LeonaBio, Inc. Common Stock 12th Annual Cantor Fitzgerald Global Healthcare Conference
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All right. Good morning, everyone. Welcome to our next session, and welcome back to the Cantor Healthcare Conference. My name is Eric Schmidt, and I am joined by my colleague, Dan Brodner. We are delighted to be hosting this webinar with LeonaBio. We have got from the company, Mark Litton, the company's President and CEO, as well as Dave Portman. A consultant still? I do not know how you introduce yourself.
Full-time helper. Something. Full-time key- Jack of all trades.
Jack of all trades and key managerial team member. Thanks, guys, for being here today. Mark, you're still relatively a newcomer to the public markets. Why don't you give a 2-minute overview on the state of the company for those who are a little bit less familiar?
Sure. First of all, thank you so much for the invite. It's been an amazing conference. Those of you that don't know LeonaBio, it's recently a new company. We started last year. Leona is lioness, and truly represents what we do. We're fiercely courageous, but leading through collaboration of the pride. Nothing represents that more than the drug that we brought in license with lasofoxifene. Lasofoxifene is a truly unique endocrine therapy. We really believe in the second line metastatic breast cancer space, that it can become the partner of choice. We will talk more about that. We brought in lasofoxifene from Sermonix. We have the father of lasofoxifene, David, with us. It was essentially a redo of Athira. We were led by Commodore, Perceptive, TCG Crossover, raised about $246 million.
I'd like to give credit to the Cantor banking team because they helped us for a year to come up with a late-stage asset of lasofoxifene. We're just so excited. Phase III is going well. We can talk more about that.
Great. Just a little intro.
Lasofoxifene has been around for a long time. Remind us of the history here and the twist of turns for this molecule.
Yes. My familiarity goes back almost two decades. I am dating myself. I was an advisor to Pfizer on their program, largely focused on prevention, a PI on 5 of their 11 phase II and III trials. It is a very well-characterized molecule. They deprioritized it after the Wyeth acquisition in 2009. While the drug went through full development for osteoporosis treatment, it was a very potent anti-resorptive. It actually had two phase III trials that showed that it treated urogenital atrophy and decreased new onset breast cancer. It was a remarkable drug for preventive health strategies. Unfortunately, it never really got to see the light of day. Rights were returned to Ligand, and that is when I founded Sermonix and in-licensed it and discovered very coincidentally that it was the most potent molecule against ESR1-mutated cell lines.
That is when we became from a women's health prevention company to a precision oncology company, taking it through phase II studies, showing activity in monotherapy and in combination. Then when the phase III needed to be funded and operationalized, that is when the opportunity to join forces with Mark and Leona materialized.
Okay, we are going to get into more details around the development and the ongoing phase III, but this is, of course, a SERM, and many in the audience who are on the webcast are more familiar with SERDs, so put that into context for us.
Yeah. We're thrilled to be the only pure SERM, or selective estrogen receptor modulator, in late-stage development for advanced breast cancer. It's a very crowded SERD space. The reason originally was because these mutations of the estrogen receptor become ligand independent, so logically it made sense to use a protein degrader to eliminate that receptor. What we found was that by binding with high affinity to those mutated receptors and inactivating them, putting them into an inactive conformation, we could do just the same, in fact, potentially better because of lasofoxifene's potency. It's the most potent small molecule. Even though it's not a degrader, it's more potent than all the degraders in development and approved. It also doesn't indiscriminately antagonize healthy estrogen receptors.
Coming from that women's preventive health world, I can certainly tell you that antagonizing estrogen in these women who are suffering from breast cancer can lead to very poor quality of life. So we think we have that unique advantage by not degrading or antagonizing estrogen receptors in the brain, the gut, the urogenital tract, but being a potent antagonist at the breast. It's the best of all possible worlds, and uniquely differentiated from the degraders.
And maybe Mark, one more high-level question before we get into the weeds. When you look at the story today and investors' attitudes, what do you think is most underappreciated or misunderstood?
Well, I think there's a lot of emphasis on monotherapy. What's interesting, the more we've interacted, to keep in mind, just to set the stage We're dealing with a complex heterogeneous tumor type that in the second-line setting, you have gone through AI, probably combination with CDK4/6, and there's uncertainty when you get that resistance, what do you do?
A lot of discussion has been about monotherapy and a lot of groups trying to go front line. But interestingly enough, I think what's underappreciated is combo is really what's needed. Not only do you have to block the estrogen, but you need to do targeted therapy as well. And the other underappreciated aspect is you can re-treat once you've had resistance with your ribo or palbo up front. You can treat with abema, is what we're doing, and you can change fulvestrant to lasofoxifene.
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