Q3 2019 Earnings Call
Good afternoon, ladies and gentlemen, thank you for standing by welcome to the Qorvis Pharmaceuticals third quarter 2019 update <unk> financial results webcast.
The conference is being recorded.
At this time all participants are in listen only mode. Later, we will conduct a question and answer session and instructions will follow at that time.
It is now my pleasure to turn the call over just.
Sure Communications. Please go ahead Sir.
Thank you operator, and good afternoon, everyone. Thanks for joining us for the Corbis Pharmaceuticals third quarter 2019 business update and financial results Conference call.
On the call to discuss the results and business highlights for the third quarter 2019, our Richard Miller, Chief Executive Officer nicely Chief Financial Officer.
And your dad, no basher Chief Medical Officer.
Also joining the call our corporate senior scientist Dr., Stephen Willingham, and Dr. drew hot.
The executive team will open the call with some prepared remarks, followed by a question and answer period.
We'd like to remind everyone that comments made by management today and answers to questions will include forward looking statements forward looking statements are based on estimates and assumptions as of today and are subject to risks and uncertainties that may cause actual results to differ materially from those expressed or implied by those statements, including the risks <unk>.
And he is described in Corpus. This quarterly report on Form 10-Q filed with the FCC and other filings the company makes with the FCC from time to time.
The company undertakes no obligation to publicly update or revise any forward looking statements, except as required by law would that I'd like to turn the call over to Mike we like.
Thank you Jack I'll begin with a quick overview of our third quarter financials, and then turn the call over to Richard for a business update.
At September Thirtyth, 2019 quarters had cash cash equivalents in marketable securities totaling $86.4 million as compared to $114.6 million at December 31st 2018.
Research and development expenses in the third quarter 2019 totaled $9 million compared to 8.4 million for the same period in 2018.
The increase of.
When Sixmillion was primarily due to an increase in C.P.I. 006 cents C.P.I.E. when they program costs and personnel costs, partially offset by reduced.
For doesn't cost.
I would like to note that we continue to carefully manage our expenses and currently expect.
Full year 2019, net cash used in operating activities to be between 38 and $40 million, where the 2019 yearend cash balance between 75 and $77 million.
The net loss for the third quarter 2019 was 11.0 million compared to a net loss of $10.5 million for the same period in 2018.
Total common stock compensation expense for the third quarter, 2019, and 2018 was $1.8 million.
Well now turn the call over to Richard.
Thank you ladies and good afternoon, everyone. Thank you for joining us today for our third quarter 2019 business update.
During the quarter, we continue to advance in all three of our clinical programs are adenosine eight to a receptor antagonist suffer a dennis or anti Cdseventy, three cpis 006, and a REIT teekay inhibitor C.P.I.E. 20.
Enrollment and all three clinical studies continues to go very well and we look forward to providing updated cpis 006 clinical data in an oral presentation and updated clinical data with sit for adamant in posters at the city meeting in November .
We're also planning to present data related to sit for Radnet and C. P. I eat one eight programs at other medical meetings over the next four months.
On today's call I will provide a brief preview of our city presentations followed by an update on our other programs sypher adamant in C.B. I eat warning.
In short, we believed that our precision medicines.
Hi, a marker driven studies and efficient clinical designs will allow us to advance multiple products deeper into clinical development.
As a reminder, Cpis 006 is a novel first of its coined anti cdseventy three antibody.
We created in our developing it because it possesses unique you know biology properties.
Dr., Jason Luke from University of Pittsburgh presented the first human clinical evidence that these properties in an oral presentation at ASCO earlier this year.
His presentation demonstrated that cpis. There. There are six has two important mechanisms of action combining immune stimulation and adenosine blockade, which are expected to be synergistic.
Briefly the key highlights for Masco included.
Oh six binds to a site on the C.D. 73 protein that blocks its enzymatic activity blocking the production of immuno suppressive adenosine.
Cdseventy three is also a co stimulatory molecule on immune cells.
<unk> 006 interacts with the site on the molecule that leads to activation of immune cells. This process is independent of adenosine.
Clinically the early results presented at ASCO demonstrated dose dependent disease control in patients with advanced refractory disease when administered as a monotherapy ends in combination with suffer ordinance.
Cpis 006 achieve tumor control and regression in patients with very advanced cancers, who is listening to current treatment approaches.
In particular, we saw early signs of activity in prostate and renal cell cancer.
We also reported a positive safety profile as O six was well tolerated at all dose levels with no dose limiting toxicities observed so far.
We continue to enroll patients with advanced cancer in the phase one one be study.
With a focus on the first two arms of the study single agent and in combination with sit for Radnet.
Since ASCO, we has we have selected our optimal dose at 18 milligrams per kilogram every three weeks for Cpis 006 monotherapy one of the main goals of the study.
Based on the experienced to date, we believe this dose provides sustained pharmacokinetic and full occupancy of the cdseventy three sites in blood and in tumors.
This dose provides the basis for the expansion cohorts in the current trial and future trials focused on assessments of efficacy.
On Friday November Eightth that 345 PM Eastern time, Dr., Luke will build on the evidence presented at ASCO with updated data from the O. Six phase one one be trial in an oral presentation at city with more patients and longer follow up for both the monotherapy.
Sit for Adnan combination arms further highlighting the immuno biology and clinical activity I've Cpis 006.
This will include dose escalation data on approximately 40 patients while the follow up is short for patients treated that dose levels near or at 80 milligrams per kilogram. The optimal dose. We are pleased to see indications of tumor activity in some of these patients.
Similar to prior results, we continue to see dramatic effects on circulating immune cells with b cell and T cell mobilization and redistribution.
B cells are specifically activated into antibody producing sells both in vitro and in vivo.
And these effects are adenosine independent and are related to the immunomodulatory properties of our Cpis 006 antibody.
We are not aware of any other agent anti body or small molecule targeting cdseventy three that has exhibited these properties.
We will highlight and discuss these results for those that are not able to 10 attend dr. Lu sits he talked at Investor reception on Friday November Eightth from six to 730 PM Eastern time for those that we'll be at the meeting the that will take place that the Gaylord National Hoteling Convention Center and we.
Also webcast the event for those that cannot attend in person.
If you would like to attend please please reach out to life.
In addition to the presentation by Dr. Lu we will also present two posters at city covering our adenosine programs Cpis. There as there are six and sit for Radnets. The first will be presented by Dr., Stephen Willingham very talented senior scientists here at Corpus Dr., Willingham and Dr. drew Hudson.
I have pioneered the identification and elucidation of our adenosine gene signature in renal cell cancer.
This work is now in press in a major medical journal.
Dr willing hams poster will be presented on Friday, the eighth and we'll highlight the scientific basis for the adenosine gene signature biomarker, which we believe can be used to predict a response to adenosine pathway therapies.
This research has deepened our understanding of the interplay between Cdseventy, three A.M.T. or adenosine mono phosphate and adenosine and has important implications for therapies targeting adenosine axis as well as immunotherapy in general.
This poster will provide an update on the correlation of our adenosine gene signature with tumor response to suffer adamant in patients with renal cell cancer.
I will touch more on this and the moment in a moment the second poster will be presented on Saturday by Dr. MARD Atmel Basher, our chief Medical officer. His poster will cover the details of the design of our ongoing trials with Cpis there as their us.
Thanks.
Overall, we anticipate that the data presented at city will reinforce our position as a leader in the development of adenosine pathway based therapeutics and in the development of second generation targeted biomarker driven immuno oncology medicines.
Turning now to sit for Radnet, our oral small molecule drugs that isn't antagonist of the adenosine eight to a receptor sypher Radnet is the most advanced candidate in development across the landscape of eight to a receptor antagonists with more than 300 patients receiving treatment to date.
It has demonstrated anti tumor activity as monotherapy.
Ends in combination with Tesla listen that in patients that have failed. The median of three prior therapies with a strong safety and PK PD profile.
This includes some patients experiencing durable responses and disease control out to over 30 months with several patients who have now been on sypher Adnan for more than two years.
We continue to enroll patients in our phase one be two clinical trial evaluating sypher radnets in combination with it says listen that.
This study has most recently been focused on patients with advanced refractory renal cell cancer and inpatients with prostate cancer.
We also continue to investigate the potential for our adenosine gene signature to serve as a predictive biomarker for patients that will respond to therapy would suffer adnan.
As we have reported previously.
In RCC renal cell cancer, we have seen both that in monotherapy ending or in combination with its has a listen had a positive adenosine gene signature is associated with the response and a negative signature is associated with lack of response, we build.
Leaves the signature reflects the presidents the presence of adenosine in the tumor micro environment.
The immunosuppressive adenosine limits existing I O therapies, such as with anti PD ones addition of an eight to a receptor antagonists counteracts. This immunosuppression.
Importantly in the Genentech study by Mcdermott published in June in nature Medicine in 2018, which involved over 400 patients with renal cell cancer patients with tumors expressing the agenda adenosine gene signature referred to as the myeloid signature and that paper had poor outcome.
With a tesla listen that therapy in front line renal cell cancer patients note. The my words signature and the adenosine signature which were discovered independently are composed of an identical eight genes.
Signature positive patients do poorly with anti PD ones, but they are the patients most likely to respond to our eight to a inhibitor sypher Adnan.
So the combination of sit for Edmonton. It says it wasn't that has a strong rationale and is as it is aimed at overcoming a resistance mechanism to PD one therapies.
With our preliminary data we believe we are seeing this play out in our studies.
We see responses in our biomarker selected patients with renal cell cancer.
The adenosine gene signature appears to be present in about 50% to 60% of renal cell cancer patients.
Its presence in many other types of solid tumors suggests that a similar strategy may apply to those tumors as well.
We're also enrolling patients with prostate cancer.
We have seen activity in this disease for both sypher, Adam monotherapy and combination with its has a listen that.
We have submitted an abstract to the ASCO genitourinary cancers Symposium a meeting in February in San Francisco, where we expect to present data in prostate patients treated with CFO and it says listen that sypher at unintended says listen that.
In short Sypher, Adnan has a known molecular mechanism a predictive biomarker and has shown activity in several different cancers. It also has encouraging potential when used in combination with cpis. There is there a six.
Outside of the adenosine pathway, we are enrolling our phase one one be study of Cpis 818 are small molecule I teekay inhibitor.
This is this trials in patients with T cell lymphomas, including peripheral T cell lymphoma, cutaneous T cell lymphoma, and other varieties of T cell lymphoma. We believe 818 has the potential to be directly cytotoxic T cell lymphomas and also may lead to enhancement of the immune.
System by increasing the T.H. one immune response.
[noise] some of our research also indicates that this drug may be an attractive candidate to examine in auto immunity.
As a reminder, the development of CP <unk> 8008 was based on a similar targeting strategy to that as BTK inhibitors and members of the scientific team that qorvis, including myself led the development of the first the BTK inhibitor Ibrutinib, which is approved for the treatment of several types of B cell lymphomas.
We continue to enroll patients in the 8.8 study at sites in the United States, Australia, and South Korea.
The drug has been well tolerated so far with no dose limiting toxicities and we're very pleased with the PK and PD findings, which to date have been asked as we predicted.
We have a poster accepted for presentation at the American Society Hematology meeting in December and a presentation at the T cell lymphoma Forum in La Jolla in January .
In summary.
We continue to believe Qorvis is well positioned with three unique candidates in the clinic. Each of these agents has precisely defined molecular targets and biomarkers that should allow for enrichments of patients most likely to benefit from therapy.
We continue to hold worldwide rights to all three agents. In addition sit for admin and Cpis 006 appear to be complementary with attractive potential as a combination therapy.
We are excited to continue presenting clinical data from sit for Adnan end Cpis. There is there a six at city in November from sit for Radnet at the G. you ASCO meeting in February and initial data on 818 at the Ash meeting in December and at the T cell Forum in January .
Our team is focused on advancing our pipeline and we look forward to 2020, when we expect to advance one or both of our adenosine programs into later stage, perhaps pivotal trials outside of our three programs in the clinic. We're also advancing our pipeline assets, but the majority of our focus continues to be on our.
Cynical work.
We look forward to providing updates on our progress progress with our pipeline at upcoming medical meetings and in future business update calls.
I will now turn the call over to the operator for questions and answer period operator.
Thank you.
Like to ask a question.
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Cost for just a moment, everyone an opportunity to signal.
First question will come from.
With Jefferies.
Hi, guys. Thanks for taking my questions Richard maybe if I could just start in terms of thresholds for.
Yeah, the prostate cancer program.
How should we think about it as we get data next year at ASCO GI you in terms of you know what is good data with suffered tenet plus as well.
In order to move the program forward into the next stage of studies.
Okay.
Thanks pairing that's a good question, we thought a lot about that we've discussed it with our experts who are involved in our clinical trials.
So we think that a response rate in hormone refractory patients with Prost with metastatic castration resistant prostate prostate cancer.
In excess of 20%, 25% objective response would be a very good result, obviously durability and safety are also key components of that durations of responsive six months or so alternatively drops and say of around 50% or so would be a senior.
In 2025% would also be good results. So I think the threshold here is 2020, 5%.
Keep in mind that you have.
Completely novel mechanism of action year also keep in mind that PD ones or whether it be anti PD, one or anti PDL. One have had very low response rates in similar pell patient populations on the order of around 5% or even less so our targets here is 2025.
Personnel are.
So when you look at 2020, 5% or are you talking about that being measured by recess inpatients with measurable disease.
Yes.
Okay. So would be and then this criteria.
Okay. That's helpful and then I guess.
It relates to the RCC program, you know last year, it's a c. you presented on yeah I think.
You know top of it has though and you know we saw PFS and the comp in the combination arm of about five and a half months across 31 patients are you going to update US you know what that cohort in terms of PFS or is that basically is that savvy basically finished now.
No the studies continuing we're enrolling.
Aaron part of your question.
Came in and out so I'm not sure I captured at all but I'll try my best answer your question I think I knew your where you were going.
So in our ongoing renal cell cancer page patient study with the Tesco and CFO keep in mind again. These are patients who've third and fourth line therapy.
Most of them, it's not all of them have failed PD ones.
There are PDL, one negatives as bad group of patients now we're using the adenosine signature I'm looking at patients who are adenosine signature positive and negative.
At the city meeting, we'll update you on the all our are in the positive versus negative and I can tell you that adenosine signature continues to hold up and predict responsiveness.
In renal cell cancer patients the target if you're looking for a target for RCC in that kind of population.
Our target for <unk> for wanting to proceed.
On this study, perhaps in a pivotal trial would be 20% or more or our by resist a in a patient population. That's similar to this or perhaps slightly earlier, because we've got a lot of really end stage patients in our current study and we probably with exclude those in the future trial. So I think we're looking for it.
20% response rate or higher by resist in the adenosine signature positives, Pat population would would which would be about 50 or 60% of renal cell cancer patients.
And what about correlation of the gene signature to duration of response in those patients are to achieve a response to expect okay. That's actually a that's a great question and it's also a discussed in our paper in press.
It turns out that the a and I forget the number exactly but the frequency of patients who are the long term.
Ritter's those who are the tail on the PFS curve those are all adenosine signature positive.
I mean, I think just about every one of them the adenosine gene signature predicts a durability and the response very well in renal cell cancer. The question that we're now beginning to look out is that signature applied a prostate and other cancers and was it's just really too early to say that.
Got it great. Thanks for taking my questions.
And once again that is star one if you'd like to ask a question.
Next we'll hear from Tony Butler with Roth Capital Partners.
The truth.
Once upon a Tom that was the notion and perhaps it's still exist so I'd like to refresh.
The molecular understanding of the need to put in a two way. In addition to anything CD 73, onboard, perhaps plus or minus PD one PDL one.
In that perhaps there is some.
Adenosine week.
If you would use one or the other I'm just curious do could speak to the notion of an oh, let's just call. It didnt seem like such that you get maximum.
Obligation of the Denison buttons and the combination thanks.
Okay. Thank you Tony.
Okay. So.
There are many sources of adenosine production not just through CD 39, Cdseventy three so we've always thought that blocking the final receptor the to a receptor was the best strategy and that's why we initiated our work in that area first.
Blocking cdseventy three will also improve upon that potentially because it will reduce the levels of adenosine, but as I mentioned there are other there are other pathways now dr. willing hams poster specifically will address this question because when you block that Dennis when you block Cdseventy, three and I don't want to go.
Yes. This poster away because he is going to give me dirty looks there [laughter] box Cdseventy three you get a buildup of MP and AMC has other consequences.
That that are interesting.
And it turns out that using.
Anti Cdseventy three and a two hour together make a lot of sense for a lot of reasons main reason be there are multiple pathways of the tendency production, but a build up as a MP also has other consequences.
That you'll hear about in his poster.
Now keep in mind that our strategy combining owes six and gateway receptor antagonists together has yet another strategy, which I think is even more important if you can block the to a receptor or adequately that's probably a very good thing to do but we think that the more important.
Thing, we're doing with those six is were stimulating immune cells and eliciting primary immune response.
That together with removing the immuno suppression of adenosine could be an awesome combination and that's sort of our strategy, which is a little bit different than than others.
So.
So I guess the summary to your question is using both in combination we feel using both in combination even if you're just focused on adenosine is a good idea, but I think were corvus has an advantage here is this other immunostimulatory ability on top of that now if you want to throw PD one anti PD.
One in there as well that's a reasonable thing to do because that's yet another pathway.
You know to block or another pathway to think about in terms of immune stimulation.
But I think I think a super willing hams poster Steven injuries poster will address and presents really new findings about the consequences of blocking cdseventy three that I don't want to divulge right here.
And my second question. Thank you for that by the way Richard My second question is around other immune cells in that microenvironment for example.
It does blocking if you were to block the anti Cdseventy three for example.
Forget about a two way for the moment inhibition, but did you actually have an increase or decrease in macrophages.
The site.
When in fact, you do get rid of adenosine and is it different.
Even in vitro if you use both agents versus one or the other thank you.
Yeah, I'm not sure we have and jump in here guys. If you have question some knowledge on this.
I'm not sure we have data show convincing data showing from biopsies, you're asking a tough question that requires biopsies.
You know, if our adenosine blockade or with they to a receptor antagonist or or Cdseventy three whether we have a demonstration of any change in my lawyer Mana Citic sell infiltrate certainly in some cases and we feel it's in our paper impressed we see in many patients and increase in T cells.
But that's really hard to study very hard to be sure about but if you recall and I'm going to let Steven comment on this.
He is just fallen out of his seat here answer. This question. The adenosine gene signature also known as the myeloid gene signature is a set of genes that are my would sell derive so you're putting your finger on the really critical cell type. The myeloid cell is probably very important and all this even you.
On add something.
Okay that yeah, we see a.
Very big differences in vitro when we use an anti 73 alone versus a anti 73, plus our age we are antagonist. That's in part will be presenting at the city conference.
Steven Richard Thanks, very much appreciate it.
Okay.
And with no further questions in the queue I'd like to turn the call back over to Richard Miller for any additional or closing remarks.
Okay, well first of all thank you very to everyone for participating in the call.
We look forward to our presentations at the society of immunotherapy of cancer or city meeting.
In November Eightth, and hope that for those who can attend you can come to our reception that evening Friday evening.
Or listen to our a webcast. Thank you very much and good afternoon.
Once again that does conclude our call for today. Thank you for your participation you may now disconnect.