Dan Junius – President & Chief Executive Officer
ImmunoGen, Inc. (IMGN) 31st Annual JP Morgan Healthcare Conference January 7, 2013 11:00 AM ET
It is my pleasure to introduce our first presenting company, which is ImmunoGen, clearly a very important year coming up with the likely approval of their first product or their partners’ first product T-DM1, which is a potentially huge one. Here to tell us about that as well as the rest of the company’s emerging pipeline and platform technologies is the President and CEO, Dan Junius. And after Dan’s presentation there will be a breakout session just down the hall on the right-hand side in the Sussex Room, so good luck fighting the crowds to get to that. And I’ve also been told to remind people to please set your phones to vibrate or silent. Thank you, and with that I’ll turn it over to Dan.
Thanks, Cory, and good morning everybody. Let me thank JP Morgan for inviting ImmunoGen to present at the conference here this year. We appreciate that opportunity. I will make some forward-looking statements over the course of the presentation. I would note that you may want to look at our SEC filings concerning the risks associated with investments in ImmunoGen.
We are in the process of developing therapies that we think have the opportunity to transform how cancer is treated. That consists of compounds that we have under development. We have three compounds in the clinic with the fourth coming into the clinic over the course of 2014. There are also some very interesting compounds under development by our partners, the most prominent and well-known is T-DM1. That’s currently in front of regulators both in the US and in Europe where approval is expected over this year and launch of sales commencing in the US hopefully very shortly.
Seven other partner compounds are also in the progress of development, and supporting all of that we have a very deep research and development set of capabilities that have allowed us to expand the portfolio and bring our compounds, our proprietary compounds forward. We have the financial wherewithal to bring these we believe to proof of concept with a rich cash portfolio of over $200 million and no debt.
Let me start just briefly with the technology. I think people are generally familiar with it. We refer to our technology as a Targeted Antibody Payload technology or TAP. Very simply, it’s using the targeting ability of an antibody to bring a highly-toxic payload into a cell, release the cell, and through that start a mechanism that results in cell death.
Some very important components here: first, the proprietary cell killing agent itself. We have a technology that has a chemotherapeutic that’s far, far more potent than standard chemotherapy – 100 to 1000 times more potent. We have two particular molecules, we work with, DM1 and DM4. These are tubulin inhibitors, and as I noted, they inhibit cells from dividing and lead to cell death.
We also have a family of engineered linkers. We have four different linkers in the clinic today. Each of these conveys a different property to the cytotoxin once it’s released from the antibody. These allow the whole compound to remain stable in the plasma but to provide activation in the cell, and we’ll talk a little bit later about the unique properties of some of these linkers.
And supporting this is a very deep expertise in both understanding targets and cell biology as well as antibody expertise. You need to understand that this is a system that we’re working with on a number of levels, a system in terms from a cell standpoint, a system in terms of a conjugate, and we have a deep awareness and understanding of the various elements that allow this to be successful.
This is truly personalized medicine, in that we’re delivering a highly-potent payload to a specific target that resides on the surface of a cell. This allows us to partition patient populations within various indications to those who robustly express the targets that we’re looking at, so therefore very much of a personalized medicine.
Another element, though, that’s very important to understand, so with the targeting nature of this, it allows us to get at cancer cells to kill cancer cells. And by using an antibody-based approach, it allows us to avoid the systemic toxicity that you normally see with broad-based chemotherapeutics. What’s also important when you think about that, so we’re targeting by using the antibody to avoid healthy tissue, but in those instances where the target does reside on the surface of healthy tissue, the fact that we’re dealing with the tubulin inhibitor – as long as this is a cell that doesn’t divide rapidly – it provides us with another layer of safety that gets us to the attractive tolerability profile we’ve seen with these compounds in many of the clinical tests.
Our approach, I think, at this point is highly validated. You’ve seen it in solid tumors with T-DM1, we’ll talk more about that later, as well as in liquid tumors. SAR3419 is a compound being developed by Sanofi for non-Hodgkin’s lymphoma. Both of these compounds have shown good efficacy and tolerability. In the instance of CD19, the 3419 target, you have a target that previously would not have been druggable. It’s not a receptor that has any known function in the development of cancer, so therefore by using this we can take a target that otherwise you wouldn’t be disrupting a signaling mechanism, but simply using it as a vehicle to get the cytotoxin into the cancer cell.
And it’s interesting to note that both T-DM1 and SAR3419 are compounds that were created by ImmunoGen and then developed by our partners. So, while we have seen this proof of concept in these two compounds from partners, we’re now at a stage where we have an expanding portfolio of ImmunoGen-owned compounds that cover a variety of cancers.
You can see on the slide here we cover both solid and liquid tumors with our proprietary compounds, a variety of different lung cancers, non-Hodgkin’s lymphoma, head and neck cancer, and that’s complemented by a variety of compounds across a number of partners that demonstrate the breadth and potential of this technology; liquid tumors, solid tumors, and some very difficult diseases that we’re looking to tackle with our TAP technology.
2013, as Cory indicated, looks to be a very eventful year for ImmunoGen. It starts with a widely-anticipated approval of T-DM1 that would lead to US sales later in the year, EU launch; and we’ll see data off of a later-stage study that would allow for first line use of T-DM1 in metastatic patients. Then across the course of the year, fresh data off of some of our compounds in the clinics and Phase II data off of our small cell lung cancer study, as well as the introduction of a new compound by ImmunoGen into the clinic, and I’ll talk more about each of these.
So let me start with IMGN901. This is a product that we have under development for CD56-positive cancers. Right now, it’s in Phase II testing for small cell lung cancer. We’ve seen activity here in a variety of earlier studies, both in liquid and solid tumors. CD56 itself is expressed on a variety of cancer types; small cell lung cancer, Merkel cell carcinoma, and it’s also on pediatric neuroblastoma. And what we have here is taking our DM1 cytotoxin and linking it to a CD56-binding antibody. Small cell lung cancer itself is a very difficult disease. Its profile is that it tends to metastasize very early, about 60,000 cases each year in the US and Europe, virtually all of them CD56 positive. It’s a very aggressive disease with median survival of less than a year in patients that are treated, and while there’s a high response rate to existing first line therapy, there’s no durability.
So what you have is for patients who are dosed with an etoposide/platinum-based therapy they have a median PFS of under six months; overall survival of less than a year. There are later line therapies, but they show little effect, and so what we’re looking for is to be able to help bring a first line therapy that will provide an extended durability benefit to these patients. And we’ve seen across a couple of different studies prolonged benefit in both liquid and solid tumors with 901 which convinces us that we here have an active agent.
What we’ve seen in solid tumors with single-agent, durable remissions in a disease called Merkel cell, it’s a carcinoma of the skin, a small cell carcinoma of the skin, plus activity in small cell lung cancer with more advanced patients. These are patients that were second line or later, so very difficult to get activity in these later stage patients. And we have our first randomized study underway looking at 901 in combination with etoposide and carboplatin, and what we’ve seen here – and you can see the waterfall plot – a high level of activity.
But of note, that in chemo-naïve patients, we’ve had two PRs but what’s been highlighted by experts who’ve looked at the data is that in patients – and again, these are later stage patients, patients who are platinum resistant or refractory – we’ve had two PRs. And you don’t typically get a response from patients who have failed and are no longer responsive to a platinum-based therapy. So, we’re excited about the potential based on the solid tumor data.
We also have looked at 901 in multiple myeloma. Here again, we saw good single-agent activity. Patients would stay on study, these are later-stage patients for an extended period of time. About a quarter of them in monotherapy stayed on anywhere from five to 24 months, and we also looked at a combination study here, looking at 901 in combination with REVLIMID and dexamethasone. What we saw was activity both with those who were REVLIMID naïve as well as those who’d received REVLIMID previously.
A couple of features: patients who were resistant or refractive to REVLIMID, we saw a good level of activity across the five patients who all showed some level of -- not necessarily a full response, but stable disease or better. And then the 13 patients with poor prognostic mutations, all of them showed some level of activity even with stable disease going all the way up to very good PRs with 901. So again, this suggests to us is the affirmation that we have an agent that’s going to be active.
I noted this is currently in a Phase II study, the first randomized study that we’ve conducted with an ImmunoGen-based compound, conducted on our own. We have it looking at here, first line small cell lung cancer patients. So given the nature of the disease, we felt that the best way to attack it was to go at patients before they’d gone through first line therapy. We are currently in the middle of this study. We are going to recruit 120 patients. We are looking at about 40 sites across four countries, and we’re recruiting this study quite well. We believe that we’ll have data from the first cohort, as you know, it’s a Simon two-stage design, and we’ll be collecting data on 59 patients. We look to have those patients enrolled very soon which would allow us to have data sometime in the back half of the year.
The primary endpoint is progression-free survival. Again, these patients respond to a platinum-based therapy but without durability, so what we are looking to do is to be able to get a more durable benefit for these patients. I should note that in the Phase I portion, we were able to dose 901 in combination with the existing first-line therapy at the same level we’ve been able to dose it as monotherapy, so again, it affirms our belief that this particular approach provides us an avenue to use this technology in combination with other therapies.
The second compound we have in the clinic is called IMGN853. This is a product candidate for folate-receptor positive cancers. That particular receptor is over expressed on a variety of carcinomas. What we have here is a design using not DM1, which I referenced earlier, but DM4 linked to a folate-receptor biding antibody. As we went through and evaluated this compound, we looked at the antibody and chose it not necessarily for its innate attributes of affinity and avidity but more for its ability to function well as a conjugate.
And I noted earlier on our linker technology what we have with our linker technology here is a new linker. This is the first time we’ve introduced this linker into the clinic. The particular attribute is that this linker allows the metabolite, the cytotoxin to resist the survival mechanism of a cell, the efflux mechanism. And we think that the antibody along with the linker should allow this to be a very interesting compound. Right now, it’s in Phase I testing looking at cancers that over express the folate receptor alpha.
The particular cancers that we expect to pursue would be ovarian and lung cancer. In ovarian cancer, you have about 22,000 diagnoses per year leading to over 15,000 deaths. One of the reasons that it’s as aggressive as it is, is it’s typically diagnosed in an advanced state. Most of the cases of ovarian cancer, however, show strong folate expression, so we think there’s good potential here.
The other disease we’re pursuing is non-small cell carcinoma, and here you have about 90,000 cases per year in the US. Again, most of these have very strong folate expressions, so we’re excited to be moving this forward through a study. Where we are right now, this is a Phase I, we will be looking to get to a dosing level to determine MTD.
We’re looking at patients who over express the folate receptor. In the dose-finding phase, it is an all-comers study but once we get to a later stage, we’ll be screening for patients with high levels of expression. Once we have that dose, we have three expansion cohorts that we have identified that’ll be looking for both additional safety and efficacy information as well as in a couple of the studies trying to identify if there are further biomarkers to help us better or more narrowly identify the population who can benefit from this particular compound. So we’re quite interested here. We think we’ll have data that we’ll be able to report sometime around the middle of this year.
The last clinical compound is IMGN529. This is a candidate for CD37-positive B cell malignancies. Those would include non-Hodgkin’s lymphoma and chronic lymphocytic leukemia. It is on CD37. The target here is expressed on the same NHL subtypes as CD20, so if you will, just looking at the same target population as Rituxan, and as you can see significant patient populations both in CLL and in NHL.
The design here is again interesting, I think differentiated from other antibody-based approaches in non-Hodgkin’s lymphoma, in that we have an antibody that has shown pre-clinically to have activity that we believe is superior to Rituxan, and taking in then an active antibody, we have added to that our conjugate technology enhancing the innate characteristics of the antibody by giving it the characteristics of an ADC. A Phase I trial here is underway. It is open to most of the NHL subtypes, and we would expect to see data here towards the end of the current year. We are taking the opportunity of the conference here to announce the target of our next compound to go into the clinic.
We refer to this compound at IMGN289, It is a candidate for EGFR positive cancers. We are doing the work to prepare an IND for submission. We think that will take place sometime around the middle of 2013, so this particular compound will be looking at head and neck cancer as well as a different type of non-small cell lung cancer as opposed to the adenocarcinoma that I referenced earlier for 853. Current EGFR targeted therapies are characterized by a level of skin toxicity as well as a level of resistance to EGFR inhibition. What we have and what we think we have come up with, with this particular compound is a novel class of EGFR binding antibody. It has, we think, the potency of Erbitux, but without the toxicity associated with Erbitux., and what we have been able to take with that antibody then is to add DM1 similar to what I referenced in IMGN529 in having active antibody to which we have then also added – in which we have also added our conjugate technology.
What we have seen pre-clinically is greater potency and including cancers that show EGFR inhibition, so we think this is a significant opportunity. We expect to have preclinical data on this compound at AACR.
Let me then talk about our partners, I think most of you are familiar with T-DM1. There has been data that has been published on the EMILIA study which looks at patients. It was a randomized study looking at patients who had failed Herceptin in an earlier line of therapy and it compared T-DM1 versus Tykerb plus Xeloda. The data that came out was most impressive. It showed a very good progression-free survival benefit. It showed a 6-month improvement in overall survival, and in a profile that I think had very attractive tolerability characteristics and that the patients showed fewer grade 3 or greater adverse events. They had fewer events that led to dose reduction or trial discontinuation, and even the grade 3 adverse events manifestations were of a profile that were not as disruptive to a patient’s life as what they were seeing in the comparator arm of Tykerb plus Xeloda. Roche took this data forward and submitted it to both the US and EU. They also have conducted a study looking at T-DM1 in a first line Phase II study in first line metastatic patients, and the outcome was similar. You saw extremely good efficacy. They actually had not designed the study to show statistical improvement in progression free survival, but they achieved that despite a very small study of 137 patients, very good tolerability.
This leads to data that we would expect to see in this disease, first line metastatic HER2+ breast cancer sometime in late 2013 or early 2014. The data that’s been generated is feeding a pretty broad registration program for Roche. You look at this compared to Herceptin, because T-DM1 would be the replacement for Herceptin as the cornerstone therapy in dealing with HER2+ breast cancer. They’re pursuing it in a broad range of indications, broader than what you have today for Herceptin. We think the opportunity is there for them to price it at a premium to how Herceptin is priced today, and plus, given the data that we’ve seen thus far with extended progression-free survival, there’s the opportunity for longer application of this particular therapy for patients.
So we’re seeing significant expansion in the registration program that we will be hearing more about over time. Over 2013 we’re looking for approvals as I noted in the US and EU. We’ll see the first line data on metastatic and then additional approvals in earlier lines of therapy including potentially one particular type of adjuvant therapy that a study will be beginning this year. So, a broad commercial opportunity that Roche is aggressively pursuing.
This is the first in a number of partner programs underway. As you can see Roche has a variety of breast cancer indications that they’re pursuing as well as gastric cancer. We have four other partners with multiple compounds in the clinic including Amgen, Bayer, Biotest, and Sanofi. You also have compounds under development from some of those partners I referenced earlier as well as from our newer partners Novartis and Lilly, who have a number of compounds in development that we would expect to see reaching the clinic in the not-too-distant future.
Lastly, in terms of sort of the three legs of this stool that supports what we’re trying to do here is the company itself. We have a very deep research and development capabilities, not just to be successful with an ADC, you can’t simply look at the conjugate as a whole but you have to have deep expertise in the subcomponents. So our ability to evaluate targets, understand not just expression but cell processing mechanisms that are important in evaluating targets is very deep. We do a lot of work around antibody development. We have a proprietary humanization technology, and as I referenced earlier, we’ve done quite a bit and continue to do work in engineering linkers and are looking at expanding our cell killing agent portfolio.
This has been very productive for ImmunoGen. With the introduction of IMGN289 in the middle of 2013, that’ll represent three INDs over the course of two years. And as I noted earlier, the company is the originator of both T-DM1 and SAR3419. All of this comes from a very deep research well and an expanding development capability. Our three senior-most PhDs which includes our Chief Science Officer have over 85 years of experience in ADCs, and we can truly look to them as being the founders of this particular technology.
At the same time we’ve been building a development organization that’s been very constructive in letting us advance our programs on an accelerated basis and come up with some unique designs. The fact that we’re deep into our small cell lung cancer study, our Phase II and we’ll be delivering results on time I think is a testament to the work that’s been done there.
Given how we’re progressing, moving deeper into the development stages with portfolios and having a wider range of compounds that are in development, we recently added Charlie Morris as Chief Development Officer. Charlie joined us from a background that includes both small and large pharma, and I think his perspective will be very important to us both in development as well as looking into the research organization and helping us select our targets for future development.
Our financial position is solid. We ended our last fiscal quarter which was September of last year with about $234 million in cash. As noted earlier, we have no debt. We projected at that time that our cash as of the end of this fiscal year, which would be June of 2013, would be between $172 million and $176 million. What’s important about that cash is we think it gives us the resources to take the existing clinical compounds,901, 853, 529, through to proof of concept, and that will then allow us to determine what the appropriate avenue is for those compounds at a time that we’ve demonstrated their full value.
As I noted, 2013 will be a very important year for ImmunoGen. We have the first clinical data coming out from 853 around the middle of the year. 901, with the Phase II first line study we will have that readout sometime in the back half of this year. Our 529 compound targeting CD37 will have its first clinical data late in 2013, and then we’ll have extensive preclinical data on our EGFR positive targeting compound hopefully at AACR this year as well as the IND becoming active around the middle of this year.
From a partner standpoint, we expect it to be a very active year for T-DM1. We think -- I think it’s widely believed that approval in the US is imminent. The PDUFA date is the end of February. The EU approval rather will come sometime in the back half of the year, and then we should hear the first data on the Phase III first line study late this year or early 2014. For early breast cancer, there are three studies that are targeted to begin over the course of 2013, and there are seven other partner compounds in the clinic that we should be hearing data on across the course of this year.
So that’s where ImmunoGen is. We think we have a very exciting technology. We do think this company has the ability to transform how cancer is treated. I look forward to speaking with you both over the course of the year and hearing your questions in the breakout room, as they said down the hall and on the right. So thank you very much.
[No Q&A session for this event]
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