ChemoCentryx's (CCXI) CEO Tom Schall on Q4 2017 Results - Earnings Call Transcript

ChemoCentryx Inc. (CCXI) Q4 2017 Earnings Conference Call March 9, 2018 5:00 PM ET

Executives

Steve Klass - IR, Burns McClellan

Tom Schall - Chairman, President and Chief Executive Officer

Susan Kanaya - EVP, Chief Financial and Administrative Officer

Analysts

Tessa Romero - JPMorgan

Eric Schmidt - Cowen and Company

Mike Englander - JMP Securities

Operator

Good morning and welcome to the ChemoCentryx Fourth Quarter and Full Year 2017 Financial Results Conference Call. At this time all participants are in a listen-only mode. Later we will conduct the question-and-answer session. As a reminder this conference call will be recorded. I would now like to turn the call over to Steve Klass, Vice President with Burns McClellan. Mr. Klass, please go ahead.

Steve Klass

Thank you. Good morning and welcome to the ChemoCentryx fourth quarter and full year 2017 financial results conference call. Earlier this morning the company issued a press release providing an overview of its financial results for the fourth quarter and full year ended December 31, 2017. This press release along with a few slides that you may find helpful while you listen to this call are available on the Investor Relations section of the company's Web site at www.chemocentryx.com.

Joining me on the call today is Dr. Thomas Schall, President and Chief Executive Officer of ChemoCentryx who will review the company's recent business and clinical progress. Following his comments, Susan Kanaya, Executive Vice President, Chief Financial and Administrative Officer of ChemoCentryx will provide an overview of the company's financial highlights for the fourth quarter and full year of 2017 before turning the call back over to Tom for closing remarks.

During today's call, we will be making certain forward-looking statements. Forward-looking statements are based on current information, assumptions and expectations that are subject to change and involve a number of risks and uncertainties that may cause actual results to differ materially from those contained in the forward-looking statements. These risks are described in the company's filings made with the Securities and Exchange Commission including the company's annual report on Form 10-K to be filed on March 12, 2018. You are cautioned not to place undue reliance on these forward-looking statements and ChemoCentryx disclaims any obligation to update such statements.

In addition, this conference call contains time sensitive information that is accurate only as of the date of this live broadcast March 9, 2018. ChemoCentryx undertakes no obligation to revise or update any forward looking statements to reflect events or circumstances after the date of this live conference call.

I will now turn this call over to Tom Schall.

Tom Schall

Thank you, Steve, and good morning to everyone listening. Thank you for joining us on our fourth quarter and full year 2017 conference call.

2017 was a watershed year for ChemoCentryx. It was a year of excellent execution both in short-term tactics and long range plan. A year in which we shaped the next stage of our destiny with remarkable progress.

Let's briefly summarize five key accomplishments as those of you following can see in Slide 3. First we took on the challenge of conducting what is by any standards a very large randomized controlled clinical trial in orphan disease indication. This trial, the ADVOCATE trial of Avacopan in patients suffering from ANCA-associated Vasculitis for an orphan indication is outsized by any historical standard.

We set ourselves the ambitious goal of 300 patients in two arms and completing this trial with unprecedented rapidity for ANCA Vasculitis. In order to do this, we activated 200 sites around the world and our momentum has been steady and inexorably accelerated so that we are now at approximately 75% of total enrollment.

Second, we launched two other clinical trials ultimately to support registration of diseases where there is currently no approved therapy. Namely these are C3 Glomerulopathy or C3G, second use of Avacopan and a trial of our next valuable unique kidney asset, the CCR2 inhibitor, CCX140 in patients with Focal Segmental Glomerulosclerosis or FSGS.

Third, we submitted an application for conditional marketing authorization or a CMA application in the European Union and the European Medicines Agency validated that application that is accepted the dossier for full review. The application reveals the maturity of our Avacopan program for ANCA-associated Vasculitis that is beyond the clinical data to-date, the maturity in terms of such things as manufacturing, toxicology and the exacting standards required for a mature comprehensive product application.

Of course approval is a high hurdle, but even getting to this point shows the sophistication of our program and teases up well for future submissions to the FDA for our end applications for full marketing authorization in Europe.

Fourth the European Medicines Agency acceptance of our CMA application has been very valuable to our commercial partner outside the U.S. Vifor Pharma, since it potentially brings forward revenues in Europe by two years. Vifor Pharma paid us $50 million for achieving this milestone. So despite all of our activity on multiple clinical trials 2017 was the year in which we took in more money than we spent.

Looking ahead, we have access to sufficient cash to get us through top-line data in the ADVOCATE trial and registration applications for that trial in the U.S. and Europe.

Fifth and last, in January, we reported updated and very promising 18-month overall survival data in patients with locally advanced metastatic pancreatic cancer using our drug CCX872. Any of these five achievements alone would have made for a good year. Together they represent a dramatic leap forward in our plan to become a fully integrated biopharmaceutical company.

Our fourth quarter was stellar. We doubled the enrollment in the ADVOCATE trial, since I reported our third quarter financial results on November 7, adding over 100 additional patients into the study. We launched the trials of Avacopan in C3G and CCX140 in FSGS. We've bolstered the strength of our balance sheet by up to $100 million additional with $50 million milestone payment that resulted from the European Medicines Agency validation of our CMA application as well as establishing a credit facility for another potential $50 million.

In 2018, we will continue to assertively execute on our plan. Today let's talk -- let's discuss and analyze briefly the five points of success as they will provide the engine of momentum for value creation in 2018 and beyond. First, the global Phase 3 ADVOCATE pivotal trial for Avacopan in the treatment of Anti Neutrophil Cytoplasmic Auto-antibody associated or ANCA Vasculitis. Those of you following the slides can see our latest progress on Slide 4 where as I mentioned earlier we are approaching 75% of full enrollment in this trial. Specifically we have activated our full target of 200 sites around the world and we have enrolled 220 patients to-date. We are well on track to achieve our goal of completing enrollment in a few months.

We are extremely pleased with how enrollment is progressing as well as with the overall conduct of the trial. We have a large majority of our target of 300 patients suffering from an orphan disease enrolled across the world in a couple of hundred sites. Why is this impressive? Because orphan diseases by their very nature are typically very difficult to enroll in randomized controlled clinical trials of any substantial scale. This is typically one of the elemental hurdles to advancing innovative medicines in orphan diseases. We believe that the ADVOCATE trial is the largest clinical trial of this nature attempted in the history of ANCA Vasculitis and we further believe that we are on pace to achieve one of the fastest ever recruitment rates in a randomized controlled trial in this important disease.

The enthusiastic welcome that physicians and patients alike are giving the ADVOCATE trial may well also be an indication of a huge pent-up need for modern drugs like Avacopan exemplifies. There we speculate that this itself is a promising sign for what may happen if Avacopan is approved and made available to patients with ANCA-associated Vasculitis. And a note about the Avacopan mechanism of action, in fact, its fundamental differentiation from other drug candidates in clinical development in what might be called the complement cascade intervention space. Since I know many of you are aficionados of this exciting and rapidly growing field of opportunity.

Eminent clinical scientists such as for example Professor Ralph Kettritz in Europe among others in the nephrology and rheumatology communities have pointed out some important features. There are two distinct C5a complement receptors, the activating pro-inflammatory destructive receptor known as the C5ar also known as the CD88 marker. This is the specific target of Avacopan. This mediates the damaging effects such as necrotizing crescentic glomerulosclerosis for example as that seen in ANCA Vasculitis. This has been shown time and again in model systems.

In addition, however, there is an anti-inflammatory C5a like receptor, the so-called C5 L2 which provides protection from the damaging actions of C5a in such Glomerulosclerosis models. Importantly in written commentary Professor Kettritz concludes the opposing actions of these two receptors indicates that neutralization of C5a itself would not be an appropriate therapeutic approach as it would eliminate the protective effects of C5 L2, in addition to the deleterious effects of C5ar.

All of this rather is by way of saying that Avacopan is unique; unique because it is the first and indeed it is the only drug candidate to selectively target and block only the C5a receptor CD88 as noted by Professor [Ketrich] [ph] in the complement cascade and you can see some details about the schematic of the complement cascade on Slide 5.

Avacopan blocks only the C5ar, the CD88 and a destructive inflammatory actions that that receptor drives while leaving untouched the beneficial actions of C5 L2. Other modalities such as for example those targeting C5a directly simply cannot make that mechanistic plain.

So in brief the ChemoCentryx approach is differentiated from other approaches in the complement inhibition field in the following very important ways with some distinct advantages. Avacopan is an orally available inhibitor of C5ar not an injectable or infusible.

Avacopan is a small molecule not an antibody which is likely in an antibody which might likely become immunogenic over time particularly if it is chimeric antibody a so-called mouse human hybrid that is not fully humanized. By specifically targeting the C5ar, we are not blocking the other C5a activated pathway through C5 L2 leaving the rest of the patients immune system functioning normally. The importance of this selectivity will I believe become ever more apparent to patients and clinical practitioners as it has already become abundantly apparent to experimental pharmacologists.

In short, our overarching principle is precise targeting leads to precision medicine. In a disease such as ANCA Vasculitis which has been treated the same way for nearly a half century Avacopan has promising potential to help patients get treated much more effectively to get better faster, stay healthy and avoid not only the physical, but also psychological side effects that come with the current standard of care regimen of high chronic doses of steroids combined with immunosuppressants.

With Avacopan we aim for the elimination of the use of chronic steroids in ANCA Vasculitis treatment thus rendering many of the safety and quality of life issues related to current therapy obsolete.

Our aim with Avacopan is to enable patients once again to live their lives to the full, spared from both the ravages of the debilitating disease itself and without the noxious effects of current standard of care used in an attempt to control that disease.

In January, we announced that the European Medicines Agency had accepted for review our registration dossier in support of a conditional marketing authorization for Avacopan in the treatment of patients with ANCA-associated Vasculitis. This acceptance for review tactically known as validation triggered a milestone payment of $50 million from our partner by Vifor Pharma together with the $50 million growth capital facility that we recently entered into. We entered 2018 strengthened by up to $100 million in new capital commitments as you can see from Slide 6.

Importantly, we believe that we now have sufficient funds available to advance Avacopan well through top-line data from our Phase 3 ADVOCATE trial and towards registration filings in the U.S. and the EU. While I am delighted by the excellent progress we made in 2017 in our clinical trials, I am equally delighted by our ability to secure the non-dilutive financing that allows us to continue full speed ahead in our mission to bring precise medicines to patients.

While the ADVOCATE Phase 3 trial is a major focus for us, it is just the beginning as you can see from our pipeline on Slide 7. We are also moving ahead with clinical trials which are designed ultimately to support registration and diseases for which there are currently no FDA approved treatments.

We are enrolling the clinical trial of Avacopan in patients with C3G a rare disorder that often affects younger patients requiring dialysis and all too often kidney transplant. There is simply no effective treatment today for C3G; immunosuppressive drugs are minimally beneficial and even kidney transplants frequently fail. For after transplantation, the new kidney will succumb to the same disease.

Ours is a multicenter 1-year trial involving of Avacopan in a cohort of 22 patients as well as a control group of 22 patients as you can see from this schematic on Slide 8. The control arm will receive placebo until they switch to Avacopan following a renal biopsy at six months. The primary endpoint of the trial is the percentage change in the C3 histological index after six months of treatment. While Avacopan continues to advance in two late stage clinical trials, we are launching trials of a second drug in our kidney franchise CCX140 in two subpopulations of the orphan kidney disease, Focal Segmental Glomerulosclerosis or FSGS a disease for which again there is no approved treatment as you can see on Slide 9.

CCX140 is an inhibitor of the chemokine receptor known as CCR2. We have a great deal of clinical experience with CCX140 having already successfully completed a one year Phase 2 study in chronic kidney disease in patients with active diabetes. In that study CCX140 treatment durably and significantly lowered proteinuria while being very well tolerated in patients over its one year dosing period.

The most dramatic decrease in proteinuria a sign of improved kidney function was found in patients with the highest levels of protein in their urine. This is very significant because those data provide the underpinnings of our current studies in FSGS, where proteinuria lowering may constitute the actual registration endpoint in certain FSGS patients.

One trial that we are launching involves primary FSGS patients who are non-nephrotic that is whose disease is often idiopathic and in most cases believed to be caused by a certain gene mutations. And the other trial is primary FSGS patients with nephrotic syndrome where patients present with a very high level of proteinuria often over 3 grams of protein in the urine per day. In this nephrotic syndrome patient population we believe a significant decrease in proteinuria from baseline can constitute an accelerated approval endpoint.

Switching to pancreatic cancer, we reported in January promising updated data from the ongoing clinical trial of our second CCR2 inhibitor CCX872 in patients with advanced metastatic pancreatic cancer. These results reported at the 2018 ASCO-SITC Clinical Immuno-Oncology Symposia. The findings demonstrated improved patient survival could result by selectively inhibiting CCR2 with CCX872. This selective blocking of CCR2 resulted in the immunosuppressing cells that CCR2 maintains in the tumor environment to be less obvious in that environment. Thus this new approach aims to mobilize the body's own potential for a powerful anti-tumor immune response. This is particularly important because other therapies such as checkpoint inhibitors do not seem to work well alone in pancreatic cancer. The mechanism of CCX872 potentially makes the checkpoint inhibitor approach more effective.

As you can see on Slide 10, the data showed overall survival in all patients randomized at 29% at 18 months, with CCX872 and FOLFIRINOX combination therapy. This is a dramatic advance over previously published overall survival rates of 18.6% using FOLFIRINOX alone to treat metastatic pancreatic cancer.

Interestingly better overall survival following treatment with CCX872 was associated with lower peripheral blood monocyte counts consistent with the model that myeloid derived suppressor cells controlled by CCR2 are being diminished in the tumor microenvironment with CCX872 therapy. We plan now to advance CCX872 in combination with other therapies.

In summary, Q4 provided a good ending to a year of impressive execution on our program as summarized in Slide 7. In short, the Avacopan trial is well on its way to full enrollment; our conditional marketing authorization was validated for review; we have initiated registration supporting trials for Avacopan and C3G and CCX140 in FFSGS.

We ended the year with a healthy cash position and indeed we were cash flow positive for the year. And our CCR2 inhibitor, CCX872 demonstrated very promising results in terms of overall survival of patients with locally advanced metastatic pancreatic cancer.

In addition to all of these advanced programs, we are constantly striving to look for new and direct indications that could offer a better life for patients and create value for our shareholders. Once one such indication, outside of renal disease is the debilitating and deforming skin disease, Hydradenitis Suppurativa which you can see explained in brief on Slide 12.

In 2018, we intend to launch our clinical development program for the use of Avacopan in patients suffering from this condition. As we move closer to potential commercialization of Avacopan in the United States, I'm pleased to say, we recently hired Bill Fairey to lead the company's commercial strategy as Executive Vice President and Chief Operating Officer. Bill brings extensive experience in commercialization, marketing and operations from his 25 years in the pharmaceutical industry and most recent position as President of Actelion Pharmaceuticals U.S., where he led sales, marketing, medical access and regulatory activities. Bill joined us as at a pivotal time in our evolution and will lead the commercialization of our drug candidates the last step as we become a fully integrated biopharmaceutical company.

Over the course of 2018, you can expect to see progress on the number of fronts as summarized in Slide 13. Completion of patients' enrollment in the Phase 3 pivotal ADVOCATE trial, which we expect around the middle of this year.

Progress in our other registration supporting trials of Avacopan for C3G and our 2 FSGS studies with CCX140, initiation of clinical studies with Avacopan in Hydradenitis Suppurativa. Potential regulatory updates and continued clinical progress with new pipeline candidates.

I will now turn the call back over to Susan to give you an overview of our strong financial picture with the main points from our fourth quarter and fiscal year end results. Susan?

Susan Kanaya

Thank you, Tom.

Our fourth quarter and full year 2017 financial results were included in our press release today and are summarized on Slide 14.

Revenue was $56.3 million for the fourth quarter and $82.5 million for the full year ended December 31, 2017 compared to $4.9 million and $11.9 million in the same period in 2016, a $50 million CMA validation milestone from our partner Vifor Pharma accounted for the majority of the 2017 reported revenue.

Research and development expenses were $12.9 million for the fourth quarter 2017 up from $9.3 million for the same quarter in 2016. For 2017 as a whole, R&D expenses rose to $49.5 million from $38 million in 2016 primarily due to higher expenses associated with activities related to the Avacopan Phase 3 ADVOCATE trial in patients with ANCA-associated Vasculitis and startup expenses related to the Phase 2 clinical trials in FSGS and C3G.

General and administrative expenses were $4.1 million for the fourth quarter up from $3.6 million we recorded in the fourth quarter of 2016. Full year 2017, G&A expenses increased to $16.5 million from $14.7 million in 2016 primarily due to higher intellectual property related expenses and accounting fees related to preparation for Sarbanes-Oxley requirement partially offset by lower travel expenses.

We recorded net income for the fourth quarter of $39.7 million compared to net loss of $7.7 million in the fourth quarter of 2016. And our full year net income of $17.9 million compares favorably to our 2016 net loss of $14 million.

Total shares outstanding at December 31, 2017 were approximately 48.8 shares. We ended the year with a 195.2 million in pro forma cash investments and receivables including remaining upfront commitments and milestone payments.

As Tom mentioned earlier in early January, we've further strengthened our balance sheet with a growth capital financing agreement of up to 50 million with Hercules Capital. We expect to utilize cash and investments in the range of $65 million to $75 million in 2018. Tom?

Tom Schall

Thank you, Susan.

To summarize, 2017 was a year of impressive execution for ChemoCentryx as we demonstrated our ability to run a landmark clinical trial across multiple sites around the globe involving hundreds of patients in an orphan disease.

We look forward to completing enrollment of ADVOCATE in the middle of this year and to working with the European Medicines Agency as they continue their review of our application for a conditional marketing authorization in Europe. We believe the unique selective targeting of the C5a receptor by Avacopan will prove to be an immense clinical and commercial differentiator.

We are advancing Avacopan and CCX140 in registration supporting trials in two other renal disease indications. We have a healthy balance sheet to fund our clinical activities and take us towards our potential registration filings in the U.S. and the EU. Our early stage pipeline remains rich with promise as the updated pancreatic cancer survival data showed. And as we intend to demonstrate with clinical studies of Avacopan in Hydradenitis Suppurativa.

We will keep you updated on our clinical progress in this and other areas. My colleagues and I, at ChemoCentryx pledged to work unstintingly to continue to create value for patients and shareholders alike. And today, we send a simple message. We believe the future of our enterprise has never been brighter.

With that, I will now turn the call back over to the operator and we look forward to your questions. Operator?

Question-and-Answer Session

Operator

Thank you. [Operator Instructions] Our first question comes from the line of Anupam Rama with JPMorgan. Your line is open.

Tessa Romero

Hi, guys. This is Tessa on for Anupam this morning. Thanks so much for the update here and for taking some time to describe sort of the fourth quarter and what happened this year. Wondering if you could maybe expand a bit on the motivation to pursue HS. Is there something in the competitive landscape and how do you think Avacopan could be particularly differentiated clinically here?

And then related to this, how should we be thinking about the target population you're going after? Is this an HS post Humira or as more of a frontline therapy?

And then, secondly, if I could ask just how you're thinking about enrollment and data timelines? Thanks so much guys.

Tom Schall

Thank you, Tessa. Those are all excellent questions. Essentially, we had a lot of interest in incoming demand if you will even from the clinical investigative community in the HS world. As you may well know there is only one currently approved therapy for HS and that is Humira, you mentioned that. Humira while it works and certainly is thought to have a modest effect among the clinical experts and the patient populations in HS. So there is a high demand for additional therapies. By the way even with the modest effects that Humira seems to have, it approaches $1.5 billion in sales in HS last year. So there is certainly opportunity there both clinically and commercially.

So with this demand and incoming interest from the clinical community, we did investigate what's going on in the HS world and not that much is going on but one very interesting feature was some early validation of C5a being involved in this debilitating and disfiguring disease with a chimeric antibody approach in some limited number of patients that has been presented.

Now that was very interesting to us. It makes perfect sense because HS is a neutrophil driven disease. Neutrophils are driven by activators in the body. But the most potent one -- one of the most potent endogenous activators is the complement fragment C5a, so all of that added up very nicely.

Now note both Humira is an antibody with again efficacy though widely regarded as modest efficacy, the clinical proof of concept data that we saw in HS patients where the rate of efficacy seemed to be even 30 points better than Humira data was with an antibody, chimeric antibody. Again that's a mouse-human hybrid likely to be immunogenic. As far as we can tell that that agent required once weekly infusions, and importantly, also short circuits the effects of C5 L2, a pathway regarded as beneficial for biology of C5a. So we thought this is a very interesting potential opportunity for an orally active small molecule that targets specifically the destructive pro-inflammatory neutrophil driver C5a receptor.

So all of that came together very nicely, the mechanism, the need and the potential to work in that landscape. As far as the approach, I think it's widely believed in the community given the modest benefits that Humira seems to accrue to patients, again, notwithstanding its enormous commercial success in that area that we could and indeed we intend to test the ability of Avacopan to work simply on its own as a potential frontline therapy.

Now HS generally is -- maybe not an orphan indication, but it is very interesting that orphan drug designation has indeed been designated for moderate to severe HS and that was given for the adalimumab approach, Humira. And so, I think that our target population would at first initially at least be skewed towards the moderate to severe. And we'll have more details to talk about as we launch those studies a little bit later on this year Tessa.

Tessa Romero

Great. Thanks so much Tom. I appreciate it. Thanks guys.

Tom Schall

Thank you.

Operator

Thank you. Our next question comes from the line of Eric Schmidt with Cowen and Company. Your line is now open.

Eric Schmidt

Good morning and thanks for taking my questions. Tom, on your discussion of Avacopan in the pivotal trial, you mentioned you thought the conduct of that trial was quite strong. Just kind of curious as to what you were referring to whether you have some indication of the compliance or dropout rates or that sort of thing?

Tom Schall

Yes, Eric. Thank you. Very good question. So as we and our team go around the world talking with investigators and the sites, overall, I think there's a huge degree of enthusiasm for the trial. You are absolutely right. I didn't quote a drop out rate the dropout rate is quite a bit lower than we anticipated for a trial of this size and this length. I think substantially lower. So I hesitate today to talk about that number, but it is in the single-digit percentages. So quite low, and that I think bodes well for the trial and the readouts.

It is also it won't surprise anyone to know that like all Phase 3 trials we have an independent data monitoring committee with 220 people already in this trial and a large leading edge of that having been in the trial for almost a year. That DMC has met more than once obviously and the trial is proceeding essentially with no change in conduct. So one can infer from that, we are not unblinded to the safety data like DMC, but one can infer from their lack of recommendation to make any changes that the drug seems to be well tolerated today.

So all of those and some other factors less tangible to me add up to a very satisfying conduct of trial to-date.

Eric Schmidt

Thanks for that color. Couple of other questions on the pipeline, I noticed that IgA Nephropathy is no longer on your slide. I think we're supposed to see some early Phase 2 data at one point there, was that program been discontinued. And then, in aHUS, what are your plans now for starting the next trial. I thought that might be a near term event?

Thanks.

Tom Schall

Yes. So Eric thank you for both those questions. In fact just a minor correction, we did present data from Phase 2 a proof of concept trial in IgA Nephropathy last year at a couple of major conferences. And we at that time it seemed that the regulatory guidance was vague about what the path forward was in IgA Nephropathy. We thought our data -- again, from a fairly small number of patients, 7, but as you know the numbers do tend to be very small in IgA and certainly in the early trials.

But our data looked really interesting and quite compelling in terms of four of those seven individuals had really quite marked reductions in proteinuria over the 12 weeks of dosing. In fact, if one is to read the guidance from other sponsors, in IgAN four of those seven went below a level that suggests that the FDA found it to be quite interesting in other studies.

It's a complicated landscape with IgAN and so I'm not sure what we might do next there but we are reevaluating our options and certainly we intend to have more discussion with regulators directly to see what the landscape looks like in IgAN and the potential for a protein lowering registration endpoint so I’ll have more to say about that soon.

aHUS you're quite correct, we are in fact dosing patients actively right now with aHUS. It's under our compassionate use protocol. So we'll have more to say about those results, I think in the coming quarter or so, but it won't surprise you of course the aHUS patient population is very hard to come by. So the number of patients that we have access to is regrettably not great. And we're struggling with that as our other sponsors. So we'll be clarifying the picture around aHUS and our approach to that as we go forward and I hope to be able to present some of the findings from our ongoing compassionate use patients in the not too distant future.

Eric Schmidt

Thanks. Appreciate the updates.

Tom Schall

Thank you, Eric.

Operator

Thank you. Our next question comes from the line of [Mike Englander] [ph] with JMP Securities. Your line is now open.

Mike Englander

Hi guys. Thanks for taking the question. Just wanted to ask about the future development plans of CCX872 in pancreatic given the nice overall survival data you guys have seen. Thanks.

Tom Schall

Yes. Thanks Mike. We'd really, really love to be able to now move forward with 872 in appropriate combinations with other therapies given the data that we have from the clinical setting as well as some very compelling pharmacological model data again revealing that the diminution of the myeloid derived my suppressor cells thought to be derived from CCR2 precursors or even directly driven by CCR2 in the microenvironment of the tumor. When they are diminished they seem to open up the immunogenic profile of the tumor in a greater fashion. We'll be publishing some of that pharmacological data, one hopes this year.

So while we'd like to do is go forward appropriate with checkpoint inhibitors that landscape as you know is not uncrowded, but we're navigating that landscape and we hope to be able to describe our forward plans with that soon. People are still in that study in fact and there will -- we may have some more data to talk about that study later this year. The one that we already reported 18-month overall survival that we'll see.

Mike Englander

Thanks a lot. I appreciate it.

Tom Schall

Certainly.

Operator

Thank you. I'm showing no further questions in queue at this time. I would like to turn the conference back over to Dr. Thomas Schall for closing remarks.

Tom Schall

Thank you, operator. Thank you everyone for joining our call today. We look forward to updating you as we execute on our plans. We will also be at the Cowen Healthcare Conference next week and I hope to see many of you there. So with that you may now disconnect and I wish you all a very good day.

Operator

Ladies and gentlemen, thank you for your participation in today's conference. This concludes today's program you may now disconnect. Everyone have a great day.