Q2 2021 Syros Pharmaceuticals Inc Earnings Call
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And future milestones and wreath and accomplishments. It's released is available on the and factors and media section upstairs. This website at www Dot Sierra Dot com.
We'll begin the call, which prepared remarks by Doctor Nancy Simonian, Our Chief Executive Officer Doctor, David Roth R. Chief Medical Officer, Gerald Quirk or Chief Operations Officer will then open the call for question.
Doctor, Eric Olson, our Chief Scientific Officer, and Christian Stevens, Our Chief Development Officer are also and the call and will be available for Q&A.
Before we begin I would like to remind everyone. Just statements. We make on this conference call will include forward looking statements actual events or results could differ materially from those express or implied by any forward looking statements as a result of various risks uncertainties and other factors, including those set forth.
And the risk factor section of our annual report on form 10-K R.
Reportedly reported on 1 and 10-Q that we filed this morning and any other filings that we may make with the S. C C and the future.
In particular, the extent to which the COVID-19 outbreak continues to impact our operations and those are the third parties and which were alive will depend on future development, which are highly uncertain and cannot be predicted with confidence.
And a forward looking statements made on this call represent our views only as of today and should not be relied upon as representing argues as of any subsequent date, we specifically disclaim any obligation to update or advise any forward looking statements.
Oh, and now like to turn the call over to Nancy.
Thank you Naomi.
The first half of 2021 was very productive for Sarah and I am pleased to provide and update on a recent progress.
[noise] and we outlined at the end of last year, we are focused on 3 strategic priority.
First we are advancing a growing portfolio of targeted therapies for hematologic disorders, each with the potential to set a new standard of care.
Second we are building on our leadership and selected TDK inhibition for difficult to treat cancers.
And third we are continuing to leverage our gene control discovery engine to fuel a robust and sustainable pipeline.
Together, we believe these efforts will enable us to build zeros and 2 a fully integrated company with medicines that provide profound benefits for people with cancer and monogenic diseases.
And the second quarter, we made great strides across all our clinical stage program.
Starting with S. Y 50, 609, as we announced this morning, we have entered into an agreement with Roche to evaluate 56 O 9 and combination with a test iliza Mab a P. D L..1 inhibitor and patients with colorectal cancer.
We are very excited to work with rose to explore this novel combination.
There was strong preclinical and mechanistic rationale for combining 50.609 with a P. D L..1 inhibitor, which David we'll discuss later and the call.
Operator: This release is available on the Infectors and Media section of Ceres' website at www.com. We'll begin the call with prepared remarks by Dr. Nancy Simonian, our chief executive officer; Dr. David Ross, our chief medical officer; and Gerald Quirk, our chief operations officer.
Notably this marks the first clinical investigation of a selective C. D. K 7 inhibitor with immunotherapy potentially could take paving the way for additional combination strategies for 50.609 with immunotherapy.
Operator: We'll then open the call for questions. Dr. Eric Olsen, our Chief Scientific Officer, and Kristen Stevens, our Chief Development Officer, are also on the call and will be available for Q&A. Before we begin, I would like to remind everyone that the statements we make on this conference call will include forward-looking statements. Actual events or results could differ materially from those expressed or implied by any forward-looking statements as a result of various risks, uncertainties, and other factors, including those set forth in the risk factors section of our annual report on Form 10K, our quarterly report on Form 10Q that we filed this morning, and any other filings that we may make with the SEC in the future.
We also announced this morning, the data from the dose escalation portion of our phase..1 study of 50.609 will be highlighted and an oral presentation at the asthma Congress and September we've.
Operator: In particular, the extent of which the COVID-19 outbreak continues to impact our operations and those of the third parties on which we rely will depend on future developments, which are highly uncertain and cannot be predicted with confidence. Any forward-looking statements made on this call represent our views only as of today and should not be relied upon as representing our views as of any subsequent date. We specifically disclaim any obligation to update or revise any forward-looking statements.
And we remain on track to move into the expansion portion of the day is 1 trial and the second half of the year and at the time of the day to read out the plan to further detail. Our next steps for advancing the development of 50.609 to further explore its potential as a transformative targeted approach, but difficult to treat cancers.
Turning now to our targeted hematology portfolio, we continue to make progress and select M. D. S..1 or phase 3 clinical trial of <unk>, formerly known as S. Y 40, and 25 and combination with <unk> and RARA positive higher risk M. D S patient.
We are also on track to initiate both select and 1 a randomized phase 2 trial of Tammy barricade, plus Venetoclax and a society as.
As well as our dose confirmation study of F Y 21, O 1 and a P. L. This year.
Together these programs put us on track for 2 potential N D A's and 2024 for <unk> and M. D S and for 21 O 1 and a P L.
Nancy A. Simonian: I would now like to turn the call over to Nancy. Thank you, Naomi. The first half of 2021 was very productive for Ceros, and I am pleased to provide an update on our recent progress. As we outlined at the end of last year, we are focused on three strategic priorities. First, we are advancing a growing portfolio of targeted therapies for hematologic disorders, each with the potential to set new standards of care.
A recent 3 part K O L. Webinar theory highlighted the opportunities for Teddy bear of teen and 21 O..1 day set new standards of care and M. D. S M L and a T O.
Nancy A. Simonian: Second, we are building on our leadership in selective CDK inhibition for difficult-to-treat cancers. And third, we are continuing to leverage our gene control discovery engine to fuel a robust and sustainable pipeline. Together, we believe these efforts will enable us to build Syros into a fully integrated company with medicines that provide profound benefits for people with cancer and monogenic diseases. In the second quarter, we made great strides across all our clinical stage programs.
Further defining the value proposition for these programs.
These 3 Webinars feature key opinion leaders, who are intimately involved and the treatment of people living with M. D. S.
M L and a P L.
These were incredibly impactful events for us at Terra.
Each position articulated a tremendous gap and the treatment landscape highlighting the urgent demand for new therapies that can provide patients with better clinical outcomes.
Or in the case and a P L a dramatically reduce treatment Burger.
The kols describe the potential of candy barricade and 21 O..1 to address these needs and also share their views and how Danny bear of teen and 21 O..1 are distinguished within the current treatment and development landscape.
Nancy A. Simonian: Starting with SI-5609, as we announced this morning, we have entered into an agreement with Roche to evaluate 5609 in combination with Tazolizumab, a PDL1 inhibitor, in patients with colorectal cancer. We are very excited to work with Roche to explore this novel combination. There is strong preclinical and mechanistic rationale for combining 5609 with a PDL1 inhibitor, which David will discuss later in the call. Notably, this marks the first clinical investigation of a selective CDK-7 inhibitor combined with immunotherapy, potentially paving the way for additional combination strategies for 5609 with immunotherapy.
Beginning with our M. D S focused event and a doctor Amy dessert of Johns Hopkins provided and overview of the higher risk M. D. S landscape.
Underscoring the need for tolerable therapies that can improve outcomes will offer and quality of life.
Hma's, including a society or the current standard of care and offer limited efficacy.
Prognosis after HMA failure is very poor.
Moreover, most higher risk M. D. S patients are elderly and either can't or don't want to undergo the intensive chemotherapy and necessary to bridge to a potentially curative bone marrow transplant.
Dr. Discern highlighted 1 of the major challenges and M. D S drug development M.
M D F often presents as a polyclonal disease, making it difficult to treat with therapy the target individual genetic mutations.
Nancy A. Simonian: We also announced this morning that the data from the dose escalation portion of our phase one study of 5609 will be highlighted in an oral presentation at the ESMO Congress in September. We remain on track to move into the expansion portion of the phase one trial in the second half of the year, and at the time of the data readout, we plan to further detail our next steps for advancing the development of 5609 to further explore its potential as a transformative, targeted approach for difficult-to-treat cancers.
And her view a combination of factors distinguishes Tammy bear a team and the current landscape.
The fact that it targets a biologic process fundamental to the differentiation of blood cells as opposed to targeting a single genetic mutation.
The ability to select for patient and most likely to respond.
The high complete response rates and a M L, which have a reasonably likelihood of translating to higher risk M. D. S.
Nancy A. Simonian: Turning now to our targeted hematology portfolio, we continue to make progress in select MDS1, our phase three clinical trial of Tammy Baratine, formerly known as SY1425, in combination with aesididine in RARA positive, higher risk MDS patients. We are also on track to initiate select AML1, a randomized phase two trial of Tammy Baratine plus Venetoclax and aza cy Together, these programs put us on track for two potential NDAs in 2024, for Tammy Baratine in MDS and for 2101 in APL.
And a favourable tolerability profile that does not exacerbate neutropenia and other complications when combined with a decided inc.
Turning now to our AML focused event.
And June be rejoined back and Doctor Daniel <unk> of the University of Colorado Doctor <unk> presentation focused on the unmet need and a M L and the paucity of options available to put people and longterm emission.
And while Ben Asa has emerged as a tremendous option for many patients a third of newly diagnosed unfit AML patients don't respond and many more via relapse, leaving them with poor options.
Dr. <unk> explained that these nonresponders tend to be patience with monothetic disease and.
Nancy A. Simonian: Our recent three-part KOL webinar series highlighted the opportunities for Tammy Baratine in 2101 to set new standards of care in MDS, AML, and APL. Further defining the value proposition for these programs, these three webinars featured key opinion leaders who are intimately involved in the treatment of people living with MDS, AML, and APL. These were incredibly impactful events for us at zero.
As we presented at Ash are translational data suggest that the RARA biomarker and richest for the Monostich disease phenotype associated with Venetoclax resistance.
Simply put by selecting Ferrara, we believe we may be enriching for the very patients who are and the greatest need for new treatment option.
Dr. <unk> also highlighted the characteristics of and optimal animal therapy.
And oral medicine, and the law allows for deep durable remissions we.
Nancy A. Simonian: Each physician articulated a tremendous gap in the treatment landscape, highlighting the urgent demand for new therapies that can provide patients with better clinical outcomes or, in the case of APL, a dramatically reduced treatment burden. The KOLs described the potential of Tammy Baratine and 2101 to address these needs and also shared their views on how Dami Veritine and 2101 are distinguished within the current treatment and development landscape. Beginning with our MDF-focused event in May, Dr. Amy Dazern of John Hopkins provided an overview of the higher risk MDS landscape, underscoring the need for tolerable therapies that can improve outcomes while offering quality of life. HMAs, including Aza Cididine, are the current standard of care and offer limited efficacy. Prognosis after HMA failure is very poor.
With minimal and manageable toxicity and that has rapid impact and disease progression, where you can tell quickly if the therapy is working.
Based on our day to day, we believe Teddy bear team they offer this product profile and.
And our phase 2 trial, Kenny barricade, plus Athos delivered high C. R. A with a rapid onset of action meaningful durability and a good tolerability profile and Aurora positives newly diagnosed unfit M L.
Nancy A. Simonian: Moreover, most higher-risk MDS patients are elderly and either can't or don't want to undergo the intensive chemotherapy necessary to bridge to a potentially curative bone marrow transplant. Dr. DeZern highlighted one of the major challenges in MDF drug development. MDS often presents as a polyclonal disease, making it difficult to treat with therapies that target individual genetic mutations. In her view, a combination of factors distinguishes Tammy Baratine in the current landscape, the fact that it targets a biological process fundamental to the differentiation of blood cells, as opposed to targeting a single genetic mutation, the ability to select for patients most likely to respond, the high complete response rates in AML, which have a Turning now to our AML-focused event. In June, we were joined by Dr. Daniel Pallier of the University of Colorado.
This gives us confidence and our triplet strategy with Tammy barricade, plus then either.
Like N D. S. M L can be a polyclonal disease by employing the triple a combination upfront we hope to achieve high initial response rates, while reducing the emergence of resistance disease by simultaneously targeting both monostich and non monothetic leukemia cells that may be present a diet.
Joseph and lead to a short duration of response and relapse.
We look forward to beginning to enroll patients and the select M. L..1 trial later this year.
Our final K O L. Webinar on a P. L was just a few weeks ago.
P. L is it clinically distinct form and AML defined by a roar of gene fusion.
We were joined by Doctor for Roger bonded Cassani, a M D Anderson cancer Center.
Highlighted how and oral therapy would represent a major advance for patients.
While I V. A T O plus acura the current standard of care is curative and greater than 80 per cent of patient and.
It comes with an enormously heavy treatment burden.
The regiment involved up to 140 lengthy infusions over nearly a year.
21 O..1 a novel oral form of a T O has the potential to deliver comparable efficacy while dramatically reducing the treatment bird.
We plan to initiate our dose confirmation study this year with the phase 3 trial to follow and 2022.
Nancy A. Simonian: Dr. Pallier's presentation focused on the unmet need for AML and the paucity of options available to put people in long-term remission. While Van Asa has emerged as a tremendous option for many patients, a third of newly diagnosed unfit AML patients don't respond, and many more relapse, leaving them with poor options. Dr. Pallier explained that these non-responders tend to be patients with monocytic disease
If you're interested in hearing more a full audio replay of each of these events as well as the company and slide presentation is available on our web site.
With that I'd like to turn the call over to David.
Thank you Nancy.
Given the proximity to the day to read out for fees warm Joseph escalation study.
Alright, and focus my comments today on S Y 56 O 9 and review the details of our study.
As you've heard the subscribe you 456 annoying is a novel targeted approach and we believe.
Nancy A. Simonian: As we presented at Ash, our translational data suggests that the RARA biomarker enriches for the monocytic disease phenotype associated with Benetoclax resistance. Simply put, by selecting Ferrara, we believe we may be enriching for the very patients who are in the greatest need for new treatment options. Dr. Pallier also highlighted the characteristics of an optimal AML therapy.
Great performance from difficult to treat cancers.
226, and Murray disrupt too important processes that cancer has changed us to survive and thrive transcription and uncontrolled soulcycle Patricia.
[noise] inhibiting C D K 7 lead to reductions and canceled driving transcription factors and and.
Nancy A. Simonian: And oral medicine allows for deep, durable remissions with minimal or manageable toxicities, and it has a rapid impact on disease progression, so you can tell quickly if the therapy is working. Based on our data to date, we believe Tamibatin may offer this product profile. In our phase two trials, Tammy baritine plus Aza delivered high CR rates with a rapid onset of action, meaningful durability, and a good tolerability profile in RARA-positive newly diagnosed unfit AML. This gives us confidence in our triplet strategy with Tammy Baratine plus Vennies.
And tried to adopt chartered per cheese and disrupt critical and the.
And so cycle and tracking cancer, and multiple ways and and multiple parents.
As part of the Josef Glacier, we're exploring 56 O 9 and breast colorectal loans, ovarium and pancreatic cancer patients as well as and patients with 2 moose and other histologies RB pathway alterations.
We chose be specific tumor checks because of the strong from clinical data.
Hi, omit need.
[noise] and mechanistic rationale based on either a high prevalence of RB password and alterations or known transcriptional and sofa.
Nancy A. Simonian: Like MDS, AML can be a polyclonal disease. By employing the triplic combination upfront, we hope to achieve high initial response rates while reducing the emergence of resistance by simultaneously targeting both monocytic and non-monocytic leukemia cells that may be present at diagnosis and lead to a short duration of response and relapse. We look forward to beginning to enroll patients in the select AML1 trial later this year. However, our final KOL webinar on APL was just a few weeks ago.
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And keeping the dark develop and philosophy of exploring both single agent and combination strategies early and development and Joseph situation was designed to assess and 50.609.
And as well and was in combination with full restaurant and neutral apology and breast cancer and.
A combination that we could explore and parallel with the situation course.
We began enrollment and the Joseph situation and January of 2020, and we shared encouraging early junior from me Joseph escalation of your T. C. M. C. I a C. R V last October.
Nancy A. Simonian: APL is a clinically distinct form of AML defined by a RARA gene fusion. We were joined by Dr. Farad Ravandi, Koshani, of MD Anderson Cancer Center, who highlighted how an oral therapy would represent a major advance for patients. While IVATO plus Atra, the current standard of care, is curative in greater than 80% of patients, it comes with an enormously heavy treatment burden. The regimen involves up to 140 lengthy infusions over nearly a year.
Importantly, those day to Jimmy Street, and pieces and recognition and told jokes shoes and pharmacodynamic activity at levels consistent with anti tumor activity and are preclinical models.
At the time, we had established B M. P. T from continuously and we drove through and had opened cohorts to begin exploring ultimate doses and schedules.
With the aim of our drinks and sorry optimal Joseph and scheduled to take 4 and 2 expansion 1 that will allow us to deliberate 56 O 9 and a jokes and scheduled.
Nancy A. Simonian: 2101, a novel oral form of ATO, has the potential to deliver comparable efficacy while dramatically reducing the treatment burden. We plan to initiate our dose confirmation study this year, with the phase three trial to follow in 2022. If you are interested in hearing more, a full audio replay of each of these events, as well as the accompanying slide presentation, is available on our website. With that, I'd like to turn the call over to data.
Would be tolerated over prolonged periods of time and that could also position those through various additional combination strategies.
And asthma.
Sure a normal Buster you say from the ongoing Joseph escalation.
This update will include safety, Tolerability and unusual clinical activity and data from patients treated and a range of dosage on multiple different contribute and schedules.
In addition, we will prove.
And 2 preclinical extracts compliments this clinical read at.
David A. Roth: Thank you, Nancy. Given the proximity to the data readout for our Phase 1 dose escalation study, I will focus my comments today on SI-509 and review the details of our study. As you've heard us describe before, 5609 is a novel targeted approach that we believe holds great promise for difficult-to-treat cancers. It disrupts two important processes that cancer cells use to survive and thrive, transcription and uncontrolled cell cycle progression. Inhibiting CDK7 leads to reductions in cancer-driving transcription factors and anti-apoptotics and disrupts critical nodes in the cell cycle, attacking cancer in multiple ways and at multiple points.
1 evaluated and you can drive tumor and pharmacodynamic activity of instrument and Joseph regiments, with 56, and learning and ovarian cancer models and.
And 1 evaluated and 50.609 as a single age and in combination with chemotherapy and models of to asking you from Kansas.
As we announced and refreshing vs. This morning, and due to changes give me development landscape with the emergency and all electric estrogen receptor graders were searched therapies.
No longer exploring the combination with 4 bedrooms, and HR per view breast cancer patients and our choice.
All Serge are expected to become the standard of care and this patient population, making the development path for a combination with investors must clear and.
As a result, we prioritize darker foods from the other cohorts and the drums, yes courage.
David A. Roth: As part of the dose escalation, we're exploring 5609 in breast, colorectal, lung, ovarian, and pancreatic cancer patients, as well as in patients with tumors of other histologies with RB pathway alteration. We chose these specific tumor types because of the strong preclinical data, High Unmet Knee, and mechanistic rationale based on either a high prevalence of RB pathway alterations or In keeping with our development philosophy of exploring both single agent and combination strategies early in development, the dose escalation was designed to assess 56 or 9 as a single agent, as well as in combination with fulvestrant in HR positive breast cancer, a combination that we could explore in parallel with the single-agent co-horse.
56, and 9 is shown preclinical synergy and Olsher and HR policy breast cancer cells, and we continue to believe it has potential and nature of positive breast cancer.
We believe that combination strategies remain T to unlock and the true power of any therapeutic cancer.
To that and we are excited to discuss the agreement with Roche to explore 56 O 9 and combination with a P. D O 1 and editor.
Under the terms of disagreement we will supply 50, 609 for a combination dosing cohort and roche's ongoing intrinsic trial.
Phase 1 <unk> evaluated multiple targeted therapies and immunotherapies as simple agents or international combinations and my wife, usually define subsets of colorectal cancer.
The cohort evaluating 56, and alright, and combination with a total loser math isn't and patients will be RAF viewed colorectal cancer.
David A. Roth: We began enrollment in the dose escalation in January of 2020, and we shared encouraging early data from the dose escalation at the EORTC NCI-A-ACR meeting last October. Importantly, those data demonstrated proof of mechanism at tolerable dose, and pharmacodynamic activity at levels consistent with anti-tumor activity in our preclinical, At the time, we had established the MTD for continuous daily dosing and had opened cohorts to begin exploring alternate doses and schedules, with the aim of identifying the optimal dose and schedule to take forward into expansion, one that would allow us to deliver 5609 at a dose and schedule that would be tolerated over prolonged periods of time, and that could also position us for various additional combination, At ESMO, we will share a more robust data set from the ongoing dose escalation.
We believe there is a strong mechanistic rush and now and and translational data to support this approach.
Preclinical day to show the C V K, 7 and nutrition and juices, do you and a replication stress and genome and stability and cancer cells trigger you responsiveness.
And the animal models suitcase 70 inhibition enhances 2 response took anti P. D..1 immunotherapy provolone overall survival and increasing immune so infiltrates.
Additionally are preclinical data shows that 50, 609 inhibit tumor growth at low tolerated doses and colorectal cancer models and cheaper responses absorbed more frequently and models will be around for mutations relative to low type.
We look forward to working with gross to evaluate the potential of this novel combination.
And parallel we remain on track to advance 56, Illinois and to the expansion portion of the face and 1 trial later this year and we look forward to share more details on our next steps for 3 to 6 O 9 at the time of our day to disclosure and September.
David A. Roth: This update will include safety, tolerability, and initial clinical activity data from patients treated at a range of doses on multiple different intermittent schedules. In addition, we will present two preclinical abstracts that complement this clinical readout. One, evaluating anti-tumor and pharmacodynamic activity of intermittent dosing regimens with 56 o'9 in ovarian cancer, and one evaluating 56 or 9 as a single agent and in combination with chemotherapies in models of K-RAS mutant cancer. As we announced in our press release this morning, due to changes in the development landscape with the emergence of oral selective estrogen receptor degrators or surge therapies, we are Oral Serbs are expected to become the standard of care in this patient population, making the development path for a combination with Fulvestrian less clear.
With that let me turn the call over to Gerald to review, our second quarter financial results.
Thanks, David we continue to operate from a position of financial strength we.
We ended the second quarter was $195.3 billion in cash cash equivalents and marketable securities compared to a 174 million as of December 31st 2020.
This increase reflects the $75 and 6 million and gross proceeds from our January 2021, and public offering partially offset by cashiers to fund our operations and the first half of 2021.
Based on our current plans, we believe we have sufficient capital to fund our plant operating expenses and capital needs into 20th twenty-three beyond anticipated day to read outs for each of our clinical stage programs.
David A. Roth: As a result, we prioritized our efforts on the other cohorts in the dose escalation. 569 has shown preclinical synergy with an oral chemotherapy in HR-positive breast cancer cells, and we continue to believe it has potential in HR-positive breast cancer. We believe that combination strategies remain key to unlocking the true power of any therapy. To that end, we are excited to discuss the agreement with Roche to explore 5609 in combination with its PDL1 inhibitor.
We recognize revenue of $5.2 million, and the second quarter compared to $3 and $2 million and the second quarter of 2020.
This consisted of $3.3 million and revenue under under our collaboration with global Blood Therapeutics, and 1.9 million under our collaboration with insight.
And the second quarter of 2020, we recognize 2.5 million and revenue from our collaboration with GDT and zero point, certainly and from our collaboration within sight.
R. A Z expenses were $25.8 million and the second quarter of 2021 compared to $14.8 million for the same period and 2020 and.
David A. Roth: Under the terms of this agreement, we will supply 5609 for a combination dosing cohort in Roche's ongoing intrinsic trial, a Phase 1, phase 1B study evaluating multiple targeted therapies and immunotherapies as single agents or in rational combinations in molecularly defined subsets of colorectal cancer. The cohort evaluating 56-09 in combination with Tazolizumab is in patients with B-Raf mutant colorectal cancer. We believe there is a strong mechanistic rationale and translational data to support this.
This increase was primarily due to the advancement of our 3 critical programs as well as increases and employee related expenses.
JA expenses were $5.5 million and the second quarter of 2021 compared to 5.1 million from the same period and 2020.
This increase was primarily due to employee related expenses.
Finally, we reported that loans for the second quarter of $22.5 million or 36 cents per share compared to a net loss of $17.22 million with 38 cents per share for the same period and 2020.
David A. Roth: Preclinical data show that CDK-7 inhibition induces DNA replication stress and genome instability in cancer cells, triggering immune response signals. In animal models, CDK-7 inhibition enhances tumor response to anti-PD1, amoeophon, prolonging overall survival and increasing immune cell numbers. Additionally, our preclinical data shows that 5609 inhibits tumor growth at well-tolerated doses in colorexal cancer models with deeper responses observed more frequently in models with B-Raff mutations relative to controls.
With that I'll turn the call over to the operator for questions. Thank you.
Thank you as a reminder to ask a question and you'll need to force star woman and his own phone.
Draw your question and press the pound keep Tuesday, and while we could probably true narrow sir.
Our first question comes from 10% off with Piper Sandler and you May proceed with your question.
Great. Thank you very much and congrats really afraid and excited to hear a rubber for about the Roche collaboration.
<unk> <unk> and talk to ultimately a value at heart 6 or not beyond colorectal. Thanks, so much.
Gerald E. Quirk: We look forward to working with Roche to evaluate the potential of this novel combination. In parallel, we remain on track to advance 5609 into the expansion portion of the Phase 1 trial later this year, and we look forward to sharing more details on our next steps for 5609 at the time of our data disclosure in September. With that, I will turn the call over to Gerald to review our second quarter financial results. Thanks, David.
Thanks, Ted for the question.
David you and take that.
Sure Yeah, no. Thanks to so high there are various correct.
Hello.
Hi, <unk>.
And it.
Where I'm very excited about the potential for S Y 50.609.
And clearly read protracted the interest a rouge and.
And the potential not only for advanced burgers and colorectal patients, but also to <unk> and you went Bam, Sir and you know therapy and broaden the opportunities that they currently have for it says it was and so so we see that you know as as a great Foundation for moving forward and we also look to our own data.
Gerald E. Quirk: We continue to operate from a position of financial strength. We ended the second quarter with $195.3 million in cash, cash equivalents, and marketable securities compared to $174 million as of December 31st, 2020. This increase reflects the 75.6 million in gross proceeds from our January 2021 public offering, partially offset by cash used to fund our operations in the first half of 2021. Based on our current plans, we believe we have sufficient capital to fund our plant operating expenses and capital needs into 2023 beyond anticipated data readouts for each of our clinical stage programs.
Where we've been making great progress and our ongoing study and since I'll be and a presentation.
From last fall and you know, we're looking forward to providing updates.
Is the September it is Moe will be focusing on and so we previously stated on the safety and Tolerability, but also clinical activity, obviously since that time, which date back to data through last August we've made progress. So you can expect and more robust and <unk>.
Gerald E. Quirk: We recognized revenue of $5.2 million in the second quarter compared to $3.2 million in the second quarter of 2020. This consisted of $3.3 million in revenue under our collaboration with Global Blood Therapeutics and $1.9 million under our collaboration with Insight. In the second quarter of 2020, we recognized 2.5 million in revenue from our collaboration with GBT and 0.7 million from our collaboration with insights. R&D expenses were $25.8 million in the second quarter of 2021, compared to $14.8 million for the same period in 2020.
Which will give us insights into her and to where we may be going and and we will provide that information to you at that point.
Awesome, a credit to hear more about it and I was looking for the progress of all the rest of the program too. Thanks, so much growth.
Thank you Ted.
[noise]. Thank you. Our next question comes from NATO and Allen.
Oh, and you may receive and your question.
What are your thanks for taking my question and so we get rid of Fresno I think the key question and 56 O 9 and people are grappling with is what is the therapeutic window kind of what what's the safety profile and.
And are there signs of efficacy it sounds like you're going to be.
Be providing data across a wide range of tumor types and a wide range of dosing paradigms. After meeting so cause how would you.
Suggest that we prepare for their as my data and how old are you.
Yourselves evaluate whether there's a therapeutic window for 56 O 9 and before how would you suggest where you kind of frame that data as we were kind of.
Gerald E. Quirk: This increase was primarily due to the advancement of our three clinical programs, as well as increases in employee-related expenses. GNA expenses were $5.5 million in the second quarter of 2021, compared to $5.1 million for the same period in 2020. This increase was primarily due to employee-related expenses. Finally, we reported a net loss for the second quarter of $22.5 million, or 36 cents per share, compared to a net loss of $17.2 million, or 38 cents per share, for the same period in 2020. With that, I'll turn the call over to the operator for questions. Thank you.
Sure. So again and thanks for that question and I think it's really important to to.
Look at the totality of the day that we're gonna be presenting it and I just you know share it with 10.
Yeah, we've we've made a lot of progress since our last on a day to update having free treated more patients from the the prior presentation and so we're gonna have a broad datasets, we at the time of the year and a meeting had really been excited to share with you that we achieved mechanism and.
Operator: Thank you. As a reminder, to ask a question, you'll need to press Star 1 on your telephone. To withdraw your question, press the pound key. Please stand by while we compile the Q&A roster. Our first question comes from Ted Tentock with Piper Sandler. You may proceed with your question.
And that we were achieving that <unk> that were tolerable I think that at this time you know we're gonna be looking at parameters, you know and <unk> and you should help and I hope you frame and way in which you and you are looking at our data.
Edward Andrew Tenthoff: Great, thank you very much and congratulations on the update. I'm excited to hear a little bit more about the Roche collaboration. Can you tell us a little bit more and whether there is the potential to ultimately evaluate five six or not beyond colonyl? Thanks so much.
And we can we identify Joseph regimen that where we can take forward based on the totality of our safety and Tolerability also are we seeing signs of biological activity or the early signals and clinical activity at those doses and that that regimen and then more importantly, what about the specific patients who've been treated.
Operator: Thanks, Ted, for the question. David, do you want to take that? Sure, yeah, no, thanks, Ted.
David A. Roth: Sure, yeah, no, thanks, Ted. So, we're very excited. Hello. Hi, yeah, we're very excited. We're very excited about the potential for SI-5609, and clearly, we've attracted the interest of Roche, who sees the potential not only for advancing this in colorectal patients but also to advance their immunotherapy and broaden the opportunities that they currently have for Tazilimab. So we see that, you know, as a great foundation for moving forward. We also look to our own data, where we've been making great progress in our ongoing study.
<unk> worthy doing prior to come and go onto our study what were the responses like and how long they were last name vs.
You may be experiencing on Orcher Island and.
If you can answer yes to those types of questions. You know, we would share with you uhm great enthusiasm about this and.
And I also think that.
You know it's important to.
I appreciate it.
<unk> the the plans and moving forward related to the type of activity. We might see you know it would be would be interpreted and that and a broader context.
David A. Roth: And since the ENA presentation from last fall, you know, we're looking forward to providing updates. This September at ESMO, we'll be focusing, as we've previously stated, on safety and tolerability, but also clinical activity. Obviously, since that time, which, you know, dated back to data through last August, we've made progress, and you can expect a more robust data set, which will give us insights into where we may be going. And we'll provide that information to you at that time. Awesome. I'm excited to hear more about it, and looking forward to progress on the rest of the program, too. Thanks so much, guys.
So you know I just.
David A. Roth: the program, too. Thanks so much, guys. Thank you, Ted. Thank you. Our next question comes from Phil Neda with Callan. You may proceed with your question.
I think that it should be very interesting presentation and hope you're looking forward to it.
And that's very helpful. And then the second question is as we think about what could happen next kiss your corporate presentation says expression cohorts as a single agent and.
Combination therapies, so it sounds like a range of where you could do anyway for his next or new tumor types or certain types of you're gonna move into as a single aging and then per.
Perhaps other combination regimens.
And it.
From missing from the other potential.
Avenues for further development and 5600.
Well, no and I smoke I think that it's it's really important to appreciate it and I I I believe you do appreciate how and oncology.
Philip M. Nadeau: Good morning, thanks for taking my question. As we get ready for asthma, I think the key question on 5609 that people are grappling with is what is the therapeutic window, kind of what's the safety profile? and are the signs of efficacy. It sounds like you're going to be providing data across a wide range of tumor types and a wide range of dosing paradigms at the meeting. So how would you suggest that we prepare for that asthma data?
Drugs are often the issue and actually tested and single age and context, and even when they work well and that contact and are often used in and various combinations and so we really technologist with your outfit and set the stage for this program at this early point in time.
To give us opportunities to move forward and and various various ways. So and that was really the critically important reason for looking at ultimate schedules got may afford us different doses. So that we can take this and unlock the power of this drug in a fit for purpose approach no I do.
Philip M. Nadeau: yourselves evaluate whether there's a therapeutic window for 5609, and how would you suggest we kind of frame that data as we go? Sure, so again, thanks for that question. And I think it's really important to look at the totality of the day that we're going to be presenting, and I just shared that with Ted. You know, we've made a lot of progress since our last data update, having obviously treated more patients than in the prior presentation. And so, you know, we're going to have a broad data set.
And want to share with you and port experience I had and my past professional life when leading the early clinical development of public <unk> C. D. K 4.6 inhibitor, which you know at that early stage of its development parallel to where we may be at this point with our C. D 370 inhibitor.
And.
<unk> single engine activity, but based on preclinical evidence from some really signals. It was clear that to truly unlock the power and that drug combination with and aromatase inhibitor was required and we all know the successful outcome on that strategy. So anticipating that we mainly many ways in which to maneuver we've really focused on studying the state.
David A. Roth: And we, at the time of the EMA meeting, had really been excited to share with you that we had achieved the mechanism and that we were achieving it at doses that were tolerable. I think that at this time, you know, we're going to be looking at parameters, you know, that, and you should help, you know, to help you frame the way in which you are looking at our data, you know, can we, can we identify a dose in the register? that we can take forward, you know, based on the totality of our safety and intolerability.
For from a robust future and approach.
That's very helpful. Congrats on the progress and thanks again for taking my question.
Think so.
Thank you. Our next question comes from Jason Button, and with JMP Security and and proceed with your question.
David A. Roth: Also, are we seeing signs of biological activity? Are there early signals of clinical activity at those doses and at that regimen? And then, more importantly, you know, what about the specific patients who have been treated? How were they doing prior to coming on to our study? What were their responses like, and how lonely were they lasting versus what they may be experiencing on our trial?
Hi, Thanks for taking my question I guess somewhat of a follow up on the next steps are 50.609, how what what would've been the factors that contributed to your prioritization for the different expansion cohorts that will learn about it is it you know potential for benefit unmet need you know obviously.
David A. Roth: And if you can answer yes to those types of questions, you know, we would share with you great enthusiasm about this. And I also think that, you know, it's important to appreciate how the plans moving forward, you know, related to the type of activity we might see, would be interpreted in that broader context. So, you know, I just think that it should be a very interesting presentation and I hope you're looking forward to it. That's very helpful.
And strategies are played and if you can help us think low and I went through how you how you prioritize where to invest.
Hey, Jason I'll I'll take that question you know 1 of the.
You know really the day. It is I'd say of the 50.609 approaches that we know it can work.
We believe it can work and many difficult to treat cancers, just based on the target and the mechanism.
And so let me think a little bit about the priorities for what we would do and I'm moving for do we think about several things and they think about.
Philip M. Nadeau: Then a second question is, as we think about what could happen next, I guess your corporate presentation says expansion cohorts as single agent and combination therapy. So it sounds like the range of what you could delineate for is next are new tumor types or tumor types that you're going to move into as a single agent and then perhaps other combination regimens. Anything else I'm missing?
Free clinical data and mechanistic rationale translational data, we think about the clinical data that's emerging from the dose escalation and.
And the safety and Tolerability profile, and then and very importantly, we think about unmet medical need.
What is the development and path and looks like.
What's the competitive intensity, where do we think you know there's a very big on net medical need that we can potentially serve with this so it's a kind of a combination of all of those factors that go into our decision about.
David A. Roth: Any other potential avenues for further development of 5609. Well, no, I think that it's really important to appreciate, and I believe you do appreciate how oncology drugs are often initially tested in a single agent context, and even when they work well in that context, they're often used in various combinations. And so we acknowledge this at the outset and set the stage for this program at this early point in time to give us opportunities to move forward in various ways.
What <unk> what to proceed with you know obviously beyond what we're doing with Roche with immunotherapy and the expansion portion.
Great and then.
And in terms of the P. D. L..1 combo can you maybe just put into context for your you know your previous your focus on the or what you've learnt about the the drug and and or be pathway alterations and teams will all be popular alterations and and put that in context of now looking and and be Ras mutations.
Mhm.
Yeah. Thanks for the for the question Jason.
David A. Roth: And that was really the critically important reason for looking at alternate schedules that may afford us different doses so that we can take this and unlock the power of this drug in a fit-for-purpose approach. You know, I do want to share with you an important experience I had in my past professional life when leading the early clinical development of Pellipurban. Obosyclip, a CDK-4-6 inhibitor, which, you know, at that early stage in its development, parallel to where we may be at this point with our CDK-7 inhibitor, had nominal single-age activity, but based on preclinical evidence and some early signals, it was clear that to truly unlock the power of that drug, combination with an aromatase inhibitor was required.
<unk>.
C C K 7 and ambition have effects as and you know, both and transcript and but also and sell cycling as <unk>. As you mentioned you know RB pathways are critical.
A critical and player and and and sell cycle. So, but what's been published is that when you inhibit TDK 7 most likely due to that effect and the cell cycle, you induce a replication stress and that stress can resolve and the formation of a signal.
David A. Roth: And we all know the successful outcome of that strategy. So anticipating that we may need many ways in which to maneuver, we've really focused on setting the stage for a robust future approach. That's very helpful. Congratulations on the progress, and thanks again for taking my question.
<unk> and <unk> and a immune signally.
And and published data it was shown is that that.
Helps a P D, 1 inhibitor and and and I'm all smile. So that was really the basis of kind of this immune signalling upon C. D K, 7 and ambition and and of course, there's you know that colorectal cancer is the place where the genome instability and.
Jason Nicholas Butler: Thank you. Our next question comes from Jason Butler with JMP Security. You may proceed with your questions. Hi, thanks for taking the question. I guess somewhat of a follow-up on the next steps for 50609. What have been the factors that contributed to your prioritization for the different expansion cohorts that we'll learn about? Is it, you know, potential for benefit?
And there is immune signalling and I mean and therapies have been shown to have some benefit there. So combined with our with a really strong activity 56 O 9 and BRAF a tumor.
David A. Roth: Unmet Need, you know, obviously combination strategies have played a role. Just if you can help us think a little more through how you've prioritized where to invest. Hey, Jason, I'll take that question.
Tumors Xena grass that we showed and ask all last year.
Basically all of those things combined and have a cell cycle interruption and a signalling and the activity and the BRAF CRC really make us excited about that combination.
David A. Roth: You know, one of the, you know, really the beauties of the 5609 approaches that we know it can work is that we believe it can work in many difficult-to-treat cancers just based on the target and the mechanism. And so when we think a little bit about the priorities for what we would do moving forward, we think about several things. We think about pre-clinical data, the mechanistic rationale, translational data. We think about the clinical data that's emerging from the dose escalation, the safety and tolerability profile.
Great. Thanks, Thanks for taking my questions.
Thank you Jason.
Thank you and as a reminder to ask a question and you'll need to press Star 100, and telephone. Our next question comes from Mark Breytenbach with Oppenheimer and May I proceed with your question.
Hey, good morning, guys and thanks for taking my questions I I'm just wondering if the collaboration with Roche will have any immediate impact on your plan and expansion cohorts for 56, and 9, especially and colorectal cancer and I'm not sure if you'll be able to answer this or not it David and I'm wondering if you can point to any clinical precedents.
David A. Roth: And then, very importantly, we think about unmet medical needs. What does the development path look like? What's the competitive intensity? Where do we think, you know, there's a very big unmet medical need that we could potentially serve with this? So it's a kind of combination of all of those factors that go into our decision about what to proceed with, obviously beyond what we're doing with Roche with immunotherapy in the expansion portion. Great, and then in terms of the PDL1 combo,
<unk> C D K inhibitor, maybe your C. D. K 4.6 or other has shown synergy with a P. D F 1 or a P. D O 1 checkpoint inhibitor.
Sure. So I think the the excitement we have for colorectal cancer. We initially share that with you last year and after <unk> when we had a preclinical presentation.
Showing the range of activity that we saw and.
Remember.
That we had about 2 thirds and what we can I think 30, pdx's and and 2 thirds of those add tumor growth inhibition upgraded and 50 per cent with about a quarter, having you know complete regression, you're 90 per cent of greater and the majority of the rafts, where the revenue colorectal cancers were.
David A. Roth: Can you maybe just put it into context for, you know, your own situation?
David A. Roth: previous, your focus on the, or what you've learned about the drug and RB pathway altering
David A. Roth: and RB pathway alterations in terms of RB pathway alterations and put that in the context of now looking at BRAF mutations.
Where responding relative to those without and so we were we really were excited about that opportunity and that contributed to our inclusion of those patients and our current study. So we're we're very excited about this it's really a difficult patient population and the application of a successful checkpoint inhibitor and like it says it was about 2.
David A. Roth: Yeah, thanks for the question.
David A. Roth: patient. You know, we've seen CDK7 in Abition have effects, as you know.
David A. Roth: transcription but also in the cell cycle, and as you mentioned, the RB pathway is a critical player in the cell cycle, so what's been published is that when you inhibit CDK 7, most likely due to that effect in the cell cycle, you induce replication stress. And that stress can result in the formation of
2 hour go forward plan and colorectal is very excited given the unmet need them the opportunity to address that <unk> with respect to the underlying mechanism and you'll be there has been published data that supports inhibition with C. D. K 7 can lead to a DNA damage and replication stress.
David A. Roth: signals that stimulate innate immune signaling. And in published data, it was shown that that That helps a PD1 inhibitor in a mouse model. So that was really the basis of kind of this immune signaling upon CDK-7 in addition. And of course, as you know, colorectal cancer is a place where there's genome instability, and there's immune signaling, and immune therapies have been shown to have some benefit there. So combined with our really strong activity of 5609 and VRAF tumors.
And that can induce and immune reaction uhm root there can be associated.
Immune so infiltrate into tumors centers exposed to see 2.7 and we think that's a clear set up for amplifying the attack with and the anti P. D. O..1 antibody. So I take it all really makes makes great great sense and there has been.
Prior work done with C. D case C. D 246, and in particular, probably <unk> and others have been combined with them and know therapies and V. The data on those and.
In certain circumstances can support Io combinations, we think that.
David A. Roth: xenographs that we showed at ASCO last year. Basically, all those things combined, kind of the cell cycle interruption, in-h signaling, and the activity in the BRAF CRC really make us excited about that combination.
Our unique mechanism, which and also involved anti transcriptional effects with a C. D..2 7 and May may really potentiate that that combination strategy. Obviously, we we attracted roche.
To bring our program forward with them and I think they have a shared view of this opportunity long and along with us and so we're really excited and we're happy that did speak your interest as well.
Mark Alan Breidenbach: Great. Thanks for taking the time to answer the question. Thank you, Jason. Thank you, and as a reminder to ask a question, you'll need to press star one on your telephone. Our next question comes from Mark Bradenbach with Oppenheimer. You may proceed with your question. Hey, good morning guys, and thanks for taking my questions. I'm just wondering if the collaboration with Roche will have any immediate impact on your planned expansion cohorts for 5609, especially in colorexyl cancer.
Okay, Great and and can you just give us a ballpark number of patients, but we should expect and there's no update if you. If you can thank you.
Yeah. So at the talk so at the time, we presented at the and a meeting which was a year ago, we had and room.
A total of 17 patients have already called 14 and and work.
<unk> and the simulation components. So that data comes back in August of 2020.
Mark Alan Breidenbach: I'm not sure if you'll be able to answer this or not, but David, I'm wondering if you can point to any clinical precedents.
Here, we are about a year later and they obviously, we've made great progress with with the trial and there'll be certainly a larger number of patients. We haven't specified the details of the actual presentation, just yet in terms of patient numbers and and things of that nature, but suffice it to say it will be a more robust dataset, we'll have another focus on safety and Tolerability, which is very important.
Mark Alan Breidenbach: Where a CDK inhibitor, maybe a CDK-4-6 or another, has shown synergy with a PD1 or a PDL-1 checkpoint inhibitor.
David A. Roth: Sure, so I think the excitement we have for colorectal cancer, we initially shared that with you last year after ASCO when we had a preclinical presentation showing the range of activity that we saw. And you may remember that we had about two-thirds, we did, I think, 30 PBXs, and two-thirds of those had tumor growth inhibition greater than 50% with about a quarter having, you know, complete regressions, 90% or
And we also will have more information on various intermittent dosing regimen and just like the 5 day to day off regiment on the $70 and 70 and you want from regimen, which were and progress at the time of the pasty and a presentation. So I think it should be very helpful and of course clinical activity that that.
And may have seen and all of this will help under help US explain all go forward plan that we're.
Planning to share with you right around the time of the day to release.
David A. Roth: And the majority of BRAFs, DRAPs, and DRAS mutated colorectal cancers were responding relative to those without. And so we really were excited about that opportunity, and that contributed to our inclusion of those patients in our current study. So we're very excited about this.
Okay and thanks, so much.
Thank you.
Thank you and our next question comes from the day of my jaw with Rock Capital Partners. You May proceed with your questions.
Good morning. Thank you for taking my question, just raise and I wanted them more clarity and they go with that which I think the first 1.
David A. Roth: It's really a difficult patient population, and the application of a successful checkpoint inhibitor like Tazilumab to our go-forward plan in colorectal is very exciting, given the unmet need and the opportunity to address that. With respect to the underlying mechanism, there has been published data that support inhibition of CDK7 can lead to DNA damage and replication stress that can induce an immune reaction. There can be associated immune cell infiltrates into the tumors that are exposed to CDK7, and we think that's a clear setup for amplifying the attack with an anti-PDL-1 antibody.
It's just how much control of high involved and you're going to be with the study that's L day writing.
Hey, thank the nice day Yep, So differently go ahead and David.
Yeah sure. So in terms of the control. So this is C. Intrinsic trial and this is their phase 1 phase won't be study under the agreement, we're gonna be providing them with drugs and we'll have we're obviously collaborating and the development of the of the the study design itself and and we'll have access to the information.
As well as retain all rights to 56 O 9, but there'll be executing the study and supporting the cost of the actual program itself.
David A. Roth: So I think it all really makes great, great sense. There has been prior work done with CDKs, you know, CDK4-6, in particular, paladicyclib, and others have been combined with immunotherapies, and the data on those, in certain circumstances, can support IO combinations. We think that our unique mechanism, which also involves anti-transcriptional effects with the CDK-7, may really, you know, potentially that combination strategy. Obviously, we attracted Roche to bring our program forward with them, and I think they have a shared view of this opportunity along with us, and so we're really excited, and we're happy that it's a peak of your interest. Okay, great. And can you just give us a ballpark number of patients that we should expect in the ESMO update?
Thanks, David and then that just had you know bright and fresh with yoga and ever too and just do a combination with and I agent and this day.
I said I bet. This is gerald so we retain all rights 250, 609, so we have access to the data and control over 50.609, So yeah no nothing further than that.
Okay, and then the last 1 and just kind of on that and I think I'll just go with a classic that's already been asked and his when you are there any ways ketchup and tender way I'll take and kind of go with this program about the victim molecule.
No. This is this is limited to this study and we have you know complete freedom to operate to be able to pursue 56 O 9 and.
David A. Roth: Ismo update if you can. Thank you. Yeah, so at the time,
On our own or with anybody else.
David A. Roth: Yeah, so at the time we presented at the ENA meeting, which was a year ago, we had enrolled a total of 17 patients, and if I recall correctly, 14 were included in the single agent component. So that data cut was back in August of 2020. Here we are about a year later, and obviously, we've made great progress with the trial.
Thank you and I.
1 last 1 and this 1 as intended decision, making about you know why and needed to kind of move is programmed to the next step I you guys are lined in terms of what you need to head to run a solid or is it there'll be a decision at that book would be making.
David A. Roth: There'll certainly be a larger number of patients. We haven't specified the details of the actual presentation just yet in terms of patient numbers and things of that nature.
Could you. Please repeat that you broke up a bit when I was listening.
So I Yeah I was just 1 day and time is you know what you need to head to kind of <unk> expert and fall. It is it Ah telling decision or is it a sign vows and Kansas.
David A. Roth: But suffice it to say it will be a more robust data set. We'll have another focus on safety and tolerability, which is very important. And we also will have more information on various intermittent dosing regimens like the five-day-on-two-day-off regimen or the seven-day-on-seven-day-off regimen, which were in progress at the time of the past DNA presentation. So I think it should be very helpful. And, of course, clinical activity that we may have seen. And all of this will, you know, help us explain our go-forward plan that we're planning to share with you around the time of the data process.
8.1 at 8 to kind of move this and the next batch.
So you know the obviously the the protocol and has been collaboratively designed we have a mutual input and interest and see a future success. We we haven't really sure. If the specific details on on some of those technical parameters are poor and future business decisions around the next steps at this time.
Thanks, all very exciting and now I've been quite excited about this that and so I think this partnership certainly gives it a lot more alrighty.
Operator: Thank you. Our next question comes from Zegh Gila with Rock Capital Partners. You may proceed with your questions. Good morning.
Thank you. Thank you <unk> me too are very very excited about this opportunity.
Zegh Gila: Good morning. Thanks for taking my question. I just want to get a little bit more clarity on the deal with Roach. I think the first question for me is just how much control or how involved are you going to be with the study that they'll be running.
Thank you and I'm not sure any further questions at this time I would not like to turn the call back over to Nancy Simonian for any further remarks.
[noise]. Thank you operator, and thank you everyone for joining us this morning.
As always and we are appreciate all of your support and look forward to update and you again soon if they continue to execute against our 3 strategic priority.
Operator: Hey, Zagel. Nice to meet you. Yeah.
David A. Roth: Yeah, so. Hear from you.
David A. Roth: Go ahead, David. Yeah, sure. So in terms of the control, so this is the intrinsic trial, and this is their phase one, phase one B study. Under the agreement, we're going to be providing them with the drug. We'll have, we're obviously collaborating in the development of the study design itself and will have access to the information as well as retaining all rights to 56 or 9. But they'll be executing the study and supporting the cost of the actual program itself.
And build Sarah and to a fully integrated biopharmaceutical company with a day portfolio of targeted medicine, that's set new standards of care and cancer and monogenic diseases.
Ya.
Thank you ladies and gentlemen. This concludes today's conference call. Thank you for participating you may now disconnect.
David A. Roth: Thanks David, and then does Roche have to, you know, write a first draft?
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Zegh Gila: You know, write a first refusal if you were ever to pursue a combination with an IO agent in this setting. Hi Zach, this is Gerald.
Gerald E. Quirk: So, we retain all rights to 5609. We have access to the data and control over 5609. So, you know, no, nothing further than that.
Zegh Gila: Okay, and then the last one is just kind of on this, and I think I'll go back to some of the questions I've already been asked. Are there any restrictions in terms of where else you can kind of go with this program, whether it's this molecule?
Gerald E. Quirk: No, this is limited to this study and
Gerald E. Quirk: This study, and we have complete freedom to operate to be able to pursue 5609 on our own or with anybody else.
Zegh Gila: Thank you. And then I should put one last one on this one.
Zegh Gila: In terms of decision-making about, you know, what is needed to kind of move this program to the next step, are you guys aligned in terms of what you need to do to move forward, or is it still a decision that will be made by me? Could you please repeat that? You broke up a bit when I was listening.
Zegh Gila: Sure, yeah, I was just wondering in terms of, you know, what you need to hit to kind of move this program forward. Is it a joint decision or is it solely based on Roche in terms of, you know, what they want to see to kind of move this to the next step? So, you know, obviously, the protocol has been collaboratively designed. We have mutual input and an interest in seeing future success. We haven't really shared the specific details on some of those technical parameters or future business decisions around the next steps.
David A. Roth: Well, really exciting. I know I've been quite excited about this program, so I think this partnership certainly gives it a lot more visibility. Thank you, Zegba. We, too, are very, very excited about this opportunity.
Operator: Thank you, and I'm not sure if there are any further questions at this time. I would like to turn the call back over to Nancy Simonian for any further remarks.
Nancy A. Simonian: Thank you, Operator, and thank you everyone for joining us this morning. As always, we are appreciative of your support and look forward to updating you again soon as we continue to execute against our three strategic priorities and build Seros into a fully integrated biopharmaceutical company with a deep portfolio of targeted medicines that set new standards of care for cancer and monogenic diseases. Thank you.
Operator: Thank you, ladies and gentlemen. This concludes today's conference call. Thank you for participating. You may now disconnect.
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