Q3 2020 Curis Inc Earnings Call
Good afternoon, everyone and welcome to <unk> third quarter 2020 earnings Conference call.
Operator: Good afternoon, everyone, and welcome to the Curis 3rd Quarter 2020 Earnings Conference Call. All participants will be in a listen-only mode.
All participants will be listen only mode.
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Please also note todays event is being recorded.
Operator: 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 Steinkraut. Sir, please go ahead.
At this time I'd like to turn the conference call over to the company's Chief Financial Officer Bill cycles. Sir. Please go ahead.
Thank you.
Bill Steinkraut: Thank you, and welcome to Curis's third quarter 2020 earnings call. Before we begin, I would encourage everyone to go to the investor section of our website at www.curis.com to find our third quarter 2020 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.
Welcome to <unk> third quarter 2020 earnings call.
Before we begin I.
I would encourage everyone to go to the investors section of our website at Www Dot <unk> Dot Com <unk> third quarter 2020 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.
Actual results may differ materially.
For additional details please see our SEC filings.
Bill Steinkraut: For additional details, please see our SEC filings. Joining me on today's call are Jim Dentzer, President and Chief Executive Officer, and Bob Martell, Head of R&D. We will also be available for a question and answer period at the end of the call. I'd now like to turn the call over to Curis' CEO, Jim Dentzer.
Joining me on today's call are Jim Dentzer, President and Chief Executive Officer and.
And Bob Martel head of R&D.
We will also be available for a question and answer period at the end.
On the call.
I'd now like to turn the call over to <unk> CEO, Jim Dentzer, Jeff.
James E. Dentzer: Thank you, Bill. Good afternoon, everyone, and thank you for joining us today. Our mission at Curis is to develop the next generation of targeted cancer therapies to meaningfully improve and extend patients' lives. In the third quarter, we made significant progress on that mission, despite the difficulties of the COVID-19 pandemic.
Thank you Bill.
Good afternoon, everyone and thank you for joining us today.
Our mission at Curis is to develop the next generation targeted cancer therapies can meaningfully improve and extend patients' lives.
In the third quarter, we made significant progress on that mission.
Despite the difficulties of the COVID-19 pandemic.
We remain on track to achieve all of our stated goals and milestones for 20 20-F.
James E. Dentzer: We remain on track to achieve all of our stated goals and milestones for 2020, as we prepare for the anticipated release of clinical results next month at AFT for CA-4948, our first-in-class IRAC TOR. We have two ongoing clinical studies. One, in patients with relapsed or refractory non-Hodgkin's lymphoma, and a second direct forest study, in patients with relapsed or refractory acute myeloid leukemia and high-risk myelodysplastic syndrome. Updates from both studies will be presented in an oral presentation and in poster sessions next month at the annual meeting of the American Society of Hematology. In addition,
As we prepare for the anticipated release of clinical results next month at Ash.
We see a 49 48.
Our first in class IRAK four inhibitor.
We have two ongoing clinical studies.
One in patients with relapsed or refractory non hodgkin lymphoma.
And the second direct for study.
In patients with relapsed or refractory acute myeloid leukemia and high risk Myelodysplastic syndromes.
Updates from both studies will be presented in an oral presentation and didn't post recession next month at the annual meeting of the American Society of Hematology.
In addition.
Earlier today, we were very pleased to announce that we have entered into a cooperative research and development agreement or credo.
James E. Dentzer: Earlier today, we were very pleased to announce that we have entered into a Cooperative Research and Development Agreement, or CRADA, with the National Cancer Institute, under which they will collaborate with us on the development of CA-4948. We are thrilled to announce this partnership as it substantially increases the number of reachable patients in a population of dire medical need without requiring an external dilutive financing or sizable financial commitment from Curis. We are eager to begin the collaborative process with our partners at the NCI, and we look forward to providing you with updates as we have them on CI 8993. Our progress has also been very exciting.
With the National Cancer Institute.
Under which they will collaborate with us on the development I see for 9.8.
We are thrilled to announce this partnership as it substantially increases the number of reachable patient population.
Population of dire medical need without requiring an external dilutive financing.
Or sizable financial commitment from cheers.
We are eager to begin the collaborative process with our partners at the NCR and we look forward to providing you with updates as we have them.
We see we see <unk> 80 993.
Our progress has also been very exciting.
Earlier this year, we announced our partnership with any next and the submission of our I N D. <unk> 80, 993, our first in class Vista inhibitor.
James E. Dentzer: Earlier this year, we announced our partnership with Immunext and the submission of our IND for CI-8993, our first-in-class VISTA inhibitor. In Q2, we announced that we received FDA clearance for that IND. Today, we are happy to report that in Q3, we were able to get our first clinical sites up and running and initiate dosing in our Phase 1a, 1b study in patients with relapsed or refractory solid tumors. All told, it was a very active quarter for Curis. We look forward to building on this progress through our year-end data updates and carrying that momentum into 2021. Now, let's dig into some detail on our ongoing clinical program. Our Phase I Dose Escalation Study of CI4948 for the Treatment of Patients with Relapsed or Refractory Non-Hodgkin's Lymphoma includes patients with diffuse large B-cell lymphoma, Waldenstrom's macroglobulinemia, and an oncogenic MITEI-88 mutation.
In Q2, we announced that we received FDA clearance of that Hi, Andy.
Today, we are happy to report that in Q3, we were able to get our first clinical sites up and running and initiate dosing in our phase 181, B study in patients with relapsed or refractory solid tumors.
All told it was a very active quarter for Curis.
We look forward to building on this progress through our year end data update.
Carrying that momentum into 2021.
Now, let's dig into some detail on our ongoing clinical programs.
As a refresher.
Our phase one dose escalation study of Cie.
For 9.8 for the treatment of patients with relapsed or refractory non Hodgkin's lymphoma includes patients with diffuse large b cell lymphoma Walton.
Waldenstrms Macroglobulinemia oncogenic Mydeighty eight mutation.
We are currently evaluating patients treated with 300 milligrams of CHF 49, 48 twice daily.
James E. Dentzer: We are currently evaluating patients treated with 300 milligrams of CA-4948 twice daily after observing clear dose response and tumor reductions at previous dose levels last week on November 4th. We disclosed clinical data from this study in an abstract that was accepted for oral presentation at the ASH conference in December, as reported in the abstract. CA-4948 has exhibited encouraging safety and pharmacokinetic properties at higher dose levels.
After observing clear dose response and tumor reductions at previous dose levels.
Last week on November 4th.
We disclosed clinical data from this study in an abstract was accepted for oral presentation at the Ash conference in December.
As reported in the abstract she a 49 48 has exhibited encouraging safety and pharmacokinetic properties.
And at higher just leveled clear single agent efficacy in a relapse refractory NHL patient population there.
James E. Dentzer: Clear Single-Agent Efficacy in a Relapsed Refractory NHL Patient Population, that had already seen a median of four prior lines of therapy before joining our study, to provide some additional context. Last year it asked.., we presented a small but intriguing data set that suggested CA4948 could potentially establish IRAC4 inhibition as a new mechanism of action, a novel way to treat patients with NHL, as it delivered a compelling safety and efficacy profile, particularly at higher dose levels in a monotherapy setting. This year's goal was to confirm that finding and also explore which of the efficacious dose levels of 200, 300, or 400 milligrams BID offered the best balance of safety and efficacy. Diving a bit deeper into the abstract data, which are from a July cutoff, we see that eight patients achieved a tumor burden decrease of 20% or greater from baseline, including four of the patients treated with 300 milligrams BID.
They had already seen a median of four prior lines of therapy before joining our study.
To provide some additional context last year at Ash, we presented the small but intriguing data set.
Suggested CH 49, 48 could potentially establish IRAK four inhibition.
As a new mechanism of action a novel way to treat patients with NHL.
As it delivered a compelling safety and efficacy profile, particularly at higher dose levels in a monotherapy setting.
This year's goal was to confirm that finding.
And also explore which I'd be efficacious dose levels of 200, 300, or 400 milligrams be I'd offered the best balance of safety and efficacy.
I think a bit deeper into the abstract data, which are from a July cut off.
We see the eight patients achieved a tumor burden decrease of 20% or greater from baseline, including four of the patients treated with 300 milligrams be I'd.
It is very encouraging the efficacy improved as dose levels increased.
James E. Dentzer: It is very encouraging that efficacy improved as dose levels increased. This was shown in both the study group as a whole and also in the case of a single patient, a Waldenstrom's patient, who, as of the July cutoff, had been on study for 18 months at multiple dose levels and achieved an objective response with a 66% tumor burden reduction. This patient started at an initial BID dosage of 50 milligrams and escalated through 100 mg, 200 mg, and 300 mg, demonstrating dose-dependent decreases in tumor burden at every level.
This was shown in both the study group as a whole and.
And also in the case of a single patient a woman's troms patient who.
Who adds up the July cut offs had been on study for 18 months over multiple dose levels.
And achieved an objective response with a 66% tumor burden reduction.
This patient started at an initial be I'd dosage of 50 milligrams.
And escalated through 100 milligrams 200 milligrams and 300 milligrams demonstrating dose dependent decreases in tumor burden at every level.
It is important to highlight again.
James E. Dentzer: It is important to highlight again that these are extremely sick patients who have received a median of four prior lines of therapy before entering the study. That we have been able to observe therapeutic effects in monotherapy, and that those effects are durable over such an extended period of time is enormously encouraging, and we look forward to the Ash Con, where we will provide an updated and expanded dataset with a later cutoff date for the data provided in the abstract, even the clear single-a We and our clinical investigators are eager to explore the combination of CA-4948 and ibrutinib in the clinic. As we mentioned on our August call, we could already see where the data were headed, and we made the decision to get the combination study up and running as quickly as possible.
These are extremely sick patients who have received a median of four prior lines of therapy before entering the study.
Yes, we have been able to observe therapeutic effect in monotherapy.
And that those effects.
Our durable over such an extended period of time is enormously encouraging and we look forward to the Ash conference, where we will provide an updated and expanded dataset with a later cut off date.
For the data provided in the abstract.
Given the clear single agent activity, we have seen in the clinic.
And the clear preclinical synergy we have seen we see a 49 40 gig is combined with a BTK inhibitor such as like Bruton Ned.
We and our clinical investigators are eager to explore the combination of see a 49 48 and that bruton it in the clinic.
As we mentioned on our August call.
We could already see where the data we're headed.
And we made the decision to get the combination study up and running.
As quickly as possible.
James E. Dentzer: Today, we are excited to announce that, working closely with our clinical sites, we have been able to amend the protocol of our existing study to include combination therapy, rather than having to file a completely new protocol and initiate a completely new clinical study. This allows us to leverage the clinical sites and staff currently active in our monotherapy study and should save significant time and resources as we speed our path to the clinic. The Combination Study has two parts, and it will be outlined in a trial-in-progress poster to be presented at the ASH Conference. Part 1 of the study design will be dose escalation, a 3x3 design with CA-4948 doses starting at 200 mg BID and escalating to 300 mg BID, and Ibrutinib doses appropriate for the respective NHL subtypes. Part 2 of this study will be an expansion basket of four cohorts. The first... in Marginal Zone Lymphoma, or MZL. The second season in ABC-DLBCL.
Today, we are excited to announce that in working closely with our clinical sites, we have been able to amend the protocol of our existing study to include combination therapy, rather than having to file a completely new protocol and initiate a completely new clinical study.
This allows us to leverage the clinical sites and staff currently active in our monotherapy study and should save significant time and resources as we speed our path to the clinic.
The combination study.
Has two parts.
And it will be designed and it will be outlined in a trial in progress poster will be presented at the Ash conference.
Part one of the study design.
We'll be dose escalation.
Three by three design with CA for nine point doses, starting at 200 milligrams, B.I.D. and escalating to 300 milligrams be I'd.
And that group does is appropriate for the respective NHL subtype.
Part two of the study will be an expansion basket of four cohorts.
First in marginal zone lymphoma or N.V.L.
The second is a b C D L Bcl.
The third.
James E. Dentzer: The third in primary central nervous system lymphoma, or PCNSL, and the fourth in NHL with adaptive ibrutinib resistance. Primary endpoints in the study will include established clinical endpoints, such as objective response rate and duration of response. But we will also explore response correlation with biomarkers we have identified that may help us enrich the patient population and help us determine the optimal path for registration, so far from scientific hypothesis, preclinical data, to clinical data. Each step of the journey has been a consistent step forward in the long-term vision for CA4948 in NHL, that IRAC-IV controls a critical pathway that is parallel to and complementary to the BTK pathway, and that inhibiting IRAC That is our vision in the NHL.
In primary central nervous system lymphoma.
Or P.C.N.S.L.
And the fourth in NHL with adaptive Ibrutinib resistance.
Primary endpoints in the study will include the established clinical endpoints such.
Such is objective response rate and duration of response.
But we will also explore response correlation with Biomarkers, we have identified it may help us enrich the patient population.
And help us determine the optimal path for registration.
So far.
From scientific hypothesis to preclinical data clinical data.
Each step of the journey.
It's been a consistent step forward in the long term vision for C. 49, 48 in NHL.
That Iraq for controls a critical pathway.
That is parallel to and complementary to the BTK pathway.
And that inhibiting IRAK four.
Provide incremental benefit to the vast population of patients.
Treated with a BTK inhibitor and may help mitigate resistance to BTK therapy.
That is our vision in NHL.
Now lets move onto leukemia.
James E. Dentzer: Now let's move on to leukemia and what many see as even more exciting than the NHL bid. Our second study of CA-4948 is in patients with relapsed or refractory AML and high-risk MDS, including those with spliceosome mutations that drive the expression of the oncogenic long isoform of IRAC4. In early July, we announced the dosing of the first patient in our open-label, phase one dose escalation study of CA4948 monotherapy in these patient populations. Since then, enrollment has proceeded particularly well.
And what many see as even more exciting than the NHL vision.
Our second study of CH 49, 48 is in patients with relapsed or refractory AML and high risk Mds.
Including those with displaces some mutations that drive the expression of the oncogenic long isoform of IRAK four.
In early July we announced the dosing of the first patient.
Our open label Phase one dose escalation study of CCH 49, 48 monotherapy in these patient populations.
Since then enrollment has proceeded particularly well.
You may recall that this study grew out with a groundbreaking work performed by Dr., Amit, Vermont and Dr. Daniel starts in ASCII presented at last year's asked conference.
James E. Dentzer: You may recall that this study grew out of groundbreaking work performed by Dr. Amit Verma and Dr. Daniel Starzanowski presented at last year's Ashcon, in which they identified the specific spliceosome mutation that drives disease in AML and MDS patients by causing the expression of the long isoform of IRAC4. We now know, based on their published work, that the long isoform of IRAC4 is oncogenic and further that IRAC 4L is overexpressed in over half the population of AML and MDS patients. This is of particular excitement to the team here at Curis. Drs.
In which the identified the specific splices on mutations that drives disease in AML and Mds patients by causing the expression of the long isoform of IRAK four.
We now know.
Based on their published work.
But the long isoforms of Iraq for his oncogenic.
And further.
<unk> Iraq for L is overexpressed in over half the population of AML and Mds patients.
A particular excitement to the team here at Curis doctors.
Doctors Burma and stars in ASCII also demonstrated.
James E. Dentzer: Verma and Starzanowski also demonstrated that inhibiting IRAC4L with a treatment of CA4948 substantially reduces leukemic blast formation in patient-derived Xenografts. Today, we are pleased to announce that the first two cohorts in the phase one dose escalation study have completely enrolled. The first cohort receives 200 milligrams twice daily, and the second cohort receives 300 milligrams twice daily. As we have previously discussed, we believe 200 milligrams is likely to be a therapeutic dose, and we will continue dose escalation until reaching the recommended phase 2 dose and Maximum Tolerable Dose. We will provide an additional overview of the study design and report initial interim data for these patients next month. We know that other drugs in single-agent studies in this late-line relapsed refractory population have struggled to show steep reductions in leukemic blast cells.
Then inhibiting IRAK four l.
With the treatment of CHF 49, 48 substantially reduces leukemic blast formation in patient derived xenograft.
Today, we are pleased to announce that the first two cohorts in the phase one dose escalation study have completely enrolled.
The first cohort received 200 milligrams twice daily.
And the second cohort received 300 milligrams twice daily.
As we have previously discussed.
We believe 200 milligrams is likely to be a therapeutic dose.
And we will continue dose escalation until reaching the recommended phase two dose and maximum and maximum tolerated dose.
We will provide an additional overview of the study design.
And report initial interim data for these patients next month.
We know that other drugs in single agent studies in this late line relapsed refractory population have struggled to show steep reductions in leukemic blast cells.
To be clear the data we will be presenting next month, we'll be early data.
James E. Dentzer: To be clear, the data we will be presenting next month will be early data. None the less... We hope to see data consistent with our preclinical findings. We remain confident that the novel approach of targeting Iraq's war... represents clear differentiation for CA 4948 in AML and MDS. Before moving on, I would like to add that this AML and MDS study, and the data we are presenting next month, are in addition to the NCI CRADA we announced earlier today. We are still in the early days of our partnership with NCI, and we look forward to providing you with updates on our partnership in the future. Now, I'd like to turn to CI 8993.
Nevertheless.
We hope to see data consistent with our preclinical findings.
We remain confident that the novel approach of targeting Iraq for.
Represents clear differentiation for C. A 49 48 in AML and Mds.
Before moving on I would like to add that this AML and Mds study.
And the data we are presenting next month.
In addition to the NC I Credo, we announced earlier today.
We are still in the early days of our partnership with the NCR and we look forward to providing you with updates on our partnership in the future.
Now I'd like to turn to see <unk> 80 993.
We believe that a therapeutic antibody such as C. <unk> 80 993.
James E. Dentzer: We believe that a therapeutic antibody, such as CI 8993, could provide potent Vista Blockade as a monotherapy in patients with certain solid tumors. Vista is a target we have long been excited about because of the critical role it plays in suppressing T cell activity when it, the Vista checkpoint, is activated. Conversely, blocking VISTA has been shown in preclinical studies to prevent T-cell suppression and thereby reactivate anti-tumor immune function.
Could provide potent vista blockade as a monotherapy in patients with certain solid tumors.
This is a target we have long been excited about because of the critical role. It plays in suppressing T cell activity went at the Vista checkpoint is activated.
Conversely, well.
Blocking that stuff has been shown in preclinical studies to prevent T cell suppression.
And thereby reactivate anti tumor immune function.
We also see significant combination potential and in the future.
James E. Dentzer: We also see significant combination potential and, in the future, may explore targeting VISTA in combination with a PD-1, PD-L1, or even a CTLA-4 inhibitor, as preclinical studies suggest that blocking VISTA significantly improves the efficacy of those checkpoint regulators. However, to date, there has been little meaningful progress targeting VISTA due to the various on-target side effects associated with pathway blockades, most notably However, progress in the development of CAR T therapy and the broader immunotherapy space over the last decade have made safe and effective VISTA regulation much more possible. To that end, we have initiated patients in a Phase 1a, 1b dose escalation study evaluating CI 8993 in patients with relapsed and refractory solid tumors, and enrollment is currently ongoing.
May explore targeting Vista in combination with the PD, one PDL, one or even a C. Chile four inhibitor.
As preclinical studies suggest that blocking vista significantly improves the efficacy of those checkpoint regulators.
To date, there has been little meaningful progress targeting Vista due to the various on target side effects associated with pathway blockade.
Most notably immune mediated toxicity and cytokine release syndrome.
However, progressing the development of car T therapies, and the broader immunotherapy space over the last decade.
Had me safe and effective Vista regulation much more possible.
To that end.
We have initiated patient dosing in a phase one a one be dose escalation study evaluating <unk> 80, 993 in patients with relapsed and refractory solid tumors and enrollment is currently ongoing.
We believe that see I 80, 993 has the potential to succeed beyond our previous PDL, One Vista program.
James E. Dentzer: We believe that CI 8993 has the potential to succeed beyond our previous PDL-1 VISTA program, a small molecule that demonstrated activity but did not provide the level of efficacy needed to compete with monoclonal antibodies in development at the time for the same target population. This is likely because large-molecule monoclonal antibodies like CI 8993 provide complete coverage of a receptor across multiple binding regions. By comparison, this small molecule interrupts only one or two contact points on a target receptor. In addition, monoclonal antibodies tend to firmly wrap around the receptor, almost like Velcro, as opposed to a small molecule which continually bounces on and off its target.
A small molecule that demonstrated activity, but did not provide the level of efficacy needed to compete with monoclonal antibodies in development at the time for the same target population.
This is likely because large molecule monoclonal antibodies like see <unk> 80, 993 provide complete coverage of a receptor across multiple binding regions.
By comparison.
Small molecule interrupts only one or two contact points on a target receptor.
In addition, one.
Monoclonal antibodies tend to firmly wrap around the receptor almost like velcro.
As opposed to a small molecule, which continually bounces on and off its target.
We believe <unk> 80, 993 is the most advanced anti Vista antibody currently in clinical development.
Bill Steinkraut: We believe CI-8993 is the most advanced anti-VISTA antibody currently in clinical development. We have received a lot of interest and excitement from the clinical community about this program. And we believe CI8993 has the potential to be a game-changing cancer therapy. We look forward to providing an overview of the study in a trial and progress poster at CITSE this week and providing additional updates in 2021. I want to emphasize how proud I am of the entire team at Curis, who, in the midst of an ongoing global pandemic, have worked tirelessly to ensure we hit every ambitious goal we set for ourselves this year. It is incredible to think that since we signed the deal to bring this new Vista asset on board in January.
We have received a lot of interest and excitement from the clinical community on this program and we believe <unk> 80, 993 has the potential to be a game changing cancer therapy.
We look forward to providing an overview of the study in a trial in Prague trial in progress posters at city. This week.
And providing additional updates in 2021.
To wrap up.
I want to emphasize how proud I am of the entire team at Curis.
Then in the midst of an ongoing global pandemic has worked tirelessly to ensure we hit every ambitious goal we set for ourselves this year.
It is incredible to think that since we signed the deal to bring this new Vista asset onboard in January.
We have written a protocol engaged the FDA.
Bill Steinkraut: We have written a protocol, engaged the FDA, secured IND clearance, opened clinical sites, trained investigators and their staff, and begun the dosing of patients, all in less than nine months. It is a testament to the team's experience, their commitment, and their passion, and it is an honor to work with you. With that, I'll turn the call over to Bill to review our financial results for the quarter. Bill?
Secured I, Andy clearance opened clinical sites trained investigators and their staff and begun the dosing of patients.
All in less than nine months.
It is a testament to the team's experience their commitment and their passion.
And it is an honor to work with them.
With that I'll turn the call over to Bill to review our financial results for the quarter.
Bill.
Thank you Jim.
Bill Steinkraut: Thank you, Jim. For the third quarter of 2020, Curis reported a net loss of $6 million, or $0.11 per share, on both a basic and diluted basis, as compared to a net loss of $6.4 million, or 19 cents per share, on both a basic and diluted basis for the same period in 2019. Revenues for the third quarter of 2020 were $2.7 million, as compared to $2.9 million in the same period in 2019. Revenues for both periods consisted primarily of royalty revenues recorded on Genentech and Roche's net sales of Arabesque. Operating expenses for the third quarter of 2020 were $7.5 million, as compared to $8.2 million for the same period in 2019. Cost of royalty revenues, for $0.1 million for both the third quarter of 2020 and 2019.
Third quarter 2020, cures reported a net loss of $6 million or 11 cents per share on both a basic and diluted basis.
As compared to a net loss $6.4 million or 19 cents per share on both a basic and diluted basis for the same period in 2019.
Revenues for the third quarter of 2000 22.7 million as compared to 2.9 million in the same period in 2019.
Revenue for both periods comprised primarily of royalty revenues recorded on Genentech and Roche's net sales of Erivedge.
Operating expenses for the third quarter 2027.
$7.5 million.
As compared to $8.2 million for the same period in 2019.
Cost of royalty revenues.
$4.1 million for both the third quarter 2000 22019.
Research and development expenses were $4.7 million <unk> third quarter 2020.
Bill Steinkraut: Research and development expenses were $4.7 million in the third quarter of 2020, as compared to $5.1 million for the same period of 2019. The decrease was primarily due to reduced clinical trial costs related to CA-170 and femoripenistat. General and administrative expenses were $2.6 million in the third quarter of 2020, as compared to $2.9 million for the same period of 2019. The decrease was driven primarily by lower personnel and stock-based compensation costs, partially offset by higher legal, professional, and consulting services costs. Net other expense was $1.3 million for the third quarter of 2020, as compared to $1.1 million for the same period in 2019. Net Other Expense for the third quarter of 2020 primarily consisted of imputed interest expense related to future royalty payments. As of September 30, 2020, Curis' cash equivalents totaled $23.6 million, and there were approximately 56.7 million shares of common stock outstanding as of June 30, 2020.
As compared to $5.1 million for the same period 2019.
The decrease was primarily due to reduced clinical trial costs related to CA, one seven day and don't Peniston.
General and administrative expenses were $2.6 million for the third quarter 2020.
As compared to the <unk> <unk>, so excuse me $2.9 million for the same period in 2019.
The decrease was driven primarily by lower personnel and stock based compensation costs, partially offset by higher legal professional consulting services cost.
Net other expense was $1.3 million for the third quarter 2020, as compared to $1.1 million with same period 2019.
Net other expense for the third quarter 2020, primarily consisted of imputed interest expense related to future royalty payments.
As of September 32020, Harrison has cash cash equivalents totaled $23.6 million and there were approximately 56.7 million shares of common stock outstanding.
Since June 32020, we.
We have extended our cash runway through our after market sales agreement with Jones trading and stock purchase agreement with aspire capital.
Bill Steinkraut: We have extended our cash runway through our At-The-Market Sales Agreement with Jones Trading and Stock Purchase Agreement with Aspire Capital, the aggregate proceeds of which have totaled approximately $10 million to date. As a result of these proceeds, we expect that our existing cash and cash equivalents will enable us to maintain our planned operations beyond our end-of-year data catalyst and through the second quarter of 2021. This forecast does not include any additional potential proceeds from our stock purchase agreement with Aspire Capital or from the Market Sales Agreement of Jones Trading.
Aggregate proceeds of which have totaled approximately $10 million to date.
As a result of these proceeds.
We expect that our existing cash and cash equivalents should enable us to maintain our planned operations beyond our end of year data catalyst.
Three the second quarter of 2021.
This forecast does not include any additional potential proceeds from our stock purchase agreement aspire capital.
Or our after market sales agreement Jonestrading.
With that I'd like to open the call for questions.
Operator: With that, I'd like to open the call for questions. Operator. Ladies and gentlemen, at this point, we will open the lines for questions. To ask a question, please press star and then 1 on a touch-tone telephone. If you are using a speakerphone, we do ask that you please pick up the handset before pressing the keys to ensure the best sound quality.
Operator.
[laughter], ladies and gentlemen at this at this point, we will be opening the line for questions to ask a question. Please press Star then one using a touchtone telephone if you are using a speaker phone only do ask you. Please pick up the handset before pressing the keys to ensure the best sound quality.
So it's all your questions you May press star and Q.
Operator: To withdraw your questions, you may press star and two. Once again, to ask a question, please press star and 1. At this time, we'll pause momentarily to assemble the roster. And our first question today comes from... Althea Young from Cancer. Please go ahead with your question. Hi guys, this is Liang from Lythia.
Once again to ask a question. Please press Star then one.
At this time, we'll pause momentarily to assemble the roster.
Yeah first question today comes from.
I'll see a young from Cantor. Please go ahead with your question.
Oh, Hi, guys isn't really I'll, probably did and for taking our question just on your upcoming Ash presentation. How many patients shall we expect that the meeting and how should we think about expectations around you know response rate and think T. and if it to early choice saturation of it Tom.
James E. Dentzer: Thanks for taking our questions. For your upcoming ASH presentation, how many patients should we expect at the meeting? And how should we think about expectations around, you know, response rate and safety? And is it too early to assess the duration of response? And then for the VISTA program, can you just provide some perspective on your trial design and how we should think about CRS management? Thank you. Sure. Bob, would you like to talk about the details?
And then quite a v. I plan can you just provide some perspective on your trial design and how should we think about Crs management. Thank you.
Sure Bob would you like to talk about the EPS conference.
Yeah, that's the.
Oh Gosh conference, we have a number of presentations coming up to trial in progress presentations in an oral presentation.
We expect on the oral presentation for the non Hodgkin lymphoma trial too.
To present, an update on our data.
Robert E. Martell: Yeah, so at this conference, we have a number of presentations coming up, two trial in progress presentations, and an oral presentation. We expect the oral presentation for the non-Hodgkin lymphoma trial to present an update on our data. As you know, in the past, we've had... [inaudible] This is part of the oral presentation that Dr. Nowakowski will present.
As you know in the past we've had.
[laughter] significant tumor reductions I'm.
And as Jim mentioned as Weve escalated to higher dose levels in our honing in on a recommended dose we continue to see activity in this way and so we'll probably be providing an update.
That trial, that's yes, that's part of the oral presentation Dr. Miller Koski will present.
The two trial in progress.
Robert E. Martell: The two trial-in-progress presentations, One would include the combination in non-Hodgkin lymphoma with the BTK inhibitor Abrutinib. There, we will describe the trial design in a bit more detail than what Jim has described today. And additionally, we'll talk about the second trial in progress. As Jim mentioned, we have already enrolled the first two cohorts in that AML-MDS study.
Jason.
One would include the combination in non Hodgkin lymphoma, with BTK inhibitor, but Ned there we will describe the trial design in a bit more detail than what Jim has described today.
And Additionally, well talk about in the second trial in progress.
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Yep.
As Jim mentioned, we have already enrolled the first two cohorts on the M.L. Mds study.
This trial was initially submitted to us.
Robert E. Martell: This trial was initially submitted to ASH prior to enrolling any patients and, therefore, was submitted as a trial in progress. We will try to update the community on some efficacy data in some manner going forward in the same time frame. Does that answer your question on the upcoming 4948 ASH data? Yeah, that's very helpful.
Prior to enrolling any patients and therefore was submitted as a trial in progress.
We will try to update the community.
The some efficacy data in some manner going forward in the in the same timeframe.
He did that answer your question on the four nine for upcoming S. data.
Hi, Yes, that's very helpful and.
On the B type program can you remind us if you are trying to dying and see our asset management.
James E. Dentzer: And on the VISTA program, can you just remind us if you're the trial design and CRS manager? Yes, so this is being designed as a Phase I dose escalation trial. We have the benefit of the prior study that was run by Janssen, and we understand some of the early dose levels and potential side effects based on that study, which we believe we can mitigate and hopefully avoid. In particular, Jim mentioned cytokine release syndrome as being one potential toxicity that's on target for hitting VISTA.
Yes. So this is designed as they are phase one dose escalation trial.
B, we have the benefit of the prior.
Study that had been run by Janssen, and we understand I love the early dose levels and potential side effects based on that study with.
But I understand he where we believe we can.
Mitigate and hopefully having a side effects in particular, it's Jim mentioned, a cytokine release syndrome is being one potential toxicity, that's on target to our hitting this stuff.
We do know that in recent years this has become much more.
Robert E. Martell: We do know that in recent years, this has become much more manageable with better understanding of how this develops and how to ultimately manage it, as well as new drugs that are available to help with that. In addition, we've done extensive research and evaluating clinical measures that we believe will additionally reduce the chance of, [inaudible] We do know that, you know, the dose escalation and dose levels that we're starting at are not too far from where we expect we would see meaningful clinical activity. Thank you very much.
Manageable with better understanding of how this develops and ultimately to manage it as was it.
New drugs that are available to help with that.
In addition, we've done.
Our partners.
In the next extensive research and evaluating clinical measures that we believe will additionally, reduce the chance of.
The side effects, causing a problem for patients are top priority is to do this dose escalation in a way that's safe for patients and also will achieve a meaningfully or high dose levels that we believe will be clinically relevant.
We do know that.
The dose escalation dose levels that were starting out or not too far from where we expect we would see meaningful clinical activity.
Operator: Our next question comes from Yeo Jen from Ledlaw and Company. Please go ahead with your question. Great, and thanks for taking the questions and congratulations on the progress. Just two more questions here.
Okay. Thank you.
Thank you very much.
Our next question comes from Yale Jen from land lot and company. Please go ahead with your question.
Oh, great. Thanks for taking the questions and congrats on the progress.
Just two questions here the first one is it.
James E. Dentzer: The first one... Could you give us a little bit more detail in terms of credit, in terms of the potential agenda, at least the planned agenda, and specifically on the clinical side? And I have another follow-up. Okay.
Did you give a little bit more detail in terms of credit in terms of regarding the potential agenda Oh.
At least the planted agenda and specifically on the clinical side and I have another follow up.
Okay and the second question Gil and thank you for calling by the way.
James E. Dentzer: And the second question, you know, and thank you for calling, by the way. Okay, no problem. The second question is that, in terms of the combo study for the 4948 for NHL, what was the anticipated, at least the planned patient size, study size that might be, Okay, thank you very much. I appreciate that.
Okay no problem in the second quarter, Washington is that in terms of the combo study for the well the knife 48.
In <unk>, you know what the anticipated the plan to a patient size study side that might be.
Okay. Thank you very much I appreciate that so I'm afraid I think we're going to hold off on updates and until we know a little bit more but we'd be happy to update you as we can I think you've seen what we can disclose at this point in time in the press release I'm not I think it just you know I just want to underscore obviously.
James E. Dentzer: So on the CRADA, I think we're going to hold off on updates until we know a little bit more, but we'd be happy to update you as we can. I think you've seen what we can disclose at this point in time in the press release on that. I think it just, you know, I just want to underscore that obviously we're very excited to have gotten that collaboration put in place.
We're very excited to have to have gotten that collaboration put in place and we think it's going to be a very help add for us to expand our our our study of these patients with the help of the NCR right and frankly in a very efficient manner.
James E. Dentzer: And we think it's going to be a very helpful addition for us to expand our study of these patients with the help of the NCI, and frankly, in a very efficient manner. On the combo study with 4948 in NHL, I think what we anticipated before is, as we discussed last year at ASH, it was really a small data set. It was about getting through those initial dose levels, improving safety and tolerability, PK, and PD, until we could get up into that efficacious range, which we expected to be 200 and, in fact, turned out to be, right? 200, 300, and 400 all looked to be efficacious doses, which was terrific. And we had six patients last year, December, and we were looking, at that time, at five out of six patients showing tumor shrinkage.
On the combo study with four nameplate in NHL, what we'd anticipated before.
As a as we discussed last year at Ash. It was really a small dataset. It was about getting through those initial dose levels and proving the safety and Tolerability PK PD until we could get up into that efficacious range, which we expected to be 200 and in fact turned out to be 200, 304 hundred all look to be EPS.
Cases doses, which was terrific.
And we had six patients on last year December and we were looking at that time at five of the six patients showing tumor shrinkage. So really what we want to do this year at ash and as we have said we have publicly said we were looking to add three to six patient.
James E. Dentzer: So really, what we wanna do this year at ASH is we have publicly said we are looking to add three to six patients. That was our goal for the year, but we wanted to add more patients at those doses and follow them for longer periods of time. Really, we have two goals. The first one is the obvious one. We want to make sure that we can confirm that finding that we've got a drug. 200, 300, and 400 are all efficacious doses. But we know that the drug is hitting the target, and the drug shrinks tumors even in this incredibly difficult population to treat, you know, four prior lines of therapy, relapsed refractory setting, monotherapy, all of it. We wanted to be So we want to try and expand on our learning to 200, 300, and 400 and try to find out if we get better efficacy as we go to higher doses. Are there additional safety signals that we're not seeing?
That was our goal for the year, but we wanted to add more patients at those doses and follow them for longer periods of time really for two goals. The first one is the obvious one we want to make sure that we can confirm that finding that we've got to drop that 200 304 hundred these are all efficacious dose.
But we know that the drug is hitting the target and the drug shrinks tumors, even in this incredibly difficult population to treat four prior lines of therapy, a relapse refractory setting monotherapy all of it we wanted to be able to show that we could repeat that finding that the drug is efficacious full stop.
After that of course, now we want to try and choose a a recommended phase two dose. So we want to try and expand on our learnings at 200, 304 hundred and try to find out.
Do we get better efficacy as we go to higher doses are there additional safety signals that we're seeing we know this is a drug that.
James E. Dentzer: We know this is a drug that is going to be used for long periods of time. We've got patients that have been on this drug for over a year in the study, over 18 months in the case of the Longstrong patient at the July cutoff. So we know that we need a drug that is not just efficacious but can support long-term dosing. So of those doses, which is the best dose, and what is the data that supports that conclusion? Those are the things that we're just talking about at ASH. Okay, that's the vet.
That is going to be used for long periods of time, you've got patients that have been on drug for over a year in the study.
Over 18 months and the kids the Waldenstrom patient at the July cut off.
So we know that that we need a drug that is not just efficacious that can support long term dosing. So of those doses, which is the best dose and what is the data that supports that conclusion. Those are the things that we're going to be just talking about at ash.
Yeah, Okay, I hope that.
Yes, that's very helpful. Maybe just I just squeezing one more question here, which is for the leukemia study the dose finding I'd just 0.0, the patient has been genetically Oh. Its you know big lease screened for having the proper mutation before they've been.
James E. Dentzer: Yes, that's very helpful. Maybe just squeezing one more question here, which is for the leukemia study, the dose finding at this point: are all the patients genetically or genetically screened for having the proper mutation before they've been treated? Show no, they haven't.
Treated.
So no. They haven't this is in fact, an all comer study. So one of the one of the terrific findings of Doctor Berman started now skis paper is that well.
James E. Dentzer: This is, in fact, an all-comer study, so one of the terrific findings of Dr. Berman-Strazanowski's paper is that... over half the population of AML and MDS patients overexpress IREC4L. And so we would expect that we've got over a 50% shot of patients that enrolled in the study that have this overexpression. And in fact, the expression of IRAC4 is suspected. It's not binary. It's not whether you have it or you don't.
Over half the population of AML, and Mds patients Overexpress directs where else.
And so we would expect that we've got over 50% shot of patients that are enrolled in the study.
That have this over expression and in fact, the expression of Iraq or is the spectrum.
Not it's not binary it's not you have it or you don't you know, it's a ratio that some patients express more some patients express less and what we want to be able to do is take all comers into that space and frankly see how they do with luck it'll be a small dataset. We were thrilled we've been enrolled more quickly than we were hoping.
James E. Dentzer: You know, it's a ratio. Some patients express more, some patients express less. And what we want to be able to do is take all comers into that space and, frankly, see how they do. With luck, it'll be a small data set. We were thrilled to be enrolled more quickly than we were hoping.
You know as I said Weve already got the first two cohorts, Phil, but we want to try and explore patients across that spectrum and in fact see how they do on the drug and the ultimate goal. Obviously would be these are all efficacious dose levels at least we would expect them to be based on the preclinical study at 200 milligrams and 300.
James E. Dentzer: You know, as I said, we've already got the first two cohorts filled, but we want to try and explore patients across that spectrum and, in fact, see how they do on the drug. And the ultimate goal, obviously, would be that these are all efficacious dose levels, or at least we would expect them to be based on the preclinical study. At 200 milligrams and 300 milligrams, are we starting to see in any of these patients the kinds of signs that we saw in the preclinical data that were so positive? That's what we're hoping for. So I expect them to look to us to talk to that data set in just a few weeks at the ASH conference, or at least around that time frame. Okay, great. Thanks, Lars.
Milligrams are we starting to see in any of these patients the kinds of signs that we saw in the preclinical data that was so positive.
That's what we're hoping for so I expect to look to us to talk to that dataset in just a few weeks at the Ash conference or at least around that time frame.
Okay, great. Thanks again, congrats on the revenue the progression program.
James E. Dentzer: Again, congratulations on the rapid progress. Thank you very much. And our next question comes from Soumit Roy from Jones Trading. Please go ahead with your question. Hi there.
Thank you very much.
And our next question comes from Sumit Roy from Jones trading. Please go with your question.
Hi, there congratulations on the nice execution.
Thank you sorry.
Kurt here looks like from the looking at the Ash abstract looks like the.
Operator: Congratulations on the nice execution. Thank you, Shani, kind of hitting the sweet point where you have manageable safety and probably maximum efficacy. Given that these patients are such late lines... What kind of translational data should we expect at the ASH presentation, or what do you look at? Are we going to see biochemical readouts or biomarkers that give us confidence that yes, this is an active drug and it is hitting the right signaling pathway the most it can? And the second question is, have you seen or have you shown efficacy in BTK mutant cell types in vitro or preclinical? Yeah, actually, Bob, would you like to chime in on this one?
300 milligram be I'd.
Kinda hitting the nice point, where you have manageable safety and probably tamaxifen because he.
Given them. These patients are such Lee applying.
What kind of translational data should we expect that the ash presentation or what do you look at.
How are we going to see biochemical read out we saw a biomarker that gives us confidence that yes. This is a active drug and it is hitting the right signaling pathways to the most it can.
And the second question is have you seen or.
Have you shown.
Casino BTK mutant cell types with you know get to any individual preclinical setting.
No actually Bob would you like to chime in on this one.
Robert E. Martell: Sure. Yes, we'll be presenting data. We've been capturing pharmacodynamic data throughout the study, as well as pharmacokinetic data, and we'll be presenting an update on that. And we do believe that, you know, as you mentioned, the 300 dose is honing in. We haven't officially declared the recommended phase 2 dose at this point, but we've had very good results, as you can see from our abstracts in the discussion today, at that dose level. But we've also seen clinical activity even at 200 milligrams.
Sure.
Yes, well be presenting data, we've we've been capturing a pharmacodynamic data throughout the study as well as pharmacokinetic data and we'll be presenting an update on that and we we do believe that.
You know as you mentioned the 300 does is honing in we haven't officially declared the recommended phase two dose at this point, but we've had a very good results as you can see from our abstract and the discussion today at that dose level, but we've also seen clinical activity even at 200 milligrams.
So we likely will declare a recommended phase two dose at some point in the near future.
Robert E. Martell: So, we likely will declare a recommended phase 2 dose at some point in the near future, and we will present pharmacodynamic data that supports... With regard to the BTK mutant, we haven't evaluated that specific question in our patient population. But we would expect that this, targeting an independent pathway that is parallel to the BTK pathway but independent of the BTK pathway, would have activity regardless of that situation. This independently inhibits activity at the NF-kappa B location, on the Vista front. Could you give us any color on what kind of tumor types you are looking at? Are you looking at strictly IO refractory, or are you looking at more IO relapse kind of cancer types? more immune-permissive cancers like RCC. Head and Neck, or would you be going more towards... for Varian or TNBC type cold or temer type? What's the initial preferred indication? Yeah, again, this is probably a better question for Bob.
And we will present pharmacodynamic data that supports that.
With regards to the BTK mutant we haven't evaluated that specific question in our patient population, we would expect.
That's it.
This targeting an independent pathway that is parallel to the D.T.K., but independent of the BTK pathway.
That we would have activity regardless of that situation.
This independently inhibits activity at the Nf Kappa B location.
Okay.
On the other front.
Could you give us any color on what kind of tumor types youre looking all that you're looking at.
Strictly.
Ill refractory all you're looking at more higher relapse kind of cancer types or more.
More immune permissive kinds of like ours.
And.
Well he had a nickel or would you be going more towards.
So Barry I know TNBC type Kroger tumor type work or any show a preferred indications it.
Yes, again this is probably a better question for Bob.
Yeah, that's okay. The actual design of the study. So this is obviously an early dose.
Robert E. Martell: Yeah, so the actual design of this study, so this is obviously an early dose-finding study, and we've opened this study to not limit the specific type of solid tumor. So it's open to solid tumor patients, so we'll be taking a variety of patients on this study. That being said, we think that the greatest opportunity for single-agent activity may be in malignancies that have a high mutational burden and that tend to be sensitive to other checkpoint inhibitors. We do know that this expression is increased following treatment with other checkpoint inhibitors. And so, you know, when we think about our long-term development strategy, at least as a single agent, we'll be thinking about those potential indications. And as we start to think about combining this drug with other checkpoint inhibitors, again, we've demonstrated very strong synergy in the ability of a combination between PI-8993 and a PD-1 antibody or others. We've demonstrated that this has the ability to overcome resistance to those other checkpoint inhibitors. So, we think that there's a strong pathway for combination therapy expanding beyond the current, very sensitive indication, and Diantha Duvall.
Dose finding study and Weve opened this study to not limit the specific type of solid tumors since up into solid tumor patients. So we'll be taking a variety of patients on the study that being said, we think that the greatest opportunity for single agent activity, maybe in malignancies said.
Hi, mutational burden and that are tend to be sensitive to other checkpoint inhibitors. We do know that Vista expression is increased following treatment with other checkpoint inhibitors.
And so you know when we think about our long term development strategy at least as a single agent.
Thinking about those potential indications.
As we start to think about combining this drug with other checkpoint inhibitors again, we've we've demonstrated very strong synergy and the ability of a combination between yeah, I mean I know.
Three and PD, one antibody or others.
We've demonstrated that so this has the ability to overcome resistance to those other checkpoint inhibitors. So we think that there's a strong pathway for combination expanding beyond the current.
Very sensitive indications. Although these are efforts that would be you know later in development right now early in development, we have a pretty broad slots that were looking at.
Robert E. Martell: Thank you so much and congratulations again on the prize. Thank you, Soumit. I really appreciate it. And ladies and gentlemen, with that, we'll conclude today's question and answer session. I would like to turn the conference call back over to the company's President and Chief Executive Officer, James Dentzer, for any closing remarks. Thank you, Jamie, 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 Origine and Immunext for their ongoing help and support. We look forward to updating you again soon. Operator? And, ladies and gentlemen, the conference has now concluded. We do thank you for attending today's presentation. You may now disconnect your lines.
Thank you so much and congratulations again on all the progress.
Thank you show me it really appreciate it.
And ladies and gentlemen, with that we'll conclude today's question and answer session.
I would like to turn the conference call back over to the company's President and Chief Executive Officer, James Dentzer for any closing remarks.
Thank you Jamie and thank you everyone for participating in todays 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 Aurigene and Imaginext for their ongoing help and support we look forward to updating you again soon.
Operator.
And ladies and gentlemen, the conference has now concluded we do thank you for attending today's presentation. You may now disconnect your life.