Latest / The BioHub - by Avetix / Episode 202 - Ben Swanson - CEO of Skeletalis

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Episode 202 - Ben Swanson - CEO of Skeletalis · The BioHub - by Avetix

0:06
So welcome back to another episode of the Biohub Diabetics
0:09
podcast. Today we're delighted to welcome
0:11
on Ben Swanson, who's the Co founder and CEO of Skeletalis, A
0:16
biotech company working to develop new therapies for
0:19
osteoporosis and other bone diseases.
0:22
Skeletalis is built around the idea that advances in skeletal
0:25
health could have a profound impact on quality of life for an
0:29
ageing population. So look Ben, it's an absolute
0:32
pleasure to have you on. How are you?
0:34
I'm doing great, Tom. It's exciting, exciting to get
0:37
to spend some time with you. And I think we're going to have
0:39
a great discussion this morning. Yeah, look, it's an absolute
0:43
pleasure to have you on as well. I was super excited about this.
0:45
So let's just start off with a little bit about your journey
0:49
through the field and how you ultimately got to where you are
0:51
today. So you've got quite a unique
0:52
path. You pursued both DDS and APHD,
0:56
which is a unique combination of clinical and research training.
1:00
Just talk us through like, why did you decide to follow this
1:03
dual path and how have your experiences treating patients
1:06
shaped your scientific questions and how your research influenced
1:11
the way you approach clinical care as well?
1:14
Yeah, You know, it's a, it's certainly a unique path.
1:16
I think I get that a lot of of, oh, you're, you're also a
1:19
dentist. But I, you know, for me, I
1:22
didn't know the world of science when I was a kid.
1:24
I had no idea where drugs were made, how it was made.
1:26
I, I thought very simply that this happened somewhere else and
1:29
it ended up on a pharmacy shelf and, and growing up in a small
1:32
town, you know, really healthcare interacting with
1:36
healthcare to me was to become a dentist or a doctor.
1:39
And so I decided to become a dentist.
1:41
And, and what was really apparent to me early as a
1:45
creative, hungry, scientifically motivated person was, well, how,
1:51
how can I be at the forefront of medicine or, or be a part of
1:56
what's coming next? And that really led me to, to
1:59
pursue my PhD, fall in love with research.
2:02
And I, I think it created such a unique combination of skills and
2:06
expertise, but also perspective on how to treat disease.
2:10
And, and you know, as a dentist, one of the things that I love
2:12
the most about being a dentist is being able to form these long
2:16
term relationships with patients and, and see what is it actually
2:19
like to live with chronic disease.
2:22
I mean that that was something became very apparent to me in my
2:24
clinical practice pretty early. One patient who I, I remember
2:28
incredibly vividly through the time she was a patient I treated
2:32
in dental school, was diagnosed with Parkinson's disease and
2:35
began in a clinical trial and, and saw her kind of decline, but
2:39
also this, this amazing result and stabilization on, on
2:44
treatment. You know, it's a privilege when
2:46
you can gain the trust of another person to actually treat
2:50
them and help them. And so I, I think for me
2:52
scientifically, then of course, my clinical practice is focused
2:56
on bone in the oral cavity and the tissues that support teeth,
3:02
particularly in periodontal disease.
3:05
And gave me a first hand glimpse of, you know, what does bone
3:06
look like in, in the practical setting of, of degeneration and
3:11
disease? How does it remodel in real time
3:14
and change and, and become affected?
3:16
And what does that do for a patient?
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So I, I think the clinic really helped me think about what is
3:23
not just an interesting scientific hypothesis, but what
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is it, what is a patient need? What can they tolerate?
3:30
What, what do they want? And it's not always a new MOA.
3:34
It's safety, it's durability, It's something that looks and
3:38
feels that it, it works, it fits into their lifestyle.
3:43
And so I think, I think it's given me a, a really keen and
3:46
different perspective on the end user who benefits, benefits from
3:52
the medicines that we get to make.
3:53
And I, I think on the flip side is a founder having that
3:59
connection to the clinic and understanding not just, hey,
4:01
we're, we're building this as a team.
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We're all super bright and hungry and creative, but we're
4:05
doing this in service of a patient who deserves better and
4:10
a patient who's waiting for a better therapy is incredibly
4:16
exciting. And I, I think specific to
4:17
osteoporosis, I saw in my clinical practice first hand the
4:23
patients who were on the existing therapies and, and had
4:26
concerns about some of the safety effects.
4:29
They didn't know exactly, you know, what they were taking or,
4:32
or whether or not it was working for them.
4:34
Of course, one of those safety concerns is a disease called
4:37
osteonecrosis of the jaw, which I I've seen and treated.
4:42
But there was another group of patients that that knew they
4:46
were at risk of fragility and frailty and they had other
4:51
chronic comorbid diseases. And I think that perspective of
4:53
what's that like to live with and experience that really has
4:57
informed the way that did I think about it and and lead my
5:00
team to think about what's the next generation of care.
5:06
Yeah, amazing. Just talk us through.
5:09
So at what point did you realize that the discoveries and
5:11
insights that you had generated in the lab could have a, you
5:15
know, a real world impact as therapies?
5:18
Was there a specific moment or patient story or scientific
5:22
breakthrough that sort of cemented the idea that you
5:25
needed to build or needed to move from research into building
5:29
a company to translate that into treatments?
5:31
Just talk us through like that moment when you thought, yeah,
5:33
I'm going to go and set up a company here instead of instead
5:36
of in the lab. Yeah, I mean, I, I think there
5:39
was for me multiple iterations of that, that I, I could see
5:43
that opportunity. And yet you're, you're trained
5:46
that the path to success is to become a professor, which, which
5:49
to me was intellectually curious.
5:50
It was exciting. I, I think two experiences that,
5:55
that stand out. The first was the first patient
5:57
that I saw and treated with osteonecrosis at the jaw was a,
6:02
which is a serious and rare, but, but you know, very serious
6:06
safety concern associated with some of the first generation
6:08
osteoporosis therapies. And I, I remember vividly asking
6:15
this patient, have you ever been on these therapies before as a
6:17
routine health history question? And the response was, yes, but
6:24
in such a timid and afraid tone. And it just made me think, you
6:28
know, here's a huge opportunity. If, if we prevented fractures
6:32
and, and never dealt with this disability in the population,
6:35
you know, using that as our North Star, that'd be
6:38
incredible. And yet patients are scared of
6:40
the tools that we have to do that.
6:41
And, and they have some real safety considerations.
6:44
And so that, that patient was the first for me.
6:48
I, I saw three patients with osteonecrosis of the jaw in my
6:50
first year of clinical practice was something that really made
6:53
me start thinking about this is a really tractable opportunity
6:58
that, that we could do a lot of good.
7:00
And at the time, my research focus was much more in
7:03
regenerative medicine, stem cell technologies, drug delivery, but
7:07
in the context of, of how do we build bone and fill holes and,
7:10
and things like that. And I started thinking about
7:13
more simply, you know, what's, what's the opportunity to
7:16
actually make a difference in the world.
7:17
If, if I got into this whole career to, to make medicine
7:20
better and, and shepherd in the next generation of therapies,
7:23
that seemed like a really compelling opportunity to focus
7:26
on systemic and degenerative bone diseases where there was a
7:31
clear unmet need. And I, I think the second piece
7:35
where I really had this in internal conviction that I had
7:39
the opportunity to do this was in going to some of the academic
7:42
bone meetings that you know, it in the academic research world,
7:48
the bone community is incredibly strong and, and incredibly
7:51
bright, doing amazing work. And I would go to these meetings
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and you and you had these animal models that had all these
8:00
different trans genes and fluorophores.
8:02
We can do lineage tracing and we, we understood so well the
8:05
mouse skeleton, yet none of this, you know, 810 years ago,
8:10
none of this was being used to make new therapies.
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And I thought, man, there's, there's such an opportunity
8:15
here. If we think about the skeleton
8:17
as as a tool, it's a scaffold that exists in the body.
8:21
And for me, again, coming from a tissue engineering background,
8:23
that was a very easy concept to, to grasp and started with the
8:28
belief of what could we, could we get drugs there?
8:30
Could we get them there and keep them there on the skeleton in a
8:34
way that allows us to modulate disease in the exact context
8:40
that it happens? And that that's really where I
8:44
became incredibly curious could see a real path forward for some
8:49
of the the work that we were working on, particularly in
8:51
targeted small molecules and therapies that treat
8:54
degenerative bone diseases. And and over the course of, you
8:58
know, a 5 to 6 year Sprint through my time at the
9:01
University of Michigan really was able to realize this from a
9:05
concept through patented technologies that that we've now
9:08
licensed into the company and are continuing to develop.
9:12
Yeah. How, how did you find that going
9:14
from being in the the lab to them being a, you know, an
9:17
entrepreneur running a company? Was it quite a, an, an easy
9:20
natural transition for you? You've obviously probably got
9:22
other components of running a company that maybe you might not
9:25
have had much experience in before, you know, fundraising,
9:29
partnership, licensing, that sort of stuff.
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Was it quite a natural transition for you or is it
9:35
something that maybe took you a little bit longer to pick up?
9:38
You know, I think the thing that that is consistent across my
9:43
entire academic and entrepreneurial journey is the
9:48
patient in need, being the North Star that every, everything I
9:52
was doing in the lab was in service of, you know, this, this
9:55
many millions of people are affected.
9:56
Here's a huge problem as every good grant starts that way.
9:59
But in, in the context of, of skeletalism and
10:02
entrepreneurship, it's that's the real result is the ability
10:05
to impact those people in a very direct way.
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And I think that was what was incredibly exciting to me was to
10:14
not just not just be able to say like, Hey, we're solving a
10:17
disease that's really hard and big, but we're doing this and
10:20
we're, we're doing it like we're actually pushing this forward
10:24
to, to those patients. And so I think it, it was really
10:30
almost freeing experience for me to to have the privilege of we
10:35
can push this fast and hard and thoughtful and assemble a team
10:39
of, you know, people who I consider some of the brightest,
10:42
most creative, sharpest scientists who I've ever worked
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with and work together on this, this shared goal.
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So certainly a lot of learning over over the last years.
10:53
We've launched the company almost a year ago, but, you
10:58
know, just an incredible privilege to be able to do that.
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And so to me, you know, this is, this is a dream job for sure,
11:06
you know, and to, to be able to both do good science, do right
11:09
by patients, but also be able to make a, a compelling impact.
11:12
And I, I think what's been the most exciting or one of the most
11:15
exciting pieces for me is just the community surrounding this
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industry and the, the support that that exists for scientific
11:22
founders And first time CE OS the, you know, belief that
11:27
amazing, rigorous creative science can change the way that
11:32
we treat patients. And I, I think that's, you know,
11:35
the reason to wake up and do this every day.
11:39
Yeah, for sure. Just to delve into the company's
11:42
platform, so the the Oasis platform, can you just explain
11:47
in detail how it actually works and how it targets areas of
11:51
active bone loss and how it, I guess how it also differentiates
11:54
from traditional systemic osteoporosis therapies?
11:58
Yeah. Just just talk us through that.
12:00
Yeah. So the, you know, as I
12:02
mentioned, the idea that we started with was quite simple of
12:07
how do you get drugs to the time and place that disease is
12:11
happening. And, and what that means is
12:13
getting drugs on the surface of the, one of the challenges, you
12:17
know, as we surveyed, where have we gone with osteoporosis
12:21
treatments over the last 30 years, is you have these
12:23
systemic drugs that, that are functioning largely in
12:27
circulation, yet the disease is happening on the bone.
12:30
And, and so there's a, a little bit of a disconnect there.
12:33
And, and yet this is a disease that literally happens on the
12:36
surface of bone as, as bone is constantly turning over and
12:40
renewing itself, even in the healthy skeleton, our bones
12:43
replace themselves about every 10 years.
12:45
So we started with this idea of how do we anchor drugs to the
12:48
surface of bone quickly getting them out of systemic
12:51
circulation. We don't need that systemic
12:52
exposure, but rather concentrating exposure to the
12:56
bone. And and what that naturally led
12:58
to then is, is what we call the Oasis platform is our core
13:02
technology, but is a tool to localize therapeutics and and
13:07
therapeutic effect to the bone microenvironment through a small
13:10
molecule delivery vector. And so this is a a small
13:15
molecule that rapidly circulates in the body, anchors to the bone
13:19
and it's either on the bone or excreted with a very short half
13:22
life, high clearance. And so traditionally you would
13:25
want a small molecule therapy that has long half life.
13:28
Of course, long half life can get you to the bone at low
13:31
exposures, but it also gets you everywhere else.
13:34
The the second piece that, and I think where we really begin to
13:37
differentiate is that our therapies are pro drugs in
13:41
circulation, meaning that they're inactive, but they're
13:44
activated at sites of bone turnover where this this process
13:48
is catalyzed by cells called osteoclasts that chew up the
13:52
bone. Again, this is a normal healthy
13:54
part of bone turnover, but it happens in an aberrant
13:56
dysregulated way in osteoporosis and as a result of estrogen
14:00
deficiency as as we get older. And so the opportunity here, we,
14:05
we really think about this as site specific pharmacology, how
14:09
do we just treat the disease where it's happening and and
14:11
limit these peripheral liabilities.
14:13
And I I think with that unlocks of course is a, a significantly
14:16
improved safety margin and therapeutic index.
14:19
But more excitingly, it's an opportunity to access new
14:22
targets and, and biology that happens in a very confined and
14:25
discreet compartment of the body.
14:28
And and so in that way, as we think about in our, our lead
14:32
program, which is a disease modifying drug for treating
14:36
osteoporosis in postmenopausal women, this is a, a real
14:40
opportunity to specifically intervene in that disease
14:45
process. And I, I think, you know, as we
14:47
survey again the landscape, this is really an opportunity for
14:50
precision medicine in bone. And, and so, you know, if we
14:54
look historically at cancer diseases, the early generations
14:58
of chemotherapy killed everything.
15:00
Now we have these very elegant precision drugs that are
15:03
specific to the tumor, specific to subtypes of, of cancer
15:07
patients in populations. Same thing is happening in
15:10
autoimmune diseases. We started with blanket immune
15:12
suppression. Now we have these targeted
15:14
approaches and and for us bone is, is on trajectory for a
15:18
similar story here that that we believe Skeletals can enable
15:22
through rather than just shutting down bone
15:25
indiscriminately and and losing that normal remodeling process,
15:28
we're compensating for the disease.
15:30
We can actually intervene very specifically.
15:32
And what that enables is the maintenance of all of the
15:36
normal, healthy, good processes that our bones require to stay
15:40
strong throughout the rest of our lives.
15:43
Yeah, for sure. How, how would you describe the
15:47
current state of the therapeutic landscape Muscos muscoskeletal
15:50
field especially for let me just start that question again.
15:55
Yeah, so the muscle muscoskeletal field so obviously
15:59
encompasses different areas of osteoporosis, fractures,
16:02
sarcopenia and and obviously more to that as well.
16:06
How would you describe the current state of this
16:08
therapeutic landscape, especially for osteoporosis, and
16:12
where do you think the biggest gaps or medical needs are in the
16:15
area as well? You know, it's, I think it's a
16:20
really exciting time to be in this field because we are at a
16:25
unique intersection between Women's Health, menopause care
16:31
that's really taken off in the last couple of years and
16:36
longevity, aging. How do we live this longer
16:38
health span and active life? I, I think what patients are
16:43
demanding is the ability to live longer, happier, more active
16:47
lifestyles. And so to really, I think about
16:49
muscle cell broadly as a mobility category.
16:53
And, and so to your point, this encompasses bone, cartilage,
16:58
muscle, even fat. And if I think if we're able to
17:01
start solving pieces of this, we want to solve the whole puzzle
17:05
on how do we, how do we stay active and not worry about
17:10
falling on a hike with your grandkids and breaking a bone
17:13
that's going to end you in the hospital for the rest of your
17:15
life? Or, you know, how do we go on
17:19
these extravagant, fun, adventurous trips and, and do
17:23
the things that we want and deserve to do?
17:25
And I, I think there's a real opportunity to seek freedom
17:28
specifically from fractures now the, the landscape today.
17:32
I, I think osteoporosis is not a new indication. 20 and 30 years
17:37
ago we had tremendous innovation in this area, the first
17:42
generation of therapies that came to the market and, and for
17:46
a long period of time osteoporosis represented 25 to
17:50
30% of major pharma's annual revenue.
17:53
So that's huge, huge, huge opportunity.
17:55
Yet there was about 10 years ago a few late stage failures and
18:00
huge trials that that really caused the field to take a step
18:05
back and, and re evaluate from the pharma perspective.
18:09
Is this really where we're working and, and many major
18:12
pharma companies stepped away from the field and, and you
18:17
know, we'll talk a little bit more about the recent changes
18:19
that have enabled this second awakening of osteoporosis.
18:23
But I, I think we are at a point because of recent regulatory
18:28
changes through the Sabre initiative, which has qualified
18:31
a new registrational endpoint and dramatically changed the
18:34
design of our registrational trials that, that we now will
18:39
see this next generation of not just blunt instruments for
18:43
treating the disease indiscriminately, but actually
18:45
what is a precision medicine for bone.
18:47
And so I, I think we are really excited about that opportunity.
18:51
And, and what that means for patients is this idea that that
18:56
we can have a more accessible, safer, more effective, more
19:00
durable therapy that it, that truly enables this freedom from
19:03
fractures is when we think about a chronic disease that is not a
19:06
one to two year problem, but it's, it's something that older
19:12
patients and you know, period and post menopausal women folks
19:15
beyond that both men and women will deal with for the rest of
19:18
their life. And so they they deserve and
19:20
need a drug that will enable them to access that freedom and
19:24
activity indefinitely. And as as you look ahead, so
19:31
like the next 12 to 24 months, what are the next sort of
19:34
critical scientific or clinical milestones for the company?
19:39
Just talk us through like what are the next inflection points,
19:42
the next milestones that you guys are particularly excited
19:45
about? Yeah.
19:47
So I mean our, our focus inside of the company is really
19:50
anchored on how do we, how do we officially get a drug to the
19:53
clinic and and you know stand behind what we're saying about
19:56
this differentiated target product profile and opportunity
19:59
to really be a disease modifying, remodeling, sparing
20:03
or or maintain the normal healthy bone processes type of
20:07
drug. And so our focus in the near
20:09
term is on development candidate nomination.
20:11
We've really been heads down on refining and lately optimization
20:14
the properties of our. Candidate, this is a really
20:19
exciting time inside of the company because it's, it's equal
20:22
parts development, commercial development, clinical
20:26
development and still this fundamental R&D process and
20:30
inability to creatively ask questions and hypotheses.
20:33
And I, I think as we reached that development candidate
20:36
nomination in the near term, that really sets us on a, a well
20:40
mapped trajectory to Ind enabling studies, Ind and, and
20:44
1st in human proof of concept for, for safety and tolerability
20:48
and efficacy. And I, I think one of the things
20:50
that's exciting is that very early in clinical development,
20:53
there's signs across osteoporosis, clear biomarker,
20:58
signs of target engagement and, and efficacy, which of course
21:01
we're very excited, you know, as we accomplish these near term
21:04
milestones to, to open that up. But I think, you know, the
21:07
second piece here is that there's a platform tailwind.
21:09
I, I mentioned that there's a shared chemical scaffolder
21:13
architecture across our assets. And as, as we develop this first
21:18
program, we have already gained tremendous learnings about our,
21:22
our platform, what it can do, what's the boundaries of it and
21:26
how far we can push it. And so, you know, I, I think
21:31
there's an opportunity, huge opportunity here for a pipeline
21:33
and we're very excited as this first asset enters the bind
21:38
enabling studies and, and into the clinic.
21:40
Now there's this opportunity to really open a pipeline approach
21:43
where we continue to take, you know, novel biology risk with
21:49
that and, and think about what else can we solve if, if we can
21:53
make a compelling case in, in osteoporosis, what else can we
21:56
do? And there's, you know, really no
21:58
shortage of opportunity and disease that did affect the
22:03
skeleton did did our critical part of how we continue to to
22:08
use our bodies, you know, as we get older, I mean, and so I
22:12
think every asset continues to be proof of the platform and
22:16
really yields benefit to the subsequent 1.
22:20
So our our focus is heads down right now on, on DC nomination,
22:23
but I think the the future of this field and of scale tasks is
22:26
is really excited on this shared architecture and design.
22:32
Yeah, amazing. Sounds exciting.
22:35
Yeah. So osteoporosis and other bone
22:38
diseases are, I think you mentioned before the chronic and
22:41
progressive conditions. From from a mechanistic
22:44
standpoint, what are some of the key challenges in achieving
22:47
durable disease remission and how does the companies aim to
22:52
maintain long term benefits without compromising bone
22:56
remodelling or or safety? You know, I, I think when we
23:01
think about this disease again, starting with the patient in
23:03
mind, this is a disease that we live with for a long period of
23:05
time. It doesn't go away.
23:07
It's not an acute infection. And and so the drugs have to be
23:10
designed in, in that lens of what's a chronic and progressive
23:14
disease. As I mentioned, you know, my
23:17
initial fascination with bone biology to begin with was on
23:20
this idea that bone is constantly adapting and turning
23:24
over and and renewing itself, adapting to the demands of the
23:27
skeleton. And we see this very clearly in
23:31
athletes. The challenge today is
23:33
durability. How do we maintain that ability
23:35
to adapt ability to renew the skeleton, yet selectively
23:41
suppress the disease process in a way that does not wane in
23:46
efficacy over time? And so that's, you know, when we
23:49
look across the clinical landscape today, I think one of
23:51
the major challenges is that we have drugs where the the
23:57
efficacy plateaus on a reasonably near term timeline.
24:02
Either it's limited in the label to 12 to 24 months or we we see
24:06
this blunting in efficacy over time.
24:09
And So what that looks like in the clinic for a patient.
24:12
And I, I think this is where it's your initial question, you
24:15
know, my clinical perspective, the, the conversation that a
24:19
healthcare provider is having with a patient.
24:22
If I tell you, hey, we're going to do this, but a year from now,
24:25
we're going to have the same conversation about what to do
24:27
next. That's not a very compelling
24:29
case for treating a chronic disease to say, hey, a year from
24:32
now, we're going to be back in the same spot trying to make a
24:34
choice. But if you can have a drug that
24:37
sustainably continues to modify the disease, shows a sustained
24:43
linear benefit without a ceiling or plateau, that's a really
24:49
exciting opportunity. I think we have to respect the
24:51
biology that our bodies have already so elegantly engineered.
24:55
And that's that's the bone turnover process with the
24:58
ability to in a very specific way intervene in the disease
25:04
process. And I think what that looks like
25:06
again is, is this idea concentrating therapy where it
25:11
matters in a very selective way and that yields that, that long
25:15
term durable profile. I, I think the other thing that
25:19
that has been a, a fun surprise to us, you know, in our
25:22
development is just how durable our technology has demonstrated
25:27
to be. And I think we, we are really
25:28
trying to push these limits right now.
25:30
What is the lowest combination of dose and frequency that you
25:33
can push on, you know, given the ability to have this skeletal
25:37
depot of drug? I think there's a an interesting
25:42
uncoupling between the the PK and PD here, which creates a
25:46
very unique profile in terms of patient experience, which you
25:50
know, as, as you know, mechanism, the science all
25:52
really matters, but patient experience is what's going to
25:55
make this a success. Yeah, for sure.
26:00
And as you look so like regulatory guidance for disease
26:03
modifying musculoskeletal therapies is is certainly
26:07
evolving, how would you assess the current environment
26:11
including opportunities like accelerated pathways or
26:15
surrogate endpoints and how does it influence your development
26:19
strategy for the company as well?
26:20
Just talk us through, yeah, on a regulatory standpoint.
26:25
So from a regulatory standpoint, I think now is the most exciting
26:29
time that there's ever been in, in osteoporosis drug development
26:33
in particular, because historically we have studied
26:37
osteoporosis in the context of fractures.
26:41
And, and what that looks like is treating a, a number of patients
26:44
and we count the number of fractures, of these rare,
26:47
reasonably rare events. And when we think about a
26:49
fracture that is truly the failure of the skeleton, it's
26:54
the failure of treatment. And so we count failures in, in
26:58
the bone community. Sometimes this is called a, a
27:00
bone attack when we count fractures and it it would be as
27:03
if you were assessing a cholesterol medication in terms
27:10
of the number of heart attacks that patients experience.
27:13
And so this is kind of an antiquated way of, of studying
27:15
disease. And again, the opportunity here
27:17
is of course preventing all fractures, but really preventing
27:20
that first fracture. And, and so the way that we can
27:23
do that is by measuring changes in bone mineral density or, or
27:28
the structural and mechanical integrity of the skeleton of
27:31
course, which which relates directly to its ability to
27:37
resist fracture. And so the Sabre initiative is a
27:43
surrogate endpoint that was approved by the FDA in December
27:48
of last year and, and really has reawakened this entire field
27:53
and, and turned the the entire biotech and and pharma
27:57
industries on to this opportunity to, to really have a
28:01
compelling impact for disease effects millions and millions of
28:04
people. But you know, what it really
28:07
means is that we have a validated tool to measure
28:15
changes in the skeleton before that failure happens.
28:19
Of course, as you know, DEXA scans now are are a household
28:23
name and term that that assess not just by fat mass, but but
28:27
total body composition including bone mineral density.
28:32
And so this was not something that happened overnight.
28:35
And I think, you know, as we think about what does this mean
28:38
as a beachhead for other clinical indications.
28:42
The Sabre initiative started more than 10 years ago and was a
28:46
incredibly robust academic effort.
28:50
There was an academic industry collaboration and and accounted
28:54
for over 150,000 individual patient data that informed our
28:59
ability to to truly qualify bone mineral density.
29:02
But this this dramatically changes the track in pathway
29:08
from innovative science to clinical impact.
29:10
And, and for context, you know, this is taking clinical trials
29:13
in osteoporosis from what historically have been 10 to
29:16
15,000 patient phase threes down to 1500 to 2000 patients, five
29:24
years down to two years. And really represents a, a
29:29
dramatically increased efficiency in evaluating our
29:33
treatments. And so I, I think it's a, a
29:36
really ripe time to be innovating in this space and and
29:39
certainly skill tasks is well positioned to take advantage of
29:43
this tailwind. Yeah, sounds like a super
29:48
exciting, exciting time for you guys.
29:51
And this is this is a question that we'd always finish with as
29:53
well. If you were to sit down and have
29:55
dinner with with any free people from past or present, who would
29:59
you go from? Why it it can be, you know,
30:02
people from biotech, people from from history, sports people,
30:06
entrepreneurs, it can be yeah, anyone you like.
30:09
But yeah, free people you'd want to sit down and have a have a
30:11
dinner with. You know, it's a, it's a great
30:15
question. I, I can tell you, I would pick
30:18
the pretty diverse matter in here of people who I find
30:21
intellectually curious and, and really who I would consider way
30:27
ahead of their time in creative. I, I think first for me is, is
30:31
Roy Vagalos who has LED Merck in, in some really exciting
30:36
times for the company's physician by training immigrant
30:41
son that started off waiting tables and diners and yet had an
30:44
incredibly successful run in leading Merck.
30:48
And I, I think for me, the, the reason he's so exciting and
30:53
interesting is that there was a, a period in the 80s of, of where
30:59
Merck had developed ivermectin, of course, for a potent
31:01
medication, but gave that drug a way to end river blindness.
31:07
And, and this was an opportunity where he saw the right molecule
31:12
that happened to work incredibly well and, and treated over 50
31:16
million people. And I, I think this is just an
31:18
incredible leadership trait, you know, that he saw the, the right
31:21
thing to do for patients and, and yet also made it an
31:24
incredibly robust and, and sustainable company and, and
31:29
enterprise. I, I think the other two for me
31:31
are non biotech people, but but personas who I, I have been
31:37
inspired by and really sought wisdom from in, in leadership.
31:40
One is Ernest Shackleton, who you may know is a explorer who
31:45
led early expeditions in Antarctic and, and there's a
31:48
Harvard Business School professor, Nancy Cohen, who's
31:51
who's written an exceptional book on him as a leadership
31:54
style and his his missions failed.
31:57
Yet he brought every person who went with him home alive.
32:01
And I think just a testament to building a team, having a a
32:05
leadership style and communication style that that
32:07
encompassed inclusivity and and diversity, was willing to take
32:11
risks, but never left his fellow band behind.
32:16
And last, miss Phil Knight from Nike, I think another incredible
32:21
entrepreneurial story, someone who is an underdog for for much
32:26
of his career and, and has created a legacy not just in, in
32:29
consumer goods, but has also used his, his position to do a
32:33
lot of good for medicine and, and through the night campus and
32:36
in a lot of the philanthropic work that he's done.
32:39
There's an incredible story there of persistence and
32:41
creativity leading to a legacy that's changed the world.
32:48
Yeah. Well, look, 3 great answers
32:49
there and thanks so much for coming on and helping us out
32:52
with this. It sounds, sounds like a super
32:53
exciting time for you guys. And I'm certainly looking
32:57
forward to following the next, the next milestones and, and
33:00
follow you guys over the coming years.
33:01
So, yeah, Ben, thanks again. It was a it was a pleasure to
33:04
hear about your story and and the company's journey that
33:06
you're going on. Thanks, Tom.
33:09
I, I appreciate it. It's certainly an exciting time.
33:11
And I, you know, I think again, you know, to close with, with
33:14
patients at the forefront, it's an exciting time for patients.
33:16
And I, I think we all should look forward to what does it
33:20
mean to, to have freedom from chronic disease.
33:23
And, and this is certainly a ripe example where the science
33:27
and regulatory tailwinds are converging in osteoporosis to
33:31
really think about what's next.