be to opt in as late as possible. Once we opt in, we then begin to share U.S. cost, not global, but U.S. cost 50/50. To the extent that we have joint control and they are paying for everything, that’s a very good arrangement and we want to carry that forward, generally speaking as long as we can.

Sara Slifka - Morgan Stanley

Okay, great. And then looking at the path forward for 6438, it seems like the prognosis for the patients with the EZH2 commutations are not really solidifying, because its not only tested for. So is this potentially a more comprehensive development plan than the 5676. Do you have to run active controlled trials study (inaudible)?

Jason Rhodes

Yes, that’s a very good question. So unlike with MLL-r patients, where it’s very clear who they are, they are diagnosed there, they have a terrible prognosis, with the EZH2 patients, non-Hodgkin lymphoma patients with the point mutation in EZH2, that’s a specific population. So it’s the GCB subtype, it’s not ADC. ADC is well treated and increasingly will be well treated going forward.

GCB, and these are diffuse large B-cell lymphoma, so DLBCL in case you want another acronym, are relatively less well treated. We also see this point mutation in (inaudible) lymphoma patients.

Within that population then, our initial focus is entirely on the U.S. refractory patients. So while the broader population conceivably has better treated and more indolence diseases in some cases at least, the patients that we are focusing on are those that have relapsed or refractory and that have the point mutation. So there is a greater unmet need in that population, than in the general non-Hodgkin informal population.

However, it is true that while the role of the point mutation and the ideology of this disease is very well understood, both in the research world and increasingly among clinical positions who treat these patients, its not a current standard of diagnostic care and so with that mind we partnered with Roche to develop an IDE, because there isn’t an existing one.

In the meantime, we essentially set up the timeline for the Roche IDE, so that it’s available by the time, no later than the time that we initiated registration study. In the meantime the clinical sites that we are working with, that are involve in the trail are actually a piece of lab based PCR.

So again, it’s a very standard office technology. It’s just a new anolyte that hasn’t been looked at before and we are very aware of the need to identify patient population in advance or at the beginning of the studies in order to pull them in.

Our expectation would be that as with the case with Xalkori and the (inaudible) location or the B-Raf mutation. For zelboraf that as you go through your clinical development and you publish results and share them with the community, that by the time the product was approved, I’m assuming we make it that far, that it has become well understood in the physician community and the diagnostic that’s available, and what we saw with both Xalkori and Zelboraf, it’s a very, very rapid up-tick, and arguably each of those drugs reached peak sales, lets say within a year, peak penetration at least within a year of launch and so we are trying to set up the same kind of dynamic for 6438.

Sara Slifka - Morgan Stanley

Okay, great. So more generally, have there been other companies that have gone after Histone Methyltransferase to such as sales, and if so what has been the biggest challenges?

Jason Rhodes

Yes, so the good news is there haven’t been failures and that’s a consequence of Epizyme being the first and so far everything has gone pretty well. So we were the first company to publish animal data for any HMT and we did it with DOT1L, EZH2 in non-Hodgkin lymphoma and also EZH2 in MRT.

We are also the first company to initiate a clinical study for any HMT and that was DOT1L, and we remain today with two programs in the clinical, the only company to have ongoing clinical development. So, we are really a leader in the field to-date.

Sara Slifka - Morgan Stanley

Okay. And then ASH is coming up in a few months. What data are we expected to see at ASH if any?

Jason Rhodes

Yes, so what we said in terms of this trial disclosure for 5676 is that we’ll provide top line dose escalation results, potentially when the data is available independent of any specific conferencing. Similarly we’ll then initiate the expansion cohort. So our disclosure of data which we do, and this could happen before the end of the year is implied to ASH or to any other specific event.

Sara Slifka - Morgan Stanley

Okay, and then do you have any sense as to the strength of the animal models that you used. Are they know well to predict human response?

Jason Rhodes

Right. So I think for good reasons people often have or do simply have skepticism about animal models and if you think about the history of cytotoxic drug discovery, animal models were often a great sort of false positive generators. You have a non-specific tumor, you have a generic cytotoxic agent, you had a very sort of artificial construct and its very forward with the disease and so as a result it wasn’t too great to model.

In our case, as I mentioned before, we are starting with human genetics. We have a very clear hypothesis and then we have tremendous continuity of that hypothesis. We take the human genetics and go into cell lines, and not a single cell line, but multiple cell lines that have the genetic alteration of interest and then we are taking those cell lines and using them to create the animal model.

So over time we’ll discovery the throughput and the power this approaches, but it’s a very different approach than what we’ve typically seen with animal model and what we have seen is remarkable consistency of the hypothesis as we evaluated it at each stage so far.

Sara Slifka - Morgan Stanley

Okay, great. And may be just in the last minute or so here, beyond 6438 and 5676, what’s next. What are the kind of the key targets you are looking at, key indication, are you kind of oncology and definitely are there other areas you might explore?

Jason Rhodes

Yes, that’s a good set of questions. So there are 20 targets that we prioritized from an oncogenic point of view. So our internal focus and effectively our focus for that current partnership is entirely on oncology.

20 targets is a huge opportunity set. There are only drugs that I think target something like 12 or 13 kinase inhibitors today and we can see that that will be a huge feel, could have 20 potential targets. Understand that not all of them are very likely to turn into drugs. It’s a very large space and so we are very happily and productively focused on that.

We have all 20 of those prioritized enzymes in what we call our cross-stream platforms. So all of them are in our platform. There’s active drug discovery at various stages against all of them.

So the way we really think about the drivers of the business are the primary indications in the two lead programs, the expansion indications that we talk about a little bit in those two lead programs. We have three targets. The specific identity of those targets we can’t disclose, but three targets partnered with GSK. All of those are moving ahead and generating 8 million milestone payments in the first year and a half or something like that of that partnership. So that’s the first five targets and then the other 15 are all being worked on in that sort of the fourth source of growth for the business.

So we haven’t specifically identified those targets. Our general approach has been to publish once we have biological insights, but the announcement is too early. So the source of some advantage, at lease for some period of time and so we are very judicious about when we share that.

That said, over time and probably going into 2014, we’ll talk more about both the expansion indications and then over time about those other 15 targets, at least the ones that are rising to the top.

Sara Slifka - Morgan Stanley

Okay, great. Well, we are out of time. So I’ll stop there and thanks everyone for joining us.

Jason Rhodes

Thanks very much.

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