ImmunoGen, Inc. (NASDAQ:IMGN)
Citi 2013 Global Healthcare Conference
February 25, 2013 11:05 AM ET
Daniel Junius – President and CEO
Thank you very much and good morning everyone. It’s a great opportunity to be here at Citi’s conference, particularly at this time and I get to that in just a moment. Before I do, as I go through the comments this morning, I will make some forward-looking statements.
I would point you to our regulatory filings about risk associated with investing in ImmunoGen. We see ourselves as being on the forefront of developing therapies that we think will be transformative in terms of how cancer is treated and we had a major event on Friday.
This is the first public forum at which I am able to say that we have a compound that’s been approved by the FDA for treatment in patients. Kadcyla was approved, it’s a compound in development by Roche for HER2-positive breast cancer. I will spend more time on that later.
In addition to being simply watershed event for the company and for the technology, obviously from an economic standpoint it affords us the opportunity, both to be realizing milestones within the transaction and generating significant royalty revenue over the life of this particular compound.
Beyond that, we are in the process of moving forward on proprietary programs. We have three compounds in development today. We have a fourth that we expect to go in the clinic over the course of 2013 and more that we are working on pre-clinically.
We do that in an environment where we think we have sufficient resources to take our clinical compounds through to proof-of-concept. We have over $200 million in cash as of our last reporting period, no debt. And the opportunity to generate additional cash from other partnerships we have with major companies who are advancing compounds in oncology.
Let me start and talk a little bit about Kadcyla for a number of reasons. One the brand name is, at this point three days old. We think it’s the start of a, what will be a new era in HER-2 positive breast cancer is treated. There is considerable efficacy that’s been demonstrated through the clinical study, the process, as well as improvement in terms of tolerability for patients.
Importantly, it’s the first antibody drug conjugate to be approved for a prevalent solid tumor and that’s important because, 90% of all cancers are represented with solid tumors. So having a compound that’s shown the benefit that we’ve seen with Kadcyla through clinical studies and getting it approved makes that a very significant event.
And from the management standpoint, I reference to revenue implications, but obviously from a technical standpoint this represents a new threshold of validation. I think that there had been technical validation as people looked at the data that was being generated through the various clinical studies but getting regulatory approval represents an entirely new threshold of validation.
As I said, Kadcyla is now approved for marketing in the US. It will be approved to treat HER-2 positive metastatic breast cancer for patients who have failed in earlier therapy of Herceptin Plus a Taxane and what that represents, it will include some patients who would have received that therapy Herceptin Plus Taxane in the adjuvant setting, if they progressed while on therapy or within six months.
So that would open up some first line metastatic patients to receive the therapy. But then for those in second line or later metastatic, they would all become eligible because the assumption is, they would have received Herceptin Plus a Taxane when first diagnosed with metastatic disease.
So the data that Roche has indicated would say that it’s at least 14,000 patients would immediately become available and importantly for late-stage patients, today who have no other targeted therapy available and then for some percentage of first line metastatic patients.
I talked about efficacy plus tolerability, what we saw in the EMILIA study which was the data that supported the filing was a significant improvement in both progression free survival and overall survival. The overall survival benefit was adding six months to overall survival versus the control of taker of Tykerb plus Xeloda, plus a more favorable safety profile and that you saw about two-thirds of the grade-3 in greater adverse events versus the control arm, as well as events that led to a reduction in dose or drug discontinuation.
The compliance rate in the study with T-DM1 and that was called then was almost 100%, 99.9% with 90 plus percent for Tykerb compliance, but only 77% complaint with Xeloda. So I think that that’s reflective of the tolerability with this particular compound versus the standard of care for those patients.
The Kadcyla approval is the first step in what we see as a broad registration pathway that’s being undertaken by Roche. This particular patient population really does represent a new segment for Roche for HER-2 positive breast cancer patients and that these are patients who failed in earlier Herceptin-based therapy.
For those who are currently receiving a Herceptin plus Taxane or even a Herceptin plus Taxane plus Perjeta therapy, there is a study underway that will read out in early 2014 that would make it – assuming the data supports it and there is approval you would have T-DM1 or Kadcyla available for all first line metastatic patients.
And then, there is a broad program underway for early breast cancer patients. So that would include your traditional adjuvant therapy but those patients also post-surgery who have residual disease as well as neoadjuvant and finally it’s also being developed for HER-2 positive gastric cancer for second line patients. So, a broad development program.
The pricing that came out, the assumption was that that Kadcyla would be priced at a premium to Herceptin and the guidance, not the guidance that’s probably, but the precedent was, what we felt with Perjeta that was priced at about 35% premium to Herceptin. What you saw and the pricing is indicated there Kadcyla is being priced at almost $10,000 a month, $1900 a month versus $4500 a month today a Herceptin-based therapy.
So a significant premium to Herceptin, reflecting both the higher level of efficacy, the tolerability and Roche’s position that Herceptin traditionally has been underpriced in the market.
In terms of just to pause on a second, the technology that’s there, how antibody drug conjugates work is, we use the antibody as the targeting vehicle and what that does is, it delivers a highly potent cell killing agent, people refer to it as chemotherapy I think that understates the value or the potency.
This is an agent that 100 to a 1000 times more potent than a traditional chemotherapeutic and we use the antibody as a targeting vehicle to deliver it to a cancer cell, where it’s internalized and the toxin is then released and activates against the cell. It includes, obviously the toxin.
But both the method of attaching the toxin to the antibody that’s very important because we have a number of different linkers that can impact the mechanism of the metabolite once it’s released from the toxin, both in terms of killing the cell as well as whether remains in the cell, whether it can resist an efflux mechanism to a number of different properties.
I would also mention here that the antibody whereas in the case of Kadcyla you have an antibody that’s marketed as an active single agent Trastuzumab or Herceptin for the patient population for which it’s been approved thus far, that antibody now has become sub-therapeutic.
So really the benefit is being delivered from Kadcyla is from the ImmunoGen agent, the cytotoxin principally and obviously are mechanisms keep it attached as opposed to getting therapeutic benefit at a meaningful level from the antibody. That adds expectable change as we are looking at earlier lines of therapy where patients are naïve to address to Trastuzumab-based therapy, but you will see.
And what this suggests is it opens up a broad range of cancers that can be addressed, because we don’t need to have an active antibody for this therapy to be effective. ImmunoGen has expertise both in antibodies themselves and in evaluating targets.
We see this as a type of personalized medicine because as we are looking at the targets we are looking at patient populations who have a cancer that specifically express the target. Beyond that, to mention a personalized medicine, we are also doing biomarkers for some of our compounds to see if we can further segment the population to identify patients most likely to respond.
Note in terms of our expertise for evaluating targets, particularly with Kadcyla, it was ImmunoGen that brought this idea to Genentech going back into the late 90s as we were looking at Her-2 as an interesting target for the technology and was out of those discussions that we ended up putting a licensing arrangement together in 2000 now has led to Kadcyla being approved today.
So with that particular compound again it is Trastuzumab, the antibody developed by Genentech, but ImmunoGen’s linker, ImmunoGen DM1 cytotoxin, As I noted, there is potential for broad application of the technology and I think we can through the various compounds under development today.
We referenced Kadcyla which is being pursued across a broad range of HER-2 positive breast cancer also for gastric cancer, but as you look at the full spectrum of compounds, either in the clinic or being developed you see that that one includes indications such as non-small cell lung cancer, hematologic disease, certainly non-Hodgkin’s lymphoma, multiple myeloma some very difficult to treat diseases where there is no effective therapy today which would include Methothelioma, ovarian cancer, glioblastoma, all of these are being developed either by ImmunoGen or by her partners.
So let me talk about what we have in the clinic, the proprietary compounds which I think represent an interesting array of indications and compounds that we are bringing forward for which we will have data over the course of this year. As I noted, we have three wholly-owned compounds in the clinic, we have a fourth that we are developing that should be in the clinic which should be in front of the regulators, roughly around mid-year and we will begin dosing patients in the back half of 2013.
The first proprietary compound is IMGN901. This is for CD56 positive cancers. We’ve studied this in a number of earlier assessments of solid and liquid tumors. Today it’s in Phase 2 testing for first line small cell lung cancer patients. The target itself is expressed on a variety of cancers. In the case of small cell for example, it’s virtually 100% of the patients, about 70% of multiple myeloma patients.
So this does afford an opportunity to pursue this compound across a broad range of disease. It’s also on pediatric neuroblastoma, so there is potentially a pediatric application here. The design is our DM1, one of our two cytotoxins that we use today linked to a CD56 finding antibody. The lead indication small cell lung cancer is a very difficult disease.
There is about 50,000 or about 60,000 metastatic cases diagnosed each year in the US and Europe, as I noted virtually all of them are CD56 positive. It’s a very aggressive disease, because it very quickly goes to metastases. The median survival for diagnosed patients is less than a year, frontline therapy will generate responses but without any durability. So, patients who are dosed with etoposide, carboplatin or cisplatin will show a PFS of under six months and overall survival of nine to eleven months.
So we view that while there is an effective first line therapy to generate responses, there is a need for more durability to these responses and we thought that 901 would apply here given the target expression, the activity we’ve seen with monotherapy and the fact that we are able to generate prolonged activity in patients in earlier monotherapy studies.
So what do we seen thus far in the CD56 positive studies that we’ve conducted in solid tumors? With a single agent, we saw durable remissions in Merkel cell carcinoma, that the small cell carcinoma of the skin that has many biologic similarities to small cell lung cancer.
We’ve also seen activity in small cell lung cancer in second line and later patients. As we looked across a couple of different studies and measured both responses as well as meaningful stable disease, we had about a 25% clinical benefit late in these later stage patients which is viewed by clinicians to be significant.
We are in a Phase 2 study, but in the Phase 1 study, we were able to extract some efficacy data that the Phase 1 portion wasn’t designed to capture a much efficacy data but what we did see was, in these patients and some of them actually were not even CD56 positive. We enrolled patients who would receive etoposide carboplatin, so we could gauge safety and get our Phase 2 dose.
But in those patients who were CD56 positive and particularly small cell patients, three of them were chemo naïve. We saw two responses, and what was noted as being significant is, that we saw seven patients who were platinum-resistant/refractory and we had two objective responses in those patients which is considered again by the clinicians to be very unusual.
So that has us enthused as we are moving now into the Phase 2 portion. We also seen 901 in an CD56 positive multiple myeloma patients, as I noted about 70% of multiple myeloma patients are CD56 positive. We’ve conducted a single agent study and what we saw there was in heavily treated patients, about 41% of them showed stable disease or better for more than three months and about 24% of them were on 901 as monotherapy or anywhere from five to twenty months.
And again, these patients had – were significantly pre-treated I believe the median therapy that these patients have been exposed to a seven. So we were – we thought it was a pretty strong indication of activity with 901. We’ve completed a combination study looking at 901 in combination with Revlimid and Dexamethasone who reported data at ASH back in December and what we saw there again was a high level of activity for patients who are Revlimid resistant or refractory.
We saw activity across all five of those patients including a PR and a VGPR. And then there were 13 patients who were presented with poor prognostic mutations and again good activity across all of those patients ranging from four patients with stable disease up to four patients with VGPRs.
So another suggestion to us that IMGN901 is an active agent.
The study that’s underway today that were on the Phase 2 is something that we call the North trial. We are looking at first line small cell lung cancer patients with extensive disease. This is a randomized study enrolling a 120 patients, 80 of them into the arm that would include 901, 40 of them into the etoposide carboplatin alone arm.
And we’ve set this up so that we’re looking at an interim cohort of 59 patients that will be able to monitor separately to see whether we get some early indication of activity that will allow us to make some decisions and therefore compress the timeline to get to a registration study.
We announced quite a month ago that we’ve completed enrollment of those first 59 patients and we are continuing to enroll, hopefully to get to the full 120 patients in relatively short order. Once we have the information from the interim cohort, we will announce that and I would expect that to be sometime in the September, October timeframe.
The second proprietary compound is IMGN853. This is for cancers that express the fully receptor alpha or fully receptor 1. We think that there are number of cancers to they are over expressed that makes it a very attractive target for this compound. The design is it’s a different cytotoxin. Same family, but we refer to this as DM4 versus DM1 and that’s linked to a fully alpha binding antibody.
Here we applied some of the knowledge that we’ve developed over time about some of the targeting. We were able to work with different antibodies and identify an antibody that was optimized for its function as a conjugate, as opposed to its function as a negate agents.
The antibody here has no therapeutic value, so we really were looking for something that will best deliver the cytotoxin to the target. In addition, what we’ve introduced with this is a new linker. This is a linker that we developed that has the properties that allow it to counter a certain type of multi-drug resistant. It resists the efflux mechanism that will allow us to get a higher concentration for a longer period of time within a cell to get the critical mass to effect cell death.
This is in Phase 1 testing on cancers that over express that fully offer the target that I referenced earlier. Those are predominantly ovarian and lung cancer, a particular type of ovarian, for ovarian cancer there is about 22,000 diagnoses each year, a very high mortality rate associated with those diagnoses. Typically the reason for that is, it’s a disease that’s in an advanced stage when it’s diagnosed.
Most of these cases show very strong folate expression. The other predominant indication is adenocarcinoma non-small cell lung cancer. Here you’ve got about 90,000 diagnoses per year. Again, the majority of these cases show a very high level of folate expression.
The study underway is a Phase 1 study. We are currently in the dose escalation phase. The study is enrolling quite well. What we are doing with the Phase 1 is, we’ll take any type of cancer, we are looking predominantly for higher expressers. Once we get to the expansion phase, we’ll look exclusively at ovarian and non-small cell lung cancer and limit it to patients that express at a hetero or greater level.
We have three expansion cohorts that we will be enrolling once we get to the MTD, one will be for ovarian platinum-resistant and refractory patients who have two or fewer prior chemotherapies. So we hope out of that getting a patient population that’s been less exposed to prior therapies. We have a greater opportunity to see efficacy.
We have two other arms that we have identified. One of them ovarian, one adenocarcinoma non-small cell lung cancer and here they can have any number of prior therapies, again we will continue to look for safety and efficacy, but we have designed these studies to also look for biomarkers that may allow us to further segment the patient population as we think about registration strategies.
The second compound, I’m sorry the third compound that we have in clinical studies is IMGN529 and this is for CD positive B-cell malignancy. So that will include non-Hodgkin’s lymphoma, chronic lymphocytic leukemia. So CD37 you can think of it as being on the same indications where you would find CD20 for non-Hodgkin’s lymphoma.
And again, very prevalent disease, there is about 70,000 cases of NHL diagnosed per year and about 16,000 cases of CLL. The design here in contrast to the prior two compounds I referenced is that we have an antibody that has a naked agent has shown a high level of activity. And to that, we have attached our DM1.
You can see on the graph, that’s a pre-clinical, out of a pre-clinical, when we look that both the conjugate and the naked antibody compared to both the control and Rituxan and what it suggests pre-clinically is that we have an antibody as a naked agent that has the potential to be as effective if not more so than Rituxan based on its pre-clinical analysis.
By then adding our conjugate technology to it, we substantially enhance the efficacy of the compound. This is in a Phase 1 study. It’s looking mostly at a non-Hodgkin’s lymphoma patients to identify where we can get the best level of efficacy to inform us as we look at a registration pathway or look to taking it further into evaluation to Phase 2 study. We will look to see the first data here in the fourth quarter of this year.
The fourth compound, this is one that we expect to bring into the clinic over the course of 2013 is IMGN289. It’s a candidate for EGFR positive disease. That would include head and neck cancer and other types of non-small cell lung cancer. The current EGFR therapies currently work only with EGR inhibition.
So that gives them a single mechanism of activity, cells eventually will sought resistance to that EGFR inhibition. What we’ve done to offset that is augment the activity of the antibody again with our ADC technology that we are adding DM1 same cytotoxin that’s used both in our IMGN901 and 529 as well in Kadcyla to the antibody to enhance its capability to kill the cancer cell.
Pre-clinically, we’ve seen very good data. The antibody itself has shown greater potency than existing naked EGFR antibodies, Erbitux for example has shown good activity against tumors that are resistant to EGFR inhibition and the tolerability profile looks to be comparable to Kadcyla.
One of the obstacles for antibody-based therapies for EGFR type of tumors is, manifestation of skin toxicity and as we’ve looked at this pre-clinically, we have evaluated it quite thoroughly, we see significantly less skin toxicity with this compound that what you would see with Erbitux.
We have significant data coming out at AACR that will look at IMGN289 from a number of different dimensions that will be published in April or just in five or six weeks.
So we talked about where we are in terms of overall pipeline development in our compounds. In terms of the company itself, as we think about it from a financial perspective, as I noted at the outset, we think that we are in a very good financial position with over $200 million in cash as of our last reporting period in December.
That should give us sufficient liquidity to take the three clinical compounds that we have today through to proof-of-concept. We have indicated that by the end of this fiscal year and June 30 year end, we expect to have cash in the neighborhood of $172 million to $176 million.
The business model that’s in place which we are seeing realized now with the approval of Kadcyla and the advance of many other partner compounds will have the partner activity generating cash to augment the development work that we are taking with our proprietary compounds.
In terms of the partners we’ve talked about Roche and all those taking place there. We have four other compounds, there are four other partners rather that has compounds in developments that would include Amgen, Bayer, Biotest and Sanofi. We have seen data on two the seven compounds that those partners have in development. We would expect to see data on the other five sometime over the course of 2013.
And beyond the clinical pipeline, there is compounds in development from some of our existing partners as well as two new partners that came on within the last two years Novartis and Lilly. So we think that we will continue to see a flow of new compounds coming into the clinic as well as those into the clinic moving into later stage.
Events to anticipate over the course of 2013 with our proprietary compounds, we should see the first clinical data on IMGN853, that’s the folate compound sometime around the middle of this year for 901 out of the small cell lung cancer study, we would expect to have the initial Phase 2 read out sometime in the back half late third quarter, early fourth quarter of this year.
And then with IMGN529, the first clinical data we would expect to see published probably at ASH. So that would be late in 2013. For IMGN289 as I noted, pre-clinical data should be available at AACR in April and then active IND sometime around the middle of this year with the first patient dosing taking place in sometimes middle of the end of the back half of 2013.
Then for partner compounds with Kadcyla, obviously the US approval has taken place that checkmark probably isn’t big enough on this slide. But in addition, we would look for approval of the European submission sometime in the back half of this year, submission has also taken place in Japan, but that process would take a little bit longer.
There are three registration studies that we will be moving into the clinic over the first half of this year for early HER-2 positive breast cancer and as I noted, there are seven other partner compounds in the clinic where we will see data and I’d note that we would expect one of those partner compound to move into a registration study over the course of 2013.
So, beyond just the significance of a big step for ImmunoGen with the approval of Kadcyla, I think we have a very exciting 2013. I think that the demonstration of the potential efficacy and tolerability of the compound with Kadcyla certainly opens up the opportunity for these compounds to make a huge difference in how patients can be treated for cancer across a broad range of disease.
So let me stop there and I’d be happy to answer any questions that you might have.
Can you please let us know, like how you plan to proceed forward with a wholly-owned compound? Would you like to go with a partnership? Or is it something that ImmunoGen will be developing on their own?
In terms of the proprietary pipeline?
The thinking is that, once we are able to get to proof-of-concept, certainly on the earlier stage compound, we’d look at some form of partnership. And that’s for a variety of reasons. So let’s think about for example, the CD56 compound that’s currently in testing for small cell lung cancer.
While we will retain a meaningful economic interest and that would anticipate some development, for example at least in the US, we do think that the opportunity for this compound globally warrant working with someone who has experienced in various jurisdictions where we will be looking to develop the compound.
In addition, the breadth of indication, if we can demonstrate efficacy and proof-of-concept in small cell lung cancer, I think we then want to look at a registration strategy that could potentially incorporate ovarian cancer, that can incorporate again pediatric nueroblastoma.
And so I think that’s a benefit of working with a larger sophisticate partner who is an expert at developing across a broad range of indications would be very beneficial. How that progresses with other compounds remains to be seen. It depends on the timing, it depends on our success with our initial compound whether our aspirations expand once we get pass the initial.
But we appreciate both the financial implications of developing compounds across a broad range of indications. The complexity of developing them globally and frankly I put it in the high class problem category but we now or by the end of this year we will have four what we believe are promising compounds in the clinic and four compounds for a company of our size frankly is a lot for us to address. We want to be cognizant of that.
Congratulations for your both catalysts.
I had a question on your linker and cytotoxin technology. I mean, clearly it’s a very competitive area in recent years and with traditional biotech companies like Genentech, Roche are developing their own linkers and forcing their own cytotoxins. We would love to hear what ImmunoGen is doing specifically to maintain its leadership in the ADC space?
Yes it is competitive although I think that there is an awful lot of value that should be placed on experience. We’ve lived and developed, lived with and developed this technology over a very long period of time and that’s given us the opportunity to gain significant insight that’s led to – in some cases, understanding of what applications are best as well as developing new technologies. So I think that’s one area that we would separate when we think about leadership and where the field is going.
Beyond that however what you’ve seen from ImmunoGen, so we brought a new linker into the clinic with a folate compound and that has particular attributes. We are looking at other earlier stage activities, we are looking at new cytotoxins because what we work with today is a tubilin inhibitor not all cancers are sensitive to tubilin inhibitor. So there may be an opportunity to apply this technology for other cancers that aren’t sensitive to an anti-mitotic.
So we are doing that, one of the other areas that we are putting more emphasis on today that probably was not terribly prominent in the past is, looking at external technologies to see whether there are technologies where we should partner with some of the smaller biotechs who have niche areas that potentially would enhance some of the things that we are doing.
And so we are spending some time on that whether we will actually see something come to pass remains to be seen. We have to do the work and understand where that we think the science is really there. But I don’t, you don’t want to underestimate competition, I think competition at the end of the day we’re all here to try to develop compounds that can benefit patients.
So I think the competition can only hope that. I do think though that our experience helps us to realize that as elegantly simple as the concept sounds of attaching a cytotoxin to an antibody and allowing it to be released in a cancer cell, it is amazingly complex. So, we’ll just see how the field does evolve.
So with the 539 to C37 positive cancers, I mean, that’s a very competitive space, right. I mean in NHL B-Cell malignancies. So I was just curious as to what you are hoping to show in a trial that would kind of validate an extra entry into that area basically?
We thought about that. Clearly, in non-Hodgkin’s lymphoma there are a number of alternatives that are available, there are more being developed. And some of our partners that are developing compounds for non-Hodgkin’s lymphoma, we felt that with the CD37 positive antibody that we develop, with CD37 as a target which is not been heavily exploited and by having an active antibody and our ADC technology that then afforded a highly differentiated offering.
And there are sub-segments of the non-Hodgkin’s lymphoma patient population who are relapse refractory to Rituxan, later stage patients, elderly patients who can’t benefit from today’s therapies.
The drug development process is one that you need to start with later stage patients working way forward, but I think when we focus on the differentiation of 529 because of having an active antibody and adding the ADC technology and the fact that even with the non-Hodgkin’s lymphoma as many therapies that are available today, patients relapse.
There are no cures today for non-Hodgkin’s lymphoma. So there is always a needy for something for later stage patients, we think 529 is a very legitimate way to try to provide a benefit to those patients.
(Inaudible) and you see some activity there. I mean, a lot of it that still seems to be going towards combo therapies now and there is a bunch of new agents showing up, looking at different targets. So what would you look to do if you show some activity? Would you look to partner it, combo studies, I mean, where do you kind of see the drugs slotting in?
Well, as I mentioned, we have four compounds, we will by the end of the year have four compounds in the clinic with 529 being one of them. You got sort of two different questions there. Let me deal with the combination side first. I think that when you think about ADC technology, certainly across the spectrum of studies that we’ve seen, we are able to dose and get what we believe to be is a very good tolerability profile. And so that in and of itself, always as you are thinking about well, what’s then going to get to the best efficacy for the patient, based on what are the therapies might be out there.
In some cases, if we are fortunate we will see activity as monotherapy but that if we need to go to combination therapy we do think ADCs afford an opportunity because of the tolerability profile you are seeing that off of Kadcyla already. So we don’t shy away from it. There are agents that are out there that you can look at either existing, have been into must being something of that nature that you could combine a 529 with potentially and we will do preclinical work to say what might be a reasonable pathway there.
On the partnering front, it’s a little bit too early specifically with 529. I think it falls into the broader comments that I made earlier that – there certainly are parties who may bring more to the table around development in a hematologic area then the spectrum that would be looking at solid tumors for some of the other compounds.
But I think we have to see what type of data we can develop over the course of this year and probably into next year to suggest what’s the potential here and what would be an appropriate development path, both in terms of disease as well as economic ownership, sharing at bringing a partner in.
One more quick one. So, we’ve seen some kind of mediocre evidence of activity with these folate offers, but we’ve all had a failure with the Morphotek compound recently and then the Endocyte had so and so data. Just your thoughts as to the target and where you might be able to differentiate yourself?
Yes, we actually think it’s a very attractive target. The Morphotek that was a naked antibody and so that sort of puts it into a different category. I think that the work that we did both to identify the antibody and look for an antibody that functions optimally as a conjugate was very important. But this was not – so we weren’t looking simply at avidity affinity in trying to optimize there. We develop some early-stage conjugate, put them in the model to see where we got the that puzzled activity.
And then the other dimension I think is significant is the use of the linker that I referenced. So whether it was the antibody design, the antibody that we selected, whether it was the new linker, whether it’s the nature of the expression. The preclinical data that we saw with 853, the folate targeting agent, our scientists would say it was the best pre-clinical data we’ve seen of any compound that we’ve worked with and that would include T-DM1.
So, we are certainly not discouraged by the Morphotek Eisai results out of the naked antibody and we think that the Endocyte data is interesting. I think it affirms something around the target itself being an attractive target, obviously we are using the different mechanism.
We are using an antibody versus using the vitamin folate going to a different epitope and so it’s early days, as I noted hopefully sometime around the middle of this year, we will have some preliminary data. But we are actually quite excited about 853. We are spending money on the early stage money on 901 to do some early development work to be prepared to have material available for a registration study.
We are doing the same with 853 probably because lead times can be very long and you’ve got to do something that risk. We are not spending the big dollars that will come in if we see compelling data. But frankly, I think that that’s the pattern that we are seeing from some of the other folates particularly Endocyte, I think reaffirms our compound that this is an attractive target to pursue.
Thank you very much.
Copyright policy: All transcripts on this site are the copyright of Seeking Alpha. However, we view them as an important resource for bloggers and journalists, and are excited to contribute to the democratization of financial information on the Internet. (Until now investors have had to pay thousands of dollars in subscription fees for transcripts.) So our reproduction policy is as follows: You may quote up to 400 words of any transcript on the condition that you attribute the transcript to Seeking Alpha and either link to the original transcript or to www.SeekingAlpha.com. All other use is prohibited.
THE INFORMATION CONTAINED HERE IS A TEXTUAL REPRESENTATION OF THE APPLICABLE COMPANY'S CONFERENCE CALL, CONFERENCE PRESENTATION OR OTHER AUDIO PRESENTATION, AND WHILE EFFORTS ARE MADE TO PROVIDE AN ACCURATE TRANSCRIPTION, THERE MAY BE MATERIAL ERRORS, OMISSIONS, OR INACCURACIES IN THE REPORTING OF THE SUBSTANCE OF THE AUDIO PRESENTATIONS. IN NO WAY DOES SEEKING ALPHA ASSUME ANY RESPONSIBILITY FOR ANY INVESTMENT OR OTHER DECISIONS MADE BASED UPON THE INFORMATION PROVIDED ON THIS WEB SITE OR IN ANY TRANSCRIPT. USERS ARE ADVISED TO REVIEW THE APPLICABLE COMPANY'S AUDIO PRESENTATION ITSELF AND THE APPLICABLE COMPANY'S SEC FILINGS BEFORE MAKING ANY INVESTMENT OR OTHER DECISIONS.
If you have any additional questions about our online transcripts, please contact us at: firstname.lastname@example.org. Thank you!