Infinity Pharmaceuticals, Inc.
Q1 2016 Earnings Call Transcript

Published: 5 May 2016

[Operator:]

Ladies and gentlemen, thank you for standing by. Welcome to the Infinity Pharmaceuticals Conference Call to discuss the Company's Financial Results for the First Quarter of 2016. My name is Kevin, and I'll be your operator for today. At this time, all participants are in a listen-only mode. There will be a question-and-answer session to follow. Please be advised that this call is being recorded at Infinity's request. At this time, I would like to introduce your host for today's call, Ms. Jaren Madden, Senior Director of Investor Relations and Corporate Communications at Infinity. You may begin, ma’am.

[Jaren Madden:]

Thank you, Kevin, and good afternoon, everyone. Welcome to today's call to discuss our recent business progress and review our first quarter 2016 financial results. With me here today are Adelene Perkins, President and Chief Executive Officer; Julian Adams, President of R&D; and Larry Bloch, EVP, Chief Financial Officer and Chief Business Officer. Following our remarks, we'll open up the call for Q&A. The press release issued earlier today details our results and is available on our Web site at infi.com. Please note that during this call we may make forward-looking statements about our future expectations and plans, including clinical development milestones, the therapeutic potential of our product candidates and financial projections. It is possible that our actual results may differ materially from what we project today due to the considerations described in the Risk Factors section of the quarterly report on Form 10-Q for the first quarter of 2016. While these forward-looking statements represent our views as of today, they should not be relied upon in the future as representing our event’s current views. We may update the statements in the future but are not taking on an obligation to do so. Now, I'd like to turn the call over to Adelene.

[Adelene Perkins:]

Thanks, Jaren. Good afternoon, everyone, and thank you for joining us on today’s call. 2016 is the year of results for Infinity, as we work to advance medicine with the potential to meaningfully impact patients’ lives. While there has been considerable progress in the treatment of patients with B-cell malignancies like indolent non-Hodgkin lymphoma or iNHL and chronic lymphocytic leukemia or CLL, there is still a significant need for new therapy that can provide these patients with deeper and more durable response and an acceptable safety profile. Our goal is to address this need and we are on track to report top line data from two registration-focused studies of duvelisib, an investigational dual inhibitor of PI3-kinase-delta and gamma with first in class potential. We anticipate reporting top line data from DYNAMO, a Phase 2 monotherapy study of duvelisib in patients with relapsed/refractory iNHL early in the third quarter of this year. We also expect to report top line data predicated on a PSF interim analysis from DUO, a Phase 3 monotherapy study of duvelisib in patients with relapsed/refractory CLL early in the second half of the year. These data, if positive, could enable regulatory submissions in the U.S. and Europe in the fourth quarter of 2016. In parallel with our preparations for data readouts and regulatory submissions, we are planning for a potential 2017 launch of duvelisib. In addition, to the potential to address patient needs through results from DYNAMO and DUO, we have the opportunity to address additional patient need and further differentiate duvelisib through other clinical studies ongoing across multiple indications and lines of therapy. To that end, initial data from CONTEMPO, a Phase 1b/2 study in first-line follicular lymphoma patients evaluating duvelisib plus Rituxan and duvelisib plus Gazyva will be presented in a poster session at the 21st Congress of the European Hematology Association or EHA in Copenhagen next month. In addition to duvelisib we are independently advancing IPI-549, an oral immuno-oncology development candidate that selectively inhibits PI3 kinase-gamma. IPI-549 represents an important extension of our oncology portfolio into solid tumors. Earlier this year, we initiated the first Phase 1 study of IPI-549 and are pleased with the progress we are making. Preclinical data supporting the rationale for combining IPI-549 with checkpoint inhibitors was recently presented at AACR, which Julian will review shortly. In summary, 2016 results are critical to advancing Infinity’s goal of bringing important medicines to patients and we expect to deliver the following seven significant milestones during the year. First, report top line DYNAMO data early in the third quarter. Second, report top line DUO data early in the second half predicated on the results of the planned interim analysis. Third, submit our NDA for duvelisib in the fourth quarter. Fourth, submit the MAA for duvelisib by AbbVie also in the fourth quarter. Fifth, report initial data from CONTEMPO, our Phase 1b/2 study in treatment naïve patients with follicular lymphoma at EHA. Sixth, advance the Phase 1b/2 study of duvelisib in combination with venetoclax, AbbVie’s BCL-2 inhibitor. And our seventh big milestone for 2016 is to advance the Phase 1 study of IPI-549 in solid tumors. With that, I’ll turn the call over to Julian to review our development programs in more detail.

[Julian Adams:]

Thank you, Adelene. I too am excited about the progress we are making as we work toward our goal of bringing duvelisib to the physicians and patients. Duvelisib has a distinct profile from our B-cell receptor inhibitors because it inhibits both PI3-kinase-delta as well as PI3-kinase-gamma. PI3-kinase-delta inhibition primarily targets the malignant B-cells and PI3-kinase-gamma inhibition primarily disrupts the tumor micro environment. It is our hope that targeting both malignant B-cells and the tumor micro environment could meaningfully improve outcomes for patients living with B-cell malignancies. Our enthusiasm for duvelisib is based on data from our Phase 1 study where we observed broad activity across a range of hematologic malignancies, including profound activity in patients with iNHL and CLL. These data led us to initiate our first two registration-focused studies of duvelisib; DYNAMO and DUO. As Adelene mentioned, we are on track to report top line data from DYNAMO early in the third quarter. This is a Phase 2 monotherapy study designed to evaluate the safety and activity of duvelisib in approximately 120 patients with double refractory iNHL. The primary endpoint is overall response rate. If the data are strong, we intend to seek accelerated approval with FDA. In relapsed refractory iNHL, double refractory patients have limited treatment options. We believe that duvelisib could address an important need for these patients. Our second potential path to approval is through DUO, our Phase 3 randomized monotherapy study of duvelisib in approximately 300 patients with relapsed/refractory CLL. This study is designed to evaluate the safety and efficacy of duvelisib compared to ofatumumab, an anti-CD2O antibody. The primary endpoint is progression-free survival or PFS. This study has an event driven interim analysis for PFS which we expect will occur early in the second half of 2016. We believe that duvelisib may offer patients with relapsed/refractory CLL the first PI3-kinanse monotherapy treatment option without acquiring combination with Rituxan. Before I review the rest of our clinical study trials for duvelisib, I will briefly comment on patient management in our studies. We have comprehensive risk mitigation measures in all of our studies including routine safety analysis. It is known as a result of the underlying disease patients with iNHL and CLL are prone to infections. To further protect against the risk of certain infections, we included prophylaxis for all patients in our DYNAMO and DUO studies and are now including prophylaxis for all patients in our other studies underway. Turning now to a review of our other ongoing clinical studies of duvelisib. These trials support our strategy of evaluating the safety and activity of duvelisib in broader patient populations. We are conducting BRAVURA, a Phase 3 double-blind, placebo-controlled study in approximately 600 patients with relapsed iNHL. This study is designed to evaluate the potential of duvelisib to improve upon chemotherapy by evaluating safety and efficacy duvelisib plus Rituxan and bendamustine compared to placebo plus Rituxan/bendamustine. The primary endpoint is PFS. To evaluate the opportunity to eliminate chemotherapy for some patients, we are conducting the FRESCO study. An analysis from several studies of patients with follicular lymphoma have demonstrated that approximately 20% of patients progress within two years upon initial diagnosis and treatment with R-CHOP, a chemotherapy cocktail commonly used for the treatment of follicular lymphoma. And that early progression is associated with significantly short survival. Given the unique and targeted biological mechanism of action for duvelisib, we are evaluating whether we can address an important medical need for these patients who do not have durable responses to chemotherapy. This Phase 2 study is designed to evaluate the safety and efficacy of duvelisib plus Rituxan versus R-CHOP in approximately 230 patients with follicular lymphoma who relapsed within two years. The primary endpoint is progression-free survival. Additionally, we are evaluating duvelisib in frontline therapy. CONTEMPO is an ongoing Phase 1b/2 study in treatment-naïve follicular lymphoma patients. This study is designed to evaluate the safety and activity of duvelisib in combination with Rituxan or Gazyva, two anti-CD20 antibodies. The primary endpoint includes safety measures and complete response rate. We are pleased to announce today that initial data from this study has also been accepted for presentation in a poster session at EHA next month. An abstract describing these data was also accepted by ASCO for online publication. We are also continuing to enroll patients in our SYNCHRONY study designed to evaluate duvelisib in combination with Gazyva and patients with CLL who were previously treated with a BTK inhibitor. The post BTK setting represents a significant medical need as there are limited treatment options for these patients who progress on or who are intolerant to do a BTK inhibitor therapy. We believe the best chance for transformation outcomes for patients with hematologic malignancies is through the combination treatment particularly by combining novel targeted therapies. AbbVie has initiated a Phase 1b/2 clinical study of duvelisib in combination with venetoclax, their BCL-2 inhibitor. This is a comprehensive study designed to evaluate the safety and efficacy of the combination in approximately 174 patients with relapsed or refractory iNHL, aggressive NHL, small lymphocytic lymphoma or CLL. The rationale for this study is based on extensive preclinical research where we observed strong synergy between duvelisib and venetoclax. Our commitment to innovation and improving patient care has led us to broaden our oncology portfolio into solid tumors with a new and exciting approach in immuno-oncology. At the AACR meeting last month, Infinity researchers in collaborations with Memorial Sloan Kettering Cancer Center presented new preclinical data for IPI-549, our potential first in class PI3-kinase-gamma selected inhibitor. The data demonstrated that IPI-549 targets immune cells and alters the immunosuppressive micro-environment promoting an anti-tumor response that leads to tumor growth inhibition. This data also demonstrated that IPI-549 enhances the effects with checkpoint inhibitors resulting in an improved survival in multiple murine models. To evaluate immune memory, mice that achieved complete responses following IPI-549 plus anti-PD1 antibody therapy were then re-implanted with the same tumor type. These animals showed low or no tumor engraftment indicating that they were immunized against the recurrent tumor growth, a significant preclinical finding. These preclinical data provide the additional rationale for our ongoing Phase 1 study of IPI-549. The first portion of this study includes a dose escalation phase to evaluate a recommended dose for IPI-549 as monotherapy and in combination with an anti-PD1 antibody. Once dose escalation is complete we are planning an expansion phase of these patients with select solid tumors, including non-small cell lung cancer and melanoma. We will evaluate IPI-549 in combination with an anti-PD1 antibody. This study is progressing well and we now expect to initiate its expansion phase later this year. In conclusion, we have a number of important milestones as we head into the second half of this year and I look forward to reporting key data over the coming months as we work towards regulatory filings in 2016 and prepare to potentially bring duvelisib to patients in 2017. With that, I will pass the call over to my friend, Larry.

[Larry Bloch:]

Thanks, Julian. I’ll now provide an overview of financial results for the first quarter of 2016. As of March 31, 2016, we had total cash, cash equivalents and available-for-sale securities of $193 million compared to $245.2 million at the end of 2015. We anticipate earning $200 million in regulatory milestones from AbbVie in the fourth quarter of 2016. This includes a $125 million milestone associated with the acceptance of our planned NDA filing, and a $75 million milestone on acceptance of AbbVie’s planned MAA filing. While the acceptance of these submissions are expected to occur in the fourth quarter of 2016, the payments of these milestones will likely not occur until the first quarter of 2017. Excluding the $200 million in anticipated milestones, we expect to end 2016 with a cash and investment balance ranging between $45 million and $65 million. While our collaboration with AbbVie is designed to fund development of duvelisib, it is not intended to fund IPI-549 or early discovery programs. Today, we filed a $50 million at-the-market or ATM offering program to provide us with the option in the future to issuing sell shares of Infinity from time to time, which consisted with our philosophy of maintaining financial optionality. Turning to our financial results for the first quarter of 2016, revenue during the quarter was $9.3 million for R&D services associated with the collaboration with AbbVie. Revenue during the first quarter of 2015 was $4.4 million also for R&D services associated with the collaboration with AbbVie. R&D expense for the quarter was $39.2 million compared to $88.4 million for the same period last year. R&D expense for the first quarter of 2015 included a $52.5 million payment related to exercise of an option to buy out the company’s royalty obligations to Takeda Pharmaceutical Company Limited for duvelisib worldwide oncology sales. Excluding the option exercise, the increase in R&D expense for the quarter was primarily due to higher clinical development expenses for duvelisib as well as increases in staffing. G&A expense for the quarter was $10.8 million compared to $8.6 million for the same period last year, primarily related to an increase in staffing as well as external commercial expenses in preparation for the potential 2017 duvelisib launch. Net loss for the first quarter was 40.7 million or a basic and diluted loss per common share of $0.82 compared to net loss of $93.3 million or a basic and diluted loss per common share of $1.91 for the same period last year. Our financial guidance for 2016 remains unchanged. In closing, we expect 2016 to be a foundational year of progress for Infinity. We expect important data this year that if positive will enable us to file approval with regulatory authorities in the U.S. and will allow AbbVie to file for approval in Europe. We also continue to make progress with IPI-549, our immuno-oncology candidate for solid tumors. We are confident we have the elements in place to bring duvelisib to patients and to make a meaningful difference in their lives. With that, we’ll open the call for Q&A. Operator?

[Operator:]

[Operator Instructions]. Our first question comes from Michael Yee with RBC Capital Markets.

[Michael Yee:]

Hi. Good afternoon, guys. For Julian, I have two topics I want to get some clarification on. The first topic was on the side effect profile of the drug. I know there’s a lot of Wall Street focus on trying to differentiate from Zydelig and a couple of things that people are trying to think about are infections, colitis, I guess, maybe hepatotoxicity. On infections, I know you’re prophylaxing but do you expect your drug to be different than Zydelig on colitis and hepatotoxicity. And can you remind us if that’s a key thing we’re going to be looking at? And why do you expect it to be different? And then secondly on CLL, you have a pivotal study that could possibly readout later in the second half. When I look at the control arm, I think that’s about eight months of PFS but Zydelig plus BR [ph] was 10.7. Can you explain to me what the one or two data points are that would support why your drug would be significantly better, just remind us on that what we should be looking at? And then lastly, would you say in your press releases whether you intend to file and would that be pretty clear to people? Thanks.

[Adelene Perkins:]

Mike, this is Adelene. Let me start on some of your questions and then I’ll turn it over to Julian to add additional perspectives around safety. And we just can’t emphasize enough that protecting the safety of our patients and our trials, which are of course intended to show the benefit of our drug is our number one priority. So, we followed closely the information that’s been made available regarding Gilead’s termination of certain drugs with Zydelig. And although we watched that, I want to remind you of two very important differences. One is that our medicines are different. Not only are they different chemical entities that are administered at very different doses but they also have different mechanisms of action. As you know, duvelisib inhibitor of both PI3-kinase delta and gamma whereas Zydelig is an inhibitor of just PI3-kinase delta only. And second, the drugs have been developed very differently. Patients with blood cancers have compromised white blood cell function, compromised immunity and are prone to infections. So to protect patients who all are vulnerable to infections, we instituted prophylaxis for all of our patients in DYNAMO and DUO and as Julian mentioned earlier are including prophylaxis in all of our trials going forward. So the data that was reported with Zydelig and their studies was that just 15% to 30% of patients were prophylaxed. So as a result of the fact of these different drugs, different doses, different mechanisms, different patient management strategies, we think the most useful way to address duvelisib is on the data that we are generating duvelisib itself. And with that, I’ll turn it over to Julian to talk about our experiences with our ongoing safety monitoring in DYNAMO and DUO.

[Julian Adams:]

Yes. Michael, so thanks for your question. I also want to – to Adelene’s comments that we have a regularly planned independent data monitoring committee, external reviews that happen quarterly that monitor the safety for our patients. And we believe that two things are important in the management for safety for our patients. One, as Adelene mentioned prophylaxis which we’ve instituted for all studies but also there’s a patient management strategy, which for the indolent diseases like iNHL and CLL, if we see a developing grade 3 toxicity, we can pause the drug, allow the adverse event to resolve and allow up to six weeks for that to occur and then we can re-challenge patients with the same dose of duvelisib. And I believe that this patient management has served us well over the conduct of the DYNAMO and DUO studies. And so we are proceeding with this believing that we are at the dose as scheduled and this is how we’re proceeding with future trials as well.

[Michael Yee:]

Okay. So do you think that they’ll be better protection against that? And I’m not really sure how to quantify that, but will wait to see the data. But also on the colitis and hepatotoxicity, I think you’re probably doing a good job on the infections. We’ll take that and we’ll see the data. But colitis is certainly a big issue as well I think just commercially too. So is there any reason to believe that that’s a differentiation as well? Just want to try and understand and tease [ph] out some of these things?

[Julian Adams:]

Yes, and the premonitory sign of colitis is the developing diarrhea which if unchecked becomes an immune base – autoimmune disease resulting in colitis, autoimmune colitis. And so we monitor patients very carefully and we have guided our investigators to immediately stop the drug and to --

[Michael Yee:]

Got it.

[Julian Adams:]

Manage those patients allowing also oral nonabsorbable steroids and we have found that in general, this is a very effective way to mitigate against GI.

[Michael Yee:]

Got it, okay. Turning to the --

[Julian Adams:]

Turning to CLL I think you have stated that ofatumumab on the expectations about eight months PFS and you asked what gives us confidence with monotherapy. I can only refer to our Phase 1 data where we have not achieved median PFS after 24 months. And so we – based on the encouraging results from the Phase 1 population, which admittedly is not the same as running a randomized Phase 3 study, we projected that monotherapy was an appropriate way to go up against ofatumumab.

[Michael Yee:]

Got it. And then disclosure, the last part of your question was just disclosure. Would you say you’re filing this stuff pretty clearly if the data is in your expectations? That’s something I think the Street will want to know?

[Adelene Perkins:]

You’re talking about regulatory filing?

[Michael Yee:]

Yes. You expect to file, so if the data is at your expectation, would you be able to tell Wall Street in your press releases that you intend to file, because I’m sure it is an important milestone because that would be an important thing for us to understand.

[Julian Adams:]

So we have to have of course a conversation with FDA about filing strategies and so as long as we have that appropriate communication, we intend to file DYNAMO based on this – as we’ve said on a single-arm study, based on the intention of an accelerated approval. In the filing with DUO, it’s predicated on a successful achievement of the interim analysis hazard ratio.

[Michael Yee:]

Okay. Thank you.

[Adelene Perkins:]

Thank you.

[Operator:]

Our next question comes from Katherine Xu with William Blair.

[Katherine Xu:]

Hi. Good afternoon. So, Adelene, when you say one study comes out in early Q3 and the other one comes out in early second half, are they pretty much the same timeframe?

[Adelene Perkins:]

Katherine, we have said in the past that they could be within very close proximity of each other and I think that’s a reasonable expectation.

[Katherine Xu:]

Okay. With regards to the safety management of duvelisib, it looks like the prophylaxis was implemented kind of halfway in a Phase 1/2. Just curious from your experience, did you see a difference prior and after of the implementation of prophylaxis in terms of the action rate?

[Julian Adams:]

Yes, so we’ve reported on our Phase 1 data and don’t want to revisit ancient history but we did have observed infections without prophylaxis and upon observing these infections, we have instituted prophylaxis. And we believe that this is the proper runway to manage these patients.

[Adelene Perkins:]

And the only thing that we do say about DYNAMO and DUO for which all patients have been prophylaxed is that as Julian mentioned the independent data monitoring committee has reviewed those patients and encouraged us to continue with the trial. But we can’t speak to specific infection rates in those trials until we have that data.

[Katherine Xu:]

Yes, I’m curious. Phase 1 last year after the implementation, did you see a pronounced difference in infection rate?

[Julian Adams:]

So, again, we have published the data and --

[Katherine Xu:]

[indiscernible]

[Julian Adams:]

Yes, we have published these data and we do not see infectious data upon prophylaxing patients. So we believe that that was the right measure. As well we amended the protocol to institute dose interruption for any adverse event. And I mentioned that we’ll allow six weeks to resolve the adverse event so that we can successfully re-challenge these patients at full dose. And we believe that this has been the appropriate way to manage this patient population.

[Katherine Xu:]

Okay. And then the other I guess characteristic of Zydelig is that the safety gets worse when it moves frontline. So I’m just curious – of course you’re reporting data on CONTEMPO soon, but from what you see so far, for example, DYNAMO and that’s second line refractory setting kind of study and it’s pretty much single arm. So you have some observations there versus your CONTEMPO. Do you see any differences on the safety side, relapses --?

[Julian Adams:]

We’re under embargo for the EHA presentation, so if you can make the trip to Copenhagen, I certainly invite you there to come and see the data. Again, I think we would implement the appropriate patient management schema in all of our trials.

[Larry Bloch:]

Also Julian, I like you all to travel to Copenhagen. There will also be an abstract online for ASCO and EHA on May 18, 19, respectively. So just a few weeks, we’ll have the beginning of that data stream.

[Adelene Perkins:]

But we’d also warn that your expectations that it’s early data. But of course we’ll be updated by the time we have a poster, but we’ll have several dozen patients and with relatively early exposure. So it’s an evolving data set.

[Julian Adams:]

So we’re very excited on the opportunity to explore duvelisib in frontline setting as you alluded to.

[Katherine Xu:]

All right. One last question is more on the science. So recently AbbVie just bought this company Stemcentrx, the lead asset is [indiscernible] expressing certain cancer stem cells. I’m just wondering any – from a biology perspective any interactions with the PI3 pathways, additives, synergistic or just not too much interaction.

[Julian Adams:]

This is fresh news to us as well. I followed this antibody drug conjugate. Primarily there’s a bright expression on these neurons [ph], tumors, small cell lung cancer and the toxin of course is the cargo to kill these cells. So I think the purpose of this antibody is simply to kill cells in small cell lung cancer based on early data. And so we’ve had no other interaction with – knowledge of PI3-kinase activity.

[Katherine Xu:]

Thank you.

[Operator:]

Our next question comes from Jim Birchenough with Wells Fargo.

[Unidentified Analyst:]

Hi. This is actually Ian [ph] in for Jim today. We have a few questions on the 549 program. First, have you talked about the timing for the data from the PD1 combo study yet?

[Julian Adams:]

We’ve just announced this afternoon that we expect to begin the expansion cohorts in the second half of this year. So we are pleased with the way that Phase 1 has progressed thus far but we’ve not really sent the data or discussed anything with IPI-549. But that would be forthcoming with more data.

[Larry Bloch:]

I’ll remind you. We just started the Phase 1 in the beginning of this year, so it really has been – we’ve been very pleased with the progress we made to-date.

[Unidentified Analyst:]

Yes, got it. And in terms of the outcome data, obviously this is single arm study studying the combo and PD1 is expected to have some activity as well. So how should we think about potential outcome of the data, any in particular? I’m interested in if you are examining some biomarkers in terms of the phenotypes of the macrophage and whether there is indeed M2 to M1 condition in the study? Thanks.

[Julian Adams:]

It’s an excellent question. First of all, I think we’ll be able to have a read of the Phase 1 because the majority of patients in a Phase 1 trial with non-small cell lung cancer, melanoma and other solid tumor types will have likely seen a PD1 antibody and either never responded or have responded and progressed. So their Phase 1 patients, so the combination will be interpretable. In addition, we have in some of the cohorts mandated biopsies to look at the change in architecture and cellularity of the micro environment in patients pre and post treatment with our combination. And of course we are very keen to look at the immunophenotyping and the reprogramming of the M2 to macrophage to the M1 phenotype to initiate a prolonged inflammatory activation CD8 positive cells.

[Unidentified Analyst:]

Got it. If I may, without getting the Phase 1 data, if we want to have some early insight into the possible mechanism of action of 549 in terms of PI3-k-gamma inhibition on macrophage phenotype, would it be possible to look into the available data with duvelisib study and look at the macrophage phenotype in patient samples to see if – obviously gamma is inhibited by duvelisib?

[Julian Adams:]

Yes, so unfortunately we do not collect samples with this understanding at the start of the duvelisib trials. In addition, the gamma selective compound is designed to inhibit greater than the IC90 for PI3-kinase-gamma in a selective mode without influencing PI3-kinase-delta. So it’s cleaner and pure study to see what IPI-549 will do. And we have a number of ways of assessing its activity including PD biomarker, looking at phosphorylation, inhibition of AKT in monocytes and T-cells as well as other flow cytometric measures that are available to us now better understanding the role of PI3-kinase-gamma.

[Unidentified Analyst:]

Got it. Lastly, would you mind comparing the interesting mechanism of turning M2s into M1s with the alternate approach of depleting macrophages through CSF1R targeting?

[Julian Adams:]

To my understanding, CSF1R will deplete all macrophages irrespective of the polarization. In our case, we are hopefully inducing a pro-inflammatory M1-2 type which we think will be more effective – we hope will be more effective and we have tested that in our murine models and feel that with getting complete responses in multiple murine models including inducing immunity or effective vaccination of these mice to the tumor in question leads us to believe that this is operating with our many controlled experiments that we know that we are operating through the M1 macrophage mechanism as well as inducing CD8 mediated killing, having no effect on the solid tumor whatsoever. We have checked. 549 has no effect directly on the tumor. It’s all for immunology of the intended treatment.

[Unidentified Analyst:]

Right, got it. Thank you very much.

[Julian Adams:]

My pleasure.

[Operator:]

Our next question comes from Anupam Rama with JPMorgan.

[Eric Holder:]

Hi, guys. It’s Eric in for Anupam. Thanks for taking the questions. Maybe just sort of a housekeeping question on the top line releases December and 3Q. Just wondering what level of detail you might expect to learn sort of beyond the primary endpoint in both DYNAMO and DUO, understanding that you might need to preserve some level of detail for a medical meeting. And then I have a follow up.

[Julian Adams:]

I think you answered your own question. We prefer to represent top line data as the primary endpoint and to the extent that we can, we would like very much to present this trial results in totality at a medical meeting and we’ll be submitting abstracts of course.

[Eric Holder:]

I guess specifically how detailed you can be sort of around safety profile?

[Julian Adams:]

I think we can report acceptable safety. I don’t think the risk benefit will have to be analyzed in the totality of the full presentation at the medical meeting.

[Eric Holder:]

Got it. And then maybe just a question on CONTEMPO, you noted that we’re looking at an early level of exposure here. But I’m just wondering whether down the line where there’s a certain sort of level of response, great or complete response that might warrant moving forward with a larger study in the frontline?

[Julian Adams:]

That’s exactly the purpose of this study. So new diagnosed patients, treatment naïve patients receiving standard chemotherapy, R-CHOP, or bendamustine-Rituxan. The response rates are very high, greater than 90% and so it’s really the complete response rate – so our primary endpoint is here safety and complete response rate. And we are looking for that to guide us as the future development in treatment naïve --

[Eric Holder:]

Okay, great. Thanks for taking the questions.

[Julian Adams:]

My pleasure.

[Operator:]

[Operator Instructions]. Our next question comes from Mike King with JMP Securities.

[Mike King:]

Hi, guys. Good afternoon. Thanks for taking the question. Can you hear me all right?

[Julian Adams:]

Yes.

[Adelene Perkins:]

Yes. Hi, Mike.

[Mike King:]

Okay, great. Just a couple questions on what I would refer to as trial execution issues with respect to DUO. A couple of things in that regard. As far as taking it interim and as far as – I hate to keep going back to the safety issue, but FDA tends to be monolithic about certain things. So I’m just wondering from sort of an all-clear standpoint, from a regulatory perspective, is an interim look on the efficacy side going to be sufficient for filing from an FDA point of view? And have you had a conversation with them about the efficacy part, is something on the order of what was seen with idelalisib [ph] going to be adequate in light of what might be a class effect or at least a perception of a class effect?

[Julian Adams:]

So in the design of DUO, this trial was presented at FDA before even starting the study. And as I said, we’ll be monitoring this study throughout the course of this study. The trial is fully enrolled. We had completed enrollment last fall and we reported that. And the statistical analysis plan had pre-specified this interim analysis for efficacy. So we have set the bar before we ever enrolled the first patient. And when we get the data, we will of course communicate with FDA.

[Adelene Perkins:]

Mike, I’ll remind you that the trial – it would like to the trial, so it’s our independent data monitoring safety planning that looks and makes the recommendation, is the benefit risk profile is such that it shows an overwhelming benefit, and then they make the recommendation to us that the trial be stopped. So that’s the first step. And then if they make that recommendation, we then go to the FDA and it’s the FDA’s decision to look at the data and determine whether we can stop early and file on that. So there’s two steps and they’re really out of our hands. It’s first the IDMC and then the FDA to make that assessment.

[Julian Adams:]

And then you made a point that I want to address, the comparison to Zydelig. There is no comparison to Zydelig for two reasons. One, it’s a different drug as Adelene has mentioned dual inhibition delta and gamma. But also perhaps more impactfully, Zydelig was not used as monotherapy, so Zydelig plus Rituxan versus Rituxan. So we did not run the same trial. They also ran Zydelig plus ofatumumab versus ofatumumab. The points of comparison are not possible.

[Larry Bloch:]

In terms of the safety question you asked is that we can’t speak to this until we actually have the data and the interim analysis. But what we can say is the independent data safety monitoring committee has recommended the trial continue without modification in their last review. So that’s the most recent update that we have to the blinded data.

[Mike King:]

Okay, great. Those are all very helpful. And then one other question. Have you spoken to the FDA as far as – what’s it like to see as far as some proportion of the patients in DUO that will have been ibrutinib failures?

[Julian Adams:]

No, ibrutinib is – prior treatment with ibrutinib is an exclusion criteria. When we started this trial, rituximab wasn’t yet available on the market. So we began this trial and excluded the rituximab and so these patients are naïve to rituximab.

[Adelene Perkins:]

We have another trial called [indiscernible] which is evaluating patients who have either progressed following the BTK inhibitor or who are intolerant to a BTK inhibitor, but it’s a different trial.

[Mike King:]

Okay, thanks for clearing me up on that. And then I had a question about the combination study with venetoclax and I may have missed this. I’ve had a tough time with my signal, but just curious with the endpoint is and I assume it’s going to be response rate but just want to get clarity on that end. Given that venetoclax can often drive MRD in certain histologies, how you would evaluate a combination of venetoclax and duvelisib in those instances? Thank you.

[Julian Adams:]

So first of all, I’ll say a broad exploration of 174 patients across five different tumor types that I enumerated during the initial remarks. And so the first order of business is to find the dose pair so there’s a drug-drug interaction Phase 1b, safety, run in and a clinical pharmacology intensive study to understand what is the right dose for the two drugs. And then after which there will be cohort expansions obviously looking for – always looking for safety and biological activity. In Phase 2 studies that are not controlled, we hoped that the preclinical data translate into synergy that we saw in the lab and so we are open to looking at all these various histological subtypes. And we may find ourselves with different dose types for different disease types. So it’s an area that AbbVie is conducting the study, so there’s not much more I can add to it, but it’s a very thoughtful program.

[Mike King:]

Thank you.

[Operator:]

I’m showing no further questions at this time. I’d like to turn the call back over to Adelene.

[Adelene Perkins:]

Thank you, Kevin. Thank you for everyone joining us today. We appreciate your interest and time. With preliminary CONTEMPO data at EHA in June, anticipated top line data from DYNAMO and potential top line data from DUO in the coming months, we expect 2016 to be a very important year for Infinity and we’ll look forward to updating you on our progress. Operator?

[Operator:]

Ladies and gentlemen, that concludes today’s presentation. You may now disconnect and have a wonderful day.