Latest / The BioHub - by Avetix / Episode 178 - Kevin Finney - Chairman, President and CEO at Autobahn Therapeutics

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Episode 178 - Kevin Finney - Chairman, President and CEO at Autobahn Therapeutics · The BioHub - by Avetix

0:06
Welcome back to the Bio Hub podcast by Avetics.
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Today, I'm joined by Kevin Finney, President, Chief
0:13
Executive Officer and Chairman of Autobahn Therapeutics.
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Kevin has built an impressive career across biotech and pharma
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with leadership experience spanning commercial strategy,
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company building, corporate development and M and A Prior to
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Autobahn, he was President and COO of Abide Therapeutics, where
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he led the company through its acquisition by Lundbeck in 2019.
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Before that, he was founder and COO of Zavante Therapeutics
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helping build the business from inception through to it's sale
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and earlier held senior leadership roles at Allegan
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where he was involved in some of the industry's most significant
0:51
transactions during a period of major growth.
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Kevin, it's a pleasure to have you with me today.
0:56
Ben, thank you for having me. It's going to be a lot of fun.
0:59
Yeah, looking forward to it. I mean, let's start from the
1:02
beginning. You've taken a rather unusual
1:05
route to the CEOC. You started in sales in pharma.
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You spent years in the field. You moved through large pharma,
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through many launches, M&A deals and through multiple biotech
1:18
companies. What were really the key
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inflection points in that journey, and how did they shape
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the way that you lead Autobahn today?
1:25
That's, that's true. Those are good questions.
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And I have had the privilege of being with seven different
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companies I believe as an operator.
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Each one of those companies I was hoping would be my last
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company and it's been my career there because they're just
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terrific organizations. But it seems like great
1:42
companies tend to come together and merge.
1:45
If I think back about those companies and really starting my
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career in the field, which is a little non traditional as you
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mentioned for ACEO in sales, carrying a bag, calling on the
1:56
customers, which are the doctors.
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I've learned that science alone doesn't get a drug into the
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hands of doctors treating patients and more importantly
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the patients themselves. And at Autobahn we built a
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patient customer focus model and that's the lens I think I bring
2:17
to the company thinking about each of those interactions and
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how to focus on the people that count most, which is the doctors
2:24
and the patients. Yeah.
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I mean unique perspectives and unique experiences is often what
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leads to to great leaders. So I guess you know coming from
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that that side of things and having that angle of different
2:37
experience will certainly be able to provide you with some
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sort of leg up in different circumstances when it does come
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to leadership. In sales and pharmaceuticals,
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when you're calling on the doctor all day, getting to
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understand the office and how they treat patients, things that
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go right and wrong on an individual patient basis enables
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you to think about how do you really design programs in a way
3:00
that are going to meet the needs not only of the patient, but the
3:04
doctor caregiver, because they are the keepers of the patient's
3:08
health. And something that came out of
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that, that we use every day at Autobahn it's not a new term,
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but it's true for us. And I hope others, the patient
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comes first and profits will follow.
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So we tried to bring that thematically into how we make
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decisions for the company, how we design our drugs.
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And I will point out that we carry that really that customer
3:30
centric perspective into the customer comes first and that
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everyone is your customer. So at work across the company,
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if you're in manufacturing or quality or research or being a
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chemist, thinking about your customers is everybody you work
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with enables you to build a better team and allows you to
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advance programs more rapidly. So all of our interactions with
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each other, our board members, our key opinion leaders who we
4:00
spend a lot of time listening to, the doctors that are leading
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the charge in psychiatry. We tried to take all them, their
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design inputs into how we thoughtfully develop our
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clinical programs, think about what kinds of things are going
4:15
to be important for patients. And you know, we're in the month
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of May, it's Mental Health Awareness Month and which is an
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important platform for patient advocacy.
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I mean, put, put on your, your sales Rep hat for a minute and
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pretend that you're back in the field speaking with
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psychiatrists. What what are you hearing about
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the primary unmet needs and residual symptoms for patients
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who are suffering from MDD and bipolar depression?
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That's probably the most important question that I can
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answer today and I can do you one better there besides just
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putting my head hat on and what things might have looked like 30
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years ago. I, I have had a couple of recent
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doctor interactions and lunches where I've had really had a
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chance to dig in again. But I think kind of the big
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picture of the space is we, we recognize that in the US alone
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and of course we can expand this globally, including for the UK.
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In the US, 21 million patients suffer from major depressive
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disorder and 7 million patients suffer from a very significant
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problem called bipolar depression.
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Combined, that's 30 million patients.
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And we all recognize that more than 50% of those patients are
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getting inadequate care. Their drugs aren't working and
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helping them, so they're going back and back into the office.
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Often it's that the groups don't have just the right efficacy for
5:34
the patient so they feel better, but often it's actually the side
5:39
effects associated with these drugs.
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So it's kind of sad if you're a patient going into a doctor's
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office to be treated, the symptom and the adverse effects
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you get feel worse than the primary symptom.
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You're being treated for things like weight gain, metabolic
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complications, fatigue. And so that is more of the big
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issue. There's a toolbox that doctors
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have and they're limited to what's in those toolboxes. 1
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practical story. Just recently I was speaking to
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a psychiatrist that is well recognized by name nationally
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and he just plainly stated that as a psychiatrist he's been
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treating his patients the same way for two decades, targeting
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neurotransmitters, serotonin, norepinephrine, dopamine, and
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that's the tools in his toolbox and that we need newer
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medications that are designed to tackle disease burden
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differently. Another example would be another
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example would be a lunch I had recently with a physician that's
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full time seeing patients. But it's also recognized as a
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national key opinion leader. And as a backdrop, you said if
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you're an orthopedic doctor and a patient's having a joint
6:56
problem, you could treat them and you want to treat them and
7:00
address both their symptoms in the underlying condition.
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And so you can give them a little NSAID pill for pain.
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If they need more, you can give them a disease modifying drug a
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little bit more. You can inject their knee a
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little bit more. You can do different degrees of
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invasive procedures. Because as a psychiatrist, a
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patient will come to me and they'll say they're having
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anxiety, they're feeling anxiety symptoms, maybe they have
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depression, or maybe they have depression and mania called
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bipolar. In each case, he wants to help
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them so he can give them a pill that makes them feel better for
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a few hours. Then everything just comes back
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again. And it's perspective was
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psychiatrists have very many tools in their toolbox that can
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help maybe tackle the underlying condition differently in a more
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substantial way and provide a different solution for these
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patients. So I think if you went in the
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field today and talked to psychiatrists, that's likely
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what you would hear or hear. Do you think that lack of sort
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of varying options then is one of the main reasons that
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patients with depression really struggle to find treatments that
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that work for them specifically? So far science is, is limiting
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us to a, a little pill that can adjust neurotransmitters.
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That's, that's all that's out there, right?
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I mean, you can go for more invasive procedures and there's
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interventional psychiatrists that do more and I think some of
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that helps. But in your garden variety 90%
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of psychiatry offices, they're limited to counseling, patient
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interactions and one of those bespoke medications, which as I
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mentioned have been for the last two decades narrowly working on
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adjusting neurotransmitters and maybe not dealing with new
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thinking on underlying the Physiology of disease.
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I will also point out that there's an, a, a sub patient
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type that I'm sure we'll talk about a little bit later when we
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get into our regulatory strategy.
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This is very interesting and it's a patient called ateical
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depression and realizing that people are diagnosed by going
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through a series of questions and getting ADSM 5
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categorization of OK, you have depression, but there are sub
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patient types. One patient's subtype is called
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atypical depression, and there's actually no medications approved
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for this patient and this patient, part of the symptoms
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that they look at besides the depression symptoms is these
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patients tend to be overeaters, maybe a little overweight,
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they're hypersomnolent, so they sleep too much and they're
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effectively called, in modern terms, couch potato.
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So you can visualize that versus another patient that comes in
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and maybe she can't sleep, she's skinny, has anxiety, and she
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also gets a, a categorization of depression.
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But there's two different patients that walk in the
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office, 1 after another. They look very different.
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And so obviously there's probably a different path of
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Physiology for their disease. And modern psychiatrists
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commonly call that patient their sleeper eater.
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They walk into the office and they know right there, you know,
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I need to find a unique treatment approach to address
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your form of depression. Nothing's approved.
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And that's a patient type that we are doing at, at, at
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Autobahn. Yeah.
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I mean, let's jump over to Autobahn for a minute.
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I mean, before joining, your career spanned major commercial
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organisations, entrepreneurial biotech and multiple successful
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acquisitions. I mean, you've really seen it
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all. What was it in particular about
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Autobahn science and the opportunity that you guys have
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here that made you want to step in and help to build this
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company? That's a great question.
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And I think maybe to approach the answer, we'll start with,
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well, it's in CNS and CNS over the last 20 years has had
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periods where there's inflows, people are very interested in
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investing in doing research and there's other areas where people
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really backed out because it's so tough.
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It, it's the brain, it's the CNS.
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You can't go take a tissue sample in a patient, right, like
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you can with cancer or some other diseases.
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It's very difficult. So the strategic answer for what
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you just said is that Autobahn is pursuing A validated target,
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which is thyroid hormone in depression, which has been used
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off label for over 50 years by psychiatrists.
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I'll say spontaneously realizing that activating hormone might
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help with the depression episodes and pairing the
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validated target with a proprietary chemistry platform
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that solves the historical problem of peripheral side
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effects. That has been the limitation
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there. So it's a rare combination of
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starting with a validated target and having a specific technology
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that can be paired to overcome the specific liability of that
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technology. And I mean that that is so
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different from the rest of the field.
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I mean, the novel chemistry platform combined with known
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thyroid hormone biology as opposed to following the more
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traditional neurotransmitter driven path, which is seen in
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depression. I mean, what what is really the
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core scientific insight behind that strategy?
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And why do you think that it could matter in a field that's
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been so hard to crack over the past, you know, 5 or so decades?
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Yeah, I will say that you know, maybe it's a summary statement
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to that. The last comments that I made is
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that after watching the field cycle through different versions
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of the same neurotransmitter story for 20 years and have a
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chance to build a new company, we can do better.
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I guess to answer your question about the science behind this,
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we take a very clear two pillar framing approach.
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The medication that we chose to advance is our medication into
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the clinic which is Eleneteron has a two pillar frame.
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The drug boosts brain energy by mitochondrial activation and is
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driving neuroplasticity and for the audience that's maybe not
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quite familiar with that term, strengthening the neuro neuronal
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connections, and we're doing both of those at once, boosting
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brain energy through activating mitochondria and driving
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neuroplasticity. It tackles the underlying cause
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of what we think is many types of CNS disorders in that besides
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just monkeying with neurotransmitters, patients with
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depression, especially serious depression and bipolar
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depression have underlying deficiencies with brain atrophy,
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synaptic junctions that are operating inefficiently.
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And the idea of a boosting agent in a drug that directly
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intervenes and drives synaptic growth together combined can
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address, as we said at the beginning, the psychiatrist that
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has few options for the patient in a different way.
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It might make sense right now just to mention our, our
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technology platform and what it is.
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And I'll, I'll tap that with a short story.
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Our thyromimetics, which are starting compounds are unique
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compounds. They're similar, but they're
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different than thyroid hormone. They're not generic versions of
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thyroid hormone. They're engineered to be
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receptor selective and to be tissue selective.
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And so if you take the oral version of our drug in its plain
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form, it can't cross the blood brain barrier.
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It gets blocked because it's a charged molecule.
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We've all heard a lot about the blood brain barrier.
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Our enabling technology, it enables making a pro drug and
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that pro drug is orally delivered and then it just makes
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its way to the CNS. It passively diffuses into the
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brain. Still it's a it's a pro drug and
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it's inactive and interesting enough, there's a naturally
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occurring enzyme in my brain. Your brain, patient's brain is
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called fo fatty acid amid hydrolase and fog cleaves and
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liberates the pro drug and enables a large amount of drug
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to deposit and target receptors only in the CNS.
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In that way you're getting high concentrations of drug into CNS
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with low concentrations of drug in the periphery and you can
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optimize that thyroid hormone signal which was just a signal
15:33
with thyroid hormone because that's a blunt instrument.
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It can't do it the same way. It enables us to get really high
15:39
concentrations, activating your thyroid hormone receptors in the
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CNS, reducing the peripheral liabilities of heart rate that
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you would see with thyroid hormone.
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And in a way, it's sort of like a Trojan horse.
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I mean, if we move forward, I, I guess a few years from your
15:56
scientific foundations that, that are backing Autobahn to
15:59
where you guys are now in terms of being in the clinic.
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I mean, you've made some pretty deliberate decisions around
16:05
study design Fuel league programme in MDD, which includes
16:09
avoiding a small exploratory path and instead aiming for a
16:12
more highly powered study in CNS where endpoints can be soft and
16:18
placebo effects can be a major issue.
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What have you learnt about designing trials that gives you
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the best chance of generating meaningful and interpretable
16:27
data? That's another really good
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question. I would say it's a company
16:32
formation and the company was started in Arch Venture's
16:36
office, which is, you know, a prominent recognised healthcare
16:39
venture investor. And we licensed technology from
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Oregon Health Science University out of Oregon, US, and then out
16:47
of the Scripps Research Clinic in San Diego.
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We have the right molecule. We are forming the right
16:53
company. And how do you design the right
16:56
studies? And so our investors have been
17:01
around for a while and they have invested in some major
17:04
blockbusters and CNS and some complete failures.
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And so if I understand your question right, how are we
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designing our clinical program in order to enable success?
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We're very deliberate. We decided to do a round of
17:23
financing and to design our phase two study to actually have
17:29
the look and feel of a phase three study and to highly power
17:34
it on the order of plus 90% to detect a drug treatment effect
17:39
with our drug versus placebo. And to answer the question that
17:43
we use in industry sometimes, do you have a drug?
17:46
So we've designed our lead program Amplify, which is
17:50
studying Elinetarom as an adjunctive agent, which means
17:56
for the common person a drug that you're giving on top of
17:58
something else that you're already taking for depression.
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So adjunctively adding it to this regimen you're already on.
18:04
And we have to prove that we're better against placebo and not
18:07
just our drug, but the drugs that you're already on together
18:10
versus placebo, which would be the baseline, whatever therapy
18:13
you're on. And we want to powerfully detect
18:17
a 90 point, at least a 90% chance of showing a change.
18:21
At the conclusion of that, we go to end of Phase 2 with the FDA.
18:26
And the way we think about it is unlike other CNS companies,
18:31
maybe they have exploratory new Moas and they hit on Phase 2 and
18:35
they'll put 100 million into phase three and then you get a
18:38
data card flip that doesn't work.
18:40
Our confidence level lies in the fact that we're starting with
18:43
validated biology that we know that off label thyroid hormone
18:47
is a blunt instrument, but it's proven it has a signal.
18:50
So we're more confident that upon successful Phase 2 success,
18:55
we'll be able to repeat that in phase three.
18:58
We also made a decision to do an exploratory second indication in
19:02
a very important disease area with very limited options and
19:07
that's bipolar depression. These patients have substantial
19:11
impacts to their lifestyles. Some of these patients end up
19:15
missing three days a week of school or work.
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And so we wanted to do an exploratory Phase 2A on top of
19:22
that that would have an earlier read and enable us to see how
19:26
this drug works in the bipolar patient population.
19:30
Yeah. I mean, can you can you touch a
19:32
little bit on how that broader sort of portfolio strategy
19:37
across both MDD and bipolar gives you know gives you a sort
19:42
of regulatory optionality moving forward?
19:45
That's a very strategic, insightful question, Ben.
19:47
And I would say we have 3 indications shot on goal with
19:55
one molecule with our first interactions with the FTAI think
20:02
our drugs mechanism of action, which we discussed previously
20:06
could work for several other indications.
20:09
But as it relates to how we approach our clinical trial
20:12
design and our future regulatory interactions for elineteron, we
20:18
started with a highly powered, as I mentioned, amplified study.
20:23
And we're intending to show that our drug works on top of an
20:27
adjunctive therapy, on top of baseline therapy in the total
20:31
population, 21 million patients. In addition to that, since we
20:36
have this atypical depression patient that we mentioned
20:38
previously, which represents about a third of all MDD
20:43
patients, we pre specified in the phase two protocol that we
20:48
want to track these patients in particular.
20:51
And I think our study is showing that we're tracking that again
20:53
about actually in fact with the real world EPI, about 1/3 of
20:57
patients are atypical. We're tracking those patients
21:01
independently as a subgroup. So this would not be a scenario
21:05
where somebody runs a study, they miss their intent to treat
21:09
population. We hope to blow that out of the
21:12
water by the way, but they miss it and then they say, oh, in a
21:15
sub analysis, look about that. Look at this.
21:18
We wanted to approach this with the agency offensively in MDD
21:21
given that there is no drugs that are currently approved for
21:24
atypical depression. It's a defined DSM 5 patient
21:29
subtype. So we get to go talk about the
21:31
total population and the atypical population in the same
21:35
meeting as we approach phase three.
21:39
In addition to that, we have our Phase 2A bipolar data with which
21:45
is called amplified BD and that's another patient group
21:49
that is suffering from depression, but they suffer from
21:52
bipolar depression and that's another more immediate shot on
21:56
goal as well. We'll be trying to approach the
21:59
agency and ask how we might pursue both indications for a
22:03
submission at the same time. So you have in a way patients
22:07
one molecule shot on goal and. Yeah, you've got two of these
22:11
data readouts coming up fairly shortly on the horizon.
22:15
Without getting ahead of the data, could can you walk us
22:17
through a little bit about what these studies are designed to
22:20
show and also why the endpoints matter?
22:23
How we design these studies and and what we're hoping to show as
22:29
it relates to the amplify MDD study.
22:32
Again, we're proud of the fact that we designed the molecules,
22:36
we did the we didn't license them in.
22:38
We've taken them through non clan phase one powered phase
22:42
two. We expect a readout for that one
22:45
in Q3 of this year. And I would say as of today,
22:50
we've actually stopped screening patients.
22:52
We're advancing now to finishing randomization and and dosing.
22:57
And so we're on track for a powered readout, which is the
23:01
data card flip. Do we have a drug in Q3 of this
23:06
year. On top of that, we also have a
23:11
bipolar readout, which is imminent and we'd expect that
23:14
bipolar readout to take place within Q2 of this year, which
23:20
we're currently in. And so we look at this staggered
23:23
data read bipolar patients, very important patient population,
23:29
coincidentally, less than 5 drugs approved to treat the
23:34
depressive episodes of bipolar. And they're all within the same
23:38
class of drugs. And they all have class labeling
23:41
that I've mentioned earlier that makes these drugs very onerous
23:44
for that patient group. That data card flip will be
23:47
within this quarter. And then we'll rally the team
23:51
and move forward after publishing that data work on a
23:57
preparation for an end of phase two meeting with the agency.
24:01
And the fun part of the job is we get to discuss with them
24:05
what's the last third of the pathway look like.
24:09
We've completed for people in pharma, all of our Clint Farm
24:13
studies, all of our talk studies.
24:16
I think everything in addition to the clinical studies will be
24:20
completed and so we can have a clear line of sight conversation
24:22
with the agency about their expectations for submitting an
24:26
NDAI mean. Yeah, it's, it's exciting times.
24:30
I think the next, the next couple of months are going to be
24:32
going to be pretty hectic on your end.
24:34
But I'm, I'm excited to keep up with, keep up with what the data
24:37
shows. I mean, you know, sort of going
24:41
back, you, you've worked across seven companies now that have
24:44
ended up either being acquired or, or or merging.
24:47
You've seen both large organisations and small biotechs
24:51
up close and in the flesh. From an operational standpoint,
24:54
when you're building a company around a novel CNS platform,
24:58
what are the key decisions that really determine whether it
25:02
becomes strategically valuable or not?
25:05
Ben, that's a good question. And you know, I, I, I will say
25:07
again that all of us in this in the pharma, in the biotechnology
25:11
industry, we're really privileged.
25:13
It's a lot of fun to advance science and move drugs through
25:18
all the way to commercial and watch those drug being drugs
25:20
being picked up at the pharmacy with, with for patients.
25:25
And the important point of your question is CNS, this is really
25:28
different. I've worked across disease
25:30
categories and five or six of them, and in this particular
25:35
case, CNS is a unique place to be.
25:38
And so for us, we think about in CNS for our company, we want to
25:46
focus on real targets, biological targets, validated
25:51
targets #1 it helps deal with the ambiguity of clinical
25:57
studies that have soft endpoints, not I'm going to take
26:02
your blood pressure and yes, you're up or you're down.
26:04
So the number one would be really focusing on the hard
26:09
endpoint that we get to anchor against this biological proof of
26:14
principle with thyroid hormone. So that's really important if
26:18
you can do that, and if you can couple that with the technology
26:21
that overcomes the actual problem with that therapy, which
26:25
in this case is we want really high CNS levels of drug and
26:29
really low peripheral levels. So that's important for the CNS
26:35
platform play #2 I'd say that drug development is the long
26:39
game. So for me, being a people person
26:42
and being with customers and growing up talking to people,
26:46
interacting with them, you have to build the right team.
26:50
To the second point, our team is designed to listen to each
26:56
other, understand the company, understand the customer, and
26:59
overcome challenges that inevitably will emerge.
27:03
And then #3 this is super important.
27:06
I think we kind of touched on this a little bit.
27:08
Even though you might have a great drug, you very well, in
27:12
fact I would argue probably you're still going to fail if
27:15
you don't design your clinical programs the right kind of way.
27:20
These clinical trial executions and psychiatry are different.
27:23
You're not testing blood pressure, putting on a cuff and
27:26
then measuring if the patient's blood pressure is up or down.
27:30
These are psychiatry studies with soft endpoints.
27:33
Many different components in that value chain can be
27:36
disrupted and so you have to design your clinical programs
27:40
with belt and suspender to ensure that you can reduce
27:43
unnecessary risk. That that's where so many,
27:47
especially within psychiatry, even as a subtext or of CNS,
27:50
that's where so many companies fall down.
27:52
I think you know you, you speak with anyone within the industry,
27:56
be that C-Suite leaders, be that VC leaders who take a look back
28:00
on psychiatry companies and psychiatry programmes that have
28:03
failed and that that's often the deciding factor.
28:07
Without getting into too much of like shop talk, we did a lot of
28:11
design considerations before we started our study.
28:14
We're we're humble enough that we want to talk to everybody and
28:18
design the right program and we hope everyone wins and gets
28:21
drugs through approval. So we spent a lot of time
28:26
speaking to CM OS and CE OS of other companies in depression
28:31
and many of them, their studies failed.
28:33
And it's not uncommon when you see a press release with a
28:37
company that didn't meet their statistical endpoints, they'll
28:39
do a sub analysis and they'll find out that one or two sites
28:43
data corrupted the whole study. It's not uncommon for patients
28:48
in psychiatry if if you hear this, it's kind of shocking to
28:52
actually sign up for two or three studies at the same time.
28:57
There's actually Reddit sites that let you go into and figure
29:01
out how to get enrolled in a depression study because they
29:05
want the income. And so we have mature AI
29:10
databases. We have different systems where
29:14
we flag and can find a patient who would maybe sign up for our
29:18
study. And they also signed up for a
29:20
competitor study at the same time.
29:24
Or even more interesting, they signed up for our same study at
29:27
two different sites. It's this kind of work,
29:30
detective work, you have to do upfront to find the real patient
29:35
suffering from disease and only and only enroll those patients
29:40
into the study. Yeah.
29:41
And and I guess you know, with with the rise of AI and, and
29:44
other forms of artificial intelligence that that all of a
29:48
sudden becomes easier and easier as things go on.
29:50
I'd imagine if you look back 1520 years ago, doing that
29:55
manually was was a hell of a task.
29:58
To your point about the use of AI and enabling clinical
30:01
studies, I think the Internet age goes two ways.
30:07
Yes, we're using AI now to help us figure out the right patient.
30:12
You can even on a site level match labs, blood work, patient
30:18
history to really detect, you know, and that's not data that
30:21
the sponsor sees, that's what the site sees.
30:24
To really identify the right patient, avoid what we call the
30:28
professional patient, which we just alluded to.
30:31
On the other end, I've been told that 10 years ago that the
30:34
number of patients that come into a study and stay in it, we
30:38
call that the screen fail rate. At one point, screen fail rates
30:41
were like 40%. Nowadays, screen fail rates in
30:46
some studies go up to 80 to 90%. So the point is, is that as
30:52
Internet's available, more patients can be aware of
30:55
studies, they can sign up and they can try to kind of play the
30:59
system. On the other hand, back in the
31:02
old days, I think patients that were showing up for sites were
31:05
more or less traditional patients that are finding their
31:08
way through a referral, and they're the real patients.
31:10
So in a way, it's just like security.
31:13
We need to have our software AI systems to keep up with modern
31:17
times. No, it, it, it makes sense, I
31:21
guess just to sort of wrap things up as, as we typically
31:23
do. If you could have dinner with
31:25
any scientist or innovator, past or present, who would it be and
31:29
why? That's a tough question.
31:33
I was thinking along the lines of science and biology.
31:37
But given that we started this conversation with me being in
31:40
the field building relationships with doctors, I think the person
31:45
that I would like to actually have lunch with or dinner would
31:49
actually be Steve Jobs from from Apple.
31:53
Don't know if you've ever heard of that before.
31:55
And if you ask why, you know, I will say that I have a
32:00
smartphone in my hand. I, I won't put it up in front of
32:02
the camera, but almost every human being on the planet has a
32:06
smartphone. And it was Apple's original idea
32:11
and totally oriented towards the end user and what they want.
32:17
And it was Steve who had the vision and the idea that we
32:21
could take computers and phones and all these things and we can
32:25
put them into a a handheld device.
32:28
And he was completely designer patient user based.
32:32
And I use that analogy as we translate to patients.
32:36
But he was the first mover visionary with just exquisite
32:40
focus on end user design to make a handheld that's portable, that
32:47
is now useful around the world to just about everybody.
32:51
And I feel like that is such a substantial invention.
32:54
And now we know that, you know, intellectual property enables
32:58
that company to keep a percent of the market on a worldwide
33:03
level. The majority of the market is
33:04
other companies. But who had the wild and crazy
33:07
and audacious idea that you could actually have this device?
33:12
And I think that that kind of visionary thinking and being
33:16
relentlessly focused on the customer enables the best
33:21
products in the world to come out.
33:22
And to connect the analogy to what we're doing at Autobahn
33:27
we're patient focused. So we're always thinking about
33:30
the end user, thinking about the doctors that pick treatments,
33:33
and designing our data and our programs with the end user in
33:39
mind. Yeah, I mean, it's, it's one of
33:42
the defining inventions of of the modern day.
33:45
So I can I can completely understand wanting to to sit
33:48
down with the man who was the was the genius behind it.
33:52
And I mean, fingers crossed that that Autobahn follow in the
33:55
footsteps of Apple and patient patients get access to to to
33:59
your drugs and it's able to help them.
34:01
Well. So, Kevin, look, it's been it's
34:03
been an absolute pleasure. I really, really appreciate you
34:06
joining me today. It's been a been a great
34:07
conversation. Ben, thank you so much.
34:09
It's been fun. Thank you for showing interest
34:11
in our industry and I look forward to watching your future
34:16
podcasts. Appreciate that and thank you to
34:18
everyone for tuning in. Make sure you you drop a like
34:22
and subscribe for any future episodes to come.
34:24
Thank you and goodbye.