Q4 2019 Earnings Call

Good afternoon, ladies and gentlemen, thank your for standing by welcome to the Corpus Pharmaceuticals fourth quarter 2019 business.

Not sure results webcast today's conference is being recorded at this time all participants are in a listen only mode.

We will conduct a question answer session and instructions will follow at that time, it's now my pleasure to tropical virtues that Kubota pure communications. Please go ahead Sir.

Thank you operator, and good afternoon, everyone.

Thanks for joining us for the corporate Pharmaceuticals fourth quarter, 2019 business update and financial results Conference call.

On the call to discuss the results and business highlights for the fourth quarter 2019, Richard Miller, Chief Executive Officer, Lately, Chief Financial Officer, and more dad, No Bastard Chief Medical Officer Executive team will open the call with some prepared remarks, followed by a question and answer period.

I would like to remind everyone that comment made by management today and answers to questions will include forward looking statement.

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 and uncertainties described in corpus. Its quarterly report on form 10-Q filed with the FCC on October 29.

2019, 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 that except as required by law.

With that I'd like to turn the call over too late.

Thank you Jack I'll begin with a quick overview about fourth quarterly and full year 2019 financials, and then we'll turn the call over to Richard for business update.

At December 31st 2019, quotas that cash cash equivalents in marketable securities totaling $78 million as compared to $114.6 million at December 31st 2018.

Research and development expenses in the fourth quarter, 2019 totaled $8.9 million compared to $8.4 million.

Same period in 2018.

Increased 1.5 million is primarily due to an increasing outside cpis virazole six and CPR eight when they go rent costs, partially offset by reduced outside set for debt costs.

He development expenses for the full year 2019 totaled $38 million compared to $38.6 million in 2018.

The decrease a $6 million is primarily due to reduced set for Doug costs, partially offset by an increase in CPR. Your zero six CPR is one eight figure on cost and personnel cost.

Like the note because we continue the carefully manage on expenses and currently expect full year 2020, net cash used in operating activities to be between 4900 $42 million compared to $37 million in 2019.

Net loss for the fourth quarter 2000, while she was $11 million compared to a net loss of $10.5 million for the same period in 2018, the net loss for the full year 2019 was $46.7 billion compared to a net loss of 46.9 million in 2008.

Total stock compensation expense for the fourth quarter and full year, 2019 was $1.7 million and $7.3 million, respectively, compared to $1.8 million and 7.1 billion in 2018.

I'll now turn the call was injured.

Thank you life and good afternoon, everyone. Thank you for joining us today for fourth quarter and full year 2019 business update.

In 2019, we made substantial progress enrolling patients we noticed studies in advancing our pipeline of precisely targeted oncology therapies.

The progress provides more clarity defining three areas that are product candidates address number one adenosine pathway inhibition and eight to eight receptor blockade and inhibition of the Dempsey production by Yeah, PCB seven three no the team immunomodulation of immune cells perfect.

We will then be cells and three modulation of T cell function to the kind age I Teekay <unk>.

The key highlights from the year include the following.

We continue to report encouraging data from the phase one two clinical trial of Super I've used in combination with it hasn't moved in that in patients with advanced refractory renal cell cancer.

Sure for at least is the most advanced candidate in development across the landscape of the tendency to waive receptor antagonists with more than 300 patients receiving treatment to date.

We reported the first data for CPR 006, our novel first of its coins you'd probably see these 73 antibody demonstrating that it may provide a new immuno oncology approach both via the activation of immune cells into the inhibition of identifying production.

The data indicates CPR 006 has potential as a monotherapy and there was a combination medicine in a variety of tumor types.

In addition, we continue to develop the adenosine gene signature, which we believe will be an important predictive biomarker for swiffer audience and for Cpis. There there are six.

Our work in the adenosine pathway was reinforced by multiple independent studies from industry and academia over the course of the year, adding to our confidence that our programs our positions for success.

Outside of the adenosine pathway at the recent American Society of Hematology meeting, we presented initial data from the dose escalation portion of our phase one study for CPR eight one they are small molecule I T.K. inhibitor, making it our third program in the clinic. This can.

I see it in January with additional clinical data presented at the T cell lymphoma Forum in San Diego.

It's working 20 <unk>, we will continue advancing our clinical studies for sypher admin for Cpis 006, NCP I eat warning.

I will begin with an update on the recent work with Super Admin and the adenosine gene signature that gives us increasing confidence in the outlook in trajectory of our lead program.

In the January 2020 issue of cancer Discovery. Our peer reviewed article was published on sit for I've missed any events. He gene signature authored by Dr., Larry fall and give you CSF one of core buses clinical trial investigators.

Article presents the safety and efficacy results from 68 patients with advanced refractory renal cell cancer and for the first party publication described the Densification and the potential to use the adenosine gene signature as a biomarker for predicting in response to therapy would suffer I've moved.

And potentially adenosine blockade in general.

This study and the adenosine gene signature were recently highlighted at the ASCO genital urinary symposium meeting in San Francisco in February.

Briefly here are some of the key sox related to the adenosine gene signature.

The signature has now been confirmed by other academic and industry groups.

The signature appears to identify a sub type of renal cell cancer that has a poor prognosis a group of patients that is unresponsive to anti PD, one therapies with a very low response rate and extremely poor PFS of less than three months, even in first line setting.

Patients with party adenosine signature, we're generally low foreign into your Genesis signature. He is your Genesis signature is an established biomarker, which predicts response favorable response to answer your Genesis inhibitors. What this means is that the adenosine signature identifies.

Group of renal cell cancer patients. We estimate that this was about 50% of patients that do quarterly with current therapies.

The signature identifies a myeloid cell population in the renal cell cancer tumor micro environment that functions as an immuno suppressive cells.

This now highlights this myeloid cell population as a potential new targets for immuno therapy that is targeting the my would component of the tumor micro environment.

The cancer discovery article demonstrates that in patients with high levels of the density gene signature expression.

There was a statistically significant association with two moving aggressively with suffer abbvie in treatment.

Identifying signature positive patients achieved a 17% response rate by resist.

Versus zero percent in signature negative patients.

These patients also demonstrated more durable progression free survival with a tail on the curve for the adenosine signature positive patients.

The the data indicate that the adenosine gene signature may be useful as a predictive biomarker to select patients more likely to respond to sit for athletes and that resistance to anti PD, one may be reversed spices radnet in these patients.

It also suggests that the signature can identify patients with low expression of the Andrew agenda since June signature, which can predict poor response, the empty injure Genesis agents.

This double enrichment.

The ability of gene signature exciting potential as a biomarker that identifies patients that will do better with fragments and have unfavorable outcomes with standard of care Teekay eyes Tyson kindness inhibitors.

Article was further highlighted in the journals editorial by Dr. Lucius It Coskey professor of immunology at North Eastern University. In addition to acknowledging the pioneering research. He noted that yes, yes that anti tumor activity was seen in highly resistant patients.

We have an oh, we have already enrolled approximately 25 additional renal care renal cell cancer patients with the goal of confirming the value of the adenosine signature.

We're also working on reforming the signature and very good progress is being made in that area. We intend to update both the critical and biomarker data at the ASCO annual meeting in June.

With these additional data we feel we will be positioned to initiate a late stage trial based on the adenosine gene signature in second third or later line renal cell cancer patients.

They are remains an unmet need for these patients and we anticipate that the signature will be capable of identifying the patient group that is likely to do better with sit for radmund compared to standard therapies.

We also presented data on for AD moving prostate cancer at the ASCO Gi cancers Symposium in February.

We are in the very early stages of this trial with a median follow up of only 3.2 months.

The highlights from that data include as mentioned median follow up of about 3.2 months. There was one partial response by resist this patient had a PS they dropped from 98 to less than 110 additional patients had tumor regression not yet meeting the criteria for partial response and seven patients have confirmed stable disease.

Ceding six months.

Many of these patients with minor response from stable disease are continuing on therapy and it is possible that their responses may deepen.

We intend to update this data at ASCO in June.

One other important finding reported in this presentation was gene expression profiling the tumor biopsies demonstrated a statistically significant correlation of tumor cdseventy three expression with the adenosine gene signature.

This correlations supports the relevance of the adenosine adenosine in prostate cancer its production by exceeding 73 any expression of adenosine induced immunosuppressive June.

Let me turn now to Cpis 006 are easy Cdseventy three antibody, we continue to be enthusiastic about this novel immuno Modulatory antibody. We most recently presented data from the phase one one the study at the society of immunotherapy of cancer meeting in November.

Similar to prior results presented at ASCO, we are seeing activity in renal cell prostate and non small cell lung cancers within acceptable safety profile.

Also continues to see dramatic effects on circulating immune cells will be selling T cell mobilization and redistribution.

These cells are specifically activated into antibody producing sells both in vitro and in vivo.

And these effects are adenosine independence.

And our related to the immuno modulatory agonistic properties of the antibody.

We are not aware of any other agents antibody or small molecule targeting cdseventy three that has exhibited these properties.

It should be noted that interest in the role of B cells in immuno therapy has intensified.

Leasing papers in nature have shown that tumor infiltration with b cells are an important predictor of response to immuno oncology therapies.

This gives us added confidence and interesting Cpis 006.

Recently, we have found evidence that some of our patients are producing antibodies to their tumor following therapy with Cpis 006, although preliminary this is a very exciting and important fighting.

In terms of the ongoing study with now selected the optimum dose of 18 milligrams per kilogram every three weeks for monotherapy and in combination with suffer adamant. We recently opened to Cpis 006 in combination with Pembrolizumab arm of the study and we expect to soon open the last farm.

This study, which is cpis 006, plus suffer Adnan plus pembrolizumab a triplet regimen.

Finally, a quick update on CP, one eight our teekay inhibitor.

As mentioned in my opening remarks, we presented the first data on this program at Ash in December and that the T cell lymphoma form in January.

We have now reach to dose that substantially inhibits the target. So we are now we are now positioned to evaluate potential efficacy.

The phase one portion of this study has met our expectations as we as we have determined safety PK receptor occupancy and we have selected the dose early signs of anti tumor activity has been observed.

In summary, we continue to believe corbis is well positions with worldwide commercial rights to three new candidates in the clinic and a leadership position in the adenosine pathway.

In addition to further characterization and confirmation of the adenosine gene signature increases our confidence that we can identify the patients most likely to benefit from therapy with super elements.

We intend to share meaningful updates on this program at ASCO in June.

I will now current turn the call back over to the operator for questions.

Answers.

Operator.

Thank you if you'd like to ask a question. Please.

Pressing star one on your telephone keypad. If you are using his speakerphone please make sure.

Well I guess exhaustive research.

Again press Star one to ask a question.

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To signal for cash.

Well first reserve Butler from Roth Capital Partners. Please go ahead.

Yes, Thanks, Richard two questions really one is around the antibodies produced.

The patients.

That's youve been able to cultivate patients treated with those six questionnaires.

Have you found any.

Common antibodies among those patients to date and consumed during the Gulf antigens, that's number one and number two when we see up and you may have said the so forgive me.

But I missed it when will we see updates with the although six dataset. Thank you.

Okay. Let me take the your first question on the antibodies.

So we have observed low tighter antibody responses in a few of these patients in one patient we've been able to identify the antigen and it is I'd, rather not say with near the gene is right now, but it was a bona fide known tumor antigens.

I mean.

Something that we will be very familiar with.

So.

What we need to be doing now of course is serially monitoring stations and and trying to figure out what happens to their tighter of this antibody now in addition to that.

We like many others are.

And the B cells from patients and looking at the individual b cells and trying to dissect out what these antibodies might be reacting with.

As as I think you're aware the nature papers back a month ago or so highlighting.

Importance of B cells infiltrating tumors as being more importantly in terms of predicting responsible T cells.

Really heightened our motivation in this area and as you know on the former antibody Guy So I love antibodies.

And they seem to work pretty well a lot of different things. So we're really excited about.

About the potential important said the usual immunity part of the Io therapy.

But really it's very early in this work and so we will have a lot of information yet as to what the importance of those antibodies are and what they might do now in terms of data on those six.

Escos going to be.

I mentioned that there's going to be mostly about 444 leno and the biomarker.

I think Oh six work, we'll wait till city in November.

Call swept through crucial.

Thank you we'll next go with it.

Team from Mizuho. Please go ahead.

Great. Thanks for taking my question.

Just two questions.

The first this is really I'm not gonna team, taking the churn just understanding tiger will incorporate that into the clinical trials are ongoing and how you see that from a clinical practice perspective, and then just on 8008 apologies, but can you confirm the dose that year settled on.

Okay, let's take the first a question so as I mentioned in my remarks.

We've already enrolled earn additional approximately 25 patients, which which had the aim of confirming what we described in new cancer discovery paper.

And so far we don't have all the data and on was 25 patients it appears to be holding up very nicely.

We're now.

Leading with Kale wells and lots of good.

Got leaders in their renal cell cancer area.

Probably in a few months, we'll we'll be in a position where we'll talk about how we will incorporate.

This biomarker into our clinical trial plans, but I can tell you Mara that it will be a very important part of our clinical trial.

Okay.

Now your question on 818.

We've recently enrolled patients that 600 milligrams the I'd.

We've just gotten through the DLC period on that we don't see any dose limiting toxicity that dose.

We've confirmed very substantial receptor occupancy.

And we're following those patients now I think that this does we have a few other measurements we have to make in addition to our receptor engagement to some other functional assays that we'll be looking at.

And also even though the make it through the DLC period is nice to get a little bit more follow up on these patients because you don't want to see side effects beyond the DLC period.

But I think that a dose of the.

I think that we have the dose of around four 600.

Okay. Thank you appreciate it.

Thank you we'll next go with GE.

From Jefferies. Please go ahead.

Yes, Hey, guys. This is cheat on for bearing Richard just wanted to maybe get a little bit more color almost 25 additional RCC patients you said you had.

I was wondering if you had any details on terms of maybe how these patients compared to the existing patient that we've already seen and I've a couple of follow up questions.

Well I mean pretty much the same kind of patients we did restrict the number of prior therapy is a little more because of course in our original 68 patients being a phase one study and thank you for raising this point there were all kinds of typical phase one patients.

In this so we did we did try to get a little better patients and of course, the other big things additional.

25 patients was that you had to have failed an io and at Teekay <unk>.

In the reason we did that is obvious in the last year or two it has now become.

Standard practice.

To give a T.K. all in I O either first line or first thing second line.

So those are the those are the differences.

Got it that's that's helpful. And then just two other questions that I had was heading into ASCO, how many more patients worth of data could we expect force Friday and in prostate cancer I believe.

On the Ascos do you poster.

There was perhaps some follow up plan at the 2020 at ASCO meeting. So just wanted to know maybe how many more patients. We can expect there for that indication and well these patients be stratified by identifying signature.

Thank you Charlie.

Okay prostate cancer patients I think there were what 33 or 35 patients on our Glasgow poster I mentioned the follow up their short I mean, our main goal now is we're following those patients and trying to get more more follow up we did not stratify for adenosine signature in that.

Obviously, we're going to be looking at that.

I mentioned this relationship of Cdseventy, three new Denison signature, which is an interesting observation, but doesn't get the exactly to your point, so but it does seem that cdseventy three makes adenosine them adenosine generates the adenosine gene signature all fits together very nicely, but basically.

I think what you're going to see at ASCO in our prostate cancers little bit more biology and more follow up.

Okay got it and then just my last question was on Oh, six when do you anticipate opening the combination dosing arm.

It's open.

Okay. Thank you very much.

Yeah.

Yeah.

Alright.

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And yet your question.

I'd like to remind everyone that in order to ask a question.

No by pressing star one.

Our next question from.

Hello.

It's C. Wainwright. Please go ahead.

Thank you.

Based on that to run right.

Thanks.

For taking my question.

Certainly goes as I've been asked but.

HM.

That.

Uh huh.

Study.

Before that.

Oh by the single agent.

Combination, but that doesn't.

Yes.

Myeloma.

Can you give us a little bit of a background I'm not an update on that.

Yes.

Thank you for that question, because I, often nickel off talking about that.

So the rationale for that study.

Which is being conducted at Johns Hopkins Medical School.

Which is.

Perhaps one of the best myeloma groups in the World.

The rationale is that.

There are two the NAV of courses anti Cdthirty eight antibody CD 38 turns out to be another important source of adenosine.

And Ah.

There.

I will go into the biochemistry, but in a view is broken down in one of the byproduct of that is adenosine.

And.

So the strategy of simply to combining adenosine antagonists like ours to fragments with their tomorrow in patients who have failed Dara.

So this isn't really nice study where patients who are growing through dara.

We'll get our 80 Ray inhibitor added to it.

Actually as a monotherapy because remember our R&D to antagonist as opposed to everyone else's has demonstrated monotherapy activity single agent activity. Many tumors. So we want to look at myeloma cells and they have some in vitro evidence for that.

And then I think within a month they come in with that there are two meb and the idea. There as you are trying to restore responsiveness to an otherwise resistant patients.

And of course, we're looking at bone marrow biopsies in London, and looking at identifying gene signature and all the all the you all the usual things so the rationale is.

Basically cdthirty eight so good source of.

Of adenosine and we want to come at that two ways, there's very nice publication on that that showed.

I think it was out of MD Anderson and various animal models that.

What they showed is that if you blockade to a receptor.

The eight to a receptor.

Together with anti Cdthirty eight you get a synergistic response in mass tumors.

We also looked at gene expression in patients in human biopsy samples and found that.

In in Cdthirty eight resistant patients.

There was the increase in a two a our into a two eight to a receptor expression. So that's the scientific rationale.

We're excited about that study because it gives us a lot of potential things that we can measure and give us a lot of good information.

Thank you. Thank you for that elaborate on so I appreciate it.

We'll next go with Tony Butler from Roth Capital Partners. Please go ahead.

Well it Clark will fall off.

Instead of 20 thoughtfully.

Paul Paul.

They will be patients who have mall.

Okay.

I'll turn it was hard to hear you, but I.

Good good 25 patients I mentioned, they have seen they have failed teekay item and an io.

But ultra based has failed to have said okay.

Just want to make sure.

Yeah, No we're clearly focusing in on the patient population look.

This our strategy is very simple.

We're going to late line.

In resistant patients were endpoints can be obtained presumably faster and so forth and then of course move up earlier as a.

As as we get more experience.

Now the interesting thing is is that.

With the success of Io.

First one renal.

And second line.

There are many many more patients who are.

Surviving to see second third fourth line.

So that is definitely becoming as we predicted by the way it is becoming a new entity or you know as a a serious patient population with unmet need.

Thank you.

Oh no.

No questions at this moment I'd like to get the conference back over to the much majors.

No closing remarks.

Okay. All this is Richard Miller. Thank you all for participating in this call. It. Thank you for those great questions.

Look forward.

Updating you on future calls and of course hopefully.

You at.

At our ASCO meeting thank you very much.

This concludes todays.

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