Merrimack Pharmaceuticals (NASDAQ:MACK)
33rd Annual Cowen & Co. Health Care Conference
March 6, 2013; 08:00 a.m. ET
Bob Mulroy - Chief Executive Officer
Eric Schmidt - Cowen & Co.
Good morning everyone and welcome to Cowen’s 33rd Annual Health Care Conference. I’m glad you could make it to day three of our sessions and we are glad to have with us to kick off the day, Merrimack Pharmaceuticals. I think this is the first time Merrimack is going to be able to present as a public company at the Cowen conference, so a special thanks to the team for making the long trip over across the Charles.
We are delighted to have with us the company’s Chief Executive Officer, Bob Mulroy. He’s going to speak for about 25 minutes and give you a company overview. If we have time, we can take a couple of questions here in this room and then there’s a break out session next door after its over.
Great. Well, good morning everyone and thank you for making it. It looks like the forecast is gloom out there for the weather. A special thanks to Eric Schmidt, the whole Cowen team for their support, not just these past few years as we’ve grown the company and developed.
So what I’d like to do is give you a quick snapshot, maybe five or 10 minutes of an overview of the entire company and then focus maybe 15 minutes on sort of two more specific issues to do with 398, one of our leads that has some Phase III data coming out this year and then 121, which also has a series of very important Phase II’s that are finishing this year. Just focus on some important attributes of those as the data gets closer to fruition.
So first off let me start with, I will talk about the future, so better beware, and let me start off with the end, which is sort of this year is going to be a very sort of important year for Merrimack in terms of the milestones we have.
We have a whole series of clinical studies that will be finishing. Two indications in Phase III monotherapy and combination therapy for a therapeutic called 398. A series of trials with 121 in breast cancer and lung cancer, they will be rapping up this year; and then early next year a whole series of additional studies in ovarian cancer and breast cancer for 121 to be finishing.
We are expecting to make progress on a number of business fronts in terms of licensing many of our compounds out in territories around the world, but we have additional new products that will be entering in the clinic this year, particularly a therapeutic called 310 and diagnostic called 929, which are important strategically to the company and we’ll also be working importantly on some supply chain and commercial development activates this year to get ready for potentially a filing on 398, with the data that will be emerging in the Phase III this year.
So lets sit back very quickly. The company started as a Systems Biology Company out of MIT in Harvard and over our 10 years we have used that Systems Biology platform to generate a platform of molecular diagnostics and we want to call micro-anatomy diagnostics to understand cancer in each patient more specifically. With that ability to stratify patients on a molecular or systems basis, we’ve also built an entire portfolio of systems based or network based therapeutics that are targeted to specific network mechanisms.
With those diagnostics and those mechanisms, together we’ve also built a company capable of delivering all the way from the discovery of the new targets, the new networks, the new ideas, the engineering drugs and designing drugs, manufacturing drugs putting them in to the clinic and we are looking to expand out all the way into delivering those commercially in the U.S. and Europe.
The whole process is something where we are looking to create fully integrated regiments in cancer diagnostics and the combinations of drugs that are optimal for certain patient populations, that’s our business model, that’s where we are headed in the future. We called that integrated solutions. So with that, we are building a fully integrated cancer company.
As I said, the core of the company is Systems Biology. What is Systems Biology in life? Well essentially, what we’ve done in the world of science is that study molecular biology, to try and take individual molecules like a specific gene or a specific protein and give it a job description.
In reality biology works by something called Systems Dynamics. It’s the interactions of the components that give rise to the functions of the system. So studying interaction of components is really what Systems Biology is about and if you get the interactions, you are really talking about Systems Dynamics, which is an engineering term that is to how the force of interactions against – of different molecules we get to function of the system; and after we study, its very different in the field of microbiology.
In order to do it, we really started with the ability to create a foundation of, both biology, computing and engineering to understand these interactions. What we do essentially is our core geography.
We started with a technology that allows us to build large datasets that study dynamics, the interactions of many, many different molecules in the system, where its borrowing its dataset for us into our computer models and translating these massive interactions in the systems into models that are not (inaudible) weather system models in Washington that predict the weather, the type of aerodynamic models that Bowing or Airbus would use to build their airplane.
Very much Systems Dynamic based models, all based on standard technology out of engineering, and then we use all the engineering principals, and obviously our dynamics to understand how these function, how they operate, where they go wrong in order to identify a right area to intercede for drugs and therapeutics.
So if you look at the history of the company, we sort of evolved following our science over time. As I mentioned, the company was founded with the invention of a technology called the high density protein array that allowed us to look at many different proteins in the same network and understand how they interacted to lead to differences in cell function or cell behavior, and so those arrays allowed us to study dynamics for the first time, which was really a breakthrough.
From studying dynamics we were able to build through a predictive model for biology. Models that actually could predict what drugs were doing in cells of animals and we believe even in patients, and those models of biology allowed us to find new targets and new ideas for drugs.
In studying those models what we discovered is that at least in the cancer field it became more difficult to inhibit signals as you went downstream from the cell purpose, inside of the cell, because of amplification, because of redundancies, because of feedback loops that get harder and harder and harder to emit sort of the signal, so indicating antibody companies stopping the signaling via the cell surface.
We have a series of papers around different antibody technologies and different antibody therapeutic identities that are singling those we discovered through the modeling processes.
When we started to study the antibody properties, what we saw about antibodies is that most of the time they are cytostatic, they don’t show true results. But what they do do is they send cells into a new state of stress that make chemotherapies much more effective, and so when we saw that we believed that really the future had to be in combinations, but not just any combinations, rational combination which we are able to build with our model, which led us to study the field of chemotherapies.
And what we saw in the field of chemotherapy is that chemotherapies are doses that are incredibly in a sub optimal way. And what I mean by that is, no chemotherapy has half-life measured in hours, but they only kill cells that are going through cell division, which happens every two to three days.
And so you have this complete mix match between the optimal dosing of chemotherapy in terms of the number of cells that are going through cell divisions, that a chemotherapy can even potentially tell, versus the window which you really need to actually kill the cells, which is much longer in terms of days as opposed to hours.
So we actually have gone into the field of neurotechnology, where we bring to optimize the chemotherapy component and the whole goal at Merrimack is to optimize the part of the antibodies together with the right optimal solutions and the neurotherapies to create the best possible outcomes in cancer.
So we see from the pipeline perspective is we have a whole series of molecular diagnostics that we are testing. There are seven different trials under way today where we’re looking at molecular diagnostics in certain patients, in multiple different areas, understanding what the inductions are in the cell pathways that are driving cell growth; understanding how the cells tend to adapt to treatment and also studying something that’s actually very, very important and we’re calling it microanatomy.
But the things that are sort of the physiology of the tumor and the micro environment the tumor sits in, actually becomes a huge influence in how the tumor normally evolves, but it becomes a huge influence over what drugs actually even get to accumulate in a tumor at all.
And so we built a set of tumors that are actually allowing to measure those, those different dynamics and we can use imaging technology to understand where drugs accumulate; we can use imaging technology where there are macrophages in the system; we can understand the whole tumor dynamics around the tumor that influence not only the patients own tumor and its evolution, but what treatments are the best choice for that patient.
So beyond electro diagnostics I believe there are therapeutics that we are developing. Right now there are six different therapeutics that are in the clinic; two more that we hope to enter in the very near term and then one of our imaging agents, which will be developed in the clinic under an IND.
And so just like the (inaudible) on Phase III, we have a drug called MM-398, which I’ll talk about in a minute. The nanotherapeutic encapsulation of irinotecan, which we believe is really changing the fundamental biology of what irinotecan can accomplish; I’ll walk you through that today.
We have two singling inhibitors and then 121, which is designed against ErbB3, which is we believe a key essential node in the perpetuation of cancer and cell survival. And then we have a drug called 111, which is actually looking to treat a specific type of cell additions we see that involve not just ErbB3, but a complex of three molecules of perpetuating patients with tumors, who have high levels of HER2 in them.
In the Phase 1 category we have a drug called 302, which is an ErbB antibody targeted version of our nanotechnology, delivering doxorubicin.
We have an EGFR inhibitor called MM-151, which is really the first full EGFR inhibitor completely inhibiting a signal there. The important theory is that our technology showed that the issue with a lot of EGFR inhibitors is not that they were handing a target, but there was some 20-fold amplification downstream of the EGFR inhibitor.
So when all the inhibitors out there are 94%, 95% or 96%, the fact that there’s not enough signal, which will be found in most situations, with 20 fold amplification the cell is getting plenty of signal to grow and survive with. And so having discovered the amplification, we don’t really have a full inhibitor.
Then we have a drug called 141 that fell through in the clinic, which is an IGF pathway inhibitor. The pathway inhibitor is about simply getting more than one node. What we discovered about IGF is not only is it a key contributor of cell growth and proliferation in cancer, but that actually was connected below the surface and a feedback moved directly over at mTOR. And so as you started to suppress the idea for an mTOR and correct for any suppression of idea form in the cell will continue selling. So we discovered that link and have booked the drug actually to knock that off.
The real sort of assembly in the pipeline, we have 11 different Phase II’s and Phase III’s underway that we are reporting out roughly in the next year and so we are very excited about the data flow we are going to have and the news flow we’ll have in the company. I’m going to talk specifically today about some of the trials underway with 398 and with 121, just as they are coming up in the near term future.
So we got a robust pipeline and a lot of robust data coming out of the proof of concept and hopefully want to build some core registration as well. We also have a whole series of drugs that are moving through the Phase I, enabling future Phase II studies, which we’ll talk about as we move through 2013.
So we’ll focus now on a couple of things; one is 398 and the other is 121. So for 398, I would say this is definitely the most misunderstood product in our pipeline. We see it often as we travel the world as a reformulation of our HETM (ph). It seems to be a popular thing to do now in the world of cancer therapeutics. This is actually how we engineer drugs, for a very specific set of patients in the world and so I’ll show you how in a minute.
Essentially there’s a whole set of tumors out there that have a very poor blood supply. They’ve grown in what’s called the Hypoxic environment with low oxygen and so with the poor blood supply any drug your going to inject in the blood isn’t really going to collect around the tumor, and so how are you going to get to that tumor, how are you going to knock it out?
So we’ve actually engineered this drug to not only collect in tumors with poor blood supply, which I’ll show you how in a minute, but actually to use macrophages, which are actually the trafficking system in these hypoxic tumors, to actually get the drug distributed, so you can actually do some damage in these hypoxic environments. So it’s built for that.
I mean you think about hypoxic, you are thinking about types of tumors like pancreatic cancer or cervical cancer or any cancer that’s got to be treated with radiation and then there are percentages of cancer cists from breast, along with the colon, who all have these properties where they are growing in this hypoxic environment (inaudible) drug.
So right now at the sort of high level, its in two Phase III indications, the trial where we are touching at monotherapy in second line pancreatic cancer in the Phase III study, while processing it in combination with 5-FU/LV in pancreatic cancers.
And then the other really important trials underway is the diagnostic study where we are looking at a couple of diagnostic tools to measure both accumulation in hypoxic environments and the level of macrophages and looking to correlate those with activity in drug and validate it.
So real quickly taking you on a tour of why this we think its going to be a hopefully a fee changer in the field of pancreatic cancer. So a little over half of all pancreatic cancers are hypoxic. Its one of the highest percentages out there, which means that’s one of the reasons its very hard to treat, because you just don’t have places with blood supply to get drugs there, right. And the reason that is, you tend to have these struggle environments and a lot of complexity in the micro environment that just make these tumors sort of hard to reach and so with a lot of complexity in the signaling pathways and we tend to have poor blood supply to start, it just becomes very, very hard to accumulate any drug there.
So what we have done is we’ve taken our nanotechnology, which is a novel nanotechnology. It’s the most stable nanotechnology out there. We can engineer it to have a half life of days or weeks, as opposed to hours, which is all the other competitors technologies today. And we’ve created a design where we can actually, through that stability have it accumulate in the drug what’s called – in the tumor environment for what’s called the EPR effect.
And so tumors, most of them tend to have very leaky vascular or blood supply. They grow fast, they don’t grow well. The blood supply that supports them has to be very leaky, so it’s a large module and a very stable one. Its stays in the blood; it doesn’t escape healthy vascular, it only accumulates in the tumor. So you get a selective deposition of what is called in the tumor environment.
But also that being stable and staying in the tumor for a while you have the slow read technology. You have a gelling side of this that actually allows you to release drug at a very specific rate and so you can get the constant supply of drug in the tumor. You’re able to get the Semax and maintain that Semax for a very long time.
And so you have this focused deposition, you have this inter tumor retention, which is unique to the technology and you have this low component, which is what we call local activation. So why don’t we use irinotecan? It’s a proto drug. It turns out that it in itself is not a very great drug, but the proto drug SN38 is one of the most potent chemotherapies around, and so by using this sort of technology to locate itself from the tumor and having local macrophages break it down, you get local activation of the drug.
Specifically when you administer irinotecan it gets broken down in the liver, so you get toxicity throughout the body. By just having it broken down right there in the tumor environment, you not only limit toxicity, but you also get the highest activity of the drug right there in the tumor. So that’s what it’s engineered to do.
But why is this important? Its important because this is the fall cycle of a tumor of any cell really and all chemotherapies really basically kill cells in a very specific phase that’s called the end-stage, as the cell is going through cell division, right, and that has to happen every two to three days in the most aggressive tumor, right; that’s why chemotherapy is actually work.
That’s why they work, because they are selectively killing cells and is riding more frequently than healthier cells that are divided less frequently. Very simple proposition right, that’s the basic concept. So you need cells that are going through cell division to really do anything.
What the other technology is out there to do, a vaccine is a great example. Because its for a large molecule, it will collectively accumulate even with the HER effect, but because its not stable, it only accumulates selectively for a few hours, for basically three hours you get this selective accumulation. After three hours it’s the same as taxane, right, and that’s truly with basically all the other reformulations that we’ve seen out there today, that are development or actually pre-clinical.
They all have this 20%, 30% more accumulations in the tumor for a few hours. The problem is, you are back at this problem. Is you need drugs for multiple days to get as many cells going through cell divisions as possible covered.
What our technology does is unique. This is actually CPT-11 Irinotecan. This is the SN38. This is the drug that you care about. This is the one with taxitone (ph) cells. What you could see here is that we’ve extend this window; this accumulation of retention of drug in the tumor and seeing about that Tmax curve tremendously. It’s not just a peak for a few hours. It’s actually extended and retained there in the tumor. So you are actually changing the area under the curve.
So if you look at a back end situation, you are not really changing the area into the curve therapeutic window inside the tumor cell. This is over a 400 fold increase in the area under the curve that you are achieving with chemotherapy in the tumor, and that’s really the big difference about that technology. So you are not getting anywhere else. It’s changing that therapeutic area of the curve 100s of folds, relative to any other nanotechnology or nano-carrier out there.
What we also have is the technology, the diagnostic technologies that go with this, which actually allows the measure; which tumors this is actually offering in, where its accumulating, where its being retained and allows to separate patients where you are going to get the benefit. And that’s really what we are doing at Merrimack; it’s very, very different. Its not a pre-formulation, you are actually changing what you can do to the cell cycles, by having a first sort of stable technology out there to really change what’s going on with accessing cells.
So in terms of data, we have put this into and completed a Phase II study, a monotherapy study in second line and third line pancreatic cancer. This is a very difficult patient population to treat. We have the first Phase III in this patient population underway in close to 20 years. It’s a patient population that people often view as just much too ill to even go after. So new therapy sends a start in the first line and referred to start a later line here.
The patients with cancer progress in a matter of weeks. The overall survivor is measured in weeks, not a very stable population. In this particular study it was done without a control and what we saw, which was promising was we had about 5.5 months overall survival average, we had 25% of the patients make it a year, we had 10% of the patients make it two years, which is impressive for that data.
The problem is in lung therapy, studies that are out of control, the patient populations can really vary, the study in oncology and it’s tough to read. What drove us going forward was that half of these patients actually had stable disease or an 80% had PR’s, which is a very high rate for this patient population, very high rate.
And if you sort of put on your lens for a second, what you notice here is 15 in the first set of patients didn’t make it a week. This is how sick this patient’s population was going in. So you are sort of correct for the fact that the six patients who didn’t make it a week and its that 15% of the study and you sort of look at the data, we actually think this is the sign that we are going to get some really great data coming out this study and coming this summer, basically what we’ve seen. So this is very encouraging data, and again we’ll have data coming up later this year in two or three setting with controls against 5-FU/LV.
So again, this is a very different technology. Its actually changing the fundamental biology of what our chemotherapy is going to accomplish, by changing that duration of exposure by 100s of folds. Its not a small incremental change in what we are doing in the micro-environmental tumor and its built specifically for the hypoxic tumors and that’s what we are doing.
So 212, is another drug that’s going to have a tremendous amount of data coming up this year. It is a monoclonal antibody. It’s the first ErbB3 inhibitor that was put into the clinic. There are now actually a whole series of folks in the cancer field with competitive entries that are in development and in pre-clinical development behind us.
What we discovered from our modeling technology was that ErbB3 was really the central node is ErbB pathway. And so just for contact, the ErbB pathway is the same pathway that herceptin verotoxin, that’s the mix I perceive are all planned. There are 12 different one to four receptors signaled through a group of roughly 40 different signaling proteins done to activate either HER or ACT, which refer to the growth and survival mechanisms for the cell.
And so what we found is that ErbB3 isn’t sailing over a spot and its not mutated within the kinase. It doesn’t mix mucus sort of like the screen of the traditional pharmaceutical world. When you put a model of signaling and you actually understand the networks, that ErbB3 was centraled in two ways and that it was actually co-opted by both the EGFR receptor where it was activated to signal in the one three dimer case. It was also co-opted by HER2 or ErbB2 to signal in the cases where you have HER2 expression as well.
And what we had found basically is that these cases, as well as the third case for when you have patients who tend to have either hormone dependent tumors or tumors that are basically just re-inactivated tumors without any sort of over expression of receptors; that ErbB2 is the central node that those tumors run thorough for resistance and so there were these many, many cases we saw where ErbB3 was implied.
This chart sort of summarizes our view of sort of the various mechanisms we have seen with the ErbB3 pathway; and so as we’ve done tumor profiles around the world of primary tumors and cell lines, what we believe we’ve seen is that the ErbB3 pathway is playing a role in about 50% of all poly tumors. That’s sounds like a huge number, and we’ll have to validate it over time.
But we continue to see the same data popping out in half of all tumors and what we also see within these pathways is that tumors can often adjust to mechanism within a pathway; they don’t always jump to another pathway to survive the end therapy, and so understanding the very specific pathway dynamics that go on inside ErbB, it becomes sort of critical to understand how to treat a patient.
So we’ve seen a pathway. There really just are five different mechanisms that tumors use and those five mechanisms actually lead to very different treatment courses, based on what you understand the mechanism to be.
So there is one family which is over here in the left hand side, which is probably the simplest family discussed and that’s the case where you have EGFR activated or over expressed and you combined with ErbB3 and the 1-3 dimer and that drives the growth and proliferation of the tumor. So there is the giant blue box up here on top and these are roughly proportional for the number of patients we’ve seen and the number of tumor surveys we’ve done in terms of where these different mechanisms play out.
So you get your wild type EDFR over here, which no one really has figured out how to treat these patients and involved the other, effectively the sealing inhibitors. This is the patient population as I discussed a little bit earlier, 151 where we discovered about business that in the wild type space EGFR has up to a 24 signal application downstream of it.
And so the traditional 95% antibody inhibitor, which everyone tends to build in this business, it doesn’t mean anything to that receptor. It doesn’t shutdown 5% of signal in 24 amplifications, there’s a 100% growth signal, right. So it’s meaningless to the pathway to put those inhibitors in the wild type setting.
What happens is when you have mutations in the pathway, the amplification tends to disappear. So you have a mutated EGFR, you have a KRAS. Other different mutations tend to alter the wiring, such that you get more than a one to one ration between EGFR signaling and downstream effect, and so when you put in the (inaudible) and drugs in the world, they actually provide a benefit there, unless we see on a full basis.
So that’s our left hand side. What we have built here is we have built a full EGFR inhibitor called 151 and then to deal with this dimmer, the ErbB3 side, we have a drug called 121, which I’m talking about now. The ErbB3 inhalator and that we see that as some of the optimal combination for this wild type situation in the signal world.
The right hand side is a little more complicated. So if you could imagine that you have an access you are going from zero HER2 receptors up to a million. So the amount of HER2 receptors you have increases. The top is the red box; this is where you have HER2 expression.
In our model, just the classic Oncogene base signaling case, you have HER2 molecules. They don’t need ligand. They can bind to each other. They fire and they grow. In this case we’ve seen a lot of the drugs that exist today, the receptant in tuvinabs and things like that are actually very effective in this case. They either inhibit HER2 through both ADDC and some signaling or they block HER2 and HER2 binding with amortization and they are effective up here; and these are tumors that are in the receptors, they are 3-plus positive, the kind of the indications up there where they work.
What we saw about these tumors though is that they tend to escape and become resistant to that over time in the presence of heregulin, and what heregulin does is it completely changes the signaling dynamics and then what heregulin’s presence you get the formation of this trimer; Heregulins2 and 3 together, and the affinity those three molecule have for each other is high enough that with no individual drug, no individual antibody, nothing blocks that.
You can hit it, the HER2 side doesn’t get effected and you can’t block the dimerization of the two, because heregulin will out compete anything for that dimerization and so you got a completely new dynamic there. And so in the resistance cases we have these cells 111 and 302, which actually threat that problem.
But we also have is an hypotheses of time, that there was a patient population who must have this mechanism up front and what we found through tumor surveys is there appears to be a population that have this little level of HER2 receptor. They don’t have the 3-plus positive test; they don’t have the Basel or low levels of HER2. They have between 200,000 and 800,000 receptors. This trimer, this presence of heregulin is actually driving the tumor.
This past fall there was a paper that came out in the oncologist from a group in Italy that looked at patients prognosis. So it was a study over 10 years, looking at prognosis of patients with breast cancer, just sorting them based of the patient receptor. Its not that the group with the poorest prognosis were the patients who were 2 positive and a bit negative. They had between 200,000 and 800,000 receptors. They weren’t responding to these therapies, they weren’t responding to these therapies.
So that doesn’t prove that we found the mechanism, but we think we found this patient population. We have a Phase II trial underway with 111 and the patient population in that study, it was also 20% of the breast cancer population, this group, this middle group. So we think its as large as the red box, which could be a huge sort of fine and a huge opportunity to improve treatment.
And then when you get down to the bottom here, we’ve grouped a whole bunch of things together. These are patients who tend to have, they are not only expecting HER2, they are not only expecting EGFR, they tend to be – they are triple negative breast cancer, they are hormone driven. It’s a whole collection of patients of different biologies.
What we found is, it was common to all of them is, once you treated them with a hormone therapy or chemotherapy, ErbB3 was the first thing they ran to for survival and the second. And so when you look at 121 today, almost all the work that we’ve done so far and published, it has been in patients who have been a very triple negative. They lack sort of these over expression profiles. They’ve been treated with chemotherapy or hormone therapy and we believe this is a gift of ErbB3.
So these are patients who are fourth and fifth line and they’ve seen 20 drugs. They have seen everything, the last resort. We are putting them in these therapies and you are seeing close to have the patients still at PR in that late stage setting, by adding 121 to taxane at that point in time.
And so we think that this is really promising data and the whole stage 2 portfolio to look at triple negative breast cancer, to look at EFGR positive breast cancer, look ovarian is underway and we are providing data on those as we go through this year.
But the one, the ErbB3 opportunity is bigger than 121 as I talked about earlier, and as these patients in this upper right where you HER2 expressed and you have the trimer where no individuals are, including 121, it really disrupt that effectively. So for that case where you have these trimers for, we built another drug called 111. It hits the sort of two three dimer situation and knocks that out.
And just quickly, you get up in the patients who have resisted the red box, so they were 3-plus positive. They become resistant over time. We put 111 in combination with different entities there and again, we saw patients in the 40% response range, sort of every effective at that late stage therapy.
So with ErbB3, I think it’s a big opportunity and it’s a really important role across what we had in all cancers and so that’s what we are on to and that’s what we are doing. So let me sort of pause there. We’ve got a lot of other stuff going on this year.
Maybe we’ll take one or two questions before we head in to Q&A. So thank you very much.
Robert, on 398, I understand why the special update in tumor could be (inaudible).
Right. Well, I guess it comes back to the pipeline, right, and that we have an opportunity where we are building other nano particles that are optimized for other situations. So for instance in this HER2 space, there’s one of the most effective type of chemotherapy is the anthracyclines, but they are co-indicated for toxicities with receptants, so they are sort of falling out of use. So like the big problem, we had more chairs in the monotherapy than these that you use today.
We’ve repackaged one of those, taken its ability that’s taken up by any cardiac tissue and then put antibodies on it, so that you’d actually, not only getting this higher differential in the tumor, but you are doubling the intake into the tumor cells. And so while 398 is a package that could be taken up by macrophages and traffic them where you don’t have day-plus supplies, these others will actually get higher up, taken into situations where you do have a more less hypoxic environment and they’ll be take up more into the cell.
So we are actually covering up these (inaudible) so to speak with other agents that will be better than that for certain indications. So because of this sort of this duration of exposure in such an order of magnitude of difference that would have brought up completely, especially using the nano particle and covering up further physiologies to get even better. So the answer is, we are going to need the technology to do what your point is, but there will be different therapies.
Anything else? All right, well thank you for your time. I appreciate it. Thank you.
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