Q3 2024 Corvus Pharmaceuticals Inc Earnings Call
Unknown Executive, Leiv Lea, Richard Miller
Speaker Change: Good afternoon, everyone. Thank you for standing by and welcome to the Cordova's Pharmaceuticals third quarter 2024 business update and financial results conference call.
Unknown Executive, Leiv Lea, Richard Miller
Speaker Change: Thank you, Operator, and good afternoon, everyone. Thanks for joining us for the Corvus Pharmaceuticals 3rd Quarter 2024 Business Update and Financial Results Conference Call.
Speaker Change: On the call to discuss the results and business updates are Richard Miller, Chief Executive Officer, Leiv Lea, Chief Financial Officer, Jeff Barquera, Chief Business Officer, Jim Rosenbaum, Senior Vice President of Research, and Ben Jones, Senior Vice President of Regulatory and Pharmaceutical Sciences.
Speaker Change: The executive team will open the call with some prepared remarks, followed by a question and answer period.
Speaker Change: I would like to remind everyone that comments made by management today and answers to questions will include forward-looking statements.
Unknown Executive, Leiv Lea, Richard Miller
Speaker Change: Forward-looking statements are based on estimates and assumptions as of today and are subject to risks and uncertainties that may cause actual results to differ materially.
Speaker Change: from those expressed or implied by those statements, including the risks and uncertainties described in Corvus's quarterly report on Form 10-Q for the quarter ended September 30, 2024 that was filed today and other filings the company makes with the SEC from time to time.
Leiv Lea: The company undertakes no obligation to publicly update or revise any forward-looking statements except as required by law. With that, I'd like to turn the call over to Leiv.
Leiv Lea: Thank you, Zach. I will begin with a quick overview of our third quarter 2024 financials and then turn the call over to Richard for a business update.
Leiv Lea: Research and development expenses in the third quarter 2024 totaled 5.2 million dollars compared to 4 million dollars in the same period in 2023. The 1.2 million dollar increase was primarily due to an increase in Socolitinib clinical trial expenses.
Leiv Lea: In addition, we recorded a non-cash loss of $32.8 million from the change in fair value of Corvus's warrant liability during the third quarter of 2024.
Leiv Lea: This compares to a net loss of $6 million for the same period in 2023, which included a $0.9 million non-cash loss from Angel Pharmaceuticals.
Leiv Lea: As of September 30th, 2024, Corpus had cash, cash equivalents, and marketable securities totaling $41.7 million as compared to $27.1 million at December 31st, 2023.
Leiv Lea: Of note, associated with our financing in May 2024, we also sold common stock warrants that have an exercise price of $3.50 per share and expire on June 30, 2025.
Leiv Lea: One investor early exercised their warrants in October, resulting in $5.9 million in cash to the company. If all the remaining warrants are exercised, we will receive approximately $54 million in additional cash.
Leiv Lea: Based on our current plans we anticipate our cash, including the recent early exercise of common stock warrants, provides runway into 2026. I will now turn the call over to Richard who will discuss our clinical progress and elaborate on our strategy and plans.
Richard Miller: Thank you Leif and good afternoon everyone. Thank you for joining us today for our business update call.
Richard Miller: We are advancing our LEAD programs with Socolitnib on multiple fronts.
Richard Miller: A registration phase 3 trial for peripheral T cell lymphoma, PTCL, is now enrolling patients and a phase 1 trial for atopic dermatitis is moving along according to plan.
Richard Miller: Socolitinib is a first-in-class oral therapy that selectively inhibits ITK to modulate and control parallel signaling pathways in the immune system.
Richard Miller: There is growing evidence, both from our own clinical efforts and preclinical research conducted by us and others, that this mechanism of action may provide a powerful new approach for the treatment of a broad range of immune diseases and cancers.
Unknown Executive, Leiv Lea, Richard Miller
Richard Miller: Our ability to move quickly and efficiently into autoimmune diseases, such as atopic dermatitis, was facilitated by our T-cell lymphoma clinical trials, which provided valuable information regarding dosing, safety, pharmacokinetics, and most importantly, effects on immune cells.
Richard Miller: Now I will provide more detail on our progress starting with Socolitinib phase 1 clinical trial in patients with atopic dermatitis.
Richard Miller: The trial is designed to enroll 64 patients with moderate to severe atopic dermatitis that have progressed on at least one prior topical or systemic therapy.
Richard Miller: The study is randomized, placebo-controlled, and patients and the treating physicians are blinded to the treatment assignment. The company is not blinded, and therefore we can evaluate the data as the trial progresses.
Richard Miller: There are four dosing cohorts that are sequentially enrolled. 100 milligrams twice per day, 200 milligrams once per day, 200 milligrams twice per day, and 400 milligrams once per day.
Richard Miller: The rationale for the dosing regimens is based on pharmacokinetic and pharmacodynamic data obtained from our lymphoma trial.
Richard Miller: Patients are randomized within each cohort at a 3 to 1 ratio to receive either active drug or placebo for a total of 16 patients per cohort, 12 active, 4 placebo.
Richard Miller: We have completed enrollment, including the entire follow-up in the initial 16-patient cohort, and the Data Safety and Monitoring Review Committee has completed its review with no safety signals observed.
Richard Miller: The second cohort is now enrolling with the same design as the first cohort, except the socolitinib dose is 200 milligrams once daily, the same total daily dose as the first cohort, which was 100 milligrams twice daily.
Richard Miller: Cohorts 3 and 4 will examine higher daily doses using the same design, 200 milligrams twice daily and 400 milligrams once daily respectively.
Richard Miller: For reference, the dose in our phase 3 lymphoma trial is 200 milligrams twice daily which provides continuous full receptor occupancy.
Richard Miller: The primary endpoint is safety and tolerability, and efficacy is measured using the clinically validated measurements of improvement in eczema area and severity index, also known as EASI score, and the Investigator Global Assessment, or IGA score.
Richard Miller: We are also measuring levels of Th2 and Th17 cytokines in the serum, such as IL-4, 5, 13, 17, and many others.
One other property of selective ITK inhibition should be noted.
Richard Miller: Published work from scientists at Cornell University this past summer in 2024 and Janssen research in 2019 have shown that the ITK protein
Richard Miller: controls a switch between inflammatory TH17 cells and anti-inflammatory T-regulatory or suppressor cells.
Richard Miller: When ITK protein is active, TH17 differentiation dominates. ITK inhibition results in a shift to Tregs and away from TH17.
Richard Miller: The Cornell Group utilized Socolitinib for their studies. The Janssen Group used siRNA to knock down ITK protein expression.
Richard Miller: because at that time selective ITK inhibitor was not available. These studies and others suggest that due to the induction of Tregs, the anti-inflammatory effects of sulcolitinib could be very durable.
Speaker Change: There is strong interest in an oral safe drug for atopic dermatitis and we are receiving positive feedback on Socolitinib's anticipated profile from our investigators and collaborators.
Speaker Change: We plan to compare our data with analogous published data from approved agents currently used to treat atopic dermatitis.
Speaker Change: In summary, we believe that socolitinib has several potential advantages for the treatment of immune diseases.
Speaker Change: An Oral Medication, Attractive Safety and Tolerability Profile, Novel Mechanism of Action
Speaker Change: durable response, and ability to address a broad spectrum of autoimmune and allergic indications. For example, comorbidities such as asthma in patients with atopic dermatitis.
Unknown Executive, Leiv Lea, Richard Miller
Speaker Change: The broad potential of Socolitinib and our next generation ITK inhibitors is supported by new preclinical data showing that Socolitinib is active in systemic sclerosis, a chronic autoimmune disease that causes fibrosis and inflammation in many organs including the skin.
Speaker Change: That data will be presented later this week at the annual meeting of the American College of Rheumatology.
Speaker Change: We continue to advance a range of second and third generation ITK inhibitor product candidates which are designed to deliver precise T cell modulation that is optimized for specific immunology indications.
Speaker Change: We are focusing our preclinical development on asthma, psoriasis, scleroderma, inflammatory bowel disease, and fibrotic diseases, with a host of additional indications identified for future work.
Now for an update on socolitinib in oncology.
Speaker Change: In September, we initiated our Registrational Phase 3 Clinical Trial for Relapsed PTCL.
Speaker Change: There are currently no FDA fully approved agents for the treatment of relapsed PTCL, and the FDA has granted orphan drug designation and fast-track designation for Socolitinib for the treatment of relapsed T-cell lymphoma.
Speaker Change: The study is designed to enroll 150 patients, randomized to Socolitinib, or standard of care chemotherapy, which is either Pralatrexate or Bolinostat. The primary endpoint for the study is progression-free survival.
Speaker Change: We are now enrolling patients at multiple clinical sites and we are on track with our plan.
Our team is working to open additional sites.
Speaker Change: with a goal of about 40 to 50 centers in the United States, Australia, Canada and South Korea participating in the trial.
Speaker Change: The vast majority will be in the United States, including centers such as MD Anderson, Memorial Sloan-Kettering, City of Hope, Washington University, and other high-profile institutions.
Speaker Change: We are delighted to have the participation of leading centers with extensive experience and expertise in conducting clinical trials in T cell lymphomas.
Speaker Change: While we are no longer enrolling new patients in our Phase 1 trial, we continue to monitor patients on therapy as they complete their scheduled follow-up assessments.
Unknown Executive, Leiv Lea, Richard Miller
Speaker Change: There are four patients who remain on therapy, including three with the previously reported complete responses, which are sustained, and one patient who achieved a partial response. The patient with the partial response continues to demonstrate tumor regression over time, but has not yet reached a complete response.
Speaker Change: Therapy in one additional patient who achieved a complete response was discontinued while in CR after 24 months on treatment per the study protocol.
Speaker Change: The objective response rate for the phase 3 patients remains at 39%, or 9 out of 23 patients. This includes 6 complete responses and 3 partial responses.
Speaker Change: The median PFS remains 6.2 months. Published median PFS for Belinostat and Pralotrexate are 1.6 months and 3.5 months respectively.
Speaker Change: We're also planning a single-agent socolitinib-solid tumor trial in relapsed renal cell cancer, or RCC, representing a new approach to immunotherapy of this disease.
Speaker Change: The Biochemistry, Mechanism of Action in Preclinical Data in Solid Tumors for Socolitinib Tumor Immunotherapy is now in press in the peer-reviewed journal Drug Discovery, a Nature Partner journal.
Speaker Change: Given our focus on our atopic dermatitis and PTCL trials, we now plan to initiate our solid tumor clinical trial sometime in early 2025.
Speaker Change: We also continue to advance our other clinical stage development programs.
Speaker Change: We have been one of the leaders in the development of adenosine 2A receptor antagonism for the treatment of cancer with cifer adenate.
Speaker Change: This includes our Phase 1B2 clinical trial that is being conducted in collaboration with the Kidney Cancer Research Consortium.
Speaker Change: The trial is evaluating SIFO as a potential first-line therapy for metastatic renal cell cancer in combination with ipilimumab and nivolumab. The study is enrolling at MD Anderson, Vanderbilt Duke, and the University of Pennsylvania.
Speaker Change: 46 patients were enrolled and the trial continues to meet our pre-specified statistical hurdle for continuation, which is the achievement of at least a 50% improvement in the deep response rate of 32% associated with IPI and NEVO combination alone.
Speaker Change: Deep response rate is the CR rate plus the PR rate only counting PRs that achieve greater than 50% tumor volume reduction.
Unknown Executive, Leiv Lea, Richard Miller
Speaker Change: Along with our partners at the Kidney Cancer Research Consortium, we have decided to continue our follow-up of patients on the trial before presenting the data. Therefore, we will not be presenting this data at the GU Malignancy Conference taking place in late November and will instead target a presentation sometime in early 2025.
Outside of RCC
New data highlighting the potential.
Speaker Change: of Cifer Adenin to Treat Prostate Cancer was presented this past weekend in an oral session at the Society for Immunotherapy of Cancer or CITSI annual meeting where it was selected as one of the top 100 abstracts.
Speaker Change: This research was led by Dr. Larry Fong from the Fred Hutch Cancer Center and UCSF.
Speaker Change: The data demonstrate the potential of CIFO to overcome immunotherapy resistance in metastatic castration-resistant prostate cancer.
Speaker Change: This includes elucidating the role of the adenosine pathway on the immunobiology of the disease, including the importance of immunosuppressive myeloid cells and the adenosine gene signature.
a biomarker discovered and published by Corvus and academic collaborators.
Speaker Change: in which PSA partial responses were observed in patients receiving SIFO alone and together with a tesolizumab.
Speaker Change: Overall, we believe these data highlight that cifer adenine could be an important advancement for patients with tumors that are resistant to checkpoint inhibitors and is supportive of our ongoing clinical trial in combination with ipi and nevo in frontline renal cell cancer.
Speaker Change: The data also underscore the importance of the adenosine gene signature as a biomarker for future studies.
Speaker Change: Summarizing the outlook for the remainder of 2024 and into 2025, we have important clinical milestones for Socolitinib.
Speaker Change: Upcoming milestones include, number one, preclinical data presentation at the American College of Rheumatology meeting later this week.
Speaker Change: Number three, final data from all four cohorts of the Phase 1 atopic dermatitis trial in the first half of 2025.
Speaker Change: Number four, initiating a phase two clinical trial with socolitinib in solid tumors in early 2025.
Speaker Change: with initial data anticipated in late 2025. Number five, continuing to activate sites and drive enrollment in the registration phase three clinical trial of socolitinib in PTCL.
Speaker Change: Our current cash plus the exercise of outstanding warrants gives us runway into 2026.
Speaker Change: Allowing us to execute on these important milestones and further demonstrate the value of our programs and in particular the significant opportunity
for ITK Inhibition in Immunology and Cancer.
Speaker Change: We look forward to providing updates on our programs in the coming quarters.
Speaker Change: I will now turn the call over to the operator for a Q&A period. Operator?
Speaker Change: Thank you. Ladies and gentlemen, we will now begin the question and answer session. Should you have a question, please press star four by the one on your telephone keypad.
Speaker Change: You will hear a prompt that your hand has been raised.
Speaker Change: And should you wish to cancel a request, please press star followed by the two. If you are using a speakerphone, please lift the handset before pressing any keys. One moment please for your first question.
Speaker Change: Your first question comes from the line of Leigh Watzak from Kantor. Please go ahead.
Speaker Change: Hey, great. Thanks for taking my questions. Rich, I wonder if you can just comment on the kinetics of IETK inhibition on the clinical scores in AD. And then do you sort of expect the EZ score to further improve after the 28 day mark?
Speaker Change: And also, can you maybe just tell us a little bit about, you know, how you're thinking about the bar for success, given it's an oral drug. Thank you.
Speaker Change: Okay, thank you for the question Leia The kinetics of the response are Are very quick. We see improvement in about the first week. I'll elaborate more of this in our in our call on in December We expect
the criteria for success to be similar what you've observed
Speaker Change: We'll be looking at 28-day data and comparing it to 28-day data for similar compounds or for Dupixent and other approved agents.
Speaker Change: We do expect that there would be a very durable effect from Socolitinib based on its mechanism of action and potential for further improvement.
Unknown Executive, Leiv Lea, Richard Miller
Unknown Executive, Leiv Lea, Richard Miller
Okay, thank you.
Unknown Executive, Leiv Lea, Richard Miller
Speaker Change: Thank you. And your next question comes from the line of Roger Song from Jeffries. Please go ahead.
Great, congrats for
Speaker Change: for the for the progress and then so a couple questions also related to the data with dermatitis, the data release.
Speaker Change: Early 2025, how should we think about the follow-up time period for those cohorts? And then in terms of the efficacy endpoint, do you see those endpoints will have a different kinetics with different follow-ups? Thank you.
We will report in December 28 day data.
Speaker Change: We'll report on the kinetics of, as I mentioned to the last question. We are seeing responses rapidly, like within a week.
Speaker Change: As we get into cohort three and four, we'll start to evaluate the kinetics and durability of the responses over the two-month period.
Unknown Executive, Leiv Lea, Richard Miller
Unknown Executive, Leiv Lea, Richard Miller
Speaker Change: Got it. Thank you. Maybe to follow up on those, based on the PK PD and then maybe preclinical modeling, do you expect to see those dependents for the forearms you're testing in phase one? Thank you.
Um.
Speaker Change: I would expect the efficacy to improve as we go higher in the dose, just based on what we've seen in lymphoma studies and getting more saturation of the target. However, atopic dermatitis is a different disease than lymphoma. So, you know, I'm not sure that that would turn out to be the case.
Unknown Executive, Leiv Lea, Richard Miller
Unknown Executive, Leiv Lea, Richard Miller
Thank you, Rich. That's it from us.
Unknown Executive, Leiv Lea, Richard Miller
Speaker Change: So, so Roger, just to just to maybe elaborate a little bit on that. We know that a hundred milligram dose
Speaker Change: So the first cohort and we know this from our lymphoma studies
gives you reasonable saturation of the target, but not complete.
Unknown Executive, Leiv Lea, Richard Miller
Speaker Change: reasonable. And we were able to, we have measurements from our lymphoma patients where we've been able to measure that immediately after taking a dose and then at the nadir, at the low point.
Speaker Change: and we know that 100 milligram dose gives you reasonable coverage but not total coverage. We know at a higher dose, for example, at 200, you get better coverage, etc.
Unknown Executive, Leiv Lea, Richard Miller
Thank you.
Unknown Executive, Leiv Lea, Richard Miller
Unknown Speaker 0
Speaker Change: Thank you. And your next question comes from the line of Edin Husanov from Lindenburg. Please go ahead.
Speaker Change: Hi, everyone. Hi, Richard. Congratulations on the progress this quarter. I've got a couple of questions. So first,
A question again on an atopic dermatitis.
Speaker Change: local regimen like loroxalitinib, is it systemic like dupilumab and is there any physician feedback in terms of the enthusiasm of the patients and et cetera, if you could share any details.
Speaker Change: Okay, so first agent, we don't have all 64 patients enrolled yet. The intent is to have 64 patients.
We're enrolling cohort number two now.
Speaker Change: The Eligibility for entry is you have to have failed a systemic or topical Therapy for your AD. You have to have moderate to severe or severe disease So far the patients enrolled
Speaker Change: Just about all of the patients that we've treated so far have discontinued their topical therapy while they're on our drug.
Unknown Executive, Leiv Lea, Richard Miller
Unknown Executive, Leiv Lea, Richard Miller
Speaker Change: Okay, understood. So mostly this is sort of topical failure, it's pre-Dupixent essentially, patient population. So far, so far, now we're in the middle of the study.
Unknown Executive, Leiv Lea, Richard Miller
Okay, that makes sense.
Speaker Change: And, yeah, so I also want to go back to PTCL indication, and maybe it's sort of an outdated question, but do you have any updates on phase 1B patients, any CRs turned into PRs, or any PRs, any sort of PRs turned into CRs, or any updates on the duration of responses for phase 1B?
Speaker Change: So the I mentioned in my remarks that there's four patients still on therapy the three of those are CRs that are oh god months I don't remember six to twelve months out there at least. One of the one of the PRs
Speaker Change: has continued tumor regression. That patient has been on treatment about 18 months now and just has slow improvement, slow continued improvement in in his disease.
Speaker Change: It is not yet a CR, but it's looking pretty promising for that. Now, one of the CRs, we stop therapy while in CR per protocol. We can't treat beyond 24 months by our protocol.
So that patient discontinued therapy while in CR.
Speaker Change: Okay, so one PR may potentially turn into CR. And how do you explain overall such a broad availability of CRs versus PRs? You have more CRs than PRs, which is unusual. So how do you explain, what does it tell us about the mechanism of action here?
Unknown Executive, Leiv Lea, Richard Miller
Well, I think it tells us that
Speaker Change: and it's effective at eradicating, remember these tumors are very heterogeneous, so they have a lot of different mutations and a lot of different clones, et cetera. And I think what this tells us is the mechanism of action is able to handle a broad spectrum of tumors and the associated mutations.
Unknown Executive, Leiv Lea, Richard Miller
Whereas if you treat with let's say a chemotherapy agent
Speaker Change: you're going to, you know, eventually select out resistant clones, we seem to be less susceptible to the emergence of resistance.
Speaker Change: And I think that's because we're inducing an immune response, and an immune response, as you know, can respond to different antigens and different diversity of antigens.
Make sense?
Speaker Change: Yes, absolutely. And the last question I have on systemic sclerosis, the preclinical data that they will present, so another hard-to-treat indication or immune indication.
Unknown Executive, Leiv Lea, Richard Miller
Speaker Change: So historically, there have been two endpoints that FDA was looking for for systemic sclerosis. One is LUNC.
Speaker Change: SVC, another one is Rodan and Skinscore. So what do you think Sokolitnev may focus? I know this is too early.
Speaker Change: but this is an active drug, one indication in oncology, one indication of autoimmune, so it wouldn't be totally unexpected if you start directly from phase two at some point, so just wanted to hear your thoughts on systemic sclerosis. Well, I mean, people die from the lung disease, the interstitial pneumonitis.
and Fibrotic Lung Disease, Interstitial Lung Disease.
Speaker Change: So that would be the thing to focus on and that's what we have focused on.
Speaker Change: So the model that's going to be in the abstract is already out on this. I think the paper is on Sunday at ACR.
Speaker Change: is a is a very interesting model, a very good model, probably the best model, animal model for systemic sclerosis.
It's a very much a Th2.
Speaker Change: Disorder and they have fibrosis, fibrotic lung disease. They get right heart failure. And All of that responds to the treatment with socolitinib.
In addition, we've also tested socolitinib in your typical bleomycin
fibrotic interstitial lung disease.
and is very active in that model as well.
Speaker Change: So I think down the line systemic sclerosis, I mean, the thing that we would focus on would be lung disease because that's what kills people. And that's the, you know, that's the biggest, the most serious part of the problem.
Speaker Change: And as you know, lung disease and right heart disease go together and arterial hypertension and so forth.
Speaker Change: So that would be, you know, that's an interesting disease for us. It also gives us a window in fibrotic diseases. Fibrosis is very much Th2. We block Th2 very well. And so this opens up a whole new...
Speaker Change: set of diseases that have to do with fibrosis. Everything from scleroderma to cirrhosis to other fibrotic diseases.
Speaker Change: Right, yeah, it makes sense. And I'm sorry, just the last question I want to ask, how do you dose differentiate between oncology and autoimmune diseases? These are two big sort of indications, just wanted to hear your thoughts on this.
I think cancer you will.
Richard Miller: Well, yeah, makes sense. Makes sense. Okay. Thanks so much, Richard. Congrats with the progress this quarter. Thank you.
Unknown Speaker 0
Speaker Change: Hi, thanks so much for taking my questions here. Congratulations on all the progress that you've been making. If I could just revisit the readout, the interim readout in atopic dermatitis.
Speaker Change: that you're expecting in December. As it relates to EASY, just if you could clarify, will you be specifically reporting on both EASY 50 and EASY 75?
And then a follow up is just going back to.
Richard Miller: Comments Richard you made in response to I think one of the first questions on the Q&A which was
Richard Miller: expectations around what the bar for success would be. I think you had mentioned
Um...
Richard Miller: You would expect something similar to approved agents such as Doobie, but I'm wondering if since you're an oral therapy if you feel the need to be as As effective as perhaps some of the injectables like a Doobie and then I have a follow-up. Thank you
Okay, so let me thank you for the question.
Speaker Change: So we expect to report for Cohort 1 and Cohort 2. Now we'll have more follow-up on Cohort 1, of course.
Speaker Change: because it was enrolled first. We expect to report on the mean percent EASYscore reduction.
Speaker Change: and for ACTIV. We expect to report on EASY 50, EASY 75, EASY 90.
Speaker Change: We expect to report on IGA zero and one. Those are very typical things. So we will be reporting on that.
Speaker Change: Obviously we report on safety as well. Now your question about oh what will we compare to? Well there is our regimen again this is the first dose we've tested it's 28 day dosing.
We can compare and will compare to, let's say, Dupiccent.
Speaker Change: Phase 1 trial where they had already optimized their dose and treated for four weeks and 12 weeks, so we can compare to things like that.
Speaker Change: And that's what we plan to do. Now your question about do we have to be as good because we're oral and safe and more convenient.
Speaker Change: You know, we're pretty excited about the mechanism of action of our drugs, so I want to be better.
Unknown Executive, Leiv Lea, Richard Miller
I plan to be better.
Unknown Executive, Leiv Lea, Richard Miller
Speaker Change: Okay, appreciate that and appreciate the confidence that you have in the potential readout there. So and then a follow-up is almost a segue from the
Obviously, the promise of having an oral
Speaker Change: Based agent for atopic dermatitis versus an injectable what the competitive landscape looks like in terms of orals that are in the clinic and kind of where, where are you relative in terms of clinical development timelines to perhaps some other oral.
Higher Profile Oral Programs that you're following closely. Thank you.
Speaker Change: Well, that's a very hard question. So as you know, there are many drugs in development for atopic dermatitis. Most of those are injectables, biologics, there are some oral compounds in the clinic.
Speaker Change: I don't know if I'm in a position to comment on those. I think they're pretty early. I don't really know what their date is. I know there's some data readouts also before the end of the year. So I'm not sure I'm able to comment on our product relative to those.
Unknown Speaker 0
Speaker Change: Thank you. And your next question comes from the line of Jeff Jones from Oppenheimer. Please go ahead.
Unknown Executive, Leiv Lea, Richard Miller
Speaker Change: Good afternoon guys and thanks for taking the question. I guess I'll switch over from AAD and go back to PTCL. In terms of the phase 3 trial in the primary endpoint of PFS, how do you deal in the trial with patients who are complete responders and go on to transplant?
Speaker Change: and then interested in your view on the bar for success here given some of the data you're we're seeing on the PI 3k inhibitors at ash right now and then I've got a follow-up
Okay, so first of all, Jeff.
Jeff Barquera: It is a randomized trial and there's an equal number of patients in the standard of care, bolinostatin, pralotrexate, and the socolitinib arms.
Now, the second part of your question was.
Criteria for success, I think.
It was.
Jeff Barquera: Statistical plan gives us about a 90% power, actually I think it's a 89% power, to see a one and a half month improvement over the control arm. So that would give you a hazard ratio of about 0.56. So that's what we need to do to win.
Jeff Barquera: Now, just getting back to the transplant question, just so people understand, I mean, most patients, most patients are too old for a transplant.
Jeff Barquera: This disease is mostly a disease of older people. Most patients are too old and patients have to get into a good remission to get a transplant.
Jeff Barquera: That's why it's been such a small subset of patients who gets to transplant, and why it's so hard to interpret the transplant data because you're selecting out a very favorable patient population to begin with.
Jeff Barquera: But in any event, in our study, we deal with that by censoring that data.
Makes sense. Appreciate that. Yeah, it does. And I guess.
Jeff Barquera: So, I mean, the data that's out at ASH right now on the PI3 kinase inhibitors, that's really it's ORR data at this point.
Jeff Barquera: But I guess just your thoughts on what you're seeing there with some of those, I guess, you know, between 40 to 60% ORRs and a couple of those studies.
Yeah, so.
Speaker Change: So, the PI3Ks have been around for a long time now in PTCL. They give you, you know, reasonable responses. They're usually very short-lived. Those drugs are highly toxic with liver abnormalities and hematologic abnormalities as well. I don't...
Speaker Change: I don't really think that that is a significant competitor to socolitinib should our trial be positive.
Speaker Change: and perhaps use it as maintenance therapy because of its safety and convenience.
Speaker Change: You're not going to do that with a PI3K. You can't just slam that together with a bunch of chemotherapy drugs. It would be too difficult to do that from a safety standpoint.
and using it as a maintenance would be also problematic.
Unknown Executive, Leiv Lea, Richard Miller
Speaker Change: Okay, I appreciate that. One quick follow-up on the renal cell study with Socolitinib.
Speaker Change: In terms of selecting patients for enrollment there, are you looking going back to looking at absolute lymphocyte counts or using prior lines of therapy? How are you sort of looking at sort of T cell health there?
Speaker Change: So I think we'll be in better shape there because I mean lymphoma patients are inherently pretty immunosuppressed.
Unknown Executive, Leiv Lea, Richard Miller
Speaker Change: from the disease as well as the types of therapy they've had. That's less of a problem in renal.
Unknown Executive, Leiv Lea, Richard Miller
Speaker Change: Okay, so you're just collecting the data and sort of look at how it pans out and for these endpoints or biomarkers post? Yes.
Speaker Change: Okay, great. Thank you very much. I'll jump back into the queue.
All right, I think
Speaker Change: I want to thank everyone for participating and we look forward to giving an update in December to everyone on our atopic dermatitis trial. Thank you very much.
Unknown .
Speaker Change: Thank you. And this concludes today's call. Thank you for participating. You may all disconnect.