Q2 2019 Earnings Call
Good afternoon, and welcome to the Curis Inc. second quarter earnings call.
Operator: Good afternoon, and welcome to the Curis second quarter earnings call. All participants will be in listen-only mode. Should you need assistance, please signal a conference specialist by pressing the star key followed by zero. After today's presentation, there will be an opportunity to ask questions. To ask a question, you may press star, then one on your touchtone phone. To withdraw your question, please press star, then two. Please note, this event is being recorded. I would now like to turn the conference over to the company's Vice President of Finance, Bill Steincroft. Please go ahead.
All participants will be in listen only mode.
Should you need assistance. Please signal a conference specialist by pressing the star key followed by zero.
After todays presentation, there will be an opportunity to ask questions to ask a question you May Press Star then one on your Touchtone phone.
To withdraw your question. Please press Star then too.
Please note this event is being recorded.
I would now let's turn the conference over to the company's Vice President of Finance Bill Steinkrauss. Please go ahead.
Thank you and welcome occurs in the second quarter 2019 earnings call.
Bill Steincroft: Thank you, and welcome to Curis' second quarter 2019 earnings call. Before we begin, I would encourage everyone to go to the Investor section of the company's website at www.curis.com to find our second quarter 2019 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.
Before we begin I would encourage everyone to go to the investors section of the company's website at Www Dot Curis Dot com.
To find our second quarter 2019 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.
For additional details please see our SEC filings.
Bill Steincroft: For additional details, please see our SEC filing. Joining me on today's call with prepared remarks are Jim Dentzer, President and Chief Executive Officer, and Bob Martell, Head of R&D. We will also be available for Q&A 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 with prepared remarks are Jim Dentzer, President and Chief Executive Officer, and Bob Martel head of R&D.
We will also be available for Q1 day at the end of the call.
I'd now like to turn the call over to <unk> CEO Jim to answer.
James E. Dentzer: Thank you, Bill. Good afternoon, everyone, and thank you for joining us today for our second quarter 2019 earnings call and business update. At the end of last year... We announced our goal of achieving key clinical milestones for each of our three clinical programs in 2019, and our first look at Advocacy Data for CA-4948 in NHL. Efficacy data in mesothelioma for CA170 and confirmation in the clinic that patients can safely tolerate a combination regimen of fimipinostat and venetocline.
Thank you Bill.
Good afternoon, everyone and thank you for joining us today for our second quarter 2019 earnings call and business update.
At the end of last year.
We announced our goal of achieving key clinical milestones for each of our three clinical programs in 2019.
Our first look at efficacy data for CA four nine full rate in NHL.
Efficacy data in mesothelioma for CA 170.
And confirmation in the clinic that patients can safely tolerate the combination regimen of independent stat and Venetoclax.
Both the stupidest Stat and CA 170 studies are on track the Big News today is our first look at efficacy for CA four I'm portrayed in NHL.
James E. Dentzer: Both the Thimipenestat and CA-170 studies are on track. The big news today is our first look at efficacy for CA-4948 in the NHL. As a reminder... CA-4948 is a first-in-class, orally available, small molecule inhibitor of IRAK4, which in preclinical studies reduced tumor burden by inhibiting midosome activity, which in turn inhibits signaling in the cancer-causing TLR pathway. In our ongoing phase one dose escalation study, we began dosing patients in the first cohort at 50 milligrams once daily, or QD, and 100 milligrams QD and BID and 200mg BID.
As a reminder.
CA 4948 is a first in class orally available small molecule inhibitor of IRAK four.
Which in preclinical studies reduced tumor burden.
By inhibiting midazolam activity.
Which in turn inhibits signaling.
In the cancer, causing T.L.R. pathway.
In our ongoing phase one dose escalation study.
We began dosing patients in the first cohort at 50 milligrams once daily or QD.
And then following cohorts at 50 milligrams twice daily or be I'd.
100 milligrams QD and be I'd.
And 200 milligrams be I'd.
James E. Dentzer: We are currently enrolling patients in the 400 mg BID cohort. CA 4948 has demonstrated good safety, dose-proportional pharmacokinetics, and clear signs of pharmacodynamic inhibition of the target. What's really exciting is that since our last update at the beginning of this year, our study has now advanced to dose cohorts with drug exposure levels in patients, where efficacy was observed in preclinical models. So we can now expand our focus from safety, PK, and PD and begin to look at efficacy data as well. To that point, we are excited to announce today that we are now seeing the anti-cancer activity we hoped for, with tumor burden reduction in multiple patients across multiple dose levels, with the caveats of small cohorts and low dosage in the initial cohorts, and, of course, that we're still in the middle of dose escalation.
We are currently enrolling patients in the 400 milligram be I'd cohort.
To date.
See a 4948 has demonstrated good safety.
Dose proportional pharmacokinetics and clear signs a pharmacodynamic inhibition of the target.
What's really exciting is that since our last update at the beginning of this year.
Our study has now advanced to dose cohorts with drug exposure levels in patients where efficacy was observed in preclinical models.
So we can now expand our focus from safety PK and PD and begin to look at efficacy data as well.
To that point, we are excited to announce today that we are now seeing the anti cancer activity, we hoped for with tumor burden reduction in multiple patients across multiple dose levels.
With the caveats of small cohorts and low dosage and the initial cohorts.
And of course that we're still in the middle of dose escalation.
It's very exciting to see clinical results in patients develop as we hoped they would.
James E. Dentzer: It's very exciting to see clinical results in patients develop as we hoped they would, as we have not yet determined the Maximum Tolerable Dose, or MTD. We are continuing dose escalation in this study until we identify a phase 2 dose or we hit MTD. In the meantime, we are working with our lead investigators to present data from this study at an upcoming medical conference, with the positive efficacy news from our NHL study. We also announced today our decision to advance CA4948 into the clinic in a study for acute myeloid leukemia, or AML, and Myelodysplastic Syndrome, or MDS. Dr. Martell will dive into the science behind this later, but we think this is another population that might benefit from CA-4948. In summary... We are excited to have hit the first of our three big clinical milestones this year with initial efficacy for CA-4948, and we are on track for the other two milestones. Confirmation in the clinic that patients can safely tolerate a combination regimen of fimopenestat and venetoclax, and efficacy data for treating mesothelioma patients with CA17. With that, I'll turn the call over to Bob Martell to review our three clinical programs in greater detail. Bob?
As we have not yet determined the maximum tolerated dose or MTD.
We are continuing dose escalation in this study until we identify a phase two dose.
Or we hit MTD.
In the meantime.
We are working with our lead investigators to present data from this study at an upcoming medical conference.
With the positive efficacy news from our NHL study.
We also announced today.
Our decision to advance CA 4948 into the clinic in a study for acute myeloid leukemia or AML.
And Myelodysplastic syndrome or Mds.
Dr. Martell will dive into the science behind this later, but we think this is another population that might benefit from CA 4948.
In summary.
We are excited to have hit the first of our three big clinical milestones. This year with initial efficacy in CA four nine for rate.
And we are on track for the other two milestones.
Confirmation in the clinic that patients can safely tolerate a combination regimen a feminist that ends venetoclax.
And efficacy data for treating mesothelioma patients with CA 170.
With that I'll turn the call over to Bob Martel to review, our three clinical programs in greater detail.
Bob.
Robert E. Martell: Thank you, Jim. Hello, everyone.
Thank you Jim Hello, everyone.
Robert E. Martell: Thanks for joining us this afternoon. Let me start with CA 4948. Jim provided a nice high-level overview of the data that we announced today, but I'd like to provide a little bit more background on the program overall. CA-4948 is an inhibitor of IRAC-4, a critical component of the midosome in the Toll-like Receptor, or TLR, pathway, which leads downstream to B-cell proliferation. This pathway, which depends on the midosome for signaling, is known to be oncogenic and tumor-promoting. Unfortunately, there are currently no approved therapies targeting this pathway. So, with CA-4948, we have a potential therapeutic that we have shown to block this pathway. In preclinical models, CA-4948 represses TLR signaling and cytokine production in vitro.
Thanks for joining us this afternoon.
Let me start with CA 4948.
Jim provided a nice high level overview of the data that we announced today, but I'd like to provide a little bit more background on the program overall.
CA 4948 is an inhibitor of IRAK four.
A critical component of the Midwest film in the toll like receptor or TLR pathway, which leads to downstream it to be cell proliferation.
This pathway, which depends on the medicine for signaling is known to be oncogenic, excuse me oncogenic and tumor promoting.
Unfortunately, there are currently no approved therapies targeting this pathway.
So with CA four nine for a we have a potential therapeutic that we have shown to block this pathway.
In preclinical models see a four nine for a repressive TLR signaling and cytokine production in vitro.
Robert E. Martell: And it exhibits anti-tumor activity in diffuse large B-cell lymphoma tumor xenograft models, as well as in patient-derived xenografts. As Jim described, we're running a phase one dose escalation study of CA4948 in patients with relapsed refractory lymphoma, including patients with diffuse large B-cell lymphoma. DLBCL, as I'll refer to going forward, and Waldenstrom's macroglobulinemia. Nine study sites in the U.S. are currently participating in the study, with at least three patients enrolled per dosing cohort. As a reminder, we've dosed patients in continuous 21-day cycles. Initially, as Jim mentioned, we started at 50 milligrams once daily and have escalated all the way up to our current dose of 400 milligrams twice daily.
And it exhibits anti tumor activity in diffuse large b cell lymphoma tumor xenograft models as well as in patient derived xenograft.
As Jim described we're running a phase one dose escalation study of CA 4948 in patients with relapsed refractory lymphoma.
Including patients with diffuse large b cell lymphoma.
Ill bcl as I'll refer to going forward.
And in Waldenstrms Macroglobulinemia.
Nine study sites in the U.S. are currently participating in the study with at least three patients enrolled her dosing cohort.
As a reminder, we dose patients in continuous 21 day cycles. Initially as Jim mentioned, we started at 50 milligrams once daily and have escalated all the way up to our current dose of 400 milligrams twice daily.
The study is evaluating the safety and Tolerability of CA 4948. In addition to pharmacokinetics Pharmacodynamics and also importantly, anti cancer activity with the goal of reaching the recommended phase two dose.
Robert E. Martell: The study is evaluating the safety and tolerability of CA-4948 in addition to pharmacokinetics, pharmacodynamics, and also importantly, anti-cancer activity, with the goal of reaching the recommended phase 2 dose. At the 200mg twice daily dose, CA-4948 has shown a clear and clean safety profile. It's also shown dose-proportional pharmacokinetics and strong evidence of pharmacodynamic inhibition of signaling in this oncogenic pathway. In addition, we've seen evidence of anti-tumor activity in several patients across dose levels, with greater activity observed as we have moved up in the dose. This initial clinical data is very promising, and we will continue our dose escalation until we define our maximum tolerated dose and, ultimately, our recommended dose for Phase 2 studies. We plan to present these data on CA-4948 at an upcoming medical conference. This quarter, we also highlighted a recent publication in Nature Cell Biology describing a cancer-causing splicing variant of IRAC4 called IRAC4L. This form of IRAT-4 is dominant in a majority of the cases of AML, or acute myelogenous leukemia, and also in myelodysplastic syndrome or MDS. The paper also noted that specific mutations of the U2AF1 splicing factor induce IRAC4L.
Through the 200 milligram twice daily dose see a 4948 has shown clear and clean safety profile.
It's also showed dose proportional pharmacokinetics and strong evidence of Pharmaco dynamic inhibition of signaling in this oncogenic pathways.
In addition, we've seen evidence of anti tumor activity in several patients across dose levels.
[noise] with greater activity observed as we have moved up in the dose.
This initial clinical data is very promising and we continue our dose escalation it until we define our maximum tolerated dose and ultimately our recommended dose for phase two studies.
We plan to present these data on CA 4948 at an upcoming medical conference.
This quarter. We also highlighted the recent publication in nature cell biology, describing a cancer, causing splicing variance of IRAK four called IRAK four ml.
This form of Iraq for his dominance in a majority of the cases ammo or acute myelogenous leukemia.
And also in Myelodysplastic syndrome or Mds.
The paper also noted that specific mutations of the you to a ask one splicing factor induce.
Rack for al.
Robert E. Martell: This represents a potential strategy for patient enrichment. These findings present that inhibition of IRAC4 with CA4948 is a potential treatment option for patients with myeloid malignancies expressing IRAC4L and also with U2AF1 mutation. Given the potential of CA4948 in this population, we've decided to bring this molecule into the clinic for AML and MDS, and we look forward to providing further updates on this program as we finalize the study protocol and initiate our first trial in these indications. Next, I'd like to move on to Fennepinistat.
This represents a potential strategy for patient enrichment.
These findings.
Present.
The inhibition of IRAK four with CA 4948, as a potential treatment option for patients with myeloid malignancies expressing IRAK four l.
And also with you today F. One mutations.
Given the potential of CA four nights for eight in this population we've decided to bring.
This molecule into the clinic for AML, and Mds and we look forward to providing further updates on this program as we finalize the study protocol and initiate our first trial in these indications.
Next I'd like to move on to fill in Penneast stat.
Robert E. Martell: This is our anti-MYC program, which targets both the genetic transcription and the protein degradation of MYC. Femipenistat uniquely targets MYC through simultaneous inhibition of both PI3 kinase and Histone Deacetylase or HDL. These two enzymes are essential to manifest MYC derangements in cancer. Myc levels are enhanced in many malignancies due to several mechanisms. For example, the overactivity of PI3 kinase, often seen in lymphomas, results in repression of GSK3, and consequently reduced MYC protein degradation. This ultimately causes a buildup of excess...
This is our anti Myc program, which targets both the genetic transcription and the protein degradation of mix.
Filippin, a stat uniquely targets Mick through simultaneous inhibition of both pithree kinase and histone deacetylase or h. deck.
These two enzymes are essential to manifest Nick the arrangements in cancer.
Nick levels, our enhanced in many malignancies due to several mechanisms for example.
The over activity of Pciethree kinase often seen in lymphomas.
Results in repression of GSK, three and consequently reduced myc protein degradation.
This ultimately causes a buildup of excess.
Robert E. Martell: Amounts of Nick in lymphoma, On the other hand, HDAC is important for the transcription of any new MYC in cancer cells. For example, when translocation of the MYC gene drives excess synthesis of MYC, that process depends on HCPCS. Inhibiting HDAC reduces MYC gene transcription, and inhibiting PI3 kinase increases MYC protein degradation.
Amounts of Mic in lymphoma.
On the other hand age stack is important for transcription of any new Mick in cancer cells.
For example, when translocation of Myc gene drives excess synthesis of mic that process depends on eight stack.
Inhibiting eight stacked reduces myc gene transcription.
And inhibiting pithree kinase increases myc protein degradation.
We and others have shown synergy in targeting both age stack Npis three kinase simultaneously.
Robert E. Martell: Although we and others have shown synergy in targeting both HDAC and PI3 kinase simultaneously, we have the additional advantage in Femapenistat of being able to target both of these in the same molecule and have shown that both enzymes are in fact inhibited both in preclinical models and in the clinic, in clinical studies to date. Finopenistat has shown a 23% overall response rate in mixed altered lymphoma, in particular diffuse large B-cell lymphoma, with a median duration of response of over a year, actually 13.6 months. This is a patient group with the most challenging prognosis. Based on our discussions with the FDA, we believe that combining Femapenistat with an anti-lymphoma agent will be the most expeditious path to initial approval for this drug.
We have the additional advantage in film a pin a stat of being able to target both of these.
In the same molecule and have shown that both enzymes are in fact inhibited both in preclinical models and in the clinic.
In clinical studies to date.
And as tenants that has shown a 23% overall response rate in myc altered lymphoma.
In particular in diffuse large b cell lymphoma.
With a median duration of response of over a year actually 13.6 months.
This is a patient group with the most challenging prognosis.
Based on our discussions with the FDA, we believe that combining feminist stat with an anti lymphoma agent will be the most expeditious path to the initial approval of this drug.
Since the strong benefit us in a tennis dad is somewhat delayed due to its mechanism of action, adding an anti lymphoma agent will also allow us to create a bridge for patients with rapidly growing lymphomas.
Robert E. Martell: Since the strong benefit of simipinostat is somewhat delayed due to its mechanism of action, adding an anti-lymphoma agent will also allow us to create a bridge for patients with rapidly growing lymphomas, slowing this growth long enough to allow Femipenistat's benefit to take hold. Because one of the most deadly types of lymphoma is this double-hit lymphoma, and this is defined by an alteration specifically Because of this, we're combining Femipenistat with Venetoclax, a drug that is rapidly acting and binds and inhibits BCL-2. By itself, venetoclax has only modest activity in diffuse large B-cell lymphoma. However, when combined with our mixed suppressor, fimipinostat, we found dramatic synergy in preclinical models of double-hit lymphoma.
Slowing this growth.
Long enough to allow semifinished stats benefit to take hold.
Because one of the most deadly types of lymphoma is this double hit lymphoma.
And this is defined by an alteration specifically in niche as well as Bcl two.
Because of this we are combining sumit penneast that with Venetoclax.
The net at KLAX is a drug that is rapidly acting and fines and inhibits bcl two.
By itself Venetoclax has only modest activity in diffuse large b cell lymphoma.
However, when combined with our mix suppressor FINMA Pinometostat, we found dramatic synergy in preclinical models of double hit lymphoma.
The current trial is designed to evaluate the safety and Tolerability.
Robert E. Martell: The current trial is designed to evaluate the safety and tolerability, the Pharmacokinetics, the Pharmacodynamics, and the anti-cancer activity of the combination in patients with relapsed refractory DLBCL, including those with double-hit lymphoma. We are planning to enroll patients in two cohorts in this study. In the first cohort, patients received 30 mg of phenepinistat and 400 mg of venetoclax daily. These are doses that have demonstrated clinical activity as a single agent for both molecules. In the second cohort, patients receive full doses of each agent, which is 60 milligrams of simipinistat and 400 milligrams of venetoclax daily. We plan to continue dose finding in this study until the recommended phase two dose has been identified. And we expect to report initial data from this study this year.
The pharmacokinetics pharmacodynamics and the anti cancer activity of the combination in patients with relapsed refractory Dl bcl, including those with double hit lymphoma.
We are planning to enroll patients in two cohorts in this study.
In the first cohort patients received 30 milligrams of cement penis stat, and 400 milligrams of Venetoclax daily.
These are doses.
That have demonstrated clinical activity as a single agent for both molecules.
In the second cohort patients receive full doses of each agent.
Which is 60 milligrams and cementing a stat and 4400 milligrams of Venetoclax daily.
We plan to continue dose finding on this study until the recommended phase two dose has been identified.
And we expect to report initial data from this study.
This year.
Our third program is CA 170.
Robert E. Martell: Our third program is CA-170, the first oral molecule targeting VISTA and PD-L1. We are currently evaluating this molecule in patients with mesothelioma because of the extremely high levels of VISTA expressed in this disease. CA-170 is the only anti-VISTA candidate in human clinical trials currently, and it is the first oral molecule targeting PD-L1 currently in the clinic. We are developing this candidate with our partner, Origene. VISTA is an incredibly important target in oncology and is highly expressed on tumor cells and infiltrating immune cells. Our Phase 1 study is evaluating the anti-cancer efficacy of CA170 in these patients with high VISTA-expressing mesothelioma. These patients have previously been treated and are not curable. We've enrolled 12 patients across six study sites within the U.S. and the U.K., randomizing patients into two cohorts.
The first oral molecule targeting Vista and PD L. One.
We are currently evaluating this molecule in patients with mesothelioma because of this extremely high levels of Vista expressed in this disease.
CA 170 is the only antibiotic candidate in human clinical trials currently and it is the first oral molecule targeting PD L. One currently in the clinic.
We are developing this candidate.
Excuse me, we're developing this candidate with our partner Aurigene.
Vista is an incredibly important target in oncology.
And is highly expressed on tumor cells and.
Infiltrating immune cells.
Our phase one study is evaluating the anti cancer efficacy of CA 170 in these patients with high Vista expressing mesothelioma.
These patients who have previously been treated and are not curable.
Weve enrolled 12 patients across six study sites within the U.S. and the UK.
Randomizing patients into two cohorts.
Robert E. Martell: The first cohort receives 1,200 mg twice daily of CA170, and the second cohort receives 200 mg twice daily. Patients who do not respond or experience disease progression at the lower dose are then crossed over to the high dose cohort. We are pleased to have completed enrollment in these 12 patients and look forward to reporting initial clinical data before year end. That sums up our ongoing clinical program. We are excited by our initial data on CA4948 and look forward to presenting detailed data at an upcoming medical meeting. We also continue to make great progress on our Femipinostat and CA-170 programs and will also report initial data in both of these programs before the end of this year. With that, I'll now turn over the call to Bill to discuss this quarter's financial results. Bill?
The first cohort received 1200 milligrams twice daily of CA 170 in the second cohort received 200 milligrams twice daily.
Patients, who do not respond or experienced disease progression at the lower dose are then crossed over to the high dose cohort.
We are pleased to have completed enrollment of these 12 patients and look forward to reporting initial clinical data before year end.
That sums up our ongoing clinical programs. We are excited by our initial data on CA 404, eight and look forward to presenting detailed data at an upcoming medical meeting.
We also continue to make great progress on our Philippine a stat in CA 170 programs and we'll also report initial data in both of these programs before the end of this year.
With that I'll now turn over the call to bill to discuss this quarter's financial results Phil.
Bill Steincroft: Thank you, Bob. Now for an update on our financial results. For the second quarter of 2019, we reported a net loss of $7.2 million, or $0.22 per basic and diluted share, as compared to a net loss of $8.7 million, or $0.26 per basic and diluted share for the same prior year period. Revenues were $2.1 million and $2.4 million for the second quarter of 2019 and 2018, respectively. Revenues for both periods comprised primarily of royalty revenues recorded on Genentech and Roche's net sales of Arabid.
Thank you Bob.
Now for an update on our financial results.
For the second quarter of 2019, we reported a net loss of $7.2 million or 22 cents per basic and diluted share as compared to a net loss of $8.7 million or 26 cents per basic and diluted share for the same prior year period.
Revenues were $2.1 million and $2.4 million for the second quarter of 2019 and 2018, respectively.
Revenues for both periods comprised primarily of royalty revenues recorded on demand Tech and roche's net sales of Erivedge.
Operating expenses were $8.2 million for the second quarter of 2019.
Bill Steincroft: Operating expenses were $8.2 million for the second quarter of 2019, as compared to $10.2 million for the same period in 2018. Research and development expenses were $5.6 million for the second quarter of 2019, as compared to... $6.5 million for the same period in 2008. The decrease in research and development expense was primarily due to decreased employee-related expenses. General and administrative expenses were $2.5 million in this second quarter of 2019, as compared to $3.6 million for the same period in 2018. The decrease in general and administrative expenses was driven primarily by lower personnel, legal, and stock-based compensation for the period. Other expense was $1.1 million for the second quarter of 2019, as compared to $0.8 million for the same period in 2018.
As compared to $10.2 million for the same period in 2018.
Research and development expenses were $5.6 million for the second quarter of 2019.
As compared to.
$6.5 million from the same period in 2018.
The decrease in research and development expense was primarily due to decreased employee related expenses.
General and administrative expenses were $2.5 million the second quarter of 2019.
As compared to $3.6 million for the same period in 2018.
The decrease in general and administrative expenses was driven primarily by lower personnel legal stock based compensation for the period.
Other expense was $1.1 million for the second quarter of 2019.
As compared to zero point $8 million for the same period in 2018.
For the second quarter of 2019 other expense primarily consisted of the non cash imputed interest expense related to the sale of future royalties that were completed with Oberland capital in the first quarter of 2019.
Bill Steincroft: For the second quarter of 2019, other expense primarily consisted of the non-cash imputed interest expense related to the sale of future royalties that we completed with Oberlin Capital in the first quarter of 2019. As of June 30, 2019, our cash, cash equivalents, and investments totaled $35.3 million, and there were approximately 33.2 million shares of common stock outstanding. We anticipate that our existing cash, cash equivalents, and investments should enable us to maintain our planned operations beyond our upcoming data catalyst for each of our three programs and into the second half of 2020. With that, we'll open the call to questions. Operator?
As of June 32019, our cash cash equivalents and investments totaled $35.3 million and there were approximately 33.2 million shares of common stock outstanding.
We anticipate that our existing cash cash equivalents and investments should enable us to maintain our planned operations beyond our upcoming bid catalyst for each of our three programs into the second half of 2020.
With that we'll open the call for questions operator.
We will now begin the question and answer session.
Operator: We will now begin the question and answer session. To ask a question, you may press star, then one on your touchtone phone. If you're using a speakerphone, please pick up the handset before pressing the keys. To withdraw your question, please press star, then two. At this time, we will pause momentarily to assemble our roster.
To ask a question you May Press Star then one on your Touchtone phone.
If you are using a speakerphone please pick up the handset before pressing the keys to withdraw your question. Please press Star then too.
At this time, we will pause momentarily to assemble our roster.
Chris Raymond: The first question comes from Chris Raymond with Piper Jaffray, please go ahead. Yes, hey, thanks for taking the question. You know, guys, Bob or Jim, I wonder if you could elaborate a little bit more on your 4948 data. It sounds like you're seeing some tumor reduction at the higher dose levels.
The first question comes from Chris Raymond with Piper Jaffray. Please go ahead.
Yes, hey, thanks for taking the question.
Yes.
Guys.
Bob or Jim I Wonder, if you could elaborate a little bit more on your.
Putting that 48 data.
It sounds like you are seeing.
Some tumor reduction at the higher dose levels.
Chris Raymond: Can you provide a little bit, first of all, maybe you could describe, are you using the Chesson criteria, I think, to measure responses, first of all? and maybe talk a little bit about the, you know, sort of the trajectory of these responses. I guess what I'm asking is are we thinking we should be or could be able to see a formal response in some of these cohorts?
Can you provide a little bit first of all maybe can you describe.
Are you using the chefs and criteria I think to measure responses first of all.
And.
And maybe talk a little bit about the.
Sort of the trajectory of these responses.
I guess, what I'm asking is are we thinking we should should be or could be able to see a risk.
Formal response.
Robert E. Martell: Thanks. This is Bob Martell.
In some of these cohorts.
Yes. Thanks this is about martell.
Robert E. Martell: So, as we mentioned, we are currently dosing at levels where, you know, we're potentially expecting to see efficacy based on our preclinical data. And so, the efficacy information that we're presenting today is sort of looking at tumor burden measurements. And we look at a variety of different factors in measuring, you know, tumor burden, one of which is tumor size. So, simply measuring a tumor and looking for a tumor decrease. And oftentimes, with, for example, diffuse large B cell lymphoma, we have measurable tumor lesions that can be monitored over the course of therapy and either reduce or increase, and so in that case, tumor size reduction is an important factor. Some of the patients that we are studying include Waldenstrom's macroglobulinemia or other diseases that have an M-spike, and so that's another way of measuring tumor burden.
So as we mentioned we are currently dosing at levels, where you know were potentially expecting to see efficacy based on our preclinical data and so sort of that the efficacy information that we're presenting today is sort of looking at tumor burden measurements and we look at a variety of different factors in measuring.
You know tumor burden one of which is tumor size. So it's simply.
Measuring a tumor and looking for.
Tumor decrease and oftentimes with for example, diffuse large b cell lymphoma.
We have measurable tumor lesions and those.
It can be monitored over the course of therapy, and either reduce or increase and so in that case.
Tumor size reduction is an important factor.
Some of the patients that we've.
Our studying include Waldenstrms macroglobulinemia or other diseases that have m. spike.
And so that's another way of measuring a tumor burden.
Robert E. Martell: So, looking at those variables, we've seen tumor reduction across multiple dose levels. For example, at the 200 milligram dose level, where we have three patients with efficacy data, two of the three are showing tumor burden decrease. We plan to present more detailed descriptions of the efficacy data, as well as the safety data, at an upcoming meeting. But in general, for each of these malignancies, we are using the standard reporting criteria for formal responses. But again, that will be presented at an upcoming meeting. Thanks for the question.
So.
Looking at those variables, we've seen tumor reduction across multiple dose levels. For example, at the 200 milligram dose level, where we have three patients with efficacy data.
Two of the three are showing tumor burden decrease.
We plan to present more detailed description of the efficacy data as well as the safety data.
At an upcoming meeting.
But in general for each of these malignancies, we are using the standard.
Reporting criteria for the formal responses, but again that will be presented at an upcoming meeting.
Thanks for the question should.
James E. Dentzer: And should we assume that it's ash?
Should we assume at ash.
James E. Dentzer: Yeah.
Yes. So this is Jim thanks for the question.
James E. Dentzer: Yeah, so this is Jim. Thanks for the question. We're generally targeting year-end, but of course, ASH is in December, so it'd be great if we could do that as well. The question is really gonna come down to where does the investigator want to present so we get, you know, all of the data updated and ready to go. So ASH makes the most sense from my perspective, but of course, that's going to be under the guidance of the investigator.
We're generally targeting year end, but of course asked us in December so it'd be great. If we could do that.
As well the.
The question is really going to come down to where do you where does the investigator want to present that we get you know that we have.
All of the data updated and ready to go so ash makes the most sense from my perspective, but of course that is going to be under the guidance of the investigator. So at that point of course, that's a much more full data of everything we've seen so far where the data. We have today is halfway through the 200 milligram cohort there'll be presumably the full data at that plus the 400 that we're already testing we don't have data in yet.
James E. Dentzer: So at that point, of course, that's much more full data on everything that we've seen so far. We are, the data we have today is halfway through the 200 milligram cohort. There'll be presumably full data on that plus the 400 that we're already testing.
James E. Dentzer: We don't have data in yet. But yeah, I think for today the answer is it's exactly what we were hoping to see for where we are. We announced earlier this year that in the first two patients, we had PK PD. And of course, what we really wanted to see that we were hoping for was, did we get more of that? Did we get safety PK PD?
But yeah I think for today. The answer is it's exactly what we are hoping to see for where we are.
We we announced earlier this year in the first two patients we had PK PD and of course, what we really wanted this what we really wanted to see that we are hoping for was did we get more of that did we get safety PK PD and of course are we starting to see tumor shrink in the answer to that is yes, now we don't want to make too much of this if it's small cohorts you're talking about three people per cohort. So.
James E. Dentzer: And, of course, are we starting to see tumors shrink? And the answer to that is yes. Now we don't want to make too much of this. It's just small cohorts. You're talking about three people per cohort. So, you know, am I going to say if we get two out of three people where we're seeing tumor reduction and that's a 66% ORR and say the answer is no? Hold that thought for, you know, future releases, future conferences, and especially expansion. But for where we are today, are we seeing exactly what we hoped? The answer is yes. That's great.
Am I going to say, if we get two or three people with.
Where we're seeing tumor reduction and that's a 66% or so the answer is no we'll hold that thought for future release, future conferences, and especially expansion, but for where we are today are we seeing exactly what we hoped the answer is yes.
That's great. One more question if you don't mind, So I think I heard Bob mentioned Waldenstrom stations could you confirm that you had waldenstrom space that study or was it just deal bcl patients.
Chris Raymond: That's great. One more question, if you don't mind. So I think I heard Bob mention Waldenstrom's patients. Did you confirm that you had Waldenstrom's patients in that study, or was it just DLBCL patients?
Robert E. Martell: Well, I did mention Waldenstrom's, and I think it's really important to emphasize that, too, because, you know, with regard to 4948, the unique thing about Waldenstrom's is that a very significant majority of those patients actually have this mid-88 mutation, which strongly activates the midosome that's oncogenic. And yes, we are enrolling Waldenstrom's patients in the study. Investigators are going to discuss in detail, obviously, at the upcoming meeting, but certainly, we're very interested in that patient population because it really doesn't require patient selection in order to have patients on the study who we know have this pathway activated.
Well, if I did mention Waldenstrms and I think it's really important to emphasize that too because you know with regards to 4948.
The unique thing about Waldenstrms is that.
Very significant majority of those patients actually have this mid 88 mutation, which strongly activates the Minnesota, that's oncogenic and yes, we are enrolling enrolling waldenstrms patients on the study.
Investigators are going to discuss in detail, obviously at the upcoming meeting but.
Certainly we're very interested in that patient population because it really doesn't require a patient selection in order to.
Have patients on the study who we know have this pathway activated yeah, it's going to be very interesting to see I mean, ideally, we'll have a broad spectrum of patients but to Bob's point.
James E. Dentzer: Yeah, it's going to be very interesting to see. I mean, ideally, we'll have a broad spectrum of patients, but to Bob's point, you know, the TOLEC receptor pathway is oncogenic precisely because when mid-88 is altered, it leads to overactivity of the midosome, which then leads to overactivity of the pathway. Since we're targeting the midosome directly, we'd love to see some patients with it, some patients without. Waldenstrom's comes right out. There are some patients, I think 95% of Waldenstrom's patients are mid-88 altered. So it'd be great if actually we could find some of both, the majority and then maybe even somebody in the minority as well, to do a compare-contrast. But to this point, we're just happy we're getting, you know, the broad swath of patients that we hoped for. And as I said, the data is really lining up exactly the way we hoped. Awesome. Thanks.
You know the toll like receptor pathway is oncogenic precisely because when mediate is altered it leads to over activity the middle right, which then leads to over activity. The pathway. Since we're targeting the mid is on directly we'd love to see some patients with some patients without Walters Troms comes right to the front.
There are some patient I think its 95% of one's troms patients RMB 88 altered.
So it'd be great. If it actually we could find some of both the majority and then maybe even somebody in the minority as well to do a compare contrast, but to this point, we're just happy we're getting.
The the broad swath of patients that we hoped for and as I said the data is really lining up exactly the way we hope.
Awesome. Thanks, guys.
Operator: Cool, thank you. Showing no further questions, this concludes our question and answer session. I would like to turn the conference back over to James Dentzer for any closing remarks. Thank you all.
Yeah, well thank you.
Showing no further questions. This concludes our question and answer session I would like to turn the conference back over to James Dentzer for any closing remarks.
Thank you operator.
James E. Dentzer: Thank you, operator. In Q4 of last year, we set an ambitious goal. We cut our staff and expenses by almost a third, and yet we promised to increase our productivity and achieve more results than we had in our 20-year history. We promised that we would see clinical execution across the board, and achieve key clinical milestones in three separate clinical studies. Frankly, it sounded a bit too ambitious, and yet here we sit, two and a half quarters later, and we're hitting or beating every expectation. We knew 2019 would be an exciting and transformational year for Curis, and it's turned out to be exactly that, and a lot of fun too. I'm very proud of our team here at Curis and our partners at Origin for their continuous success, and I'm thrilled for the patients and families who are benefiting from participation in our clinical trials. Thank you for joining us on our call today, and we look forward to updating everyone again soon.
In Q4 of last year, we set an ambitious goal.
We cut our staff and expenses by almost a third.
And yet we promise to increase our productivity and achieve more results than we had in our 20 year history.
We promised that we would.
C clinical execution across the board.
Achieve key clinical milestones in three separate clinical studies.
And frankly, it sounded a bit too ambitious.
And yet here, we sit two and a half quarters later, and we're hitting or beating every expectation.
We knew 2019 would be an exciting and transformational year for Curis and it's turned out to be exactly that.
And a lot of fun too.
I'm very proud of our team here at Curis and our partners at Aurigene for their continuous overachievement and I'm thrilled for the patients and families who are benefiting from participation in our clinical trials.
Thank you for joining us on our call today, and we look forward to updating everyone again soon.
The conference has now concluded. Thank you for attending today's presentation you may now disconnect.
Operator: The conference is now concluded. Thank you for attending today's presentation. You may now disconnect. Once again, the conference has concluded. You may disconnect from your lines at this time. Thank you.
Oh.
Once again the conference has concluded you may disconnect your lines at this time. Thank you.
Oh.
Oh.
No no.
No.