Array Biopharma (NASDAQ:ARRY) Q3 2012 Earnings Call November 5, 2012 4:30 AM ET
Tricia Haugeto - IR
Ron Squarer - CEO
Kevin Koch - President & CSO
Eun Yang - Jefferies
Howard Liang - Leerink Swann
Stephen Willey - Stifel Nicolaus
Matt Lowe - JP Morgan
Welcome to the Array Biopharma Conference Call to discuss accepted abstracts ASH abstracts. My name is Kim and I will be your operator for today’s call. (Operator Instructions).
I will now turn the call over to Ms. Tricia Haugeto. Ms. Haugeto, you may begin. Tricia Haugeto.
Thank you Kim. Good morning and welcome once again to Array Biopharma’s Conference Call to discuss the Abstracts on ARRY-520 and ARRY-614 accepted for presentation of this 2012 ASH Annual Meeting. You can listen to this conference call on Array’s website at www.arraybiopharma.com. Also we are using slides today to accompany our remarks. The slides can be downloaded on the Investor Relations homepage of our website. In addition the replay of the conference call will be available as a webcast from our website. I would like to introduce Array’s Chief Executive Officer Ron Squarer, I would also like to introduce Kevin Koch, our President and Chief Scientific Officer. Mike Carruthers our Chief Financial Officer and Karsten Witt, our Vice President of Clinical Sciences who will be available to answer your questions as needed.
But before I hand over the call to Ron, I’d like to read the following Safe Harbor statement. The matters we are discussing today include projections or other forward-looking statements about the future results, research and development goals of Array and its collaborators and future financial performance of Array. These statements are estimates based on management’s current expectations and involve risks and uncertainties that could cause them to differ materially from the actual results. We refer you to risk factors discussed in our filings with the SEC including our Annual Report filed on Form 10-K for the year ended June 30, 2011 and in other filings Array makes to the SEC. These filings identify important risk factors that could cause actual results to differ materially from those in our projections or forward-looking statements.
Now I’d like to turn it over to Array’s CEO, Ron Squarer.
Good afternoon everyone. And for those who live and work in the New York areas. We continue to track the aftermath of the devastating storm that they came through the area and your loved ones and friends and family rapid recovery. This call was originally scheduled to describe the abstracts on ARRY-520 and ARRY-614 which have as of this morning been posted to the ASH website. In addition to the ASH abstract there is a great deal of progress emerging across our broad portfolio. At this point Array is evolving into a late stage development company with full five programs having the potential for pivotal trial decisions by the end of calendar year 2013.
And as of this morning, we actually had a one more product to our Phase II line up with VentiRx having dosed the first patient with our toll-like receptor 8, VTX - 2337 in a Phase II study in ovarian and related cancer. So this brings the total number of Array products currently in Phase II to a remarkable 11.
I’m on slide three now and on this slide we summarize our value drivers, the components of our value can be separated into three clear buckets and while these buckets are roughly similar in value from a risk adjusted point of view. We sense that many in the investment community, value Array mostly on our MEK inhibitors alone and that’s in the middle bucket on the slide which includes the MEK programs which we have already, which have already demonstrated impressive multi-tumor activities. These, of course, include Selumetinib, partnered with AstraZeneca, and MEK162, partnered with Novartis, both of which we believe to be progressing towards pivotal trial.
You may recall we stayed on our quarter call just last week that Novartis has scheduled an R&D Investor Day for this Thursday, November 8, at 8 a.m. Eastern Time and we expect to providing an update on forward plans for MEK162. We encourage our investors to listen in to their presentation this Thursday this morning. Next to the MEK bucket on this slide, we listed the all presentation topics from ASCO 2012 all of which could represent forward registration pathways for these products. Although MEK in general has shown even broader tumor activity than listed here. OK.
In the lower left bucket on the slide, this includes our existing partnerships beyond MEK as well as ARRY-797 our pain program and ARRY-502 asthma program, which we plan to partner given internal focus on hem/onc. So we are planning to partner with both of those. We were actually very pleased to hear earlier today and again exciting times at Array that the late breaking 797 abstract which we submitted to ACR it was accepted for presentation on Tuesday November 13.
The late breaking abstract was posted on the ACR website this morning and refers to our randomized placebo control Phase II study of ARRY-797. In which patients with osteoarthritis pain, which was refractory to NSAID treatment, showed statistically significant improvements in the WOMAC pain scale. What is really important and new in this abstract is our data regarding biomarkers of cartilage, COMP, and bone CTX1 degradation, which also were accessed and in fact with 797 treatment that they both were reduced statistically with comp and CTX-1 at week four down 10% and 38% respectively.
These are statistically significantly results. The top bucket on the right includes our two wholly-owned hem/onc products, 614 and 520 for or multiple myeloma and we will be discussing the multiple accepted abstracts regarding these products today. To summarize this topic as an investor or analyst if you focused your evaluation on Array on only one or two of these buckets we would encourage you to consider our full portfolio going forward. Quickly on slide four, this summarizes our upcoming catalyst for the product specifically for the products that are being developed by Array and so 520 and 614 tracking on similar timelines both with the dated ASH, the timing of top line results early next year and the potential to initiate Phase III 2013.
Both MEK162 which we are co-developing with Novartis and 502 for asthma should see their data mature on a similar timeline in the first half of next year with success MEK162 is likely to proceed to registration trials and as I mentioned we will be seeking a partner for ARRY-502.
Finally we have already initiated partnership discussions with ARRY-797 and do look forward to discussing the new disease modification data in 0A at the ACR meeting in addition to the statistically significantly efficacy data. So I’m now moving on to slide five, here we list the ASH abstracts for hem-onc programs. We'll be presenting four abstracts including one oral presentation as you can see we are providing data on the benefit of adding 520 to DEX. The further potential benefit of our newly identified selection biomarker AAG and the benefit of combining 520 with carfilzomib. Also, we’ll be sharing data on the improved PKPD profile for ARRY-614 in MDS.
So moving on to slide seven, just as a background multiple myeloma is the second-most common hematologic cancer, with the prevalence of about a 122,000 patients, very significant and highly unmet need. In existing therapies fall into two classes IMiD, like Revlimid and thalidomide, and proteasome inhibitors, like carfilzomib and Velcade. But the disease remains incurable, and ultimately, all patients go on to progress and die from multiple myeloma.
Flipping to slide eight, ARRY-520 represents a new mechanism for the treatment of multiple myeloma. It's highly selective allosteric inhibitor of KSP. The KSP protein is not found and differentiate itself so there is no expectation of neuropathy with this mechanism which has been a significant problem with other commonly used treatments. Because it is a novel mechanism we believe there would be less or no cross resistance to other mechanism in this space.
KSP appears to be highly active because of the role of MCL1 in melanoma, specifically in the dependence on MCL1 levels on KSP activity. We have also demonstrated preclinically that 520 has synergistic efficacy with both synergistic efficacy with both lenalidomize and bortezomib both standards of care in this disease. So slide nine actually details lot of the new data that we are presenting at the ASH meeting. Just to recount we reported a last ASH that 520 this was in 2011 had compelling activities as a single agent in relapsed or refractory patients.
Now in the updated data to be reported at ASH this year, 16% of the patients had a partial response with a median duration of greater than 8.4 months. This data, this single agent data is highly comparative with a single agent data presented on other drugs and heavily pre-treated refractory patients. It's been previously observed, as with pomalidomide, that the addition of DEX could enhance the response rate and the durability of response and relapsed and refractory in myeloma patient. With this in mind we initiated combination of trial of ARRY-520 with low-dose DEX in patients who were documented triple-refractory to IMiDs, bortezomib and DEX itself.
In the data to be reported at ASH this year, patients enrolled in the 520 study were more heavily pretreated than most studies reported to-date with a remarkable median number of 10 prior regimens. OK we observed a partial response rate of 22% for the combination of 520 index in these patients with enhanced time on study relative to single agent alone. The safety profile in the single agent and combination arms were similar arms were similar. This response rate was comparable to the response rate seen when pomalidomide was combined with low dose DEX as seen in this table. During our evaluation of the PKPD and response relationships for drug treated patients, we evaluated the binding of 520 to readily measure plasma protein. Binding of drugs to plasma protein has been shown to affect the response rates of other cancer drugs like Gleevec and Docetaxel. By selecting for patients who had non-elevated levels of the plasma protein AAG we could enhance the partial response rate to a full 33% more mature data regarding the duration of response and the time on study will reported at the meeting.
Now on slide 10, we are talking a little bit about AAG or alpha-1 acid glycoprotein. It is a member of class of plasma proteins that can be up regulated in diseases like multiple myeloma. 520 was found to bind reversibly to AG whereas other marketed myeloma agents were not shown to interact with the protein. The binding of this protein may have an effect on response seen in cancer studies. High levels of AGG and patients will decrease activity of drugs that bind strongly to AGG resulting in shorter time on study and decreased response rates. Since AAG is readily measured prior to the treatment of multiple myeloma patient. In fact patients with non-elevated AAG can be selected with the expectation of higher response rates for 520 treated patients.
Now turning to slide 11, ARRY-520 has a unique mechanism of action so we’re summarizing. Here is one might expect for a novel target given differing resistance mechanism, we have demonstrated durable response as a single agent in relapsed and refractory patients with minimal non-hematologic side effects. The combination of 520 with DEX increase the overall response rate in particularly heavily treated patient population relative to the single agent data as expected without comprising safety in patients who have few or no other treatment option.
By selecting patients with non-elevated AAG we can enhance response rates and ensure that only patients who are likely to benefit from 520 will in fact be treated. Finally, more mature data and data on more patients from our 520 with carfilzomib study will be reported, showing that the combination has manageable safety, has a manageable safety profile and encouraging early signs of efficacy.
On slide 12, we are pleased with the results regarding 520 and the recent approval of carfilzomib has in fact provided clarity regarding the regulatory hurdles for late stage multiple myeloma. We have three trials ongoing all of which provide potential paths to approval that would be a ARRY-520 with DEX and dual refractory patients 520 with elcade or bortezomib in relapse refractory patients of 520 with carfilzomib and relapsed refractory or refractory or intolerant to bortezomib patients. Given the appropriate results from our ongoing study we anticipate pivotal trials to initiate in 2013.
And so that represents the exciting and new information on our 520 multiple myeloma program. I’m just going to touch briefly or more briefly or ARRY-614 in in myelodysplastic syndrome. Also, on Slide 14 as you can see a very large patient population over a 150,000 patients and the disease is in fact a syndrome of aberrant cell death in the bone marrow of typically elderly patients.
The transformed cells within the bone marrow are called blasts, and aberrant cell death leads to the decrease in cells such as platelets, neutrophils and erythrocytes, which lead ultimately to a wide range of disease such as fatigue, bleeding, cardiovascular issues and infections. There are significant quality of life and economic burden associated with the disease including costly and frequent transfusions ultimately the disease progresses to AML disease progresses to AML, which is lethal, and there are limited treatment options in this populations. There are actually has been very little work on the disease, only in last few years have people really recognized the size of the patient population and the unmet need including the very high economic burden.
And so we actually have seen an increase I diagnosis with greater awareness and on slide 15, we have targeted with 614 initially, patients who are low risk in Int-1 which represents the majority of MDS patients and specifically have focused early studies on HMA failures. After HMA failures these patients have no other approved treatment option and simply receive supportive care including significant amount of transfusions.
The prognosis for these patients are very poor, there is a published data out there representing median survival of sort of in the range of 12 to 15 months, so very poor prognosis specifically in the Int-1 HMA failure population and in fact at ASH there is a publication expected from Moffitt/M. D. Anderson on their database indicating that while using the IP as a scale they are also sort of confirming that median survival above 15 months. So extremely poor prognosis for these patients with a no real approved therapeutic option. On 16 we recount our data from ASH last year where we saw full nearly 40% HI rate response rate at our highest dose and these are patients which you would not expect to see any spontaneous response at all at the highest dose. We also saw a greater than 2/3rds multi-lineage response. So more than two types of cytopenias impacted. On 17, we also recount our data indicating what appears to be clear disease modification as we see a decreased aberrant cell apoptosis upon additional cycles of 614. Now moving on to slide 18, what we are doing at ASH is providing an update of our formulation work and PD markers that will be further described at the meeting this year.
We will show that formulation has roughly tripled the bioavailability of the older formulation where we saw a bit of pill burden or capsule burden in that study at the highest dose. We have also observed improved intra and inter patient variability and we will also report further confirmatory data on our biomarker work and we will report on interim clinical data using the new formulation. So we’re very pleased with the clinical result of the initial formulation and we continue to be encouraged with the performance of the new formulation going forward and in fact on slide 19, we just summarized as a dual P38 Tie 2 inhibitor with a unique mechanism of action. We are excited about the potential for impact in this disease. As far as we know there are no other trials ongoing in this particular patient population of low-blast count and multiple cytopenia that have failed hypomethylating agents. We did demonstrate for that very nearly 40% very strong and response rate at our highest dose and we demonstrated PD effects that are consistent with bone marrow normalization which is a very powerful disease modifying effect with the drug. The compound was certainly well tolerated up to 1200 milligrams q.d and we are currently conducting our Phase IB to evaluate the new commercial formulation and plan to meet with the FDA this year to talk about registration endpoints for this exciting program.
So as you can see we have been carefully narrowing and this is statement we made at our last two quarter calls, we are carefully narrowing our internal focus specifically on development and commercialization of our wholly-owned hem/onc programs -- our internal focus. So we look forward to presenting further data at ASH and hope to see you there and this concludes the prepared portion of our presentation. And with that I will turn the call back to the operator for Q&A.
(Operator Instructions). At this time we have a question from Eun Yang from Jefferies. Please go ahead.
Eun Yang – Jefferies
Questions on 520, you mentioned that the duration of response data while you presented on ASH. So can you talk a little bit of reference and based on the 33% response rate, what kind of duration of response that you would expect little while to see?
And so I think the 33% you’re referring to is with the AAG cut, OK so I’m going to turn this over to Kevin to give you whatever color we could about duration. Although that may be challenging.
The abstracts were not supposed to really release, thing that are not in the abstract but we know we saw a duration of eight months in patients with only six prior median therapies. These patients were the median of 10 prior therapies and were strictly triple refractory with other agents it's typically on the order of only four months in this patient group and in double regimes. We would anticipate somewhere you know north of four to five months would be interesting. Of course we would hope for that it would be out in the eight month range which would really provide a significant patient benefit. Now I should point out again with 520 is that the response takes as much as three or four months to fully mature.
So in reality these patients maybe on as much as a year when they do have responses and that I mean the total time on study, I think is an important factor in determining the benefit of these patients.
So let me add to provide context to your and we referred sort of precedent sent by carfilzomib with the recent ODAC recommendation and approval. And we continue to suggest that a response rate in the sort of 20% to 25% range and a duration of sort of 8 to 9 months qualify for accelerated approval and we would assume that would be true, certainly anything better than that would even raise the or smooth the path and that can certainly provide us an opportunity to get to market and treat the heavily pre-treated refractory patients. We are very much, though looking forward to our carfilzomib data and maturing and certainly would hope it would be positive because we believe that with carfilzomib and ultimately, bortezomib, as our data emerges we will have the opportunity to move certainly further upstream by combining with and providing a synergistic benefit to those patients. So we kind of think DEX as the way to market quickly and then see a lot of earlier line and great commercial line of longer durations in combination with carfilzomib and bortezomib.
Eun Yang – Jefferies
Sure and then in the (inaudible) multiple myeloma about 51,000. If you look at the AAG elevated patient population, what percent of those 51,000 will there either have an elevated AAG level.
From what we know from the literature and this has been studied to some extent but not extensively, we would anticipate about a third of the patients would have elevated AAG.
Eun Yang – Jefferies
Would you actually in your registration trials, would you actually select a patients based on AAG levels?
Well that’s under study and we have not made a decision on whether we would actually use that as a selection marker or would we recruit both groups of patients and use it as have a dual primary end point.
Eun Yang – Jefferies
Okay and in terms of primary end point for registration trials for 520 I’m assuming that it's going to be response rate and the duration of the response but for 6012. Is it that same online number that I’m looking at?
614 you mean?
Eun Yang – Jefferies
Yes 614 and yes would you use over (inaudible) as a primary end point?
So our current plan Eun is to speak to the FDA about HI hematologic improvement -- which is a composite measure. As a full approval we have spoken to quite a few experts and thought leaders in this area and believe there is a very strong argument to be made about the very substantial clinical benefit of hematologic improvement. There is a possibility that we will also discuss if needed with the FDA which is to use HI as a surrogate endpoint and perform a confirmatory study in OS if that’s required but we would make the argument that HI is a very important endpoint in itself. There we go.
Yes and I think there is actually new data from an abstract ASH describing the differences in survival for patients with low to intermediate one MDS and patients that have who are transfusion dependent, have almost a 4X increase or decrease in overall survival. So they having transfusion independent is a very major risk factor for progress in low risk and intermediate one risk MDS. So I think that’s more data to confirm from the ASH presentation that decreasing transfusion rate is very important and we believe HI and transfusion rate are very similar and will be important in the discussions with the FDI. The more data that comes out talking about how HI is a surrogate for survival the better off we are.
Thank you. Our next question comes from Howard Liang from Leerink Swann. Please go ahead.
Howard Liang - Leerink Swann
I have probably three varied questions, first, is AAG saturable? In other words, can high-AAG be overcome by -- with a higher dose? Second, is do we know whether AAG is a prognostic in multi-myeloma and lastly if you understand why 520 to AAG.
Okay so I will take the last one first. I think that’s probably a physiochemical property of the drug, of course, it's a basic drug binding with a an acidic glycoprotein. So that’s probably one rationale but that’s probably a property of the drug.
In regards to the prognostic factor of the AAG prognostic for progression, I would say that it's mildly linked but not linked as well as CRP, IL-6 or beta-2 microglobulin. So I would say that that data is not all that strong that AAG levels will predict progression but there is maybe some evidence I think there is evidence on both sides. And the third question was – and we will report data in the poster with a direct correlation of AAG levels and 520 activity and so that yes you could increase the dose of ARRY-520 and you might be able to overcome that and that would of course require Phase I dose titration study, which we would ultimately do as a post marketing strategy.
Howard Liang - Leerink Swann
Let’s follow-up on that, so if that was the case do you envision doing both sets of patients two-thirds with high-AAG, you would use regular dose than the one third with high…
I don’t anticipate that will be a path we would take initially. It's certainly something that we would want to study in subsequent trials, but the initial path we will go is rapidly as we can to registration and which I think to if you know as successful we would initiate the carfilzomib combination study to drive towards a complete approval. And that I think is important goal.
Howard as Kevin indicated you know fortunately the vast majority of patients would still be eligible based on this selection market. So we are selecting for the majority of patients and only would be deselecting a small relatively small number but with potentially substantial improvements in our profile so we are excited about that.
Thank you. Our next question comes from Stephen Willey from Stifel Nicolaus. Please go ahead.
Stephen Willey - Stifel Nicolaus
Kevin I know you mentioned the kinetics around 520 responses you have seen today. Is it safe to say that by adding on these additional agents whether it be DEX or carfilzomib that we are seeing those kinetics accelerate with respect to time to response.
I would say Steve I don’t think we have enough data to be able to say definitely. Yes I would say somewhat more rapidly but at this point I don’t think I can say.
Stephen Willey - Stifel Nicolaus
Can you also confirm and I understand that you guys are constrained with respect to what you can or can’t say but can you confirm that you have seen responses at least in the cohort 2 in combo with DEX and with carfilzomib and patients that have (inaudible).
We will have all of that data at the ASH poster and I’m very enthusiastic and optimistic about the possibility of combining carfilzomib with 520 and you have to wait for the data though.
Yes the timing of the submission of the carfilzomib data was such that I think it points to a manageable safety profile but was certainly too early at that point to provide insight on efficacy and so right as Kevin said. We are looking forward to seeing more robust and mature data and more patients at the actual meeting and so we know we continue to be optimistic about carfilzomib as an additional path on top of the sort of DEX accelerated approval path as we go forward with the program.
Stephen Willey - Stifel Nicolaus
And then just one more, is the next dose escalation core within the carfilzomib trial going to be at 1.25 mg per meter squared and I guess just given the fact that it looks like you had I believe what is in and your complete response at the 0.75 dose. Do you feel like you need to maybe step on the doses as hard as you’re in the DEX combo and would you be willing to maybe trade off a little bit of the drug activity to kind of abate some of the hematological talks.
I think that we’re satisfied with the toxicology. We have done kind of a head to head comparison with some of the other agents that are approved of carfilzomib and what we know of the AE profile of the pomalidomide/DEX combination. And we are as good or better. We have patients that have been on study from greater than 12 months as a single agent. We are now patients who have been quite a while in the DEX study which we will report and we are quite happy with the safety profile today and I think that we will be able to report those at the ASH presentation.
Stephen Willey - Stifel Nicolaus
It is the next dose cohort in the carfilzomib combo study 1.25?
Yes and the MDT (ph) is a single agent for ARRY-520 is 1.25 mg per meter squared and we have virtually identical schedule as the carfilzomib schedule. So I think it works up very well for us.
Thank you. Our next question comes from Cory Kasimov from JP Morgan. Please go ahead.
Matt Lowe - JP Morgan
Hi there it's Matt Lowe in for Cory today. I’m just wondering at what point do you think you may need a partner for the registration program I guess how many Phase III studies you think you can take on yourselves and I guess I’m indicating well including kind of lifestyle studies in this also. Thanks.
So at this point as you known as we have stated these programs both 520 for multiple myeloma and 614 for MDS are wholly-owned. Currently our plan is with our now internal focus on hem/onc, to take these forward on our own and if there was a population to pick in going at loan you would want to pick hematology within oncology and oncology in general. So we believe these studies especially the initial studies that are focused on accelerated approval and combination with DEX and potentially also in combination with carfilzomib. We believe these are manageable on our own. Although I will say our relationship with Onyx is positive and we have had discussions about co-founding or sharing the cost of trials going forward, but you know it is our intention to maintain these programs as wholly-owned at this point and take them to commercial stage on our own but you know we will certainly consider that as we move forward specially from some of the geographies that are outside of let’s say U.S. and Europe and we will continue to assess that as we progress forward and you know we will see how that goes but that’s our current plan. Does that help Matt?
Thank you. (Operator Instructions). And at this time I show no additional questions. I will turn the call back to Ron Squarer for closing remarks.
Great. Well thank you all for listening in and for providing questions today. Again we have a lot going on within Array, a lot of momentum and a lot of activities. Today we have provide an update on our single agent data with 520 and heavily pretreated patients indicating it is comparable to other newer agents in the space. We have also indicated the favorable impact of adding DEX in a unusually heavily pretreated patients this is patients 10 median lines of prior therapy.
Also the further potential positive impact of utilizing AAG is a very broad selection marker and some early insight into carfilzomib and an indication that we will expect to have more robust data pointing towards efficacy results at the meeting itself. Just because of the timing we also informed you about a another Phase II program, the toll-like receptor 8 with VentiRx, bringing our total Phase II count at this time 11 and very exciting disease modification data that we indicated or the biomarkers related to disease modification in OA and the late breaker that was accepted at ACR and so we look forward to speaking to you about that in the future and I will also remind everyone on the call to mark the Thursday morning Novartis R&D Analyst Day on the calendars and listening to see what kind of update they may provide on MEK162 which, as I indicated our MEK inhibitors do drive a lot of our value and that is our most valuable deal from a deal terms of point of view, royalty point of view between the two deals although they are both AstraZeneca and Novartis are attractive. So with that all of us on the call here at Array would like to thank our employees for their commitment, ingenuity and diligence that continue to fuel Array's success. I also want to thank our patients, partners and shareholders for their continued confidence and support. Thank you very much and with that I will close the call.
Thank you ladies and gentlemen. This concludes today's conference. Thank you for participating. You may now disconnect.
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