Episode Transcript
[00:00:03] Speaker A: Welcome to power to the Patients, a LinkedIn live and podcast series hosted by Power, where clinical research leaders across sponsors sites, CROs, and patient advocacy groups discuss patient centricity in clinical trials. We explore the bottlenecks in today's system, challenge the status quo, and talk about future opportunities for innovation. Let's dive in.
[00:00:31] Speaker B: Well, Dan, hey, thank you so much for taking the time to have this conversation. Really excited about this for the listeners. Dan is the chief medical officer over at Mindmed, doing some incredible work in psychedelic research. He also teaches at Tufts in his spare time and has founded a few companies, all at the intersection of next generation medicine and mental health and neuroscience. So I've been keen to have this conversation for quite some time. Dad, thank you for being on the show.
[00:00:56] Speaker C: Yeah, it's great to be here, and thanks for that comprehensive introduction. It's always funny to hear other people walk through some of the things you've done.
[00:01:04] Speaker B: Totally.
[00:01:05] Speaker C: Well.
[00:01:05] Speaker B: We're going to ask you to walk through some of the things you've done in just a minute. If you give us maybe a thumbnail sketch of your career and how you ended up where you are today, we'd love to kind of start there.
[00:01:14] Speaker C: Yeah. You know, my primary training is psychiatry, and I've tried to keep that as my orientation, as I've done everything else I've worked on. I take a broad view of psychiatry. I think that psychiatry has often been sort of limited in its scope to some extent, and particularly in the current era, psychiatry can be largely seen as sort of pill pushing and prescribing SRis and things like this. And so I've tried to take a broader view of the role that psychiatry can have both in the world, but also in individual patients lives, that no matter what someone is suffering from, their experience of that suffering is mediated by their experience, by their brain, by the things the psychiatry is interested in. That's always been where I've tried to be oriented. I'm also trained in addictions, so I'm an addiction doc and trained in clinical informatics, which is the use of computers in medicine. It kind of grew out of the early growth of electronic health records and I, electronic decision support tools and things like this, and is now a full medical field with departments around the country and its own board certification. So the intersection of psychiatry and technology has been an area where I've also been focused.
[00:02:32] Speaker B: Yeah, absolutely. And maybe take us on a bit of a journey through your career here. How has the kind of state of the art evolved as you see it, as far as psychiatry, addiction and treating mental health.
[00:02:44] Speaker C: Yeah, it depends how far back you want to go to answer.
[00:02:46] Speaker B: Sure.
[00:02:47] Speaker C: The question about the evolution of psychiatry. Some might say that the de evolution of psychiatry. You know, when we think about early thinkers, the early almost philosophers of psychiatry, you think back to people like Freud and Jung and other early psychoanalysts. Also think about people like Kreplin and jaspers and early phenomenological observers of. Of how people with mental illness are, how they feel, what they do, how they trend over time. Psychiatry has this incredibly rich history, and the modern version of psychiatry, even to some extent modern popular culture, tells us we're supposed to ignore that history.
Freud was wrong about almost everything, and I don't think that's true at all. I think that many of the observations from the beginning of moderating psychiatry bring a lot of value forward into understanding people. At the same time, we've seen a growth of attention to neuroscience and neuroscientific techniques, things like fMRI and EEG, which, while incredibly interesting, often don't provide us a ton of value in the clinical space. So we've got these old tools that may be really valuable being sort of denigrated and these new techniques that may someday bring us more value clinically being elevated. And a lot of that comes from this transition of psychiatrists being providers of dynamic psychotherapies to psychiatrists being sort of relegated to the prescriber role. And that's largely speaking in payer spaces. So in environments where the patient's care is being funded by a third party payer, generally you're going to not be able to access, say, a psychotherapist who is trained as a psychiatrist.
You might be able to access a psychotherapist who's trained to a master's level. And then the psychiatrist role becomes a brief med management visit, because that's how the payer dynamics work best. So the last 30 or so years of psychiatry, the Sri era, we've seen this increasing trend toward a psychiatry that seems more oriented towards symptom suppression than it does toward expansion of capacity and thinking about how one lives their best life. Something like CBT, cognitive behavioral therapy, that's been elevated as the evidence based psychotherapy. Well, it's not really about expansiveness. It's not about finding yourself, is not about knowing yourself better. It's about using thoughts to suppress feelings. And that works to some extent, but that doesn't reach the full capacity of what something like psychotherapy can do. Similarly, Sris, which I never want to focus only on the negatives of an intervention, because there are hundreds of thousands, if not millions of people have benefited, some enormously from sris. But Sris are about bad feelings being suppressed, right? They don't people to experience their best feelings. They tend not to elicit strong, like, stronger positive feelings, but they. They can, for some people, help the bad feelings be less bad. And so what we're entering now with the drug I'm working on, one of the drugs I'm working on, and drugs that others are working on are. Are drugs that maybe have more of an auto therapeutic mechanism, where the acute experience that one feels from these drugs may be more akin to what someone gets from really good psychotherapy in terms of the changes that it can help induce in a person. So I think that these drugs get the attention they get in the popular imagination and certainly in psychiatric circles, because they seem at some level to offer a return to hopefulness, a return to psychiatric intervention that helps people to feel and be better in the world, maybe to feel more like themselves.
[00:06:50] Speaker B: Even so, almost like a shift from suppression as a treatment modality to, I don't know, fundamental curative effects.
I probably don't have the right words. You have better words than I do for that.
[00:07:04] Speaker C: We talk about this all the time, that in the current era of psychiatry, the idea of cure has almost been discarded. And now language always creates difficulties, because when we have uncomfortable things in society, we try to come up with words that make them less uncomfortable. So you'll notice that just in your lifetime, the good word for something uncomfortable becomes the bad word. And then we need a new good word, and pretty soon that good word becomes the bad word. Psychiatry, we call that the euphemism treadmill. And it's actually an interesting mirror of an internal process. So I talked about Freud and psychodynamics, and we have defensive mechanisms. We employ defensive mechanisms to protect ourselves. And that's probably good, right? The world can be dangerous. Other people can be hurtful. We probably need defenses. The trouble comes when we bring defenses often, that we learn when we're very young, forward into adult life, and apply them, maybe inappropriately, or apply them in situations where they don't accomplish the protective effect that they set out to accomplish, but do something that's deleterious. And what ends up behind those defenses, the thing that is repressed or suppressed or put away in one way or another is still there. It just comes out in strange ways. Right? It emerges. The repressed always returns. Freud pointed that out to us. And so when something is repressed, it's not really gone. And so the mirror to that is when we have something in society. The other day, I was teaching residents, and I talked about the fact that we have homeless people, right? And in healthcare circles, the word for homeless people has gone through, like, three or four iterations, you know, unhoused, undomiciled.
There's always the word du jour, because we change the word to try to make the thing feel better. But the thing that feels bad is that we let people live in poverty on our streets, and calling them something different doesn't actually change that. That's. That's something we've tried to repress. And these folks still exist. They still come into ers. Changing the word for them every year or two doesn't actually make the situation any better. Right? So the word becomes bad. You can't ever have a good word for something that persists when the bad thing is still there, when the thing that makes us uncomfortable is still there.
[00:09:25] Speaker B: Well, Dan, I want to pull on a thread that you just. You left out there, which was almost looking to the future a little bit. You mentioned that one of the drugs you work with in this kind of domain of psychedelic assisted therapies, maybe tell me a little bit more about what got you so excited about this is the path.
[00:09:41] Speaker C: I'm very excited about it now. I hope that comes through.
This isn't where I was even four years ago.
If you'd asked me again four years ago if I thought I'd be manufacturing or not directly manufacturing, but in part responsible for the manufacturer of very large amounts of LSD, I would have said probably no. That does not seem likely where my career path is headed.
And I developed shortly after my training in psychiatry. I kept a faculty role at Tufts in the school of Medicine there. But I also started working at Pfizer, developing psychiatry drugs there. So I got trained in and learned the sort of processes, procedures, and the art of drug development. Pfizer subsequently left psychiatry and wasn't developing psychiatry drugs anymore.
And I stuck around and worked on something called digital medicine advisor. We built out this concept of digital medicine there.
Eventually, when I left Pfizer, I started creating companies of different sorts of types. But digital therapeutics and digital measurement companies continued to do some consulting into pharma and then encountered mindmed through a psychiatrist friend who introduced me to the CEO. It turned out someone who I'd known many years earlier in a very different context. And ultimately, mindmed acquired this company health mode that I had built, and that put me until that acquisition I had been sort of on the sidelines. I'd been looking inward curiously, watching the companies in the space do their work and very interested in the potential of these drugs and the way people were talking about the sort of academic studies that had recently started cropping up. But I was as outside of it as anybody else. I'm just sort of casually curious and interested and excited about the potential.
When I joined the company as chief medical officer, that put me in sort of fully in the pool as it were, jumped in with both feet. And since that time my enthusiasm for and hope for the class has only grown. So the inside view of these things, public company. So the inside view and the outside view are pretty similar. We have to disclose just about everything. But my set, particularly with our phase two data. My sense of the potential for these drugs and for this drug in particular for mm 120, which is lsd, has only grown.
[00:12:13] Speaker B: And was there like an aha moment once you got on the inside there? Like what was the realization or turning point for you?
[00:12:21] Speaker C: Anytime you run a blinded study and you don't know what the results are going to be until you know what the results are going to be. And when I finally got to see the analysis of our phase two data, particularly when we saw the twelve week analysis and we saw that for patients starting with what we call the Hamilton anxiety scale, their hema scores, with a mean of 30, we started with people. And that if you don't know that scale, which reasonable for most people not to know that scale 30 is well in the category of severe. So this is sickest folks with a gad.
And when I saw that twelve weeks after a single dose of mm 120 with no concurrent psychotherapy and as a monotherapy, so we took people off their background drugs, just a single dose of this drug put 48% of patients in remission. Twelve weeks later, all of my hope and belief that this would probably work played out and data like those just change your whole vantage on the thing. It's led us move forward towards phase three with real confidence in what this drug is capable of doing.
[00:13:42] Speaker B: And for the folks at home here, twelve week 48% total remission.
What do people experience today as status quo? What are we comparing this against? When you get.
[00:13:55] Speaker C: It's hard to draw comparisons between drugs when you're not testing them head to head. And we, as is standard in drug development, we're not doing drug versus drug testing, we're doing drug versus placebo. And so the drug has to stand on its own. What we can do to compare between studies so that when you haven't studied a drug in the same study, but drugs have been in other studies, you can calculate something that's called the Cohen's d, which is a standardized effect size in essence. And the Cohen's d for pooled studies of other GAD treatments is around 0.3 to 0.4. For sris it's 0.36.
In our study, our phase IIB study, we saw Cohen's d of 0.8.
So that's more than double the effect size of current standard of care.
[00:14:58] Speaker B: Incredible. Now there's, you know, a lot of ink has been spilled on psilocybin and other psychedelic or psychedelic adjacent therapies.
Why do you believe so strongly in LSD versus some of these other ones? How should we be thinking about that?
[00:15:14] Speaker C: You're exactly right. There's been a lot of attention paid to psilocybin. There's been more recent research in psilocybin. And when you see that it's reasonable to ask the question why did this early renaissance of psychedelics focus on psilocybin? And we've had the opportunity to talk to folks who were involved in pulling these molecules back out of sort of research obscurity let's say. And the answer was well it seemed like a much easier academic political request to say I'd like to work on psilocybin than I'd like to work on LSD. LSD picked up more cultural baggage in the sixties, leading to their illegalization and the creation of the DEA and all these things that led to them not being particularly accessible for research.
In part that was because the interest in psychedelics in the fifties and sixties was to a large extent spurred by the discovery of LSD in the late thirties and the discovery of its effects in the forties. So that LSD kind of became the poster child for big bad psychedelic. And all the risks and all the different.
You talk about the socio political, socio cultural impacts of all this and you can see their impacts on the left and impacts on the right. The hippies were using, CIA was using it, who knows who was giving it from where to where. These stories get pretty muddled. So it just seemed like a bigger lift to start working with LSD. The reality though is that in that early psychedelic period of interest LSD was far more studied. It was the drug that sort of offered the best promise of the class. And so for us LSD is like an obvious choice. It seemed like iT's a place where other folks weren't going. It is a very potent molecule it has some difficulties with manufacturing and stability and things like this that we've been able to solve for, but it's a drug that I think offers promise that maybe even exceeds what the class. Though drugs in the class have similarities in their acute effects, they certainly also have differences in their acute effects. And there's every reason to think that there may be differences in their long term effects. Some research has shown that LSD has. We talk about neuroplasticity as one of the effects of these drugs, and the period of neuroplasticity from LSD seems to be longer than with other drugs in the class. So there are some specific promises that LSD offers, and what we're trying to do is research that can reveal those.
[00:17:52] Speaker B: Fascinating. Now, as I dig deeper into the landscape here, I'm seeing MDMA for PTSD, psilocybin, ketamine for depression, LSD for GAd. How should I be thinking about these different kind of intervention types and why they're mapping to specific indications? What's the logic there?
[00:18:12] Speaker C: Yeah, you're getting into a really interesting question in this space.
First, let's step back and say, well, why would we list MDMA, psilocybin, LSD, and ketamine, s ketamine in even the same list? Right? MDMA is in pathogen or intactogen ketamine and s ketamine or dissociative anesthetics. Now, I mean, I guess we can safely say S ketamine is also an antidepressant.
And then psilocybin and LSD or classic psychedelics. There are other drugs in the class of classical psychedelics, like DMT, five Meo, DMT, mescaline, ayahuasca, classical psychedelic. So even that class sort of clumping that's happening, sort of obfuscates the differences. Right. And I said before, even amongst the classic psychedelics, the differences between them, MDMA, specifically, the way it's being used in lycosis development, it's a psychotherapy adjunct. So you take the drug as a way of enhancing the efficacy of psychotherapy. It's a challenge because now you're studying a combined intervention. The intervention depends on two parts, and those parts connect to one another. Ketamine and s ketamine do not seem to have their antidepressant effect mediated by the experience. It seems like that's probably more just whatever the receptor based effect is, it has an antidepressant effect like an srideh. The experience of taking the SRI doesn't mediate its long term effect. The classic psychedelics seem to have a two part mechanism. One is mediated by that acute experience. And then there's this downstream neurobiological change that maybe allows for a differential encoding of what happens during the acute experience. Others with classic psychedelics have attempted to accentuate that effect through a program of psychotherapy that involves psychotherapy before the dose, maybe psychotherapy during the dose, psychotherapy after the dose.
We didn't do that. We ran much more conventional trials where we just let the drug effect stand on its own and used the folks in the room as safety monitors.
[00:20:19] Speaker B: Now, there's a few additional threads I want to pull on here. You mentioned neuroplasticity earlier, and I think you're starting to hit on potentially there being an effect range or time period in which LSD may be more potent. Here I've seen you kind of write about a talk about this idea of neuroplasticity being split into positive plasticity or negative plasticity. How do you even encourage one form or the other? How does that even work?
[00:20:47] Speaker C: I don't think that neuroplasticity on its own has a curative effect. We've known about many psychoactive drugs, or neuroplastic lithium, for example, promotes neuroplasticity. Us talking depends on neuroplasticity for you to remember anything we talked about. So just the big word neuroplasticity, that gets thrown around a little bit loosely, I think, isn't enough to explain kind of anything that's happening here.
What seems to be this is. And again, we've been using SRI for 30 plus years clinically, and ten more years than that in clinical trials, and we don't know how they work. So when anyone claims to have a thorough understanding at a molecular level of how psychiatry drugs create change, there are a few that we get better than others. So like gabaergic drugs, like benzodiazepines, we have pretty good acute understanding of what they do. But when it comes to depression and anxiety, we don't know the mechanism of the diseases. There are clearly multiple diseases. They don't have a single underlying cause. So if we hear someone say, well, the serotonin hypothesis of MDD is wrong, let's kind of silly, because if MDD is not one thing, how could there be one molecular hypothesis for what causes it?
Yeah, that we're going to ever discover a thing, that molecular thing, a neurobiological thing that is the cause of all depression is just a silly idea.
So take what I say about mechanisms somewhat as hypothesis, right, and somewhat as my best.
My best model to describe what I think is happening.
[00:22:31] Speaker B: But better you than me to hypothesize. So let's go there.
[00:22:34] Speaker C: Yeah. And it's all models, right? Our way of conceiving of the world is model based. We use language to form models of the world so that we can interact with it in a meaningful way. It's okay that models aren't completely true. They never conveniently, we don't have access to that reality.
When we go through development, when we form the defense mechanisms that end up causing us distress in adult life, when elements of our character get encoded in ways that are distressing to us, a lot of that must be encoded in the filters that allow us to translate the world into something understandable to us, right?
We exist as a story we tell about ourselves. That story can have distressing elements. Our relationship to the past and the future is based on a linguistic story we tell ourselves. We worry in this way about the future.
We look back on the past with regret and call those anxiety and depression. Maybe if we think of our distress also being encoded in the filters that allow us to experience the world in a meaningful way. Those filters are what LSD turns off, right? So you can call it the default mode network if you want, because we sort of know from neuroimaging studies that this is the part of the brain that's firing when we're not doing anything, whatever that means. But if you look at enough people trying to not do anything over enough time, eventually you can kind of coalesce onto circuits that seem to be those.
I would argue that when we're not doing anything, what we're doing is filtering. We're turning the world into sense that has to happen all the time. And that's the part of the brain that we know from neuroimaging and that we know from experience that gets turned down, right? So that people under the influence of mm 120 or another psychedelic experience, a disintegration of the usual models that allow them to organize the world. Things look different, they sound different, senses might get crossed up, but the. And the story starts to not be told in the same way. The story about the world around you, the story about your internal world as well, is told differently. It's told without the usual filtering mechanisms. That experience could be described as quite akin to what happens in long term psychotherapy. You learn to understand your relationship to yourself and the world around you differently by breaking through those encoded defense mechanisms, the encoded ways you see the world and seeing the world without them. My sense is that people who have that experience on MM 120 or another psychedelic then leave, having experienced the world differently. Now, we saw in our study that as soon as the next day, people are statistically and clinically better. So something about that mediates that, and then they stay better in many cases. Right? 48% remission, twelve weeks later. And I think that's because now we get to this neuroplasticity thing. The parts of the brain where we encode this filtering and the self story and character, all of the adaptive and maladaptive parts of who we are, then is more prone to being modulated. And the modulation ultimately can be the storage of this changed experience, this experience of change that someone had during the session. So that is the most common description of a relatively high dose psychedelic experience, is ineffable, unable to be put into words. It exists outside of this filtering mechanism that is our linguistic translation into words. And people remember the experience. They encode it in the usual places where we encode episodic memory. But my argument would be that the neuroplasticity allows it to be encoded in parts of the brain, usually much less prone to change, and that that accounts a lasting change from the session.
[00:26:30] Speaker B: And, you know, you also mentioned that you made an intentional decision not to do a drug assisted therapy version of this, this kind of treatment. Maybe talk to me a little bit about why this works without any additional kind of prompting or stimulation.
How did you land on that?
[00:26:50] Speaker C: I think that we need to conceive of that as almost a three part choice. One, we're a biotech company. We develop choices. We don't develop therapies. We don't regulate therapies. The FDA doesn't regulate therapies. Psychotherapy is notoriously, really hard to study. It's one of the reasons that CBT thing I said earlier, like CBT, is the evidence based psychotherapy. Well, it's just an easier psychotherapy to study manualized, so you can standardize it and deliver it in a repeatable way. So introducing psychotherapy into a drug study makes the drug study harder to execute with high fidelity.
We wanted to demonstrate that this drug has a drug effect independent of some secondary intervention. That's for regulatory reasons. It's much more facile to bring a drug forward that you've introduced as a monotherapy, and then ultimately it's for commercial reasons. Right? And I say commercial, but of course, it's not about, necessarily, drug sales so much as it is making sure that everyone who could benefit from the drug is able to access it. And the higher the requirement for trained psychotherapy in the environment where the drug is being given, the fewer people will have access to the drug. So that if we can show, and again, I hope it comes through in this conversation. I'm pro psychotherapy. I, in my clinical practice, I practice almost exclusively, in fact, right now, exclusively psychotherapy. I try to avoid prescribing the current, currently available drugs to people who don't really, really need them, because I think that psychotherapy is the best tool we have. It's such a good tool that we kept it out of our clinical trials, and we know that in the real world, if we've developed the drug in such a way that it can be given without psychotherapy, then it can also be given with psychotherapy. Sri is better when people are also getting psychotherapy right, and so slow will our drug. But we wanted to be sure that we gave providers the option to do the drug in the way that fits with their practice and that patients could access both, access the treatment at all, but also access the treatment in such a way that it suits what they want for themselves and that they can find a good match with a provider who wants to do what wants to do with the patient wants, provider wants to do what the provider wants, and that's a good match. So we tried to open up the broadest landscape that the drug could be given in by showing that as a standalone intervention, it's safe and efficacious, a.
[00:29:20] Speaker B: Kind of combination of the practical realities of, I guess, kind of logistical constraints are trying to do research like this, but then kind of married with, again, commercial maybe being a loaded way to say it, but like the, that market access kind of constraints that might be applied by doing research that's combined like this.
[00:29:38] Speaker C: We were trying to be the best scientist we could be and make sure the drug had the chance to show what it was capable of. And when we think about, you said market access, I think it's critical to point out that we know that people do LSD. We know that this is a thing that happens in the world.
This is not just for them, or it's not even necessarily for folks who can get LSD today. This is probably people would ask us, you know, are you worried that you're just gonna have people enrolling in your trials to get acid? Like, no, I think if you know how to buy LSD today, our clinical trial is the least efficient way to get access to drug. We have people enrolling in our trial because they are profoundly anxious and they want to experience relief and the same is true for when we think about real world clinical use. The goal here is to make this incredible drug that has gone through all the regulatory hoops and hurdles and is then something that is acceptable to people who would never in a million years consider accessing street trucks or buying, you know, buying and taking LSD on their own. The point of this is to make this accessible both from a sort of sense of safety and sense of efficacy standpoint, but also from a payer coverage standpoint point. If we don't get broad payer coverage for this, we haven't done our jobs very well. So it's on us to be sure that we're demonstrating the value of the drug to society, to individuals, and to payers.
[00:31:06] Speaker B: And that kind of maybe is a nice intro into MM 120. And I can't believe we're almost at the end of our show here. And I'm just starting to ask you about MM 120. But, like, how is this specific version of LSD different from what you might be getting on the street or elsewhere?
[00:31:25] Speaker C: It's manufactured to pharmaceutical standards, which is a starting point, which, you know, this is probably the highest quality LSD that's ever been manufactured because it's made to the same standards as any other pharmaceutical agent. We also have a proprietary oral dissolving tablet formulation. LSD, on its own, is notoriously unstable, so it breaks down in the presence of light and moisture. And so by creating this oral dissolving tablet formulation, we make a shelf stable, highly shelf stable version of MM 120 that's quickly absorbed and as a reliable and knowable. What's called PK curve. Right. Pharmacokinetic curve. So we're able to describe the way that the drug enters the body through absorption and the way it's broken down by metabolism and how long it sticks around in the. In the interim, really tightly.
[00:32:19] Speaker B: Are there any things that you had to maybe strip out or specifically change as you thought about producing a pharmaceutically optimized version of LSD?
[00:32:28] Speaker C: The chemical itself stays the same. But all of this formulation work we did to get to the ODT. This was challenging, and we have a very talented manufacturing group who worked on this process. We have a good partner in Catalint who is the. The manufacturer of the zytis formulation. But getting to this formulation, even to bring the formulation into phase three, we had to test it against the formulation we used in phase two. That was capsules. So we've done additional studies to characterize the PK of the drug in the different formulations. So there's a lot of background work that goes on, including clinical pharma studies, clinical pharmacology studies, that inform our ability to get to a regulatory outcome that we want.
[00:33:14] Speaker B: This is a nice place for us to start to converge here at the end. How do you think about threading the regulatory needle for something like this that's, frankly never been done before. How do you think about that?
[00:33:26] Speaker C: Well, we certainly organized the phase three programs and our phase two program around regulatory approval, around making this seem as approvable as possible. And to do that, we ran studies that, aside from the intervention being an unusual one, the rest of the study should be really familiar to regulators. We've just had an end of phase two meeting with FDA and have come to agreement on a phase three program that we think will be able to bring us to a regulatory approval. And so everything we do in these clinical studies is meant to be familiar, recognizable, and generate robust evidence for safety and efficacy. We talk a lot about psychedelic exceptionalism and that there seem to be people in this space who think psychedelics are categorically different from any other psychiatry drug that's existed. They certainly have some differences, and as we've shown, they have some real differences when it comes to efficacy. But that, that doesn't mean that the development process should look different. The process of developing these drugs ought to look like the process of developing any other psychiatry drug, and the evidence base really ought to be the same.
[00:34:36] Speaker B: Is there. Is there, like, a certain amount of, I guess, expert bias that you need to overcome here, public bias being one thing, but you're probably also playing to win the hearts and minds of practitioners and the kind of advisory committee as well, right? How do you think about that?
[00:34:54] Speaker C: Well, I'll say among psychiatrists, there's just a ton of enthusiasm for drugs in this class, and we've heard increasing enthusiasm for MM 120 specifically. So when I teach residents and ask people what they're excited about psychiatry, this is. This is it, right? This is why people there, I've now met a number of residents who pick psychiatry as a specialty because psychedelics are coming down the tracks. We watched the last Adcom, again, not for psychedelic and for a drug with assisted therapy with a lot of interest, and feel really confident that the issues that were encountered at the ADCOM are issues that we've been planning to encounter and working to ameliorate, to mitigate since the beginning of our development program. So we're really confident that what we are putting together from phase two through to phase three is a package that will be satisfactory and address each of the concerns that's been raised in the prior ADcom. And we were able to front run a lot of this because these issues were predictable.
[00:35:59] Speaker B: Sure. And let's imagine this phase three goes according to plan. We're post approval now and maybe we're a few years post approval. I'm curious now about competitive landscape. How do you think about that evolving post approval? Assuming you and a lot of the kind of other smart people operating the space kind of figure that out, how do you think about competing post marketing in a world where all these things are now available against all these locations?
[00:36:25] Speaker C: Yeah, I mean, it's not going to be all that many things. There are a few programs working during development, many of them with the same psilocybin drug or similar psilocybin drugs. There are enough people in distress.
We tend to think in terms of demonstrating the best data we can for our drug, showing how efficacious it can be, showing good durability of effect, doing the legwork to make sure we have payer relationships as quickly as possible. What we want to do is make our drug the obvious choice when someone walks into a psychiatrist's office or a clinic in distress. So for us, it's not so much about competition as it is about building just the absolute best evidence for the use of our drug that we can, and providing tools and guidance to providers so that they feel comfortable with using the drug, they feel comfortable prescribing it, they feel comfortable monitoring sessions if that's the role they take on, that, they're confident they'll be reimbursed for the time they spend doing those things. For us, it's all about making as low friction a path to uptake as possible, and having generated a data set that shows providers and ultimately patients that this is something that could be helpful with their distress.
[00:37:46] Speaker B: Well, Dan, I feel like I could sit here and learn from you all day.
My closing question for you here is, is there anything I didn't ask about that I should have?
[00:37:57] Speaker C: Well, I think there's always more. We can always say more about these drugs, but no, I think for where we're at now and for our first conversation we covered the important stuff.
[00:38:08] Speaker B: Yeah. Well, dad, hey, again, thank you for spending the time with me here today. I learned a lot and I'm sure folks who are listening along are appreciating it as well.
[00:38:16] Speaker C: It's a total pleasure to be here and I suspect we'll have more to talk about in the future. So happy to come back.
[00:38:22] Speaker B: Absolutely. We should plan on a on a revisit once things are thoroughly in the works.
[00:38:27] Speaker C: Awesome.
[00:38:28] Speaker B: Perfect.
[00:38:29] Speaker A: Thank you for tuning in. If you haven't already, please follow power on LinkedIn. Sign up for our live events and engage with us in the conversation. We hope to have you join us next time on power to the patients. Take care of.
