Latest / The BioHub - by Avetix / Episode 65 - Robert Ross - CEO of Clasp Therapeutics

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Episode 65 - Robert Ross - CEO of Clasp Therapeutics · The BioHub - by Avetix

• 0:04
  Welcome back to the episode of the Bio Hub.
• 0:06
  Today, we're delighted to be joined by Rob Ross, who's the
• 0:09
  CEO of Class Therapeutics, A biotech company pioneering
• 0:13
  position. Immunotherapy is designed to
• 0:15
  harness the power of T cells to fight cancer and other serious
• 0:19
  diseases. Before taking the helmet class,
• 0:22
  Rob served as CEO at Surface Oncology, leading the company
• 0:26
  through its acquisition at Caheris.
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  And prior to that, he's the Head of Oncology at Bluebird Bio,
• 0:32
  where he helped advance innovative selling gene
• 0:35
  therapies as well as roles at Genentech and Infinity
• 0:38
  Pharmaceuticals. Trained as a medical oncologist,
• 0:41
  Rob completed his residency at UCSF and his fellowship at Dana
• 0:45
  Farber Cancer Institute, and he also holds his MD from Columbia
• 0:49
  University. So join us today as we'll talk
• 0:52
  through the origin story behind class, the differentiation in
• 0:57
  the pipeline and his journey from a medical oncology to CEO.
• 1:01
  So Rob, thanks so much for coming on.
• 1:03
  How are you? Yeah, Thanks so much, Tom.
• 1:05
  It's great to be here. I I appreciate you taking the
• 1:09
  time and getting to know the story.
• 1:12
  Yeah, for sure. It's an absolute pleasure to
• 1:14
  have you on. So look, let's just start off
• 1:16
  with a bit about your journey through the field.
• 1:19
  So what What inspired you to pursue a career in the biotech
• 1:22
  space? Yeah.
• 1:24
  So it, it really goes back to my decision to go into medicine in
• 1:29
  the 1st place and oncology in the 1st place.
• 1:31
  I when I was in college, my grandfather was fighting,
• 1:37
  fighting through ultimately dying of prostate cancer.
• 1:41
  And I was very close with him. I named my first born child
• 1:45
  after him and I was very affected by that.
• 1:48
  At the same time, I found that in college.
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  I love science and I really loved the, the sort of mystery
• 1:58
  of understanding human biology and the way all of our, all of
• 2:04
  our organs and all of our systems integrated.
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  And I also found that I love working with people.
• 2:11
  And so that that got me very interested in medicine.
• 2:14
  I went to medical school and in medical school, one of my most
• 2:19
  profound mentors was a medical oncologist.
• 2:21
  And what I was most influenced by was the way he worked with
• 2:26
  patients. Interestingly, he was a former
• 2:28
  Episcopalian priest. So before he was an oncologist,
• 2:31
  before he was a doctor, he was a priest.
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  And he was just so good at the bedside and so good with
• 2:37
  patients who were, you know, as you can imagine, dying of awful,
• 2:42
  awful cancers. And at the same time, he was a
• 2:46
  basic scientist and did a lot of work on the underpinnings of
• 2:50
  leukemia and lymphoma. And so I saw this as a great way
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  to integrate my my enjoyment working with people, with
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  science. And so I went and did my
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  medicine residency and then my oncology fellowship because I
• 3:03
  found that oncology was at this great Nexus of innovative
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  science and helping people in in desperate, desperate need.
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  Interestingly, between my residency and my fellowship, I
• 3:18
  had a year because my wife had my wife's also a physician and
• 3:22
  had an additional year for her residency.
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  And my attending in the CCU when I was a third year resident was
• 3:32
  a guy named Hal Baron. And Hal happened to be a senior
• 3:35
  executive at Genentech at the time.
• 3:37
  And so I went to Hal and said, Hal, I, I, I need a job for a
• 3:41
  year, I need something to do and I'm really interested in
• 3:44
  oncology. I'm going to go get do an
• 3:45
  oncology fellowship and Hal said, well, why don't you come
• 3:48
  over to Genentech, You can come and work with us and work on
• 3:52
  this drug, this antibody we have that binds to VEGF that's in
• 3:55
  late stage clinical trials. And that was the drug that
• 3:58
  eventually became Avastin. I had a year there and was just
• 4:02
  overwhelmed by just how much fun it was, how exciting the science
• 4:07
  was, how great the people were and just the leverage it had to
• 4:13
  really help huge numbers of patients, huge numbers of
• 4:16
  patients. I happened to be there an
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  incredibly exciting time. The trials that I worked on were
• 4:22
  ultimately positive. And this was a, a huge win for
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  the field and you know, frankly a huge win for for Genentech and
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  sort of continued on the trajectory that that that made
• 4:35
  it a world leader in oncology drug development.
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  So then I went and did my oncology fellowship.
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  I tore myself away even though I thought I could stay, but I
• 4:43
  thought I really wanted the oncology training, did my
• 4:46
  oncology fellowship and then stayed on faculty at the Farber,
• 4:49
  seeing patients and doing clinic research, running, running
• 4:53
  clinical cancer trials. And I found that I really love
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  seeing patients, but I missed, I really missed the clinical
• 5:03
  development intellectual challenge that you really saw
• 5:07
  when when I was a Genetech and I missed that part.
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  And so I was trying to figure out how I could do that yet
• 5:13
  still be able to see patients. And after thinking about it for
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  a couple years, I decided to move back into industry.
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  And that's when I started Infinity Pharmaceuticals and
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  small biotech. But I maintained a clinic at the
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  Farber and I maintained a clinic at the Farber for the next
• 5:27
  decade. So I'd see patients about once a
• 5:30
  week. So not a super intense clinic,
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  but I still was able to see patients, yet was able to work
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  on incredibly interesting and fascinating integrated teams on
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  novel drugs and oncology, trying to do something different,
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  trying to do something that could benefit huge numbers of
• 5:49
  patients. Eventually I had to stop seeing
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  patients. Eventually, by the time I got to
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  Bluebird, I was traveling too much and I just couldn't make it
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  work anymore. But, but by that point I was,
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  you know, I, I'd really just, you know, fallen in love with,
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  with the work of, of developing drugs, oncology and moving into
• 6:09
  more of a leadership role at that point.
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  So, so that was my story. That's how, that's how I got
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  there. I, I do miss seeing patients.
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  I miss that part of my, that part of my brain.
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  Having said that, I've also now really enjoy the leadership
• 6:26
  positions and, you know, being in charge of groups of people,
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  teams, companies to move these drugs forward.
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  And at the end of the day, I'm in this for the same reason that
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  I got into oncology, for the same reason that I got into
• 6:42
  medicine, to help people like my grandfather, right?
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  To help people who need innovative treatments.
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  And that's what I feel like I've been been able to do.
• 6:52
  Very good. So you launched Clasp just over
• 6:56
  a year ago. Can you talk us through the
• 6:58
  origin story behind the company and the inspiration behind its
• 7:02
  founder? Yeah, yeah, Happy to.
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  It's, I'd love to take credit for it, but really the
• 7:08
  inspiration came long before I got involved.
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  This was Burt Vogelstein, Drew Pardal and their labs at Johns
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  Hopkins. And Burt Vogelstein is one of
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  the fathers of genetics and also very, very interested in
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  immunity and cancer, along with Drew Pardal, who's obviously one
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  of the one of the fathers of that field.
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  And the underlying question was how can you use the immune
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  system to fight cancer cells, but in a very precise way such
• 7:43
  that you're not at the same time attacking and killing normal
• 7:47
  cells. So we know that problem, right?
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  That fundamental problem of how do you kill cancer cells and not
• 7:51
  kill normal cells? That is the primary problem in
• 7:55
  all of oncology, right? That goes back to the use of,
• 7:58
  you know, mustard gas and mustard gas derivatives, right?
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  How do we kill cancer cells and not normal cells?
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  And when we're utilizing something as potent as the
• 8:07
  immune system, that question becomes even more important
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  because when the immune system attacks normal cells, you can
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  you can get horrible, terrible toxicity and unfortunately,
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  sometimes patient deaths, which we've seen in in oncology drug
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  development. And So what Burt and Drew
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  focused on was can we use the specific genetic changes that
• 8:36
  make a cancer a cancer, right? So this is the same thing we
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  talked about with precision oncology with small molecule
• 8:41
  inhibitors, yet use those to stimulate the immune system.
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  So we know that those genetic drivers are intracellular
• 8:50
  proteins for the most part, right?
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  This is mutations in P53, mutations in K Ras, mutations in
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  B RAF. These are the who's who of of
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  mutations that cause cancer. The problem is that they're
• 9:04
  intracellular proteins. So how can you get the immune
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  system to attack them if they're intercellular proteins?
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  Well, the immune system has a system for that.
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  That is the what we call the major histocompatibility complex
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  or MHC proteins. These we call them in humans, we
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  call them the HLA proteins. And the HLA proteins sample the
• 9:24
  inside of the cell and put it on the outside of the cell.
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  So they are, you know, it's like a chef and tasting its food as
• 9:31
  you're cooking the food, tasting it along the way and seeing do
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  you need more salt? You need more pepper.
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  So the HLA system, one of the things it does is it will
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  present these mutated peptides, these mutated peptides that come
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  from mutated P53, mutate K Ras, mutated B RAF that just aren't
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  on normal cells and then will present it on the cell surface.
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  And if you can get the immune system to identify and attack
• 9:57
  those cells, then you have a beautiful way of avoiding on
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  target off tumor toxicity because these complexes the HLA
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  protein complex with the mutant peptide, that complex just does
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  not exist on normal cells. And so that was their that was
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  their idea. And really their breakthrough
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  was demonstrating that we can use antibody like technology to
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  make these binders, these binders that bind the mutant
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  peptide in the context of the HLA.
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  So you need both, you need both the mutation and the HLA to bind
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  and then we can use that as a way of triggering the T cell to
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  attack the tumor cell. And so the entire company was
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  born of that idea. And we've now shown that you can
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  do this with multiple different mutations.
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  So we've shown we can do it with P53.
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  We're doing the same work in K Ras as well and multiple
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  different K Ras mutations. And that's the the underlying
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  genius here is developing these off the shelf molecules that can
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  distinguish absolutely between a tumor cell and a normal cell
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  based on these underlying mutations that make the cancer a
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  cancer. Very good.
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  And the CEO of a company that launched just over a year ago.
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  I think building out any early stage company has its
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  challenges. Can you talk about what it takes
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  to build a biotech and what does it take to make the shift from
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  preclinical to a clinical stage company?
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  Yeah. It's, it's really interesting
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  and I've been a part of this now, but multiple different
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  biotechs moving from very early through with two of them going
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  public and getting into the clinic and now with clasp
• 11:43
  getting into the clinic. We're very proud that we entered
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  the clinic a few months ago with our first with our first
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  potential therapeutic. It's funny because 50% of it is
• 11:56
  purely internal, right? 50% of it is setting up the
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  systems and the procedures, making sure you have the right
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  people around the table, working with people that you love
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  working with. And the more you do it, the
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  easier that becomes because you get to know the people you love
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  working with and the people that you might not.
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  And you do a better job of finding those people and
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  preparing internally folks for the idea that this is a company
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  that's going to involve, right? This is a company.
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  We're not going to be discovery stage forever.
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  We're going to be moving into the clinic, right?
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  That's going to involve some gives and some takes and laying
• 12:27
  the groundwork for that, right? And setting, setting out your
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  vision. And for me, my vision and I
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  think for anyone with a clinical background, your vision is
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  getting these drugs, the patients need them, right?
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  That's, that's, that's where you got to go.
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  And that it takes time and effort.
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  You get better at it, right, as you do it more.
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  And I think as long as you're authentic, as long as you're
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  straightforward, reasonably transparent and surrounding
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  yourself with great people, then it's a lot of fun.
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  The other 50% is the external environment, right?
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  And so I've done this in the context of a boom.
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  I've been a part of this in the context of an external
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  environment that was, you know, unicorns and rainbows, which is
• 13:09
  the early days of Bluebird bio. I've done this during the time
• 13:13
  of ups and downs, but overall, a reasonably positive trajectory
• 13:18
  for the biotech community. And that's where we were with
• 13:20
  surface and then now at class where you know, the external
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  environment in the last 18 months has been rough, right.
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  And I think you have to, you have to make choices about how
• 13:35
  you're going to build the company based on the probability
• 13:38
  of the markets being there. And you may say, look, five
• 13:44
  years ago we could raise money on an Ind filing, two years ago
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  we could raise money on early, early clinical data.
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  But frankly now what the market is saying is we want to see more
• 13:56
  clinical data, reproducible clinical data before you can
• 13:59
  raise in the kind of raise you want to do in order to generate,
• 14:04
  to generate real investor return.
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  And you have to be aware of that and cognizant of that.
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  The good news is we have very supportive investors, right?
• 14:11
  And we're in the clinic. So we're generating the clinical
• 14:14
  data that we're going to need. But how you build the company is
• 14:18
  in part dictated by what the external environment looks like,
• 14:22
  what the M&A environment looks like now and where you see it
• 14:25
  going over the next, you know, two to three years.
• 14:28
  Yeah. And you, you mentioned about a
• 14:30
  successful I and D and getting into the clinic.
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  Can you share some of the other recent milestones and
• 14:35
  achievements that clasp have have achieved?
• 14:38
  Yeah. I'd be delighted to.
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  So the biggest achievement was the timing from the A to getting
• 14:46
  into the clinic was just about a year.
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  So now this is because a lot of the work on this lead program
• 14:52
  class 1025 came from Hopkins. So this is AT cell engager.
• 14:57
  So this is a molecule that binds the mutation in P53 in the
• 15:02
  context of HLAA O2 and then binds T cells and get makes the
• 15:06
  T cells kill the tumor cells with that mutation.
• 15:09
  And this is the first T cell engager ever in this space.
• 15:14
  So in the in the mutant P53 space or really any mutant, any
• 15:19
  genetic mutation that we are attacking using AT cell engager
• 15:25
  that I and D was filed in the early part of this year and
• 15:28
  we're now enrolling patients throughout the United States.
• 15:30
  So we're very excited about that and we executed beautifully on
• 15:36
  this initial program. The other thing that I'm very
• 15:39
  proud of that we've been able to do is now take this technology
• 15:43
  of making these binders right, which are which are highly
• 15:47
  specific and sensitive to these mutations in the context of HLA
• 15:52
  and now applying it to our next pipeline program.
• 15:55
  So applying it to new mutations, including mutations in K Ras.
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  And so our expectation is that our next suite of programs will
• 16:03
  be focused on KRAS and those will those will be those are
• 16:07
  moving forward quickly and we expect to have more news around
• 16:10
  those in in the middle of next year.
• 16:13
  Exciting and class, we're looking to address some of the
• 16:15
  most significant challenges in oncology.
• 16:19
  Can you share more about what the company's differentiated
• 16:22
  approaches as well? Yeah.
• 16:24
  So, so it is a, we talked about this a lot with investors.
• 16:30
  We have a dual selection approach.
• 16:34
  Every patient we treat on clinical trials and eventually
• 16:38
  commercially, we'll have to have both the mutation and the right
• 16:42
  HLA. So for class 1025, the mutation
• 16:46
  is the P53R175H mutation, right. So they have to have that
• 16:50
  mutation in the same way that if you have a e.g.
• 16:53
  Fr small molecule you have to have an EGFR mutation or if you
• 16:56
  have you know a kit small an anti an anti kit small molecule
• 17:01
  you have to have the kit translocation right.
• 17:05
  You also though, have to have the right HLA.
• 17:07
  And so the HLA for the first program for, for 10/25 is HLAA
• 17:13
  O2. That means every patient who
• 17:15
  enrolls has to have HLAA O2. And in the US that's a little
• 17:21
  under 50% of the population. Actually it's, it's around 40%
• 17:24
  of the population in Europe, in Northern Europe is a little
• 17:27
  higher, it's about 50% of the population.
• 17:29
  And then it changes based on the racial and ethnic makeup of the
• 17:32
  country, of the country you're going after.
• 17:35
  So obviously it puts guardrails around the size of the
• 17:39
  population, right, because every patient is dual selected.
• 17:43
  Having said that, with P53, this is still a very large
• 17:45
  opportunity both in the US and outside the US.
• 17:48
  What I love about it though is that it means that every patient
• 17:53
  we treat, even from the earliest part of the phase one trial has
• 17:57
  the underlying biology to respond because they have both
• 18:01
  the mutation and the HLA. So this from a clinical
• 18:05
  development standpoint means you start to get actionable clinical
• 18:10
  data and actionable efficacy data reasonably early in your
• 18:13
  Phase 1. So you don't have to wait until
• 18:16
  phase two. You don't have to wait until
• 18:18
  combinations in order to in order to demonstrate whether or
• 18:22
  not the drug is working. So for our phase one, this is a
• 18:25
  monotherapy dose escalation and a monotherapy expansion in
• 18:29
  patients that are dual selected as I described.
• 18:32
  And we will learn a huge amount about the drug just from the
• 18:35
  phase one. And then at the same time, we'll
• 18:38
  do some combination work, particularly focused on colon
• 18:41
  cancer combinations because this mutation is highly prevalent, is
• 18:45
  most prevalent in patients with colon cancer.
• 18:48
  OK. And you mentioned P53 a couple
• 18:51
  of times. Can you like just talk through
• 18:53
  what the significance of the P53 mutation is in oncology and how
• 18:58
  does class platform target these mutations and what could that
• 19:01
  mean for potential treatments of cancer?
• 19:05
  Yeah. So P 53 is really interesting.
• 19:07
  It is, you know, one of the hallmarks of cancer is P53
• 19:11
  mutation. There are many different P53
• 19:12
  mutations. P53 is the single most highly
• 19:18
  mutated gene in all of oncology, all right.
• 19:21
  But there are many different mutations in P53.
• 19:24
  The R175H mutation that we're that we're targeting is the most
• 19:29
  common of all of those mutations.
• 19:31
  We have in drug development been trying to target P53 mutations
• 19:36
  for decades and for the most part we've been unable to.
• 19:41
  This is one of the first, not the first, but one of the first,
• 19:47
  one of the first attempts to really try to target the
• 19:50
  underlying mutated peptide. So the way this works is the
• 19:54
  R175H mutation, which just means that where there was an
• 19:58
  arginine. In the 175 position, there's now
• 20:01
  a histidine, right? It's a single amino acid change
• 20:04
  and that peptide is now presented in H on on the surface
• 20:08
  of the cell in the HLA protein. So our approach is not targeting
• 20:16
  the activity of P53, right? So we're not targeting how P53
• 20:22
  works in, in helping to cause cancer.
• 20:25
  We're just using it as a flag. We're using it as a flag that's
• 20:29
  on the cell surface that is saying, hey, this is an abnormal
• 20:34
  cell. This is a cell that has this
• 20:36
  mutation. So by definition, this is not a
• 20:38
  normal cell. And we're using that flag as a
• 20:42
  way to then get T cells to attack and kill the tumor cell.
• 20:46
  So it's a, it's a very different approach than other people have
• 20:48
  taken to target P53. The nice thing about it or one
• 20:53
  of the nice things about it is that this P53 mutation is
• 20:57
  truncal, meaning it happens very early in the development of
• 21:01
  cancer. So every tumor cell in the body
• 21:05
  that comes from this, that comes from this initial mutated cancer
• 21:12
  with the P53 mutation, they all share the mutation, right?
• 21:16
  Moreover, the P53 mutation is critical for the cancer to be a
• 21:21
  cancer. So you can't down regulate, you
• 21:24
  can't lose the mutation. This means that when we treat a
• 21:28
  patient, we're treating every cancer cell in the body, not
• 21:31
  just some of them. And one of the common ways of
• 21:35
  developing resistance down regulation of P53, we think, we
• 21:39
  think there's at least a reasonable chance that that
• 21:41
  can't happen because P 53 is so necessary in the cancer being a
• 21:45
  cancer. Fine.
• 21:48
  And it's just a question back to you actually.
• 21:50
  So your background you went from medical oncologist to CEO, I
• 21:55
  guess it's a less of a traditional route to get to to
• 21:58
  being a biotech CEO. Can you talk us through that
• 22:02
  transition and how did you find it from been so heavy on the
• 22:05
  clinical side to to running the yeah, the company?
• 22:09
  So, so I've loved it. It's been, it's been great.
• 22:12
  And I have, you know, people in this field that I look up to,
• 22:15
  people like David Shenkind who come from the same, you know,
• 22:18
  from the same lineage, the same, the same approach.
• 22:21
  I think where it's really useful is in helping set the vision and
• 22:29
  the mission for the company because coming at it from the
• 22:33
  perspective of having taken care of patients, having enrolled
• 22:36
  patients on clinical trials, having given them these very
• 22:39
  toxic medications, having dealt with informed consents, having
• 22:46
  dealt with toxicities from different investigational drugs.
• 22:50
  You can in a very genuine and sincere way layout a vision and
• 22:54
  mission for everybody in the company that feels very genuine
• 22:58
  and feels very authentic because it is, it's very close to, it's
• 23:01
  very close to my heart, but very close to the heart of anybody
• 23:04
  who spent time taking care of patients.
• 23:06
  So that's a real, that's a real benefit.
• 23:08
  And honestly, you know, 95% of people who work in small
• 23:11
  biotech, they'll they'll never take care of a patient.
• 23:15
  And the reason they're there is because they want to feel like
• 23:17
  they're part of something that's bigger than themselves and their
• 23:20
  job. And laying that out, coming from
• 23:24
  a clinical background is I think second nature.
• 23:28
  The part of it that is intimidating I think for a lot
• 23:31
  of physicians, it certainly was for me is the it's basically the
• 23:38
  language of business, right? So I don't have a background or
• 23:42
  training in finance or accounting.
• 23:45
  I don't the world of investors was one that was very new to me
• 23:50
  and that I had to learn. But I found that it's not that
• 23:55
  hard. It just takes time and effort
• 23:58
  and intellectual curiosity. You got to ask a lot of
• 24:00
  questions. You got to be OK being wrong.
• 24:03
  You got to get a lot of advice from a lot of different folks.
• 24:05
  But there are lots of folks out there who will need you advice,
• 24:07
  right? And some of it it's, it's just
• 24:11
  like, you know, early medical school in that the concepts
• 24:16
  aren't hard, but the language can be hard.
• 24:20
  And so you got to learn the language.
• 24:21
  And then when you learn the language, like, oh, that's what
• 24:24
  that means that that wasn't that hard to figure out, right?
• 24:26
  I just didn't know what the word meant, right?
• 24:28
  And, and I found that to be, I found that to be very true in my
• 24:34
  experience. Like you got to be
• 24:35
  intellectually curious, you got to be excited to learn, and you
• 24:38
  got to be willing to tell people that you don't know and you need
• 24:41
  help, right? But it's not like it's, it's not
• 24:45
  like learning, you know, X-ray crystallography, right?
• 24:49
  It's it's. It is.
• 24:51
  It's, it's much more like, you know, like memorizing the Krebs
• 24:55
  cycle, right? It seems intimidating, but it's
• 24:57
  really not. It's just language.
• 24:59
  Yeah, good. I love that.
• 25:01
  And this is a question we always finish with on the Bio Hub.
• 25:03
  And I know I wanted to give you a heads up on this, but if you
• 25:07
  were to have dinner with three people past or present, who
• 25:10
  would it be and why? It doesn't necessarily need to
• 25:12
  be biotech innovators or a company if you like, but yeah.
• 25:16
  Yeah. So I'm interested in your
• 25:19
  experience here because I think many people ask this question
• 25:24
  are going to revert back to something that happened
• 25:27
  recently, right? So I was just recently in Paris
• 25:29
  with my family, with my kids, and I was reading up a lot about
• 25:35
  Mary Curie and about Louis, Louis Pasteur.
• 25:38
  And Louis Pasteur in particular, a brilliant scientist, but also
• 25:43
  one of the fathers of immunology, right?
• 25:45
  And certainly a clasp in the Fort surface.
• 25:48
  We're all about immunology. So Louis Pasteur would certainly
• 25:51
  be one of them. I, I recently finished reading
• 25:55
  American Prometheus after seeing the movie Oppenheimer.
• 25:58
  And it's hard to be a leader of a biotech or a scientific
• 26:03
  endeavour. And you have to be impressed
• 26:06
  with Robert Oppenheimer, no matter what you think morally,
• 26:09
  no matter what you think scientifically, just the fact
• 26:12
  that he was able to lead and get all of those folks pointed in
• 26:15
  the same direction and end up where where we ended up is
• 26:22
  amazing. And I'd love to have dinner with
• 26:23
  proper Oppenheimer. And then finally, you know, I
• 26:27
  would be saying this third person since I was, you know, 8
• 26:30
  years old. So I grew up in Maryland.
• 26:33
  I grew up a huge Orioles fan and my grandfather's favorite player
• 26:38
  and my favorite player because of that was Cal Ripken, still is
• 26:41
  Cal Ripken, even though he's obviously hasn't been a player
• 26:43
  for a long time. And so, and it's not just that
• 26:47
  he was the Iron Man and showed up every day.
• 26:49
  His consistency, his resilience, and his humanity I to this day
• 26:58
  find incredibly, incredibly compelling.
• 27:01
  So, you know, Louis Pasteur, Robert Oppenheimer and Cal
• 27:04
  Ripken would be the three folks that I would imagine having
• 27:06
  dinner with right now. In a year, that'll probably
• 27:08
  change. I'll be influenced by some other
• 27:10
  movie and some other trip. So, but it'll it'll always be
• 27:12
  Cal Ripken. He'll always be one of them.
• 27:14
  Yeah, well, look for three terrific answers there and
• 27:18
  certainly I'm very excited to follow class journey going
• 27:21
  forward. It sounds like you guys are,
• 27:24
  yeah, doing some exciting stuff at the moment.
• 27:26
  So yeah, thanks so much for helping us out with this.
• 27:29
  It was a pleasure to have you on.
• 27:30
  And yeah, looking forward to to following you guys even more.
• 27:34
  Thanks so much Tom. I really enjoyed the time.