Septerna, Inc. Common Stock 12th Annual Cantor Fitzgerald Global Healthcare Conference
Review the key takeaways and the transcript of this earnings call.
Transcript
Preview the first fifteen paragraphs, organized by speaker.
Welcome, everyone. I'm Josh Schimmer from the Cantor Biotech Equity Research team, and very pleased to introduce from Septerna, we have Jeff Finer, co-founder and Chief Executive Officer, and Liz Bhatt, President and Chief Operating Officer. Welcome. Jeff, maybe set the stage for us. Give us a quick overview of where Septerna is today and where we're headed.
All right. Well, real quick, I do have a few slides to just share. Septerna's a company focused entirely on G protein-coupled receptors. We found a new way to do drug discovery for GPCRs that has allowed us to find novel binding pockets and novel compounds for traditionally difficult to drug GPCR problems, like finding small molecule agonists for peptide GPCRs or finding allosteric modulators. That has quickly evolved into this pipeline that I'm sure we're going to spend most of the time talking about today. Our lead program is called SEP-479. It's in a phase I study for hypoparathyroidism. We'll have a lot of discussion there. SEP-631 targets MRGPRX2 for mast cell-driven diseases. It's a negative allosteric modulator. That one is through phase I. We showed that we had a profile that we think is a best-in-class profile there. It's between phase I and phase II.
Behind that, we've got our thyroid-stimulating hormone receptor program. This is one that's been on our pipeline for a long time, but one where we now believe we've got line of sight to a development candidate and hope to have a lot more to say about that in the coming months. The newest addition to our pipeline is the fourth line there. We announced that we've got a very early stage, it's discovery stage as an osteoporosis program. That whole area is getting quite hot. Here, we want a short-acting PTH agonist compared to the long-acting PTH agonist for hypoparathyroidism. We've also got a really quite a substantial deal with Novo Nordisk focused on metabolic targets. There we discovered novel binding pockets for a whole variety of different incretin receptors. Got Novo excited. We're sitting in an excellent cash position. At the end of the second quarter, we had about $516 million, which gives us runway at least into 2029.
We're in heavy execution mode at this point.
All right. A lot to talk about then. Why don't we start with SEP-479? One of the most common questions I get, which is actually a really telling question, which is, by the time that SEP-479 gets to the market, will the injectable PTH replacement therapies for hypoparathyroidism be so entrenched and so sticky that there isn't necessarily a role for an oral drug? What's so interesting about that is we're already jumping to the assumption that the development is going to go very smoothly, and you'll hit all the clinical hurdles and regulatory hurdles. What gives you the confidence that this is the molecule that really can go that distance?
Yeah. First off, maybe I'll say a little bit about the molecule, and then Liz can frame how it fits within the space. We've got a molecule that from the very beginning was designed to basically phenocopy a PTH peptide. It's proven to do so in all of our assay systems. Cell-based assays, animal models, it's doing everything indistinguishable from what a peptide does. PTH receptor's been a traditionally very difficult one to hit from a small molecule standpoint, but we think we've cracked it. The effects that we've seen in animal models for all other PTH agonists have translated to healthy volunteers, and those have translated to patients. Back to your point. I think we've got a lot of confidence going from animals to now healthy volunteers.
Hopefully we'll see in the coming months that data to show that we can hopefully go the distance. In this particular program, the healthy volunteer data should be actually quite predictive of working in patients. Healthy volunteers are just a little bit different than hypoparathyroidism patients in that healthy volunteers have intact parathyroid glands. The endocrine system is so efficient that the first thing we expect to see is decreases in PTH secretion to counteract anything that would push calcium up, and then calcium consequences after that. Back to your main question. Liz, do you want to comment on?
Actually, maybe before we get there.
Sure if you can finish out the development milestones and walk us through the key steps ultimately to being in a position to file for approval.
Yeah. So maybe I'll just quickly go here, flip ahead to this slide, which is an outline of our phase I study. It's a single ascending dose, multiple ascending dose design. It's a very standard study. We are looking obviously at safety, tolerability, PK. We gave a preview of the PK. We've got a very long half-life. So the half-life is about 3-4 days, which is, we think, in an absolute sweet spot. If you look at Yorvipath, their effective half-life's about 2.5 days, and so this is quite nice. So from this phase I study, we want to see, as I mentioned, PTH going down, calcium going up. We want to be in a zone that we think would be an appropriate starting dose for a hypoparathyroidism patient.
We will try to pivot from this study as quickly as we can to a patient study. This study is being done in Australia. We are thinking currently about a global phase II study, and in order to do that, we'd go into different regions. We will need phase II ready IND to be in the U.S. That will have to include all the phase I data. We've also decided to go forward with trying to get chronic toxicology studies out of the way. The reason for that is that once we are in patients, we would like those patients to be able to continue on the drug. So we are going to be planning for an open label extension on that phase II study. The goal of the phase II study, they're fairly focused goals.
One is to show that it works in hypoparathyroidism patients, but also we want to know what the starting dose would be for a pivotal study. So we'll probably test a couple of different starting doses. Most agents have tested 2 or 3 starting doses in that first patient study. We want to know, importantly, what the titration protocol is. Fortunately, since our half-life's on about the same scale as Yorvipath, we can kind of leverage their learnings there.
Okay. Then we would go into a pivotal study.
These studies aren't that large in the grand scheme of things, on the scale of about 100 patients or so.
Okay. You don't feel like you could size up phase II to turn it into a pivotal, or?
FULL TRANSCRIPT
Continue the full translated transcript in StockNow.
Access every statement, the English original, and speaker-by-speaker history with StockNow Pro.
View the full transcript with ProCall participants
3 people spoke on this call — only 1 are shown here.
PARTICIPANT LIST
View participant details in StockNow.
Log in to see executives and analysts, their roles, and complete speaking history.
Log in to view all participantsKeep exploring
