ImmunoGen, Inc. (IMGN)
31st Annual JP Morgan Healthcare Conference
January 7, 2013 11:00 am ET
Dan Junius – President & Chief Executive Officer
Previous Statements by IMGN
» ImmunoGen's Management Presents at Lazard Capital Markets 9th Annual Healthcare Conference (Transcript)
» ImmunoGen's CEO Discusses F1Q13 Results - Earnings Call Transcript
» ImmunoGen's CEO Presents at UBS 2012 Global Life Sciences Conference (Transcript)
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.