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Curis, Inc. (CRIS)
The Wall Street Analyst Forum
September 20, 2007 1:20 pm ET


Daniel Passeri - President and CEO



Good afternoon, ladies and gentlemen. In our ongoing attempt to adhere to the public schedule, I would like to introduce the next company in this afternoon's program, a Massachusetts company from Cambridge, Massachusetts. A global company, I should say. A global company with the corporate headquarters in Cambridge, Massachusetts. Curis is a drug development company that is committed to leveraging its innovative signaling pathway drug technologies to seek to create new medicines primarily for cancer.

Curis' pipeline includes proprietary small molecule cancer drug candidate, that Curis is developing under its targeted cancer drug development program, including a lead development candidate, CUDC-101, in which Curis expects to file an IND during the first quarter of 2008. In addition to its proprietary cancer assets, Curis maintains three Hedgehog signaling-based drug development programs including a systematically administered small molecule antagonist of the Hedgehog signaling pathway, that is currently in Phase I clinical testing in collaboration with Genentech and Hedgehog antagonist programs for stroke and cardiovascular disease under development with Wyeth.

So, without any further introduction, I would like to introduce Daniel Passeri, President and Chief Executive Officer of the company.

Daniel Passeri

Thank you very much and good afternoon. Curis is a NASDAQ-listed company, symbol CRIS. I would address first our pipeline in our overall corporate development. We have endeavored to continue to build a broad portfolio of assets, principally focused in oncology, but not exclusively, the Wyeth relationship is in neuro and cardiovascular.

The dates you see up at the top denoting 2003, 2007 and 2009, they represent our corporate evolution. When we entered into the relationship with Genentech to exploit and further develop our Hedgehog platform, we consummated that transaction in 2003, and the reason the date is towards early preclinical, is that's where the program was when we partnered and that also represents where the company was in terms of it's core competencies.

And one thing we have then a very deliberate is our systematic evolution as a company. We have resisted the pressure from the financial markets to rush toward the clinic. We felt that that was not the prudent way to develop the company. We knew what we did well and we knew what we did not do well. So, we stayed focused on executing on fundamentals of what we were quite proficient in and have evolved competencies through these collaborations.

So, through our relationship with Genentech were we had a substantial amount of financial support supporting our scientists. We met with them formally and informally on an ongoing basis. That relationship really allowed us to evolve a much deeper understanding of how a company like Genentech identifies a lead clinical candidate, and designs and goes forward towards IND filing.


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Where we are today in 2007, as we have through that relationship as well as our others evolved a very deep proficient understanding of preclinical development. We are now at a level where we have a deep pipeline of our own proprietary preclinical assets and we are very proficient and professional at preclinical development. We are now preparing for an IND filing and our objective is by 2009, so that is the remainder of this year, 2008, we intend to file our own IND and evolve competencies of clinical trail development.

I am now going to go through briefly. Our partnered programs and the majority of this presentation I am going to focus on our proprietary oncology pipeline. First, I am going to touch upon the Hedgehog antagonist platform that’s exclusively licensed to Genentech.

Hedgehog pathway has been shown by multiple third parties, and it's a partial list of publications there at the bottom. The Hedgehog is involved in a number of solid tumors. The way this pathway works is -- it is what is classically known as a morphogen. So, during embryonic development, its expression coordinates a cascade of events with surrounding cells, surrounding tissues, but then will release a myriad of growth factors, angiogenetic factors, to faster tissue development. Then the [adult] that are typically quiescent are expressed at very low levels and tissues that are being replaced.

Except in the case of cancer, where you have aberrant expression, plays basically the same role, but usually during embryonic development and now that the tumor is expressing, this morphogen and paraffin loop. It's a means of communicating to the surrounding tissues basically saying we need growth factors and we need blood vessels, we need blood supply. So, it's a paraffin loop. The protein is secreted by the proteins communicating to adjacent stromal stronger cells. The stromal cells then in response to that signal will make a myriad of factors inducing blood vessel growth, and fostering proliferation, and growth of the tumor.

So, we have developed a series of small molecule antagonist, as well as a blocking antibody, and this is exclusively licensed, now in the control of Genentech. The basic concept is that this is an upstream sort of master switch that if we can block the signal from being emitted by the tumors, or received by the stromal cells [yield] end up blocking the downstream cascade of other factors in response to that signal.

This program is currently in Phase I for a small molecule antagonist. The Phase I began in January 2007 for systemic administration. The Phase I is expected to enroll approximately 50 patients, and to all comers, in a dose-escalation study. The IND was filed in October 2006 that resulted in a $3 million cash payment to Curis and subsequent clinical development milestones including Phase II would result in further cash payments to Curis.

And we will switch now to the Wyeth program. This in the inverse, were the agonist is met to augment the natural antagonist response to tissue damage. So, they stated the protein Hedgehog is involved in embryonic development, than typically quiescent in the adult, where you see is upregulation and the abnormal situation such as cancer but under normal circumstances, you also see it up regulator when there's trauma or damage to a tissue. And there is a recapitulation of the embryonic process to try to minimize damage and faster repair.

So, in this slide which shows a classic bell curve response, this is the typical response you see in the body when there is damage. You have a quite dramatic upregulation of Hedgehog, but then it is down regulated in a pretty tight time curve, and this is because it’s such a powerful molecule, body has a self regulation built into the pathway. And the reason I’m getting into this is that it explains where we are right now with the search for small molecules that can turn up the amplitude of the signal and maybe extend up the longitude, the length at which the signal is expressed, if you want to retain this self regulation mechanism.

We had previously identified small molecules that bypass the self regulation of pathways, stayed on too long and although, we showed very impressive neuro protection and stroke models, Wyeth was concerned with potential systemic toxicity, because the pathway stayed on too long. So, we are now searching for small molecules that achieved the upregulation, but retained the self regulation of the pathway.

So, we are currently conducting research on small molecule agonist for stroke, as well as a second program involving a protein agonist for cardiovascular disease. There is also the potential for using the protein for stroke because we have some preliminary evidence that the blood brain barrier is comprised, and the protein actually crosses the blood brain barrier.

We are entitled to cash payments upon the achievement of development objectives, as well as royalties should product sales occur, and cash payments could total approximately $170 million, assuming there is at least two product that are successfully developed.

Under the stroke program, the first small molecule compound class proved efficacious in preclinical models, but as I stated, because it did not have that self regulation, it also demonstrated systemic toxicities at high doses. So, Wyeth delayed selection of a lead compound in favor of searching for agonists that have a more attractive profile. So, preclinical studies are currently being conducted seeking the identification of different classes.

And then, Wyeth recently initiated a cardiovascular program. Early preclinical models of acute heart attack yield promising results that basically validated previously published data.

I am now going to turn to our own proprietary program. This is a very deep pipeline of Curis controlled, Curis owned oncology programs. In terms of the way I am going to present this, I am going to discuss the rationale for the design of these drug candidates. They are multi-target inhibitors. They have been specifically designed to address validated targets. And this is our basic approach and then I am going to go through our portfolio with an in depth discussion on our lead candidate, which is an EGFR/Her2 and Target A inhibitor.

As a background to the rationale for this approach, what I want to underscore is the evolution of cancer therapies. As we are all aware, traditional chemotherapies are basically toxic compounds that are more toxic for rapidly dividing cells. And a lot of progress has been made in that front, but the disadvantage is they are not selected for cancer and, they are toxic to any cell which is rapidly dividing. There is recently been an emergence of a more targeted approach and these are drugs that specifically inhibit, identify targets that have a validated role in the biology of cancer. Examples for this are, Gleevec and Tarceva. They are efficacious in some clinical settings and the real promise is that they are less toxic and most specific for tumor cells.

However, the overall response for it has been relatively poor and drug resistance is a challenge. What I want to underscore is the reason why the response rates are lower than anticipated, is that tumor cells have a repertoire of many pathways that they are using. If you intervene with one, there is typically a small sub population, where the cancers of those patients are addicted to that one pathway, and they will respond favorably. Other patients may have a minor response and then are able to rebound because the tumors are able to use other pathways.

So, there has been an emergence of kinase inhibitors that hit more than one kinase. So, if you do in stressing the tumor out at more than one intervention point and this is proven to be more efficacious. The current trend is actually combination therapy much like what we have seen with HIV therapy by the way, where its a manageable disease if you provide cocktails of different agents that are stressing out the virus at different intervention points, because the virus evolves and will respond. Tumors do basically the same things. If you hit it at one intervention point, it will respond by up regulating other pathways.

So, the current paradigm is cocktail combination therapies where they are trying to find synergistic combinations, synergistic targets that when you hit the cancer with more than one target, it induces the cancer to go into that program's cell death. That’s the current paradigm. So, these targeted therapies hold tremendous promise, and they are in the clinic being used widely in combinations, and the data has been emerging on what combination it's synergistic. This is what our scientists says, and try to exploit and take advantage off it. The observation that some of these validated targets if you combine them, they provide synergistic effects that the effects are greater than just being additive.

So, our drugs are designed to engage more than one key target. So, they are designed to engage synergistic targets. They are expected to be more efficacious and work against a broader range of cancers that inhibit several pathways, in the same cells, at the same time. This is one drug entity. The basic concept is the drugs have been designed where target area -- and I apologize we have not been able to disclose the target a year. We are hopefully going to be able to start disclosing that within the next couple of weeks. We keep it proprietary, because of patent considerations. We filed the provision when we had a one-year grace period to build up a patent applications. We didn't want to compromise that.

And what we did is, we took a chemical structure that Target A, and inhibits Target A. And we synthesized drugs that have active moieties of other drug prototypes. So, this drug is designed to hit more than one target. It's designed to hit drug A and a myriad of Target Bs. We have gone after clinically validated targets, with potential synergistic inhibition.

The real attractive aspect of this is it takes advantage of the observations and combination therapy that’s emerging, and gives us proprietary compounds. So, we have a broad suite of platform of proprietary drug structures, that were currently in preclinical development, showing very promising results and we hope to be in the clinical with our first lead in Q1 '08.

The objective here is that this dramatically lowers the development risk. We are looking at indications with established clinical paths for validated molecular targets based on prototype drugs that we going to be following suit with. And has potential for accelerated market acceptance because of our proprietary position, we should have long market exclusivity.

And the objective is that these drugs should prove efficacious, hit a broader range of drugs and because of the enhanced potency and the synergism, we are expecting lower effective doses. Therefore also extrapolating that we should have fewer dose-limiting toxicities, particularly off-target toxicities.

So in terms of Target A, the reason we selected Target A as the back bone for this platform, it’s a validated non-kinase target. There have been numerous enormous publications suggesting a broad range of cancer activities for Target A inhibitors and showing also simultaneous activation by inhibiting Target A of several [apoptosis] that way. So by inhibiting Target A, you are increasing the likelihood that the cancer cells are going to be induced towards cell death. Also selective killing of tumor cells and it lowers the apoptotic threshold when you treat in combinations with other drugs. That’s a very important observation.

Regarding the synergy with other anticancer agents, and there have been multiple publication showing that this target when inhibited is synergistic with kinase inhibiters, conventional chemotherapies as well as regulated proteasomal degradation and radiation. So, these broad anticancer activities basically suggest that Target A inhibitors may be have a greatest therapeutic benefit in the clinic, when in combination with other therapies, and the real key observation that was made as our scientist noted that the active Target A inhibitor moiety on a series of these is one that’s approved and they are several that are in the clinic, the active moiety appeared well suited for integration into other anticancer drug skeletons resulting in proprietary compounds with combination inhibitory activities.

As a result of this approach, we have built a very broad platform. What you see in the top quadrant, color coded in purple. These are all multi-target inhibitors with Target A build-in with a series of Target Bs. The top one is EGFR/Her2/Target A. We anticipate selecting another lead candidate towards the end of this year. Most likely either the HSP90 Target A or the Bcr-Abl Target A inhibitor.

Now we have been able to build such a broad platform in a series of drug candidates without increasing our burn rate because we have opened operations in Shanghai, China. We use a CRO extensively there doing our medicinal chemistry. So, our scientists in Cambridge, Mass do all the drug design. They then send over the Medicinal Chemistry Schema and we have synthesis performed in Shanghai. We have a web portal that allows us to keep track of this seamlessly. And I want to underscore we should take the intellectual property issue very seriously. The chemists and scientists in China, never sees a structural activity relationship that's preserved in Cambridge, Mass and that's what your IP is based upon.

The most important commentary on the China operations is the fact that it doesn’t just afford us significant cost savings but to our surprise, its dramatically truncated the amount of time required to develop drugs, because we basically have a 24/7 operation because of the time difference.

I’m now going to go into some depth on our lead program. This is an EGFR/Her2/Target A inhibitor. We are currently doing IND-enabling studies right now and anticipate filing an IND towards the end of Q1, '08. And the reason we focused on EGFR and Her2 is that these are well validated tyrosine kinases with a lot of clinical experience. These pathways play a central role in tumor cell proliferation, survival and metastasis. So, the promise of inhibiting these pathways and providing efficacy was great. There are already several EGFR/Her2, as well as combination EGFR/Her2 inhibitors on the market, both small molecules as well as antibodies.

We’ve been able to use the observation of those drugs to guide our own development. So, the thinking is that this targeted approach should be less toxic than traditional chemotherapy. However, growing body of evidence from the clinical study has shown us an -- inhibition of these pathways has provided overall a poor response rate in the terms of the number of patients responding.

Now, this does not reduce the significance of these drugs. What it shows is that the tumors are adaptive and they are highly responsive. So, if you hit the tumors and interfere with just one pathway, the tumors will be able to respond by up regulating alternative pathways. These drugs still hold tremendous promise in combination. That's really where the field is moving.

The other important issue is the rapid emergence of drug resistance. There has been growing body of evidence that EGFR inhibitors have initial success, but the tumors are responding by up regulating alternative mechanisms of using the same pathway.

So, there remains a compelling unmet need to be able to utilize the observations and targeted therapy in a more robust manner, and we believe it’s a combination therapy, and our approach is single agents that are hitting these targets simultaneously.

There have been reported synergies between Target A inhibition and EGFR/Her2 inhibition, potentially addressing the low response rates. There have been studies showing that you can enhance or restore the sensitivity to EGFR inhibition by the multiple mechanisms that are turned on via inhibition of Target A. It lowers the apoptotic threshold and it's also been shown as a bio-marketed upregulation of Target A results -- in inhibition of Target A results and upregulation of E-cadherin, and that's been correlated with an improved enhanced response rate to EGFR inhibition. And that's shown here. What you see are EGFR positive yet resistant cells and what you have is an EGFR inhibitor on the top line here. This is a (inaudible) MS-275. That is a Target A inhibitor.

In combination, you are seeing a much greater response and those cells are responding to the EGFR inhibitor. So, this is basically conveying that inhibiting Target A increases the sensitivity to EGFR inhibition.

In terms of creating a durable response, one of the reasons these tumors are able to develop drug resistance is, observations that there are downstream responses. Well, there is an upregulation of Akt phosphorylation. We have shown that our drug inhibits Target A and inhibits EGFR, and results in durable inhibition of both EGFR and Akt phosphorylation. So, we are hopeful that we will have a more efficacious drug, and one single agent hitting multiple targets that is durable. So, we are hoping that it attenuates if not reduces or eliminates drug resistance.

So schematically, the basic observation we've made is this one single agent is providing synergy because it is targeting the same molecule, and the same cell is hitting the EGFR target Her2, and it is hitting a different target which results in a synergistic affect of upregulation of (inaudible) and a durable reduction of phosphorylated Akt.

We've done studies trying to assess the right optimum combination of Target A inhibitors and EGFR inhibitors and it turned out the best ratio for synergy was a one-to-one ratio, and fortunately, this is serendipity for us but it turns out our molecules are one-to-one ratio in terms of the way its designed.

Molecule, this is a single chemical structure. It is a small molecule. It actually has a lower molecular weight than Tykerb which is an EGFR/Her2 inhibitor. Our molecule is sensitive in inhibiting EGFR/Her2 as well as Target A.

And what I want to underscore in this next slide is we have unanticipated results. We derivatised this chemical structure, we made over 80 derivatives. So, we really did a lot of work at optimizing the potency. So, this one molecule has enhanced potency against the prototype drugs. For Target A, the Target A inhibitor is an approved drug currently in the clinic. It has a potency of 40 nanomole. That means if the concentration were you have a kill rate 50% or you are inhabiting 50% of the target, so you need 40 nanomoles of Target A inhibitor to inhibit Target A and our drug its 4.4 nanomole. So, we have single digit nanomole of potency.

On EGFR, we have basically achieved the same thing. Erlotinib, which is the OSI/Genentech/Roche drug. It has IC50 for EGFR 48 nanomole. We have driven the potency on that down to single-digit nanomole. So, you have seen a nice correlation single-digit nanomole or inhibition of both Target A and EGFR and Her2, it's basically comparable to the prototype drug.

So, we have done an extensive series of in vitro test looking at enhanced potency. And what we have done is we have compared our drugs potency against the approved Target A inhibitor, against our Lapatinib combination, where they may be synergies and combination of this drug. And we compared the activity and potency of our drugs against the combination and you are seeing on the right hand column, showing improved potency. This is a series of non-small cell lung cancer cell lines, wild type as well as mutated, ranging from an equivalency in the wild type H2122 up to nine fold enhancement of potency against the mutant type.

And this is the corresponding in vivo data that we have generated showing a nice dose response curve. This purple bar at the bottom denotes period of treatment. So, we went on treatment for six days, off for six, seven days and treatment for five day. And you see a nice dose response curve, in fact you see tumor regression during initial treatment period and on the right, the reported data of same cell line being treated by erlotinib.

This is against another cell line 549 and its published data on the right showing us statistical significance. When treated with erlotinib, you see a nice statistical spread with our proprietary compound.

This is our proprietary compound compared with erlotinib and lapatinib\, which is the EGFR/Her2 inhibitor against a series of apoptosis cellular carcinoma cell line, which is liver cancer and again showing nice enhancements of potency. And then the real nice dose response on -- this a in vivo study where we see spaces and one can argue some regression in tumor size. And this is in liver cancer, which has really no affected treatment currently on the market.

This is against other major cancer types that could be focused here on prostate cancer. We had up to a 20 fold enhancements of potency and activity and again a nice dose response curve and in vivo models.

And this is looking at -- versus erlotinib and lapatinib against resistant breast cancer cell lines, by the way, lapatinib is the number drug I think for breast cancer, because of Her2 involvement. And again, we see either equivalency or up to a 23 fold enhancement of potency against these various cell lines.

This is the induction of apoptosis, induction cell death and this is SKBr 3, breast cancer cell line in 24 hours. You will see no affect of combination of erlotinib in Target A inhibition. We think that's because of the Her2 response to our drug and you are seeing a four fold increase over the colon cell lines. We did see some synergy by the way in EGFR inhibitor and the Target A inhibitor.

We have looked out the pharmacodynamics and the biological response of this drug. We have seen induction of apoptosis. This is the area of cell death after three days of treatment and on the bar curves, we have see a nice regression of this tumor mask after three days of treatment. We are seeing induction of apoptosis. This is non-small cell lung cancer xenograft. It's difficult to see, we removed the background staying those brown spots on the right hand quadrant. Those are cells that are undergoing program cell death.

We have also shown suppression of tumor proliferation. And as I stated earlier, there have been observations that inhibition of Target A results in upregulation of (ina33.00udible) here in, which correlates to enhanced sensitivity to EGFR inhibition.

So, we show a nice upregulation of (inaudible) in response to our compound. We have filed very broad patent applications. We have over 20 patent applications on file. We continue to file on specific chemical compositions. It's the reasons we have not disclosed the identity of Target A over the past year was to preserve our one-year period under the provision of application to -- [both to the] application with additional data. So, we will be disclosing Target A over the next couple of weeks. We have met that one-year period.

It terms of the overall model, our upcoming milestones. Our program is under collaboration. The first one is Hedgehog systemic antagonist exclusively licensed to Genentech. That’s currently in Phase I and we are hopeful if that hits a Phase II entry that would trigger milestone. The Hedgehog, a small molecule agonist under Wyeth. We continue to research and look for the class of agonist. If they select a development candidate, that will trigger a milestone and we are also hopeful with the protein that continues to make progress, its currently in preclinical studies, showing promise for both cardiovascular and potentially for stroke.

Regarding our internal programs, under our multi-targeted platform, we are anticipating IND filing on our lead candidate, which is the EGFR/Her2/Target A inhibitor towards the end of Q1. We are currently in discussions with pharmaceuticals companies in for the potential collaboration. We will not license this the way we had previously just handing over control, so we are looking for a relationship that affords us some control in the clinic. We'd like to have co-development at least to Phase II for greater upside and greater control over our portfolio. We are going to be selecting our second development candidate from this portfolio by the end of '07.

And then on the BMP-7 protein, this was earlier this year returned by J&J. We are in discussions with several pharmaceutical companies right now and we are optimistic that we should be able to consummate another license on this program by the end of '07.

Our financial situation, we reported in June that we had approximately $30 million in cash subsequent to that on August 8, we raised money under a [pipe], we raised $14.5 million that's not reflected in the numbers you see here, so at present we have enough capital to have approximately two years of runway without any other infusion of capital for milestones, etcetera. Okay and thank you for your attention, I'd open up to questions.

Any questions? Yes.

Question-and-Answer Session

Unidentified Audience Member

Does that $30 million reflect the 14?

Daniel Passeri


Unidentified Audience Member

Or is it 45 or the 30?

Daniel Passeri

No. It was 30 prior to raising the 14. Any other questions?

Unidentified Audience Member

How much equity did the 14 get?

Daniel Passeri

It was at market. There was no discount. It was at a $2.00. Any other questions? Yes?

Unidentified Audience Member

(Question Inaudible)

Daniel Passeri

Well, that's the objective. That's our hope. It's under control of Genentech. The question by the way for webcast is, what's the status of the Genentech relationship? Genentech has exclusive control over the Hedgehog Antagonist at this point. We collaborated preclinical development and now with clinical there, it's under their control.

Unidentified Audience Member

Okay. I am sorry. What I am trying to really ask is, is it a single protein or a single molecule at this point and that's it or there could be other?

Daniel Passeri

Yeah. The question is -- is it a single molecule or are there potentially others. Well, that's actually a whole platform. It's the Hedgehog Antagonist platform. They have a small molecule in Phase I under evaluation now. They have been working on backups and our hope is that they will even look at developing the backup.

And they also have the blocking antibody, so they are looking at possible synergism with the antibody in small molecule, so this could result in several clinical programs simultaneously.

Unidentified Audience Member

And will all those different developments trigger any (inaudible)?

Daniel Passeri

Depends on how it's structured, so it's a prospect of one more than milestone. Yes?

Unidentified Audience Member

(Question Inaudible)

Daniel Passeri

Okay. So the question was, we had reported that we lost a couple of collaborations and what's the future prospect for additional collaborations. So the J&J relationship that wasn't a collaboration, we had exclusively licensed the entire BMP-7 portfolio to them, so we had no active role. We were very disappointed with the rate of progress on that program and it was actually under our evaluation of progress and compelled them to return the program. We are hopeful that we'll be able to consummate our license or even assigning those rights to another company. We are not active in that field but we want to see that asset exploited. So we are hopeful that we're making progress on that front and as I stated in the milestone that we are hopeful that we could possibly even announce something in '07.

The other program was PNG for the (inaudible) program. It is highly unlikely that that program would be reinitiated unless we make some break through in the Wyeth program where we find that activate the pathway, but provide the self regulation. So the same toxicity that Wyatt observes in systemic was the concern that PNG had even in topical application. Because when you give large doses for an extended period of time the pathway was not regulated properly.

Okay. And then under our proprietary pipeline we're evaluating strategic alternatives now in terms of collaborations that provide us with the deal structure that we are looking for.

Okay any other questions. Thank you very much for your attention. Thank you.


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