Corvus Pharmaceuticals, Inc. 12th Annual Cantor Fitzgerald Global Healthcare Conference
Review the key takeaways and the transcript of this earnings call.
- Corvus Pharmaceuticals is a clinical-stage company developing novel immune modulators for cancer and immune diseases.
- Their lead program, SOCALITNIB, is an oral ITK inhibitor in a registrational phase 3 trial for peripheral T-cell lymphoma and a phase 2 trial (CR1) for moderate to severe atopic dermatitis.
- SOCALITNIB has strong composition of matter patents through November 2037, with pharmaceutical extensions to 2042.
- The drug blocks TH2 and TH17 pathways, rebalances the immune system by increasing Treg cells, and has shown a safety profile similar to placebo.
- Biomarker data supports clinical outcomes, showing dose response effects in reducing TH2 cytokines and increasing Tregs, with durable effects off therapy.
- Phase 2 CR1 trial enrollment is ongoing, with data expected in Q3 2027.
- The company plans additional studies in asthma and hidradenitis suppurativa (HS) starting this year.
- Corvus raised several hundred million dollars in January and had $214 million in cash as of June 30, providing runway through mid-2028.
- They expect to complete the phase 3 PDCL trial and phase 2 CR1 and HS trials within this funding period.
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Transcript
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Hi, everyone. Welcome to day 2 of the Cantor Fitzgerald Global Healthcare Conference. My name's Li Watsek, a biotech analyst here at Cantor Fitzgerald. I'm very pleased to welcome our next company, Corvus Pharmaceuticals, for a fireside chat. With me today is Jeff, our Chief Business Officer from the company. Jeff, how about we turn it over to you to walk us through the story?
Sure. Maybe we'll start with who's Corvus.
Yeah. We're a clinical stage company.
We're focused on developing novel immune modulators for the treatment of cancer and immune diseases. Our lead program, soquelitinib, is a novel oral ITK inhibitor.
It's in a registrational phase III trial for peripheral T-cell lymphoma. In addition, we're in a phase II trial called the CR-01 trial for moderate to severe atopic dermatitis. Our partner, Angel Pharmaceuticals, is also studying soquelitinib in an AD trial as well. Soquelitinib represents a pipeline and a product opportunity for us. We have a number of studies planned, including asthma and HS, that will start this year. We have strong composition of matter patents that go through November of 2037, and with pharmaceutical extensions, 2042. The ITK is a platform technology for us, so we have a number of next generations and backups in development.
Okay, great. Maybe let's start with ITK. I think this is a little bit of a novel biology for a lot investors, and you guys have shown some pretty nice data in atopic dermatitis, and we're still learning about how the drug works. I wonder if you can just tell us a little bit about the ITK inhibition and how that differentiates from the other classes that we have seen in the space, for example, like STAT6.
Sure. How are we different? I would say three things. We're an oral tablet, the mechanism of action, as you mentioned, and also the selectivity and safety of the drug. We're an oral tablet, which is important to note because obviously in atopic dermatitis, the primary therapies are injectables, so there's an unmet need for a novel and safe product. In terms of the mechanism of action, ITK stands for interleukin-2-inducible T-cell kinase. It's involved in T-cell receptor signaling and differentiation.
Essentially how we work is that we block Th2 and Th17 and those respective cytokines. Think IL-4, 5, 13, like DUPIXENT, think IL-17 like Taltz. In addition, what we've shown is that we can shift or switch Th17 cells to become Treg cells. So we feel like we are actually rebalancing the immune system, not suppressing it. In addition, in terms of differentiation, ITK has very limited tissue distribution. It's found only on T-cells and NK cells.
We are highly selective just for ITK, so we expect limited off-target effects, and we've seen that to date in our clinical data. We've had a very good safety profile.
Mm-hmm. I want to follow up on some of the biomarker data that you guys shared, which I think provided pretty interesting insights into how ITK inhibition works in autoimmune diseases.
I wonder if we can just share a little bit about the findings there, the recent data, and how do we match that with the clinical outcomes?
Sure. Well, maybe to start with the clinical outcomes because we've had very strong data to date. Our safety profile is similar to placebo in atopic dermatitis. Our efficacy profile is similar to a JAK or a biologic. It depends whether you're looking at EASI 75 or IGA 0/1.
Relating to the biomarker data, it does support the clinical profile. We showed at the SID data, we had data showing a dose response effect in reducing Th2 cells- and those respective cytokines, so we reduced IL-4, 5, 13, and TARC.
In terms of Th17, we actually showed a reduction in RORγt, which is a transcription factor for IL-17. And we showed an increase in Tregs both on therapy and off therapy, and we saw an increase as well in Bach2, which supports Treg survival. So we think now this biomarker data is supporting our clinical data.
Mm-hmm. I think, Jeff, you mentioned Treg upregulation is a pretty unique aspect of ITK inhibition because that contributes to sort of immune rebalance. Tell us about in your own study, do you see the upregulation just from absolute number perspective or percentage perspective? After you discontinue the drug, do you still see the elevated Treg- Yeah upregulation?
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