ChemoCentryx (CCXI) Q4 2017 Earnings Conference Call Transcript

ChemoCentryx (CCXI)
Q4 2017 Earnings Conference Call
March 9, 2018 8:30 a.m. ET

Contents:

• Prepared Remarks
• Questions and Answers
• Call Participants

Prepared Remarks:

Operator

Ladies and gentlemen, please stand by your conference call will begin momentarily. Again thank you for your patience and please stand by.Good morning, and welcome to the ChemoCentryx Fourth Quarter and Full Year 2017 Financial Results Conference Call. [Operator's Instructions] 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 -- Vice President, Investor Relations

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 website 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 and chief financial and administrative officer of ChemoCentryx, will provide an overview of the company's financial highlights for the fourth quarter and full year 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 the call over to Tom Schall.

Thomas Schall -- Chief Executive Officer, President and Chairman

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 us 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 an 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 in diseases where there is currently no approved therapy. Namely, these are C3 glomerulopathy or C3G, a 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 ANCAassociated 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 -- and applications for full marketing authorization in Europe. Fourth, the European Medicines Agency acceptance of our CNA (sic) [ 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 a 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 5 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 bolstered the strength of our balance sheet by up to additional $100 million with the $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 5 points of success as they will provide the engine of momentum for value creation in 2018 and beyond. First, the global Phase III 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 four, 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, Prof. 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 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 C5L2, which provides protection from the damaging actions of C5a in such glomerulosclerosis models. Importantly, in written commentary, Prof. 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 C5L2 in addition to the deleterious effects of C5aR. All of this is by way -- 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 Prof.

Kettritz, 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 or CD88 and the destructive inflammatory actions that, that receptor drives while leaving untouched the beneficial actions of C5L2. Other modalities, such as, for example, those targeting C5a directly, simply cannot make that mechanistic claim.

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 -- an antibody which might likely become immunogenic over time, particularly that is a 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 pathways through C5L2, leaving the rest of the patient's 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, technically known as validation, triggered a milestone payment of $50 million from our partner 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 III ADVOCATE trial and toward 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 III 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 in diseases for which there are currently no FDA-approved treatments. We are enrolling a 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 avacopan in a cohort of 22 patients as well as a control group of 22 patients, as you can see from the 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 6 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 nine.

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 1-year Phase II 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 1-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 endpoints 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 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 three 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 antitumor 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 seven. 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 in C3G and CCX140 in FSGS.

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 indirect -- indications that could offer a better life for patients and create value for our shareholders. One such indication outside of renal disease is the debilitating and deforming skin disease, hidradenitis 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 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 a number of fronts, as summarized in Slide 13: completion of patients' enrollment in the Phase III pivotal ADVOCATE trial, which we expect around the middle of this year; progress in our other registration-supporting trials, avacopan for C3G and our two FSGS studies with CCX140; initiation of clinical studies with avacopan in hidradenitis 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 -- Executive Vice President, Chief Financial and Administrative Officer

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 periods in 2016. The $50 million CMA validation milestone from our Vifor Pharma -- 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 2016, primarily due to higher expenses associated with activities related to the avacopan Phase III ADVOCATE trial in patients with ANCA-associated vasculitis and start-up expenses related to the Phase II 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 requirements, 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 $40 million. Total shares outstanding at December 31, 2017, were approximately 48.8 million shares. We ended the year with $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 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?

Thomas Schall -- Chief Executive Officer, President and Chairman

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 toward 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 hidradenitis suppurativa.

We will keep you updated on our clinical progress in this and other areas. My colleagues and I at ChemoCentryx pledge 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?

Questions and Answers

Operator

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

Tessa Romero -- JPMorgan Chase

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 4Q 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 sort of related to this, how should we be thinking about the target population you're going after? Is this an HS post-Humira or as a -- more of a front-line therapy? And then secondly, if I could ask just how you're thinking about enrollment and data timelines.

Thomas Schall -- Chief Executive Officer, President and Chairman

Thank you, Tessa. Those are all excellent questions. Essentially, we had a lot of interest and 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's Humira, you mentioned that.

Humira, while it works and certainly has some -- certainly is thought to have modest effects 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 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 within antibody, a chimeric antibody.

Again, that's a mouse-human hybrid, likely to be immunogenic. As far as we can tell, that agent required onceweekly infusions and, importantly, also short-circuits the effects of C5L2, 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 it 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 front-line 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 toward the moderate to severe. And we'll have more details to talk about as we launch that -- those studies a little bit later on this year, Tessa.

Tessa Romero -- JPMorgan Chase

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

Thomas Schall -- Chief Executive Officer, President and Chairman

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 -- Cowen & Co.

Hello, good morning, and thanks for taking my question. 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're referring to, whether you have some indication of the compliance or dropout rates or that sort of thing.

Thomas Schall -- Chief Executive Officer, President and Chairman

Yes, Eric. Thank you. Very good question. So as we and our team go around the world talking with investigators in the sites, overall, I think there's a huge degree of enthusiasm for the trial.

You are absolutely right. Though I didn't quote a dropout 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. And 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 III 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 the DMC, but one can infer from their lack of recommendation to make any changes that the drug seems to be well tolerated to date. 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 -- Cowen & Co.

A couple 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 II data at one point there. Has that program been discontinued? And then in aHUS, what are your plans now for starting the next trial? I thought that might be a nearterm event. Thanks.

Thomas Schall -- Chief Executive Officer, President and Chairman

Yes. So Eric, thank you for both those questions. In fact, just a minor correction. We did present data from a Phase IIa 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 IgAN, 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. 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 not -- it is 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 distant future.

Eric Schmidt -- Cowen & Co.

Thanks. Appreciate the updates.

Thomas Schall -- Chief Executive Officer, President and Chairman

Thank you, Eric.

Operator

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

Mike Englander -- JMP Securities

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.

Thomas Schall -- Chief Executive Officer, President and Chairman

Yes. Thanks, Mike. We'd really, really love to be able to now move forward 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 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 what we'd like to do is go forward appropriately 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 they are -- we may have some more data to talk about that study later this year.

The one that we already reported, the 18-month overall survival, but we'll see.

Mike Englander -- JMP Securities

Thanks a lot. Appreciate it.

Thomas Schall -- Chief Executive Officer, President and Chairman

Certainly.

Operator

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.

Thomas Schall -- Chief Executive Officer, President and Chairman

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.

Duration: 43 minutes

Call Participants:

Steve Klass -- Vice President, Investor Relations

Thomas Schall -- Chief Executive Officer, President and Chairman

Susan Kanaya -- Executive Vice President, Chief Financial and Administrative Officer

Tessa Romero -- JPMorgan Chase

Eric Schmidt -- Cowen & Co.

Mike Englander -- JMP Securities

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