Daniel R. Passeri - Chief Executive Officer and Director
Curis, Inc. (CRIS) Citi 2013 Global Healthcare Conference February 25, 2013 3:00 PM ET
Great. Welcome, everyone. I would like to introduce the next company, Curis. It's my distinct pleasure in introducing the speaker, CEO, well we've got right here, Dan Passeri. Curis is a very exciting oncology company. They recently got approval for Erivedge for basal cell carcinoma, and now they have a very exciting pipeline that's starting to emerge. And I'll turn it over to Dan to tell you more about it.
Daniel R. Passeri
Okay. Thanks, Winston [ph], I appreciate it. First, I'd like to thank Citi for giving us an opportunity to present. Welcome.
Before I begin, just want to remind everyone that Curis is a NASDAQ listed company, symbol CRIS. This presentation may contain some forward-looking statements. I read that as our attorney would like us to all use up 15 minutes of the presentation.
All right, so just starting off with investment highlights. My first few slides are going to just talk about the pipeline and an overview as to what they mean from an investor standpoint the potential milestone inflections.
So Curis is focused in oncology. It's a drug development company that's well-capitalized. We ended 2012 with approximately $60 million in funds, and we have funds -- basically, they're adequate to get us well into the first half of 2015. That does not include the prospect of additional milestone payments that we have potentially coming due as a result of a few upcoming milestones, and I'll touch upon it later in the presentation.
We have a Curis-controlled proprietary pipeline, as well as partnered drug candidates, and as well as the approved drug, Erivedge. And we have a balanced business model as a result of this approach, and I'll get into that in a moment.
Our proprietary programs, we have CUDC-427, which is an IAP antagonist, recently in-licensed from Genentech. That's a Phase II-ready program. CUDC-907 is a PI3 kinase HDAC inhibitor. It's a 1 chemical entity that has 2 active moieties built into it for what we believe will be a more durable and broader coverage in oncology, as a result of blocking the PI3 and HDAC, concurrently. And again, I'll touch upon those 2 programs in quite a bit of detail in a moment. And then thirdly, we a proprietary program, CUDC-101. Presently, we're looking at making a decision on going -- go/no-go on this program based on whether we're successful with an oral formulation that we're working out with some folks at the University of London.
Our partnered programs in terms of products and product candidates, Erivedge is obviously our lead the program partnered with Genentech and Roche. We believe this is a testimony to the quality of the science that we conduct. As has been recently approved last year for the use in advanced BCC. This is under collaboration, they're doing all of the marketing through Genentech and Roche. Again, we had U.S. approval in early 2012, and we're waiting for a decision on EU and Australia in the first half of this year. And again, those will trigger a cash milestone payment to the company.
Then we have the potential of significant market expansion in the current label, and that's based on ongoing Phase II studies in operable modular. I'll touch upon that when I go over Erivedge. And then finally, I'll give you a brief overview of our Hsp90 inhibitor partnered with Debiopharm.
This is an overview of our pipeline, which is a broad, diversified pipeline, and we believe the pipeline development has basically given us an ideal situation for going into 2013, '14, in terms of potential value inflection points for investors, which is what I'll touch upon here.
Starting with CUDC-427, again, this is the IAP antagonist we in-licensed from Genentech. We have the prospect of initiating a Phase II campaign by mid-2013. We, at this time, anticipate initiating studies in combination with Xeloda in breast cancer as well as others. And we're also looking at the prospects of using the drug as a monotherapy, and this is predicated in some of the observations that came to the Phase I study, and that will be presented at an upcoming conference mid-year by Genentech on the PI.
CUDC-907, we expect to complete the Phase I during 2013. This is an open label, so we do anticipate having the prospect of getting insight on the drug's absorption rate and exposure, the drugs PK in terms of its t1/2 and hopefully, we'll also get some sign of clinical signal well before the end of the year that we could discuss publicly.
As I stated, with CUDC-101, we have presently an IV formulation that we're surveying in head and neck, and we anticipate making a go/no-go decision in 2013. And more importantly, based on the culmination of data that we have supporting this program, we're looking at an oral formulation, which is really important to be able to expand out and exploit the promise of this drug, and that we should know, I think by midyear, as to the prospects of the oral formulation work.
Again, with Erivedge, we have upcoming approval for Europe and Australia. It's already been approved in the U.S., Israel and Mexico. And what's most important about Erivedge is the expanded market potential in terms of territory expansion, but also the potential expansion into the operable but suboptimal patient group, and that's going to be predicated on the read-out of Phase II trial, which is currently pending with 3 cohorts, and that will read-out by mid-year. And then finally, with Debiopharm, it's presenting on the Phase Ib results, and the start of Phase I, II in renal cell carcinoma.
I'm going to start off now with a brief overview of Erivedge. Just to remind everybody, this is a first-in-class Hedgehog pathway inhibitor. Drug is now approved for use in basal cell carcinoma. Now this is the actual label that Genentech was successful in achieving. In terms of the advanced basal cell carcinoma indication, based on data that Roche has released, it's anticipated that approximately 40,000 patients would benefit from the drug in the advanced -- that's a restrictive reading of the advanced basal cell category that covers metastatic substantial deformity and in operable, which is about 1.5% of the total BCC population. That turns out to be about 40,000 patients for the U.S. and the top 5 European markets.
What's important about this, and it really underscores the logic and deliberate strategy that Genentech deployed, they went after an unmet medical need, although a smaller market, to get rapid approval. This drug was approved, and I'll remind everyone, on pivotal Phase II data. So that data is now the objective of the ongoing Phase II, is to supplement that data with a survey of 3 separate cohorts in the operable modular category. And that would allow the drug, we believe, under the existing label, to expand into the poor surgical candidate category, where the drug could be used as a neoadjuvant. And that's a really important point to underscore.
So the current label is that the drug can be used in adults for metastatic BCC or recurrent disease after surgery. We believe that would also encompass Gorlin patients, which are not included in these numbers. That would be an additional approximately 4 to 5 patient prevalent in the U.S. or not amenable to surgery or radiation, and that's important to underscore because that third category is in the doctor's discretion. And we believe that would allow the current label to expand into the poor operable surgical candidate, where the physician could make the decision to use Erivedge as a neoadjuvant prior to surgery.
And that would potentially bring an additional 55,000 patients into the market potential. So we believe this is a very significant opportunity for our shareholders to benefit from, but most importantly, for patients, who, without this drug, wouldn't have an alternative. And we believe that Genentech and Roche are looking at surveying this indication in a very strategic and intelligent manner.
So again, the objective during 2013 and '14 is to expand the market potential through marketing -- global marketing. The drug has been approved presently in the U.S., Israel, as well as Mexico. It's presently under review for European and Australian health authorities, and we expect that decision to be made by midyear. Upon that decision, if it is approved, we would receive additional milestones, and that would extend our cash lifeline out even further.
I wanted to just underscore for a moment the importance of the operable BCC Phase II study. This is currently involving 3 separate cohorts. The first is already read out, and we're expecting Cohort 2 and 3 to read-out by midyear. Now this is, we believe, a very intelligent way of supplementing the existing data from the pivotal Phase II.
Phase I -- Cohort 1 has already read out, and that was in 25 patients, where they saw a 42% complete histological clearance. So that is the surgeon did a serial excision and looked at it microscopically and saw no detectable lesion. And then 96% of the patients had either complete or partial response. So this bodes extremely well for the prospect of the drug being used as a neoadjuvant if the next 2 to cohorts are similar in the type of data presented.
The second cohort is to treat the patient for 12 weeks and then wait for 24 weeks before doing surgery, and that's to look at durability, but also to see if the therapeutic response can be enhanced, because the drug is still active after you stop therapy. Its t1/2 is over 7 days. But also, some of the lesions appear, when you look at them histologically, they look pre-apoptotic. So it could be that by waiting, you get an even more impressive complete clearance of lesion and a better response.
And then the third cohort is to see if the physician could alter the dosing regimen and ameliorate and attenuate the adverse events. So rather than 12 weeks of receiving the drug daily, it would be 8 weeks on, a 4-week drug holiday, followed by an additional 8 weeks of therapy. And that's extremely important because it would basically educate the physician for taking also the dosing regimen to ameliorate DAEs without diminishing the therapeutic effect. So this operable study Phase II should be reading out in completion by midyear, and we think this is extremely important for the prospect of expanding the market potential.
Now I'm going to move on to CUDC-427, which is an antagonist of the inhibitor of apoptosis or IAP protein. This is a Phase II-ready program that we just in-licensed from Genentech. Now cancer cells are known to evade apoptosis or programmed cell death. This, in fact, is a hallmark of cancer itself. It's a fundamental resistance mechanism to many of the chemotherapies and anticancer treatments being used. These therapies normally are meant to induce apoptosis and it turns out IAPs are blocking that process from being completed.
So IAPs play a critical role in the evasion from apoptosis, both intrinsic and extrinsic. Intrinsic is from intracellular signals, typically from mitochondria. Extrinsic is from tumor necrosis factor binding to the receptor and it should induce apoptosis, IAPs prevent that from happening. So clearly, this is an attractive target if one can find a chemical entity that prevents that blockade from occurring.
So Genentech, among others, Novartis is another company that invested heavily in this, they have a program in clinical development now. Invested quite a bit of effort into this program. We have to say, it's an extremely well-performed package of -- compiled package of data, both preclinical and clinical. It's the first-ever drug out-licensed by Genentech and I want to underscore that. We take that as a testimony to the relationship we have with Genentech, as well as their confidence in the quality of our development capabilities.
We received an exclusive worldwide license for the development and commercialization, and we'll have to pay milestones on first commercial sale, and there's a tiered single-digit royalty on net sales.
The program is completed. Phase I clinical development, in terms of a dose expansion study. 42 patients were treated with solid tumors of off [ph] lymphoma. Drug appears to be very well-tolerated. The full results on that Phase I are going to be presented at an upcoming conference mid-year by Genentech in PIs. We have to respect their desire to do so, so we're not disclosing any of the details until after that.
In parallel, we're working on our development strategy, which we will relaunch shortly after that presentation. We tend to initiate a Phase II development campaign by midyear. And we're going to be using the drug in combination with chemotherapies. I'll elaborate upon that in a moment. We're also looking at the prospects of using the 427 as a monotherapy in selected patient populations, which may have a particular genetic mutation, which would represent a patient stratification approach. Data is still early and we're evaluating the merits of that.
Again, in overview, it's an oral small molecule peptide mimetic drug candidate that hits the 4 isoforms of IAP that are involved in blocking apoptosis. So that's really important as much as hitting 1 or 2 of these isoforms. It's mechanism of action is to induce apoptosis by interfering with the intrinsic blockade for apoptosis, as well as the extrinsic signaling from TNF-alpha death receptor, et cetera.
The key differentiating factors of CUDC-427 is its high potency. It is orally administered. A number of these IAPs are IV administration, so we have ease of use in the prospects of every day dosing, which is what Genentech has done, and we intend to do going forward.
Importantly, it's a monomer, where a number of these drugs are heterodimers or dimers, and they are known to have more toxicity associated with them. So the drug is very well-tolerated. And as I stated, as an oral drug, we have the prospect of daily dosing, and that's been established and it provides for expanded development opportunities, giving us greater flexibility.
The drug has demonstrated its biological activity that one would expect. When you block IAP, you see induction of caspase, which is a metric of apoptosis. And you can see after 4 hours post single dose, you see induction of cleaved caspase-3, as well as caspase 8.
This is from Genentech pre-clinical data. The drug also has shown to synergize with drugs you would expect it to synergize. These are drugs that induce TNF-alpha. And you should see apoptosis as a result exposure to these drugs, and it's obviously not as effective as one would expect because of IAPs blocking the caspase cascade. So if you liberate that blockade, you should see enhanced apoptosis and efficacy, and that is in fact what we see. And these 2 models, one is a breast cancer model with 5-FU; the other is a pancreatic cancer model with gemcitabine. And you can see on both of those synergy, when you use the chemotherapy in conjunction with CUDC-427.
In terms of its clinical development path, Phase I, again, has been completed by Genentech. Drug has been well-tolerated, and the data on that will be presented midyear. We anticipate launching a Phase II development campaign, mid-2013. We'll first be looking at the treatment of Her-2 negative breast cancer patients in combination with Xeloda. Xeloda is known to induce TNF-alpha, so this fits the thesis of how this drugs works and where we should see synergies.
And CUDC-427 is on the modulate TNF signaling towards apoptosis, and that's been demonstrated on multiple pre-clinical models. There's also some data that's recently been published by Novartis on their IAP inhibitor, also supporting this basic premise.
We're also looking at other cancer indications, treating with 5-FU and Xeloda GI cancers in particular. And as I stated earlier, we're also evaluating the prospects of using CUDC-427 as a monotherapy in patients with a particular genetic mutation.
So in summary, this is a potent antagonist of IAP that has a very attractive preclinical data package supporting mechanism of action. It's gone through Phase I, so we feel it's a de-risk from that standpoint, that's orally available. Active in-vivo and clinically, based on biomarket data, where we see the drug's activity through the following biomarkers. Synergy with chemotherapies has been demonstrated preclinically, and if you look at the Novartis data, that supplements that.
Phase I trial, dose escalation has been completed. The results, again, are going to be presented midyear. Daily dose has been established, well-tolerated in patients. And again, we anticipate launching a Phase II trial campaign by midyear. Just to remind everyone, also, we have exclusive worldwide rights for this program.
I'm not going to switch to our second propriety program, which is CUDC-907. This is a dual PI3 kinase HDAC inhibitor presently in Phase I clinical testing. PI3s have recently gained a lot of attention with the success that we've seen with some delta inhibitors. There are a number of pan inhibitors in development.
Our strategy is to overcome the limitations of some of the current inhibitors, both through the fact that we're hitting not just delta, but alpha, beta and delta, and also the fact that we're concurrently inhibiting HDAC. And I'll elaborate on why we think that's going to be advantageous, shortly.
So the PI3K delta, alpha and beta functions have been demonstrated to function in lymphocyte proliferation and survival. PI3K delta isoforms have clearly shown activity, clinically, despite to say that we think it's somewhat of an oversimplification to think that deltas are going to resolve all of the hematological cancer issues that are presently faced by patients.
It's been shown, for instance, that alpha is involved as an escape mechanism in mantle cell lymphoma. That's a recent publication out of a group in London, where they showed that an alpha-delta inhibitor has superior clinical effects from a delta-only inhibitor. And that's because you have initial response, and the tumor adopts by bypassing with alpha. There have also been publications showing that alpha and beta are involved in multiple myeloma. In fact, the clinical data observed to date with the delta's isoform-specific compound have not been that impressive in multiple myeloma.
So we believe that CUDC-907 has a number of advantages, where we have high potency for alpha, delta, beta, and descending auto, and it's a weak gamma inhibitor. So we believe we'll be getting broader coverage and should give us more durable therapeutic response as well by blocking bypass mechanisms.
And then concurrently, we're also inhibiting HDAC which has also shown -- HDAC inhibitors have shown to have therapeutic effect in hematological cancers. And Curis, as well as third parties, have published on the synergistic effects of blocking -- concurrently blocking PI3 kinase and HDAC. In fact, a recent ASH abstract showed that CAL101 plus HDAC gave superior efficacy and durable response.
So we believe that our drug captures these attributes of both broader coverage on PI3, and with HDAC, a more durable response, because blocking the bypass mechanisms through HDAC inhibition.
So it's presently in Phase I development for lymphoma and multiple myeloma patients. Again, it has compelling rationale for the pan PI3K and HDAC combination. It's an oral small molecule, combining 2 anticancer mechanisms that have been validated. It's a PI3 alpha, delta, beta in descending order of potency. And it also blocks HDAC 1, 2, 3, which is intranuclear for transcriptional alteration, and HDAC 6, which is involved in cytoplasmic alteration of protein, such as Hsp90 and HDAC10. Its mechanism of action is that it interferes with cell proliferation and survival through the PI3 kinase of mechanism and cellular stress response through HDAC. We believe that should give us a more durable therapeutic benefit.
Key differentiating features are that we have combined 2 proven activities in 1 molecule. It's the only candidate in its class. Has the potential to overcome drug resistance mechanism, giving us a broader application into a number of hematological cancers, including B- and T-cell lymphomas, as well as multiple myeloma.
And that's captured here in this preclinical, cell-based assay, where you can see that we've surveyed a number of compounds, compared to 907. So we have exempt 2 prototype PI3 kinase inhibitors. Where you don't -- the first one, you don't see much potency across a whole panel of hematological cancer cell lines. The second PI3 kinase inhibitor, certainly some activity in leukemias and lymphomas, but modest activity. HDAC inhibitor is the most potent one that's on the market presently. What's important there is you don't see representation in multiple myeloma cell lines. They're actually off the chart way up on the top. Even when you combine the PI3 kinase inhibitor 2 and that HDAC inhibitor, you see a slight shift in potency, but not that dramatic. And then with 907, we're hitting a much broader, very potent sampling of hematological cell lines.
And we have good representative data in-vivo. Here, we have 2 lymphoma models at the top. This is non-Hodgkin's Lymphoma, as well as a diffused large B-cell lymphoma model. Dose escalation -- nice dose escalation data showing good regression.
And importantly, at the bottom there, you see a good response with multiple myeloma. So the drug appears to have broad application in hematological cancers and again, presently in Phase I dose escalation.
We'll be treating refractory, relapsed lymphoma or multiple myeloma patients. We expect to enroll up to 36 patients. Obviously, primary objective is to determine the maximum tolerated dose and then the recommended dose for going forward into Phase II. And secondary objectives are to look at safety, tolerability, PK, PD, patient benefit, et cetera. Remind everyone, this is open label, so we should be seeing data as it emerges, and we're hopeful that by mid-year we have some insight on some of these metrics that can disclose.
The study status, we have enrolled the first 3 patients, so the first cohort has been enrolled. We will be, on a cohort-by-cohort patient assessment, looking at tolerability, drug exposure, biomarkers and disease status. And again, being open label, we'll disclose that data as we have comfort with it and feel it's appropriate to update the investor base based on the data that we see.
So the summary is this is a pan inhibitor of PI3 kinase. Again, very potent against alpha and delta, mildly potent against beta and have a weak inhibitor against gamma. And then very potent against HDAC 1, 2, 3, 6, and 10. It's orally available. Has potent activity and lymphoma and multiple myeloma models, which I think clearly differentiates this compound. It's active and engineered models that are resistant to prototype PI3 inhibition.
Phase I trial has been initiated. First cohort completely enrolled, and we expect the Phase I completion in 2013. Again, where it's open label, we should be able to disclose that -- some of that data by mid-year Q3. Phase II trial campaign should be initiated again 2014, first half. And again, we control this program 100%.
Give you a brief overview on Debio 0932, which is our small molecule Hsp90 inhibitor, presently in Phase I/II development. It's in development presently for non-small cell lung cancer patients. Debio has notified us they also intend to expand into renal cell carcinoma Phase I/II. This is an oral small molecule.
As a second-generation, Hsp90, i.e., it's not a geldanamycinand derivative, so it has not shown any of the ocular toxicities associated with that class. Its mechanism of action is that it blocks a protein that protects client proteins from being degraded, particularly mutated proteins that are destabilized or unstable. Hsp90s protect them from degradation and we believe that's why certain mutations are more amenable to Hsp90 inhibition.
DebioPharm has an exclusive worldwide license from Curis that was established in 2009. The deal value is $90 million in total, including upfront and milestone payments. We've received $13 million out of that $90 million to date, and we would get royalties on net sales if the drug is approved.
The next milestone due would be 5th patient treated in Phase I. DebioPharm has progressed 0932 in clinical development. Phase II portion of the HALO study is anticipated to begin in first half of 2014, and we anticipate initiation of a Phase I/II in renal cell carcinoma in the second half of this year.
Overview of our financials, and then again, highlighting our investment thesis and milestone inflections. We ended 2012 with approximately $60 million in cash. Based on our present burn rate and forecast budget going forward, without additional milestones, we have enough cash presently to get well into the first half of 2015. And that does not include milestones that we would anticipate with EU approval, Australian approval, as well as DebioPharm going into Phase II.
I started off with this slide, and I'll end with this in a pipeline overview of these milestones. We're well-positioned right now, well-capitalized with a number of proprietary programs, as well as partnered programs, which give us the prospect of multiple inflections throughout 2013 and into '14, and we are well-capitalized to realize these inflections. And so the company really is extremely well-situated right now both from the standpoint of increasing market potential and value-creation from the improved drug, Erivedge, which Genentech and Roche are handling. But also with our proprietary pipeline, we believe we're very well-positioned with our PI3 kinase HDAC inhibitor for competitive positioning, in a space that has gained a lot of attention as of late. And then IAP inhibitor 427, we look forward to launching the Phase II campaign mid-year.
Thank you very much for your attention. I'll turn it over to Winston if you have some questions asked.
Great, thanks for the presentation. Any questions from the audience?
Regarding 907, can you expand on why it's beneficial to have both of those activities in the same molecule? So the alternative would be to take your pan PI3 and have the flexibility to combine it with other spectrums, other doses or other administration protocols for HDAC and get the effect separately with more flexibility.
Daniel R. Passeri
Yes. It's a very good question and an important one. So the question is, why have one molecule as opposed to using 2 or 3, where you can alter the dose in a controlled exposure, et cetera. From a practical standpoint, using 2 or 3 compounds is not a trivial matter. They usually have a family of different aggregation rates. So it's actually quite difficult to control exposure. They also have very different PD effects. So physician has to continually monitor, and patients may have various PK profiles. So they have to monitor each patient very closely. Also, the toxicities tend to -- can be exacerbated, and this has been shown with HDAC inhibitors when use them in combination with other compounds, because of this oscillating exposure profile, you're going to have 2 Cmaxs that are different. You may have to give the drug at different times, inconvenience for the patient. SO it's not a trivial matter. What we have seen pre-clinically is the drug is one chemical entity, you're hitting all 3 targets of, I should say, all 2 targets with multiple isoforms, concurrently. And the t1/2 of the drug, the first thing you lose is the HDAC effect. And a positive aspect of that is HDAC has a prolonged PD effect. Its biological activity lasts for quite a long time because it's a stress adaptor, it alters transcriptional access, et cetera, where kinase signaling is an ongoing function where you need to hit the target on an ongoing basis. So it's too early to convey with any certainty, but preclinically, we've seen that the first part of the compound to be degraded in animal models as the HDAC moiety, where one of the metabolites appears to still be active on the PI3 side. So in terms of animal efficacy that we've seen, the single agent actually appears to be advantageous in terms of controlling exposure. We also think, from a toxicity standpoint, it might have an advantage, but that remains to be seen clinically.
Any other questions from the audience? We'll have one final question for you, Dan. As you think about the PI3 space obviously alluded to as being a competitive space, and it's great that you now advanced the program where it is, how do you see the landscape shaping out? How do you plan to differentiate the program? Obviously, there are some properties now that are starting to look that interesting, but how would you plan to carry that forward?
Daniel R. Passeri
Okay. So, we think it's an ideal time to have 907 in clinical development. And clearly, these delta isoforms, CAL101 for instance has a lot of attention affinity with their delta inhibitors gaining a lot of attention. The PI3 space is being focused upon right now because of the efficacy that's been seen. I think, clearly, we are learning to delineate and differentiate patients populations based on which isoforms they are expressing. I think it's a gross oversimplification to think one particular isoform is going to apply to all hematological cancers. Biology is much more complex than that. And we've seen a number of groups report, that some of these lymphoma groups of multiple myeloma have different isoforms being manifested. So we believe that 907 will have the advantage of not only hitting delta, so we may be able to position within the same market that those drugs are demonstrating efficacy, but have a broader application, for instance, in multiple myeloma or lymphomas that are -- turn out to be refractory to just delta. And there has been a recent publication in mantle cell lymphoma where alpha is a bypass mechanism. So I think the key is to survey the clinical data very carefully, be able to characterize the patients' isoforms that are being expressed, and we think there'll be front-line possible applications and then applications to patients that become refractory to standard of care or some of these other emerging PI3 kinase inhibitors. I think it's early days and there's a lot to learn in these targeted therapies. And I think that's the whole point of precision medicine, is knowing where to apply the characteristics of the drug under different contacts and scenarios.
Great. Are there any more questions? If not, I want to thank you for coming to our conference and presenting, and thank you.
Daniel R. Passeri
Okay, thanks, Winston. Thank you.
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