Q2 2021 Curis Inc Earnings Call
[music].
Good afternoon, and welcome to the Harris second quarter, 2021earnings call.
Operator: Good afternoon, and welcome to the Curis second quarter 2021 earnings call. All participants will be in a listen-only mode.
All participants will be in a listen only mode.
Operator: Should you need assistance, please contact a conference specialist by pressing the star key followed by zero. After the company's prepared remarks, call participants will have an opportunity to ask questions. To ask a question, you may press the star key and then 1 on your touchtone telephone.
And you need assistance. Please I know conference specialist by pressing the star key followed by zero.
Yeah.
After the company's prepared remarks call participants will have an opportunity to ask questions.
I ask a question you May press Star and then 1 on your Touchtone telephone.
Operator: To withdraw your questions, you may press star and two. Please also note today's event is being recorded. At this time, I'd like to turn the conference call over to the company's Chief Financial Officer, Bill Steinkrauss. Please go ahead.
To withdraw your question you May press Star and 2.
Please also note today's event is being recorded.
At this time I would like to turn the conference call over to the company's Chief Financial Officer Bill Steinkrauss. Please go ahead.
Thank you and welcome to cure.
Bill Steinkrauss: Thank you and welcome to Curis' second quarter 2021 earnings call. Before we begin, I would encourage everyone to go to the investor section of our website at www.curis.com and find our second quarter 2021 earnings release in related financial tables. I would also like to remind everyone that during the call, management will be making forward-looking statements, which are based on our current expectations and beliefs. These statements are subject to certain risks and uncertainties, and actual results may differ materially.
Second quarter 2021 earnings call.
Before we begin I would encourage everyone to go to the investors section of our website at Www Dot <unk> Dot com.
Find our second quarter 2021 earnings release and related financial tables.
I would also like to remind everyone that during the call.
Management will be making forward looking statements, which are based on our current expectations and beliefs. These statements are subject to certain risks and uncertainties and actual results may differ materially.
Bill Steinkrauss: For additional details, please see our SEC file. Joining me on today's call are Jim Dentzer, President and Chief Executive Officer, and Bob Martell, our Head of R&D. We will be available for a question and answer period at the end of the call. I'd now like to turn the call over to Jim.
For additional details please see our SEC filings.
Joining me on today's call are Jim Dentzer, President and Chief Executive Officer and.
And Bob Martell, our head of R&D.
He will be available for a question and answer period and the.
The call.
I'd now like to turn the call over to Jim.
Yeah.
Thank you Bill.
James E. Dentzer: Thank you, Bill. Good afternoon, everyone, and thank you for joining us. At Curis, we are focused on developing the next generation of targeted cancer therapies that will meaningfully improve and extend patients' lives. In the second quarter of 2021, we made concrete progress towards that goal and laid the foundational groundwork to expand into additional areas where we believe we can make a difference. As a reminder, our lead asset, a novel small molecule IRAK4 inhibitor called CA4948, is currently being evaluated in nine distinct patient populations, two AML and MDS populations in monotherapy for patients with spliceosome or FLT3 mutation, two AML and MDS populations in combination therapy of CA4948 with azacitidine and venetoclax, and four B cell cancer populations, in combination therapy of CA-4948 with ibrutin.
Good afternoon, everyone and thank you for joining us today.
And curious we're focused on developing the next generation of targeted cancer therapies that will meaningfully improve and extend patients' lives.
In the second quarter of 2021, we've made concrete progress towards that goal and laid the foundational groundwork to expand into additional areas, where we believe we can make a difference.
As a reminder, our lead asset and novel small molecule Iraq for inhibitor called CA $49.48 is.
<unk> is currently being evaluated in 9 distinct patient populations.
2 AML and Mds populations and monotherapy for patients with spliceosome or flit 3 mutations.
2 AML and Mds populations and combination therapy of <unk> 49, and 48 with as decided Inc, and vanilla clocks.
And for B cell cancer populations and combination therapy of CA 494, 8 with Ibrutinib.
In addition, we are working with Dr. Ebay, plus Becker of the University of life stage.
James E. Dentzer: In addition, we are working with Dr. Uwe Plossbecker of the University of Leipzig on the Lucas IST to study CA4948 in monotherapy in patients with lower-risk MDS, as many of you have been following. The long isoform of IRAC4 or IRAC4L has been identified as the key driver of disease in the majority of patients with AML and MDS.
And the Lucas I S. T..2 studies CH, $49, 48, and monotherapy in patients with lower risk Mds.
As many of you have been following.
The long isoform of Iraq for or Iraq for L.
Has been identified as the key driver of disease in the majority of patients with AML and Mds.
James E. Dentzer: Curis has the most advanced drug that directly targets IRAC4 in clinical testing for these patients, and with each new batch of data, our excitement for CA-49-48 grows even further, with its manageable and predictable safety profile and demonstrated ability to show deepening efficacy the longer patients remain on treatment. At the IHA meeting in June, we were especially pleased to share updated data from the monotherapy arm of the Phase I-II AML and MDS study
I'm curious has the most advanced drug that directly targets Iraq for in clinical testing for these patients.
With each new batch of data.
Our excitement for CH 49, 48 grows even further.
And with its manageable and predictable safety profile.
And demonstrated the ability to show deepening efficacy the longer patients remain on treatment.
At the <unk> meeting in June we were especially pleased to share updated data from the monotherapy arm of the phase <unk> AML and Mds study highlighting efficacy at multiple study doses are potentially differentiating factor that may enable us to help even the most.
James E. Dentzer: Highlighting Efficacy at Multiple Study Dose, a potentially differentiating factor that may enable us to help even the most extremely sick patients in this historically underserved population. Our second program, our first-in-class monoclonal anti-VISTA antibody, CI8993, has also been making good progress. We've been pleased with patient enrollment in the phase one dose escalation study in relapsed or refractory solid tumors and are on track to provide a substantive initial report on safety by year-end, including what we hope to be signs of early success in managing the CRS side effects known to be associated with antivista therapy. All told,
Extremely sick patients in this historically underserved population.
Our second program.
Our first in class monoclonal anti Vista antibody Ci 80.993.
<unk> also been making good progress.
We've been pleased with patient enrollment in the phase 1 dose escalation study in relapsed or refractory solid tumors.
And are on track to provide a substantive initial report on safety by year end.
Including what we'd hoped to be signs of early success in managing the Crs side effects known to be associated with anti Vista therapy.
All told we continue to progress through 2021.
James E. Dentzer: We continue to progress through 2021 as a year of execution for Curis. With that, Let's dig into some detail on our ongoing program, starting with the IRAC-IV program in leukemia. At EHA earlier this summer, we were pleased to present updated data from the monotherapy arm of our AML and MDS study, which reinforced previously observed findings of single-agent efficacy across the spectrum of late-line AML and MDS patients, despite these patients having already experienced several unsuccessful prior lines of therapy.
A year of execution procure us.
With that.
Let's dig into some detail on our ongoing programs starting with the Iraq program in leukemia.
And <unk> earlier. This summer we were pleased to present updated data from the monotherapy arm of our AML and Mds study, which reinforced previously observed findings of single agent efficacy across the spectrum of late line AML and Mds patients.
Despite these patients having already experienced several unsuccessful prior lines of therapy.
As a reminder, the data in our <unk> presentation identified a subset of patients with specific genetic mutations that make their disease highly amenable to treatment with CA 4948 based on the drug's mechanism of action.
James E. Dentzer: As a reminder, the data in our EHA presentation identified a subset of patients with specific genetic mutations that make their disease highly amenable to treatment with CA4948 based on the drug's mechanism of action. Of the four valuable patients with a spliceosome or FLT3 mutation, all four achieved an objective response. This early success provides a key validation of the scientific thesis that U2 AF1 and the SF3B1 spliceosome mutation are specific drivers of the oncogenic long isoform of IRAC4, which CA-4948 is explicitly designed to target.
Of the 4 evaluable patients with a spliceosome or flip 3 mutation.
All 4 achieved an objective response.
This early success provides a key validation of the scientific thesis.
And that Youtube F 1 and.
And <unk> spliceosome mutations are specific drivers of the oncogenic long isoform of Iraq for which see a $49.48 is explicitly designed to target.
In the broader patient population and those patients without a spliceosome <unk> 3 mutation. We also saw encouraging signs of efficacy.
James E. Dentzer: In the broader patient population, in those patients without a spliceosome or FLT3 mutation, we also saw encouraging signs of efficacy. 9 of 11 evaluable patients in this group achieved tumor reduction or were able to maintain a blast count in the normal range. The next step in our clinical plan is to address this population in combination therapy of CA4948 with azacitidine or venetoclax. We hope that CA-4948, with its unique mechanism of action and demonstrated disease-modifying capability, will prove an important addition to the combination therapy tool set in the battle against AML and MDS.
9 of 11 Evaluable patients in this group achieved tumor reduction.
And we're able to maintain a blast counts and the normal range.
The next step and our clinical plan is to address this population and combination therapy of <unk> hundred 4900, 48, with Azacitidine or venetic locks.
We hope that CA $49.48, with its unique mechanism of action and demonstrated disease modifying capability will prove and important addition to the combination therapy toolset in the battle against AML and Mds.
The data presented at <unk> also highlighted the strong safety profile of CA 49, 48, with no dose limiting toxicities related to Milo suppression and no overlap in dose limiting toxicities with <unk> or venetic blocks, which are planned where combination studies.
James E. Dentzer: The data presented at EHA also highlighted the strong safety profile of CA4948 with no dose-limiting toxicities related to myelosuppression and no overlap in dose-limiting toxicities with azazitidine or venetoclox, which are planned work combination studies with CA4948. The dose-limiting side effect at higher doses consisted of uncomplicated rhabdomyolysis or elevated CPK and muscle soreness, which was manageable, quickly and easily detected, readily reversible, and did not limit further treatment at a reduced dose level, of Nodes, those patients who did experience rhabdomyolysis at higher doses, generally had predisposing facts, such as taking satins or strenuous exercise, and last.
We see a $49.48.
The dose limiting side effect at higher doses consisted of uncomplicated rhabdomyolysis or elevated CPA and muscle soreness, which was manageable.
Quickly and easily detected readily reversible and did not limit further treatment at a reduced dose level.
Of note those experience those patients who did experience rhabdomyolysis at higher doses.
Generally had predisposing factors, such as taking sentence or strenuous exercise.
And lastly.
James E. Dentzer: We were also pleased to report at EHA an update on the pharmacokinetic analysis for CA4948. At the 300 milligram BID dose, we are achieving pharmacokinetic exposure in patients that correlates to 98% target inhibition in preclinical models. These impressive data further our confidence in CA4948 as a novel and robust IRAC4 inhibitor that has the potential to significantly advance therapeutic options for patients with AML and MDS, in first-line patients whose bone marrow has not been irrevocably damaged by cancer or by prior cytotoxic treatment. It has been shown that clear and substantial hematologic recovery is achievable within a few months if leukemic blast levels are effectively reduced.
We were also pleased to reported Bihar and update of the pharmacokinetic analysis for CA $49.48.
At the 300 milligram IV dose.
We are achieving pharmacokinetic exposure in patients that correlates to 98% targeted inhibition in preclinical models.
These impressive data further our confidence and CA 4900, 48, as a novel and robust Iraq for inhibitor that has the potential to significantly advance therapeutic options for patients with AML and Mds.
And first line patients, whose bone marrow has not been irrevocably damaged by cancer.
Or by prior cytotoxic treatments and.
It has been shown that clear and substantial hematologic recovery is achievable within a few months if leukemic blast levels are effectively reduced.
James E. Dentzer: In contrast, for the late-line patient in our study, it is important to remember that they already have deeply scarred dysfunctional marrow, which may delay or even prevent successful hematologic recovery. GA4948, like other cancer therapies, addresses the underlying cancer, but it is not by itself a marrow stimulating agent. We are therefore very pleased to see signs of hematologic recovery in these extremely sick patients after only a few months of treatment. From a regulatory perspective, our goal is to have 10 to 20 patients with spliceosome mutations on the drug by year end. Assuming that the data remained consistent.
In contrast for the late line patients in our study.
It is important to remember that they already have deeply scarred dysfunctional mero, which may delay or even prevent successful hematologic recovery.
Ta 4900, 48 like other cancer therapies.
Addresses the underlying cancer.
But it is not by itself.
Stimulating agent.
We are therefore very pleased to see signs of hematologic recovery.
And these extremely sick patients.
After only a few months of treatment.
From a regulatory perspective.
Our goal is to have 10 to 20 patients with spliceosome mutations on drug by year end.
Assuming the data remain consistent.
James E. Dentzer: We hope to be in a position to reach out to the FDA in the first half of next year to discuss the potential for a rapid approval path, given the compelling data observed to date and the impressive pace of enrollment. We are optimistic that we can meet this goal. The spliceosome population is only one of the nine population groups we are studying with CA4948, but we believe this may be the data which matures the quickest, enabling the earliest discussions with FDA.
We hope to be in a position to reach out to the FDA in the first half of next year to.
To discuss the potential for a rapid approval path.
Given the compelling data observed to date and.
And the impressive pace of enrollment we are optimistic that we can meet this goal.
The spices and population is only 1 of benign population groups. We are studying with CA 4948, but we believe these may be the data, which mature the quickest, enabling the earliest discussions with FDA.
While the monotherapy studies push ahead.
James E. Dentzer: While the monotherapy studies push ahead, the Incremental Positive Safety Find showing no overlapping dose-limiting toxicity with azacitidine or venetoclox was an important next step in the development of CA4948 in combination therapy for the broader population of AML and MDS patients. These findings underscore the relevance and importance of the updated preclinical data also presented at EHA, which highlighted CA4948's synergistic anti-tumor activity when used in combination with azacitidine and venetoclax in leukemia cell lines before moving on from Leukenia.
The incremental positive safety findings.
No overlapping dose limiting toxicity with is decided in orphan and clocks, where and important next step in the development of $49.48, and combination therapy for the broader population of AML and Mds patients.
These findings underscore the relevance and importance of the updated preclinical data also presented at Ehealth, which highlighted CA $49.48, synergistic anti tumor activity when used in combination with azacitidine and <unk> and leukemia cell lines.
Before moving on from leukemia.
James E. Dentzer: I would like to briefly touch on the ongoing Phase 2 lupus IST trial for patients with lower risk NDS being led by the co-chairman of EHA's Scientific Working Group on MDS, Dr. Uwe Plotschbeck. As a reminder of the study's rationale, if successful, it could lead to a potential breakthrough in the MDS field. Current Standard of Care with EPO Stimulating Agents can be effective for patients with lower-risk MDS. However, this effect is often transmitted.
I would like to briefly touch on the ongoing phase 2 Lucas <unk>.
And for patients with lower risk Mds fees.
Being led by the co chairman of Ehealth scientific working group on Mds, Dr. <unk> Becker.
As a reminder of the studies rationale.
If successful.
It could lead to a potential breakthrough and the Mds field.
Current standard of care.
Epo stimulating agents.
Can be effective for patients with lower risk Mds. However, this effect is often transient.
James E. Dentzer: It is not disease-modifying, and it does not affect further disease complications and progression to AML. With its direct targeting of IRAC-4 and strong safety profile, we believe CA-4948 could potentially offer a safe and disease-modifying alternative for patients at earlier stages of disease. With that, let's move on to lymphoma. We reported updated clinical data from our phase 1 dose escalation study of CA4948 for the treatment of patients with relapsed or refractory NHL or other hematologic malignancies at ASH last December.
And is not disease modifying.
And it does not affect further disease complication and progression to AML.
With its direct targeting of Iraq, 4 and strong safety profile. We believe CA 49, 48 could potentially offer a safe and disease modifying alternative for patients at earlier stages of disease.
With that.
Let's move on to lymphoma.
We.
Ported updated clinical data from our phase 1 dose escalation study of CA $49.48 for the treatment of patients with relapsed or refractory NHL or other hematologic malignancies at Ash last December.
These data highlighted durable reductions in tumor burden in 6 of 7 evaluable patients treated with 300 milligrams of CA 4948 twice daily.
James E. Dentzer: These data highlighted durable reductions in tumor burden in six of seven evaluable patients treated with 300 milligrams of CA4948 twice daily following a median of four prior lines of therapy. It is important to reiterate that seeing clear efficacy with a novel monotherapy agent and seeing that this efficacy is durable over such an extended period of time for these extremely sick patients is enormously encouraging and has provided powerful affirmation of our intention to launch the current combination study evaluating CA4948 with ibrutinib. As a reminder, enrollment in the combination study began in Q1 of this year, with CA-49-48 doses starting at 200 milligrams and escalating to 300 milligrams BID.
Following a median of 4 prior lines of therapy.
It is important to reiterate that seen clear efficacy with a novel monotherapy agent and.
And seen that this efficacy is durable over such an extended period of time, because these extremely sick patients.
Is enormously encouraging and provided powerful affirmation of our intention to launch the current combination study evaluating CA $49.48 with Ibrutinib.
As a reminder, and.
Enrolment and the combination study began in Q1 of this year.
With CA 4948 doses, starting at 200 milligrams and.
And escalating to 300 milligrams PID.
We expect to report initial data from this study at a medical meeting and the first half of 2022.
James E. Dentzer: We expect to report initial data from this study at a medical meeting in the first half of 2022. Now, I'd like to turn to our VISTA program with CI 8993, our first-in-class monoclonal antibody for the treatment of patients with relapsed or refractory phlegm. We believe CI-8993 is the most advanced anti-VISTA antibody currently in clinical development and has the potential to be a game-changing cancer therapy.
Lastly.
I'd like to turn to our Vista program with Ci $89.93 or.
Our first in class monoclonal antibody for the treatment of patients with relapsed or refractory solid tumors.
We believe Ci $89.93 is the most advanced anti Vista antibody currently in clinical development.
And has the potential to be a game changing cancer therapy.
In June we hosted a virtual symposium.
James E. Dentzer: In June, we hosted a virtual symposium, gathering industry thought leaders and respected academics to discuss the emerging understanding and opportunities surrounding this immune checkpoint. The excitement and interest in our program in both the clinical and academic communities are very high, and we look forward to reporting an initial update by year end. Briefly, I'd like to give you a sense of why we're so excited about this program. Existing Major Checkpoint Inhibitors, Function to Enhance T-Cell Priming, such as anti-CTLA-4 antibodies, or Relieve T-cell Exhaustion, such as anti-PD-1 or PD-L1 antibodies; all of these have two key limitations.
Gathering industry thought leaders and respected academics to discuss the emerging understanding and opportunities surrounding this immune checkpoint.
The excitement and interest in our program in both the clinical and academic communities is very high and we look forward to reporting and initial update by year end.
Briefly.
I could give you a sense of why we're so excited about this program.
Existing major checkpoint inhibitors.
Function to enhance T cell priming.
Such as anti <unk> 4 antibodies.
Or relief T cell exhaustion.
As anti PD, 1 or PD lone antibodies.
All of these have 2 key limitations.
James E. Dentzer: First, CTLA-4 and PD-1 Checkpoint cannot act on T-cells that are stuck in a quiescent state. Second, it is known that the CTLA-4 and PD-1 effect is actively impaired by myeloid-derived suppressor cells, or MDSCs, which promote T cell exhaustion and suppress pro-inflammatory macrophages.
First <unk>.
<unk> 4 and PD, 1 checkpoint cannot act on T cells that are stuck and acquire and state.
Second.
It is known that <unk>, 4 and PD, 1 effectiveness is actively impaired by myeloid derived suppressor cells or Mds fees.
And which promote T cell exhaustion and suppressed pro inflammatory macrophages.
In Vista.
James E. Dentzer: In VISTA, we find the checkpoint whose primary role is enforcing T cell quiescence. In addition, Vista is a known driver of MDSC, with this dual-pronged effect. It can sequester a large proportion of T cells in a quiescent state and prevent them from being acted upon by anti-CTLA-4 or anti-PB1 antibodies. Finally, we know that the expression of VISTA can increase dramatically as a compensatory mechanism during treatment with anti-CTLA-4 or anti-PD-1 or PD-L1 therapy for these reasons. We believe that therapeutic targeting of VISTA will be a crucial addition to the Immune Oncology R-Seq.
We signed and the checkpoint, whose primary role is enforcing T cell quite awesome.
In addition.
This is a known driver of Mds fees.
With this dual pronged effect.
Mr <unk> and sequester, a large proportion of T cells, and acquire and state and prevent them from being acted upon by anti <unk> 4 or anti PD 1 antibodies.
Finally.
We know that the expression of Vista can increase dramatically as a compensatory mechanism during treatment with anti <unk>, 4 or anti PD, 1 or PDL 1 therapy.
For these reasons.
We believe that therapeutic targeting of Vista.
Will be a crucial edition.
To the immune oncology Arsenal.
James E. Dentzer: To wrap up, I'd like to extend my utmost appreciation to the entire Curis team, who continue to work tirelessly in pursuit of these paradigm-altering breakthroughs. We're eager to build upon our efforts in the quarters to come and Advance Our Next Generation Targeted Cancer Program to help patients. With that, I'll turn the call over to Bill to review our financial results for the quarter. Bill?
To wrap up.
I'd like to extend my utmost appreciation to the entire curious team.
Who continue to work tirelessly in pursuit of these paradigm altering breakthroughs.
We are eager to build upon our efforts and the quarters to come and advance our next generation targeted cancer programs to help patients in need.
With that I'll turn the call over to Bill to review our financial results for the quarter Bill.
Thank you Jim.
Bill Steinkrauss: Thank you, Jim. For the second quarter of 2021, we reported a net loss of $10.8 million, or $0.12 per share, on both a basic and diluted basis, as compared to a net loss of $6.7 million, or 17 cents per share, on both a basic and diluted basis for the same period in 2020. Revenues for the second quarter of 2021 and 2020 were $2.3 million and $2.4 million, respectively. Revenues for both periods comprise primarily of royalty revenues recorded on Dementek and Roche's net sales of Aravid.
And the second quarter 2021.
We reported a net loss of $10.8 million or <unk> 12 per share on both a basic and diluted basis.
Compared to a net loss of $6.7 million or <unk> 17 per share from both the basic and diluted basis for the same period and 2020.
Revenues for the second quarter of 2021, and 2020 were $2.3 million and $2.4 million respectively.
Revenue for both periods comprised primarily of royalty revenues.
Courted on <unk> and Roche's net sales of urban edge.
Operating expenses for the second quarter of 2021 were $12.9 million as compared to $7.8 million.
Bill Steinkrauss: Operating expenses for the second quarter of 2021 were $12.9 million, as compared to $7.8 million for the same period in 2020. Cost of royalty revenues. $0.1 million for both the second quarter of 2021 and 2020; research and development expenses were $8.8 million for the second quarter of 2021 as compared to $5.3 million for the same period in 2020. The increase in research and development expenses for the quarter is primarily attributable to increased clinical and manufacturing costs for our program, as well as increased employee-related costs as a result of additional headcount.
The same period in 2020.
Cost of royalty revenue.
$1 million for both the second quarter of 2021 and 2020.
Research and development expenses were $8.8 million for the second quarter of 2021.
As compared to 5.3.
$3 million for the same period in 2020.
The increase and research and development expenses for the quarter is primarily attributable to increased clinical and manufacturing costs for our programs as well as increased employee related costs as a result of additional head count.
General and administrative expenses were $4.1 million the second quarter 2021, as compared to $2.4 million the same period from 2020.
Bill Steinkrauss: General and administrative expenses were $4.1 million in the second quarter of 2021 as compared to $2.4 million in the same period in 2020. The increase in general and administrative expenses was driven primarily by higher costs for stock-based compensation, personnel, professional and consulting services, and legal services.
The increase and general and administrative expense was driven primarily by higher cost for stock based compensation personnel professional and consulting services and legal services.
Bill Steinkrauss: For the second quarter of 2021 and 2020, total other expense was $0.2 million and $1.3 million, respectively. Total other expenses primarily consisted of imputed interest expense related to future royalty payments, partially offset in the second quarter of 2021 by a gain related to the extinguishment of debt. As of June 30, 2021, there were approximately 91.6 million shares of common stock outstanding. As of June 30, 2021, Curis' cash, cash equivalents, and investments totaled $160.7 million.
And the second quarter of 2021, and 2020 total other expense was $2 million and $1.3 million respectively.
Total other expense Pri.
Primarily consisted of imputed interest expense related to future royalty payments.
Largely offset and the second quarter of 2021.
Gain related to the extinguishment of debt.
As of June 32021, there were approximately 91.6 million shares of common stock outstanding.
As of June 32021, curious as cash cash equivalents and investments totaled $167 million we.
Operator: We expect that our existing cash, cash equivalents, and investments should enable us to maintain our planned operations into 2024. With that, I'd like to open the call for questions, Operator. Ladies and gentlemen, at this time, we'll begin the question and answer session. To ask a question, you may press the star and then one on the touch-tone telephone. To withdraw your questions, you may press star and two. If you are using a speakerphone, we do ask that you please pick up the handset before pressing the numbers to ensure the best sound quality.
We expect that our existing cash cash equivalents and investments so and enable us to maintain our planned operations and.
Into 2024.
With that I'd like to open the call for questions operator.
Ladies and gentlemen at this time, we'll begin the question and answer session to ask a question and you May Press Star and then 1 using a touchtone telephone to withdraw your question you May Press Star 2.
If you are using a speaker phone we do ask you. Please pick up the handset before pressing and numbers to ensure the best sound quality.
Operator: Once again, that is the star and then one to ask a question. We'll pause momentarily to assemble the roster. Our first question today comes from Justin Walsh from B-Riley Securities. Please go ahead with your question. Hi guys.
Once again that is star and then 1 to ask a question.
And we'll pause momentarily to assemble the roster.
Our first question today comes from Justin and Walsh from B Riley Securities. Please go ahead with your question.
Hi, guys. Thanks for taking my question and congrats on the progress.
James E. Dentzer: Thanks for taking the questions. Congratulations on the progress. To start off, as the VISTA safety data approaches, can you remind us what changes were made to this trial versus prior Janssen trials that increase your confidence that the asset will prove safe? And what would you view as a good outcome for the safety readout? Thanks, Justin. Really appreciate the question. Bob, you're probably the best person to talk to about that. Yeah, thanks, Justin.
To start off as the safety data approaches can you remind us what changes were made to this trial versus prior Janssen trials that increase your confidence that the asset will prove safe and what would you view as a good outcome for the phase II readout.
Thanks, Jess and really appreciate the question Bob you are probably the best person to talk to that.
Yeah. Thanks, Justin So as you know the Janssen trial was run a number of years ago and.
Robert E. Martell: So, as you know, the Janssen trial was run a number of years ago. Since that time, there's been a lot of study of cytokine release syndrome, which was the dose-limiting toxicity that they experienced in one patient on that study. With the CAR-T therapies coming out in the oncology field, cytokine release syndrome has been much more manageable, and clinicians understand much better how to deal with this. In fact, a number of guidelines have been published since that time, including NCCN guidelines and others. So we've implemented a number of factors around those guidelines into our protocol.
Net time.
And there's been a lot of study.
And released syndrome, which was the dose limiting toxicities of day had experienced and 1 patient and that study.
With the car T therapies coming out and the oncology field.
Medical and release syndrome has been much more manageable and clinicians understand much better how to deal with this.
In fact, a number of guidelines have been published since that time, including <unk> and CCN guidelines and others.
So we've implemented a number of them.
Factors around those guidelines into our protocols.
Robert E. Martell: I think also very importantly, we've done quite a few preclinical experiments to better understand cytokine release and how to potentially mitigate that. So to that end, we've determined that performing a fairly quick desensitization for patients, at least in preclinical models, in those models, we were able to reduce or even completely mitigate cytokine release findings. And so we've implemented a brief sort of desensitization or dose escalation that takes about a week for patients on a couple of different infusions.
And also very importantly leaves and.
In the next 2 have done quite a few preclinical experiments to better understand the cytokine release and how to potentially mitigate that so to that and.
And we've determined that.
Performing <unk>.
Fairly quick desensitization for patients.
At least in preclinical models and.
And those models, we were able to reduce or even completely mitigates.
Cytokine release.
Findings and so we've implemented a brief.
And sort of desensitization, our dose escalation that takes about a week for patients.
And a couple of different infusions, and we do that prior to starting the dosing and believe that that will help mitigate this.
Robert E. Martell: And we do that prior to starting the dosing and believe that that will help mitigate the, You know, the end result that we hope to see is that we're able to manage these patients who have a brief cytokine release syndrome at the beginning, during, and slightly after their infusion. Generally, this goes away fairly quickly. And what we've found, and what Jansen actually found also, is that the intensity and frequency of getting some cytokine release symptoms after dosing reduces with subsequent doses. So initially, we'd like to see that we can get through that initial dose and then continue on with treatment of these patients once they become desensitized.
The end result that we hope to see is that we're able to manage.
These patients who have agreed <unk> syndrome.
At the beginning during and slightly after their infusion.
Generally this goes away fairly quickly and what we've found and what Janssen and actually found also is that the.
Intensity and frequency and getting some cytokine release symptoms after dosing reduces and subsequent doses. So initially we'd like to see that we can get through that initial dosing and.
And then continue with treatment of these patients once they become desensitized to the cytokine release.
James E. Dentzer: You mentioned what would be the success factor really for year end on this. There are really two big catalysts for VISTA.
Yes.
Yes, yes.
You mentioned what are the what would be the success factor really for year and for this they are really 2 big catalysts for this the first 1 is the 1 we're going to address this year that safety of course to the longer term loan will be efficacy.
James E. Dentzer: The first one is the one we're going to address this year; that's safety. Of course, the longer-term one would be efficacy. The first one was, obviously, in Jansen's study, they ran into CRS early on, and our thesis is that CRS is manageable for all the reasons Bob said.
First 1 was obviously and Janssen study.
They.
They ran into Crs early on and and our thesis is Crs is manageable for all the reasons Bob said.
James E. Dentzer: So this year, by year end, what we wanna be able to fundamentally de-risk that program from a safety perspective. Effectively, with five more years under our belts, both Curis, Dartmouth, and Immunex, but also the industry as a whole and our knowledge of CRS, we can manage CRS, and we can get this drug up into the therapeutic range. And then, of course, the next goal will be sometime next year, and that is now we begin the hunt for... somewhere in between that 0.5 and 2.0 mg per kg.
So this year by year, and what we want to be able to do is fundamentally derisk that program from a safety perspective.
Effectively that with 5 more years under our belts, both curious chart within and index, but also the industry as a whole and our knowledge of Crs that we can manage Crs and we can get this drug up into the therapeutic range and then of course. The next goal will be sometime next year and that is now we begin the hunter per EFT.
You can see.
Somewhere in between that 5 and to point out makes per day, but first things first this year is all about derisking. The program hitting that first really important catalysts for value creation and that is proving that this drug can be dose escalated and the crs can be managed.
James E. Dentzer: But first things first, this year is all about de-risking the program, hitting that first really important catalyst of value creation, and that is proving that this drug can be dosed escalated and that CRS can be managed.
Got it thanks.
James E. Dentzer: Got it, thanks. And one last question for me. So we previously expected the CA4948 plus Brutonib data by the end of this year, but it looks like we won't get it until the first half of next year now. Has enrollment been challenging, or are we just seeing the timelines being honed as we move forward? No, I think everything is moving really quite a pace.
1 last question from me. So we've previously expected the CH 49, 48, plus ibrutinib data by the end of this year, but it looks like we won't get it until.
The first half of next year now has enrolment and challenging or are we just seeing the timelines being honed as we move forward.
No I think everything is moving really quite a pace. We're really pleased with that I think it's a reflection of and we want to make sure to present. These data at a medical conference and just the timing of the medical conferences means if youre going to get the data submitted and all of that that's going to be a first half of 2022 conference.
James E. Dentzer: We're really pleased with that. I think it's a reflection of how we want to make sure to present these data at a medical conference. And just the timing of the medical conferences means if you're going to get the data submitted and all that, that's going to be a first half of 2022 conference. I think our focus for this year end continues to be on the spliceosome patients in the AML and MDS study. But all nine studies, I think we're really pleased with the pace of movement on them all, and specifically in enrollment with the combo with the hybrid.
I think our focus for this year and.
<unk> continues to be on the spliceosome patients and AML and Mds study, but all 9 studies.
I think we're really pleased with the with the pace of moving on the mall and specifically and the enrollment with the combo with Ibrutinib.
Operator: Perfect, thank you. That's all the questions for you. Sure. Our next question comes from Alethea Young from Cancer Fitzgerald. Please go ahead with your question.
Perfect. Thank you that's all the questions here.
Sure.
Sure.
Our next question comes from Alethia Young from Cantor Fitzgerald. Please go ahead with your question.
Hi, Thanks for taking our questions and congrats on the progress this is neena on for Alethia.
Operator: Hi, thanks for taking our questions and congrats on the progress. This is Nina from Aletheia. We were wondering about Vista, can you just like characterize where you are in the dose escalation process?
And I'm wondering for feedstock can you just characterize where you are and the dose escalation process.
Operator: And then, oh, sorry. Go ahead. No, no, no. Go ahead. Sorry. And second, if you could just share more on why you picked these particular monotherapy populations for CA-948 and the rationale behind that.
Yes.
Oh, sorry go ahead no no no go ahead sorry.
And and second if you could just share more on why you pick. These particular monotherapy populations for CA, 4.9 and freight and.
And the rationale behind that.
Sure well first and foremost thank you for joining the call I appreciate it and for the questions and of course.
James E. Dentzer: Well, first and foremost, thank you for joining the call. I appreciate it.
James E. Dentzer: And for the questions, of course. So, let me address the dose escalation question in VISTA simply by saying that we're really going to postpone any discussion of our progress in that until year end. We've been pretty consistent, you know, over the course of this year, that our goal is to have that update at year end. And we, we frankly want to make sure that while we're very pleased with the progress to date, we want to make sure we've got enough experience under our belt by the time we get to year end to definitively say that we have de-risked the asset, that it can be managed and safely dose escalated.
And so let me address the dose escalation question and Vista simply by saying that we're really going to postpone any discussion of our progress and that until we get to year and we've been pretty consistent.
Over the course of this year that our goal is to have that update at year end and we frankly want to make sure that while we're very pleased with the progress to date, we want to make sure. We've got enough experience under our belt by the time, we get to year end to be able to definitively say that we have derisked the asset that it can be managed.
And safely dose escalated and I frankly want to.
James E. Dentzer: And I frankly want to, you know, wait and give any sort of progress update on that program until we get to that point. On the next question on CA 4948, there are a couple of things that are important about the different populations that we're testing in and why we're selecting the ones that we did. So I'll start with.
Weighted and giving any sort of progress update on that program that until we get to that point on the next question on CA 4.9 and 4.8.
There are a couple of things that are important about the different populations that we're testing and and why were selected and the ones that we did too.
I'll start with.
The data on this program has been really exciting not just for us and of course for investors, but the.
James E. Dentzer: The data on this program has been really exciting, not just for us and, of course, for investors, but the investigators have been really excited about it, and that's why we've blown the doors open on investing in this program. It's why we've got nine separate populations ongoing, and all of this work was really initiated leading up to ASH last year. But with the positive data at ASH and the money we were able to raise, we were able to put our foot on the accelerator and run all of these studies simultaneously. So that's the first really exciting thing.
And the investigators.
And I've been really excited about it and it's why we've blown the doors out on investing and that this program. That's why we've got 9 separate populations ongoing all of this work really being initiated lean.
Leading up to ash last year, but with the positive data at ash and the money we were able to raise we were able to put our foot on the accelerator and run all of these studies simultaneously. So that's the first really exciting thing and the next thing is all of these studies really.
James E. Dentzer: And the next thing is all of these studies really, I think, have the ability to generate an incredible amount of value and represent a significant Value Creation Opportunity and Therapeutic Options in and on MDS. The focus for monotherapy is going to be on those patients who are part of a population that's directly targeted by the drug. And you may remember the drug has a dual targeting mechanism for MLMDS purposes. It's IRAC4 and FLT3.
I think had the ability to generate and and.
Accretable amount value and represent a significant.
Value creation opportunity and therapeutic option.
For these patients.
In AML and Mds.
And the focus for monotherapy.
And is going to be for those patients who are part of our population that is directly targeted by the drug and you may remember the drug has a dual targeting mechanism for AML and Mds purposes, It's Iraq for inputs right. So of course, the patient populations we've chosen there.
James E. Dentzer: So, of course, the patient populations we've chosen there are the IRAC4 population or the splice cell mutation patients and patients with a FT3 mutation. Everybody else is going to get this in combination therapy, in AML and MDS, that is, with Aziz Zaiduddin and Veneda Clark because, you know, those are the drugs the clinicians would look to today. We want to make sure that we can combine it safely with them, and then our unique mechanism of action would further their improvement in that broader population. As you go to ibrutinib in B-cell cancers... we look to use this drug wherever you find dibrutinib is being used, period. For the long term.
Our.
And the Iraq, <unk> population or the spices and mutation patients.
And patients with a <unk> mutation.
Everybody else is going to get this and combination therapy.
In AML and MBS, that's what <unk> and been and clocks.
And those.
So the drugs the clinicians would look to today, we want to make sure that we can combine safely with them and then our unique mechanism of action would further their improvement in that broader population and should go to ibrutinib.
And b cell cancers.
We look to use this drug.
Wherever you find Ibrutinib is being news period long term, that's the commercial strategy.
James E. Dentzer: That's the commercial strategy, that if you're on iBrutenib today, you are on it precisely because it down-regulates NF-kappa B. Well, there are two pathways that drive NF capital. One is the BCR pathway. That's addressed with A. Bruton
And that if you're on Ibrutinib today.
You're on it precisely because it downregulates Nf Kappa B.
Well there are 2 pathways that drive Nf Kappa B.
1 is the <unk> pathway.
That's addressed with Ibrutinib.
James E. Dentzer: Second is the toll-like receptor pathway. That's addressed by our drug, 4948. In our view, if you want to downregulate NF-kappa-B, you want to stomp on it as hard as you can with both feet. That's with BTK, and it's with 4948.
The second is the toll like receptor pathway.
That's addressed by our drug by $49.8 and.
And I'll review, if you want to down regulate Nf Kappa B you want to stamp on it as hard as you can with both feet, that's with a b teekay and it's with 49, correct. So everybody longer term in our view ought to be considering hitting Nf Kappa b as hard as you can and going on combination therapy for Knight.
James E. Dentzer: So everybody longer term, in our view, ought to be considering hitting NF-kappa-B as hard as you can and going on combination therapy, 4948, and iGrud. For regulatory purposes, it gets a little more complicated because of what you want is to get the highest probability study going in as fast as you can, get an answer as fast as you can. So you want to try and identify comparatively aggressive indications, meaning indications where you can see an effect of the drug more quickly, and also a subset of those indications where Ibrutinib gets used where it doesn't work as well.
And I agree with it.
For regulatory purposes, it gets a little more complicated because of what you want is to get the highest probability study going in as fast as you can get an answer as fast as you can see you want to try and identify comparatively.
Gressett indications, meaning aggressive indications, where you can see and effective the drug more quickly.
And also a subset of those indications where ibrutinib gets used.
And where.
And frankly, ibrutinib doesn't do as well so think of those those applications are those indications where the Nf Kappa b activity is being driven on balance more from the toll like receptor side and the PCR side.
James E. Dentzer: So think of those applications or those indications where the NF-kappa B activity is being driven on balance more from the toll-like receptor side than the BCR side. So that's why we chose the three first indications of the four being assessed in combination with ibrutinib. So there's the BTK-naive bucket for marginal zone lymphoma; there's primary CNS lymphoma, and, of course, ABCD, and DLBCL. These would be three comparatively aggressive indications where ibrutinib is used, but they're also indications which have been associated with either toll-like receptor activity or MID-88 activity, activities which should be amenable to therapy with an ARIC4 inhibitor.
So that's why we've chosen the 3 <unk>.
And first indications of the 4 being.
And combination with Ibrutinib, so theres the BTT naive bucket for marginal zone lymphoma, There's primary CNS lymphoma and of course ABCD <unk>. These would be 3 comparative.
Comparatively aggressive indications, where ibrutinib gets us, but there are also indications which have been associated with either toll like receptor activity or mid 88 activity.
Activities, which should be amenable to therapy with and IRAK 4 inhibitor and then of course the last bucket is.
James E. Dentzer: And then, of course, the last bucket is anybody who has responded to ibrutinib in the past who has since become relapsed refractory. Those patients, of course, if you had gotten a response in the past on ibrutinib, you know that shutting down NF-kappa B was effective, and for whatever reason has stopped being effective, if you can add 4948 to that register, attack NF-kappa B from a different angle through the Tolec receptor path and bring that patient back under control, we think that's a really compelling case where you could say clearly the difference was adding 4948.
Anybody who has responded to ibrutinib and the past who has since become relapsed refractory those patients of course, if you used if you had gotten a response and the past on Ibrutinib.
You know that shutting down Nf Kappa B was effective.
And for whatever reason has stopped being effective if you can add 494.8 to that regimen.
Attack Nf Kappa B.
From a different angle through the toll like receptor path and bringing that patient back under control. We think that's a really compelling case, where you could say clearly the difference was adding per night.
James E. Dentzer: So that's really the walkthrough. The story is, of course, a complex one as you look across the breadth of AML and MDS and B-cell cancers. But in all cases, it's taking advantage of 4948's properties as a novel targeting drug going after IRF.
So that's really the walk through it. The story is of course, a complex 1 and you look across the breadth of AML and Mds and B cell cancers.
But in all cases, its taking advantage of <unk> 49 per <unk>.
Properties as a novel targeting drug going after Iraq book.
Okay that makes sense and and thank you for the detail.
Operator: Okay, that makes sense.
Operator: Once again, if you would like to ask a question, please press star and 1. Our next question comes from Yeo Jin from Ledlaw and Company. Please go ahead with your question.
Sure.
Okay.
Once again, if he would like to ask a question. Please press star and 1.
Our next question comes from Yale Jen from Laidlaw and company. Please go ahead with your question.
Operator: Good afternoon and thanks for taking the questions as well as congratulations on the progress. I'm just going to follow up the previous question regarding 4948 in lymphoma. You have naive patients, or you also have a root and nip resistant patient. [inaudible] What's your sort of expectation of hope, the kind of improvement you would like to see considered as a very positive outcome even at this early stage of the trial? Yeah, first, thank you for the question. I appreciate that. Actually, Bob, if you wouldn't mind, you might be a good person to talk to about that.
Good afternoon, and thanks for taking the questions congrats on the progress.
I was just going to fall off the previous question regarding.
For the day 48 and lymphoma.
And you'll have your patients are also you'll have a good day.
And net resistant patients.
What's your sort of expectation and hope that.
And.
Improved and you would like to see.
Considering.
A very positive outcome, even at this stage of the trial.
First thank you for the question I appreciate that actually Bob If you wouldn't mind you might be a good person to talk to that.
Thanks.
Robert E. Martell: So if we think about the different populations that Jim mentioned, let me start with the last population he mentioned, adaptive resistance. In this case, the patient's disease has been altered, ultimately, such that the BTK inhibitor is much less or not effective. Yet, as Jim mentioned, we know that the disease is driven by NF-kappa B. We also know from a variety of preclinical studies done by both us and outside academic investigators that have shown really strong synergy in multiple different systems by targeting IRAC4 or the midosomal pathway in combination with targeting the BTK pathway.
So if we think about the different populations that Jim mentioned, let me start with the last population and you mentioned the.
Adaptive resistance in this case the patient disease has been.
And alter and ultimately such that the <unk> inhibitor is much less or not effective yet as Jim mentioned, we know that that disease is driven by Nf Kappa B. We also know from.
A variety of preclinical studies done by both us and outside academic investigators that have shown strong synergy in multiple different systems by targeting.
Iraq for or the Minnesota pathway in combination with targeting the <unk> pathway, and so and that situation as a patient has developed resistance and on Ibrutinib. For example, and then we continue with Ibrutinib and 448.
Robert E. Martell: And so in that situation, if a patient has developed resistance to BRUTENIB, for example, and then we continue with BRUTENIB and add on 4948, what we would expect to see would be actual responses. By adding this additional hit on NF-kappa B and knowing that that has synergy, we'll hope to start to see objective responses in that study. And that's in a population that's resistant or refractory to BRUTENIB or another DTK inhibitor.
What we would expect to see with the actual responses.
By adding an additional hit on Nf Kappa B and knowing that that has synergy.
And we'll hope to start to see objective responses on that study.
And that's in a population that's resistant and refractory to ibrutinib or other <unk> inhibitor.
Robert E. Martell: In other settings, for example, ABC, DLBCL, or primary CNS lymphoma, these are populations where the midosomal pathway is favored. So, for example, in primary CNS lymphoma, we know that the majority of patients have a mid-ADH mutation; in ABCDLVCL, probably 40% of those patients have a mid-88 mutation.
And the other settings for example, and <unk> or primary CNS lymphoma. These are populations where.
And the <unk> pathway is favored.
So for example, and primary CNS lymphoma, we know that the.
The majority of patients have a mid 88 mutation.
And <unk>, probably 40% of those patients have a mid 88 mutation.
Robert E. Martell: And in these populations, abrutinib and other VTK inhibitors are somewhat effective but tend not to get very deep or durable responses. And so here we would expect to see a significant number of durable and deep responses. We ultimately will, once we get those data, discuss them with the FDA in terms of ultimately what type of benefit the patients are seeing, so we haven't made a statement of what specific response rate we want to see at this point.
And in these populations.
And and other PTK inhibitors are somewhat in fact effective but.
<unk> tends not to get very deep or durable responses and so here, we would expect to see.
A significant number of durable and deep responses.
<unk>.
We.
Ultimately, we will once we get those data.
Discuss them with the FDA in terms of ultimately what type of benefit the patients are seeing so we haven't.
Made a statement of what specific response rate and we want to see at this point.
Robert E. Martell: But those are the types of endpoints that we'll be looking for. Okay, that's very, very helpful. And maybe one more question here. In terms of 4948 and all this leukemia study, which is anticipated to start in the second half of this year, do you guys have any sort of timeline or refine the timeline in terms of when some of these studies might start? And thanks. Yeah, thank you, Gail.
But those are the type that would.
And we're looking for.
Okay. That's very very helpful and maybe 1 more question here in terms of 49.48 and all of these.
Give me a study which are anticipated to start in the second half of this year are you guys, having a sort of the timeline or what.
Fine tuned and timeline in terms of when some of this.
These studies might started and thanks.
Yes. Thank you, yes, so as you can imagine.
James E. Dentzer: So as you can imagine, we are moving as aggressively as we can across the board. So, as you know, we've got these nine studies moving. On the leukemia side, I think we're especially interested in getting data on the targeted monotherapy crowds, the spliceosome mutation, and FLT3 mutation populations. So those are moving, of course, the fastest.
We are moving as aggressively as we can across the board so and.
And as you know we've got these 9 studies moving.
In the leukemia side.
We are especially interested in getting the data on the targeted monotherapy crowds spliceosome mutations and flip 3 mutation and populations. So those are moving of course the fastest.
James E. Dentzer: I think we're also very excited about the studies that you mentioned that are starting in this second half in combination with azazitamine and venetoclox. The data that we've been able to present at EHA that are in our current corporate deck, you can see the combination data in preclinical studies is really compelling. We think we've got a very strong case for rapid approval, a rapid approval path with monotherapy, for spliceosome and FLT3. We should have data in spliceosome patients, as they say, by year end.
I think we're also very excited about the studies that you mentioned that are starting.
The second half the combination with <unk> and venetic clocks, the data that we've been able to present at <unk> that are and our corporate.
And our current corporate deck you can see.
The combination data.
Pre clinically is really compelling we think we've got a very strong pace.
For rapid approval, a rapid approval path with monotherapy with with spices and flit 3 we should have data and splicing zone patients as I say by year end.
James E. Dentzer: And then the combination therapy, that will take a little longer. But, of course, that gets to every other population, the broader commercial story, where every patient that's with AML and MDS ought to be looking for an IRAC4 inhibitor. And we, of course, have the lead. So our view would be, let's get all of these studies going simultaneously. The one that goes the fastest is probably the spliceosome crowd, but they're all really important. And we wanna make sure that as we're sprinting down the fastest regulatory path, we are following it up very quickly with data that will support broad application across the spectrum.
And then the combination therapy that will take a little longer but of course that gets to every other population and the broader commercial story, where every patient.
And with AML, and Mds ought to be looking for and IraQ4 inhibitor and we of course have delete. So our view would be let's get all of these studies going simultaneously, but 1 that goes the fastest is probably displace and some crowd, but they're all really important and we want to make sure that as we're sprinting down the fastest regulatory path. We are following it up very quickly.
Lee.
With data that will support the broad application across the spectrum.
Okay, Great that's very helpful and again congrats on the rapid progress.
James E. Dentzer: Okay, great. That's very helpful. And again, congrats on the rapid progress.
Thank you so much I really appreciate your support.
James E. Dentzer: Thank you so much. I really appreciate your support.
James E. Dentzer: And ladies and gentlemen, with that, we'll conclude today's question and answer session. I'd now like to turn the floor back over to the company's president and chief executive officer, James Dentzer, for a closing remarks.
And ladies and gentlemen, with that we'll conclude today's question and answer session.
And I'd like to turn the floor back over to the company's President and Chief Executive Officer, James Dentzer for closing remarks.
James E. Dentzer: Thank you, operator. And thank you, everyone, for participating in today's call. And, as always, thank you to the patients and families participating in our clinical trials, to our team at Curis for their hard work and commitment, and to our partners at Origin, Immunext, and the NCI for their ongoing help and support. We look forward to updating you again soon.
Thank you operator, and thank you everyone for participating in today's call.
And as always thank you to the patients and families participating and our clinical trials to our team at curious for their hard work and commitment.
And to our partners at origin, and Immunex and the NCI for their ongoing help and support we.
We look forward to updating you again soon.
Operator: Ladies and gentlemen, with that, we'll conclude today's conference call. We do thank you for attending today's presentation. You may now disconnect your lines.
Operator.
Ladies and gentlemen, with that we'll conclude today's conference call and we do thank you for attending today's presentation.
You may now disconnect your lines.